BCS + PPS Flashcards
ECG interpreta’n ✓
Normal ECG
- Pulse = 300 ÷ # of big boxes btw adjacent R’s
- Sinus rhythm = regular pulse + P waves are round, of same shape + precede EVERY QRS complex
→ If not sure if u see P wave before every QRS, check if RR = consistent !
⚠️ Think Vtach if u see absent P wave + tachycardia + high amplitude QRS complex (especially if pt has Hx of MI)
⚠️ Absent P wave + tachycardia + short amplitude = Vfib
- P wave width = 2-3 little squares (represents atrial depolariza’n)
- QRS complex width = < 3 little squares (represents ventricular depolariza’n aka closure of mitral valve)
→ prolonged QRS (i.e >120ms) + dominant S wave in V1 = suggestive of LBBB - ST segment = from point right after S to beginning of T wave, should be a perfectly straight line
-T wave = upright except in leads aVR, aVL, III + V1, represents repolariza’n
- QT interval = count # of small boxes + multiply by 40
→ 350-450 for men + 360-460 for women
→ prolonged QT interval = sign of HYPERCa
→ short QT interval = sign of HYPOCa - PR interval = beginning of P wave to point just before Q, width should be 3-5 little squares (represents time btw atrial + ventricular depolariza’n i.e conduc’n by AV node)
→ prolonged PR interval = > 1 large box
ECG Leads
- V1, V2 = Septal / Posterior = LAD
- V3, V4 = Anterior = LAD (most commonly occluded artery)
- 2 + 3 + aVF (“ferior right”) = Inferior = right coronary in most ppl + left circumflex from left coronary in 10% of ppl
- 1, V5, V6, avL (“15 6 avL” + left lateral”) = Lateral = left circumflex
Axis Devia’n
-30° 0° 30° 60° 90° = Normal
< -30° = Left axis devia’n = +ve QRS complex in Lead 1 + -ve QRS complex in inferior leads
→ ex’s : LBBB, left ventricular hypertrophy, inferior MI
> 90° = Right axis devia’n = -ve QRS complex in Lead 1 and +ve QRS complex in inferior leads
→ ex’s : RBBB, right ventricular hypertrophy, lateral MI, HyperK, P.E, COPD, right sided heart strain, WPW syndrome, ventricular tachycardia
- Know for OSCE *
Coronary anatomy ✓
RCA supplies . . .
- RA
- SA node in 60% of ppl
- AV node in 80% of ppl
LCA supplies . . .
- LA
- most of LV
- SA node in remaining 40% of ppl
Ischemic Heart Disease ✓
Def - IHD = term used to describe the spectrum of heart diseases that results from coronary artery atherosclerosis
→ angina = crushing chest pain radiating to left arm or jaw, characteristic of MI
→ ischemia = ↓ed perfus’n to tissues = when tissue O2 demand > supply = reversible but if persists can cause infarct i.e myocyte death which is irreversible
⟹ Partial occlus’n → ischemia
⟹ Complete occlus’n → ischemia → infarct
Pathophys - gradual but slow enlarg’nt of STABLE plaque (contains mainly smooth muscle cells)
→ GRADUAL occlus’n of coronary vessel(s)
→ GRADUAL ↓ in blood flow → mismatch btw O2 supply + demand to myocardium → ischemia OR . . .
- gradual but slow enlarg’nt of STABLE plaque (contains mainly smooth muscle cells) → COMPLETE occlus’n of coronary vessel(s) → SUDDEN ↓ in blood flow → Infarct
Types
- stable angina / angina pectoris = pain upon exer’n (means there’s at least some blood flow to whatever part of heart) = for STEMI, lasts 1-2 min, pain = relieved by GTN spray
- unstable angina = pain @ rest (means there’s very little blood flow), lasts 3-5 min OR is severe + of new onset OR occurs w/ crescendo pattern
→ could be SSX of N-STEMI or could be diagnosis of its own - Know for OSCE *
Infective Endocarditis ✓
Def - infec’n of endocardial surface of heart including valvular structures + chordae tendineae
RFs
- artificial heart valve
- post heart transplant
- acquired valvular heart disease
- structural congenital heart disease
- previous Hx of infective endocarditis
- hypertrophic obstructive cardiomyopathy
Eti
- Staph. aureus colonizing normal valve OR fungi such as candida albicans / aspergilus fumigatus
- weakly pathogenic bacteria like Strep. viridians colonizing an abnormal valve i.e prosthetic valve / prolapsed mitral valve
SSX = “FROM JANE”
- Fever
- Roth’s spots = white retinal hemorrhage (seen on fundoscopy)
- Osler nodes = on tip of fingers / toes + are painful
- Murmur
- Janeway les’ns = on palm / soles + are NOT painful
- Anemia
- Nail SSX i.e splinter hemorrhage
- Emboli
Ix’s = urgent trans-thoracic echocardiogram (trans-esophageal echo instead if pt has prosthetic valve / intracardiac device OR TTE = -ve but there’s a strong clinical suspic’n of IE) + 3 blood cultures taken 12 hrs apart from each other + from diff sites + a serum sample
Criteria for diagnosis (i.e Duke’s Criteria) = 1 major + 3 minor OR 5 minor
→ Major criteria = persistently +ve blood cultures OR vegeta’n on echo
→ Minor criteria . . .
⟹ Predisposi’n i.e IV drug use / heart valve pathology
⟹ Fever > 38°C
⟹ Vascular phenomena i.e splenic infarc’n / intracranial hemorrhage / janeway les’ns
⟹ Immunological phenomena i.e Osler nodes / Roth spots / glomerulonephritis
Tx = IV broad-spectrum Abx such as amoxicillin or gentamicin for 4 wks for pts w/ natural heart valve + for 6 wks for pts w/ artificial valve
Complica’ns
- acute heart failure
- disturbance of valve func’n
- stroke b/c part of vegeta’n can detach → get transported via circula’n + cause an embolism
- forma’n of antigen-antibody immune complexes which can impair kidneys + hence cause AKI / glomerulonephritis
- Know for OSCE *
Acute Pericarditis ✓
Def - new onset inflamma’n of pericardium lasting < 4-6 wks
RFs
- male
- 20-50 y/o
- neoplasm
- Cardiac Sx
- transmural MI
- uremia or on dialysis
- viral / bacterial infec’n
- systemic autoimmune disorder
Eti
- TB
- uremia
- post MI
- idiopathic
- viral infec’n such as coxsackie
- systemic autoimmune disorder
SSX = chest pain worse when pt is supine i.e leans back + better when they lean forward + serial electrocardiographic Δs + pericardial fric’n rub i.e sound of walking on snow heard when diaphragm of stethoscope = placed over left sternal border (especially @ end-expira’n w/ pt leaning forward)
Ddx
- MI
- P.E
- pneumonia
- pneumothorax
- costochondritis
Ix’s
- ECG → upwardly concave ST-segment eleva’ns w/ PR-segment depress’ns in most leads
- troponin → if elevated = suggestive of myopericarditis
- CRP → will be elevated
Tx
- NSAID for pain
- PPI for gastric protec’n due to NSAID use
- long term colchicine i.e 3 months to prevent recurrence
→ order FBC before starting colchicine b/c can cause neutropenia + bone marrow suppress’n
→ avoid in pts who are very frail or have impaired mobility due to high likelihood of Tx-related diarrhea
- restrict strenuous physical activities until SSX have resolved + CRP = back to normal
Complica’ns
- chronic constrictive pericarditis (rare + usually occurs 3-12 months later)
- pericardial effus’n due to accumula’n of exudate in pericardial sac → cardiac tamponade (life-threatening)
- Know for OSCE *
Constrictive Pericarditis ✓
Def - chronic condi’n where granula’n tissue forma’n in pericardium results in loss of pericardial elasticity
RFs
- male
- cardiac Sx
Eti
- idiopathic
- after viral infec’n
- TB (in endemic reg’ns)
Pathophys - loss of pericardial elasticity → ventricular filling = restricted → ↓ in end diastolic volume, SV + consequentially CO as well
SSX
- RHF SSX
- fatigue + dyspnea on exer’n due to ↓ in CO
+ve Kussmaul’s sign i.e ↑ of JVP on inspira’n
Ix = 2D echocardiography → may show ↑ed pericardial thickness w/ or w/o calcifica’n
Tx = pericardiectomy i.e removing as much pericardium as possible
Complica’ns
- renal failure
- hepatomegaly
- pulmonary HTN
- metabolic acidosis
- Know for OSCE *
Myocarditis ✓
Def - inflamma’n of myocardium in the absence of ischemia / CAD
RFs
- HIV
- infec’n
- auto immune condi’n
- peri partum / post partum
Eti
- systemic disease
- viral / bacterial / fungal infec’n
- toxins such as snake venom, arsenic, CO, cocaine or heavy metals i.e Cu / Fe / Pb
SSX
- SOB
- fatigue
- palpita’ns
- chest pain
- tachypnea
- orthopnea
- S3 sound (usually when CHF develops as a result)
- rales / crackles “ “
- hepatomegaly “ “
- prominent neck veins “ “
Ddx
- ACS
- pericarditis
- dilated cardiomyopathy
Ix’s
- CXR to check for SSX of CHF
- ECG + CK-MB / troponin to r/o MI
- BNP to confirm whether or not pt has heart failure
→ can be falsely low in obese pts + falsely high in pts w/ CKD
- 8F-FDG PET-CT if it’s chronic
- 2D echo → will show RV dilata’n
Tx
- if hemodynamically stable w/o evidence of LV systolic dysfunc’n → supportive care + treat underlying cause
- if hemodynamically stable w evidence of LV systolic dysfunc’n → treat as u would chronic HF
- if hemodynamically unstable → arterial vasodilator such as Na nitroprusside (may precipitate CN- toxicity especially in pts w/ renal dysfunc’n) + invasive hemodynamic monitoring
Complica’ns
- Afib
- Vtach
- sudden cardiac death
- dilated cardiomyopathy
- Know for OSCE *
Hypertrophic Cardiomyopathy (HCM) ✓
Def - genetic disorder characterized by LVH w/o any identifiable cause i.e ↑ in thickness of wall of LV = most common cardiomyopathy + most frequent cause of sudden cardiac death in young ppl
→ pts = classified as obstructive or non-obstructive based on presence or absence of left ventricular outflow tract obstruc’n @ rest on echocardiography
RF = FHx of HCM or sudden cardiac death
SSX
- SOB
- angina
- palpita’ns
- dizziness / syncope
- systolic ejec’n murmur
- double apical pulse / carotid pulsa’n
- left ventricular lift i.e left parasternal heave
Ddx
- athlete’s heart
- LVH due to HTN
- discrete sub-aortic stenosis
Ix’s
- ECG → will show prominent Q waves, LVH + ST-T wave abnormalities
- CXR → will show cardiomegaly
- echocardiogram → will show LVH
Tx
- asymptomatic but not @ high risk of sudden cardiac death = just monitor
- asymptomatic but @ high risk of sudden cardiac death = ICD (implantable cardio-defibrilator) + pt should avoid intense physical activity
- symptomatic but not @ end-stage heart failure = -ve ionotropic + chronotropic agents i.e β blocker or non-dihydropyridine CCB such as verapamil / diltiazem
- symptomatic + @ end-stage heart failure = β blocker + ACE-I / ARB
Complica’ns
- Afib
- ischemic stroke
- infective endocarditis
- sudden cardiac death
- Know for OSCE *
Dilated Cardiomyopathy ✓
Def - enlargement + dila’n of 1 or both ventricles along w/ impaired contractility i.e LVEF < 40%
Eti
- 1° = idiopathic → only when all possible causes have been excluded
- 2° = due to HTN / infec’n / ischemic disease / medica’n such as anthracyclines
Pathophys - progressive dilata’n of ventricle(s) → mitral + tricuspid insufficiency → EF further ↓
SSX
- SOB
- PND
- fatigue
- orthopnea
- SSX of CHF
Ddx
- acute pericarditis
- cardiac tamponade
- hypertrophic cardiomyopathy
Ix’s
- echocardiogram for diagnosis
- CXR → cardiomegaly + Ψly signs of CHF
- coronary angiography in pts w/o known Hx of CAD to r/o occult ischemic disease as the cause
Tx = treat like acute HF if it’s acute + like chronic if it’s chronic
Complica’ns
- congestive HF
- sudden cardiac death
- valvular heart disease
- abnormal cardiac rhythms
- thromboembolism b/c when ventricle(s) = dilated blood flow through heart = slower than normal
- Know for OSCE *
Pericardial Effus’n ✓
Def - fluid in pericardial sac beyond its physiological amt i.e ≥ 50 mL
Eti
- trauma
- malignancy
- idiopathic for ex post cardiac Sx
- renal disease i.e uremic pericarditis
- infec’n i.e viral / bacterial pericarditis
SSX
- palpita’ns
- chest pain
- cough / SOB
- syncope / light-headedness
Ddx
- MI
- P.E
- cardiac tamponade
- constrictive pericarditis
Ix’s
- FBC to check for infec’n
- U + E to check for uremia
Tx = pericardiocentesis
Complica’n = cardiac tamponade
- Know for OSCE *
Cardiac Tamponade ✓
Def - when pericardial effus’n gets to the point where it leads to ↑ in intra-pericardial pressure ∴ restricting cardiac filling + leading to ↓ in CO = medical emergency !
RFs
- malignancy
- aortic dissec’n
- purulent pericarditis
Eti = same as pericardial effus’n
Pathophys - ventricular filling = impeded all throughout diastole
SSX
- SOB
- tachycardia
- pulsus paradoxus i.e severe ↓ in BP during inspira’n
- Beck’s triad i.e hypoTN + muffled heart sounds + elevated JVP
Ix’s
- ECG
- TTE for diagnosis → will show pericardial effus’n > 20 mm of echo-free space during diastole btw visceral + parietal pericardium
Tx
- if hemodynamically stable i.e SBP > 110 mmHg → NSAID + gastro-protec’n
- if hemodynamically unstable + eti = unknown → pericardiocentesis
- if hemodynamically unstable + eti = known → surgical drainage
Complica’ns
- cardiac arrest
- organ hypoperfus’n
- Know for OSCE *
Inflamma’n + Atherosclerosis ✓
- Inflamma’n = body’s physiological response to any kind of tissue injury i.e infec’n / trauma / hypoxia / radia’n in order to eliminate injurious agents, remove damaged tissue + initiate healing process
→ Acute inflamma’n = vascular Δs + neutrophil accumula’n @ site of injury = controlled by cytokine release which was triggered by injury
a) vasoconstric’n
b) vasodila’n ∴ ↑ in blood flow → ↑ in permeability of capillaries → leakage of plasma proteins through gaps btw endothelial cells so coagula’n cascade can begin
→ ↑in blood viscosity → blood flow slows down i.e STASIS of RBCs → b/c of slow blood flow, neutrophils get pushed to margins i.e NEUTROPHIL MARGINA’N
c) leukocytes loosely attach + detach to endothelial cells @ inflamma’n site via selectins (ROLLING)
→ leukocytes express integrin + bind tightly to integrin ligand (ADHES’N)
→ leukocytes squeeze in btw endothelial cells (DIAPEDESIS / TRANSMIGRA’N)
→ leukocytes move towards injury site or pathogen via chemotaxis
c) macrophages secrete IL-6
→ Liver produces CRP (acts as an opsonin = molecule that makes foreign matter recognizable for immune system by coating it)
→ CRP binds to bacterial cell wall (in the case of bacterial infec’n but could still be produced in other cases of inflamma’n like burns or trauma)
→ macrophages recognize CRP (High CRP = RF for atherosclerosis)
→ PHAGOCYTOSIS
d) REGENERA’N i.e replac’nt of damaged cells w/ the same types of cells but new ones ∴ original structure + func’n = restored (there are scenarios where scar tissue is able to replace damaged cells structurally but not func’nally - see below)
→ for COMPLETE restora’n to happen, there has to be limited tissue destruc’n w/o substantial damage to connective tissue matrix OR damaged cells need to have capacity to regenerate (for ex liver cells)
⟹ when neither condi’n = met, we have scar/fibrous tissue forma’n (= produced by fibroblasts, main component = collagen)
⟹ scar = mechanically strong so structure = preserved, but func’n ≠ preserved b/c scar can’t perform func’n of previous cells
→ sometimes doesn’t end at scarring but instead proceeds to chronic inflamma’n
⟹ in acute inflamma’n exudate i.e what comes out = fluid, fibrin + neutrophils
→ cardinal signs of inflamma’n = heat, redness, pain, swelling + loss of func’n (due to pain)
→ Chronic inflamma’n can either occur as a sudden onset OR as a result of unresolved acute inflamma’n
⟹ usually ends w/ tissue destruc’n + scar forma’n rather than regenera’n
⟹ has high E demand so nutrients get diverted ∴ pt can experience weight loss, anemia of chronic disease + ↓ed host resistance
- Pathophys of atherosclerosis :
- Endothelial damage → LDL accumula’n in tunica intima → recruit’nt of macrophages → LDL = oxidized by ROS → engulf’nt of oxidized LDL produces foam cells → collec’ns of lipid-laden macrophages identified macroscopically as yellow eleva’ns known as fatty streak → death of foamy macrophages
→ release of intra-cytoplasmic lipid
→ forma’n of lipid debris
→ prolifera’n of smooth muscle cells + migra’n from tunica media = last step of atheroma forma’n so what will be seen in arteries
→ secre’n of collagen + other ECM proteins
→ develop’nt of fibrous cap over core
(fibrous cap = thick in stable cap + thin in unstable cap → represents body’s attempt to repair injured vessel wall by scarring)
→ gradual but slow enlarg’nt of STABLE plaque (contains mainly smooth muscle cells)
→ gradual ↓ in blood flow → angina
OR instead of gradual but slow . . .
→ sudden rupture of UNSTABLE/VULNERABLE plaque (contains mainly inflammatory cells)
→ thrombus forma’n
→ MI if it causes partial or complete occlus’n at site of ruptured plaque + ischemic stroke if thrombus dislodges to brain i.e becomes an emboli
OR instead of gradual but slow . . .
→ enlarg’nt of atherosclerotic plaque + weakening of tunica media → aneurysm forma’n → aneurysm rupture
Atherosclerosis = chronic inflamma’n b/c meets the 3 criteria : persistent injury + on-going inflamma’n + repair w/ scaring (that’s what the fibrous cap is)
- Know for OSCE *
Pathophys of Edema + Lymphatic System ✓
Fluid mov’nt across capillary wall = dependent on balance btw hydrostatic + oncotic pressure gradient across capillary
→ hydrostatic pressure draws fluid into tissue from blood
→ oncotic pressure = mainly due to plasma proteins i.e albumin → draws fluid OUT of tissue into blood
→ lymph = fluid that has leaked from blood into tissues → lymphatic vessels return that “leaked” fluid i.e interstitial fluid back to bloodstream to prevent fluid imbalance ∴ causes of edema = anything that . . .
- ↑ hydrostatic pressure i.e in heart failure
- ↑ capillary permeability i.e in inflamma’n
- ↓ oncotic pressure i.e hypoalbuminemia
- obstructs lymph drainage such as a tumor
STEMI + N-STEMI ✓
RFs
> 65 y/o
- HTN
- obesity
- smoking
- diabetes
- dyslipidemia
- physical inactivity
Eti = complete occlus’n of coronary artery due to one of RFs
Pathophys
1. Myocyte necrosis (0-12hrs)
2. Neutrophil accumula’n for acute inflammatory response (12-72 hrs)
3. Organiza’n i.e replac’nt of dead cells by granula’n tissue = 1st step of repair process (3-10 days)
4. Progressive scar tissue deposis’n = 2nd + last step of repair process (wks to months)
SSX
- SOB
- sweat
- nausea
- angina = crushing chest pain due to lactic acid accumula’n that radiates to left arm or jaw (usually happens in an MI)
→ stable = pain upon exer’n = for STEMI
→ unstable = pain @ rest = for N-STEMI
Ix’s
- ECG :
→ STEMI = ST segment eleva’n in ≥ 2 contiguous leads aka raised line (not straight + flat) +/- pathological Q wave +/- T wave invers’n
→ N-STEMI = ST segment depress’n +/- T wave invers’n
- Cardiac troponin for 1st MI + CK-MB for reinfarc’n → will be high
⟹ Troponin rises after 4-6 hrs, peaks @ 24hrs + returns to normal by 1-2 wks
⟹ CK-MB rises after 4-6 hrs, peaks at 24hrs + returns to normal w/in 48-72hrs - FBC → high WBC + maybe high ESR/CRP
- Lipid profile → high LDL + high ttl cholesterol
- Glucose → could be high
Tx for either = statin b/c prevents already present plaques from dislodging ∴ ↓ morbidity + ↑ survival
Immediate Tx for either = “AATGMOPP”
- Aspirin 300mg PO + anti-emetic
- Anticoagulant i.e unfractionated heparin
- Ticagrelor
- GTN
- Morphine IV
- O2 if O2 sat < 94%
- PPI for gastroprotec’n
- PCI or Fibrinolysis w/in 12hrs if PCI can’t be delivered w/in 2hrs for STEMI + coronary angiography for N-STEMI
→ coronary angiography = inject contrast to visualize blood flow in arteries via x-ray
⟹ can be used to identify occluded vessels in any part of the body + sites of hemorrhage, aneurysms or stenosis
⟹ risks = bleeding, aneurysm, stroke, heart attack, death
- Aspirin MOA - irreversibly inhibits COX ∴ ↓ produc’n of thromboxane → can’t do platelet aggrega’n → less clotting → risk of arterial occlus’n ↓
- side effects - GI bleeding, ulcers, irrita’n + tinnitus
- C/Is - hypersensitivity, 3rd trimester, < 16 y/o
- Ticagrelor MOA - prevents platelet aggrega’n ∴ ↓ing risk of arterial occlus’n
- side effects = bleeding, GI upset + thrombocytopenia
- C/Is = active bleed
- end in “GREL” or “GRELOR”
- Nitrates MOA - cause release of NO → guanylate cyclase = activated → GTP = converted to cGMP → ↓ in [intracellular Ca] in vascular smooth muscle cells which causes them to relax → venous vasodila’n + a bit of arterial vasodila’n
- side effects = dizziness, HA + hypoTN
- C/Is = hypoTN, severe bradycardia, inferior MI, aortic stenosis, pt took phosphodiesterase inhibitor in past 24-48 hrs
- ex = GTN spray
→ Morphine / Opioid MOA - binds to mu opioid receptors in CNS ∴ blocking pain signals
→ side effects = pruritus, ↓ed peristalsis which can lead to constipa’n, pupil constric’n, bradycardia
→ SSX of morphine toxicity = resp. depress’n
⟹ Tx = Naloxone
Tx on discharge = “3A’s + 1B”
- ACE / ARB
- 80mg atorvastatin
- Anticoagulant i.e fondaparinux
- β blocker
→ MOA of β blocker - block β adrenergic receptors in heart hence ↓ heart contractility + suppress release of renin
→ side effects = insomnia, cold extremities, HA + GI disturbance, abrupt w/drawal of β blockers can cause rebound tachycardia
→ C/Is = bradycardia, asthma + heart block
→ end in “OLOL”
→ SSX of β blocker overdose = bradycardia, hypoTN, HF, syncope
⟹ Tx = atropine if pt is bradycardic + then glucagon if bradycardia still persists
Short term complica’ns
- Vfib (24hrs later) = due to release of K from necrotic myocytes that induced arrhythmia in hyper-excitable tissue around infarct → results in sudden death
- other arrhythmias → usually in inferior infarcts (ex’s- ventricular tachycardia = w/in 4hrs post MI, supraventricular tachycardia + bradycardia)
- acute cardiac failure (can be left or right sided or bi-ventricular) → can lead to cardiogenic shock if very severe + BP maintenance ≠ possible
- cardiogenic shock = when substantial amt of affected myocytes can’t contract anymore
- acute pericarditis (w/in 48hrs post MI)
- mural thrombus
- myocardial rupture (effects depend on site of rupture . . .)
→ Rupture of free wall will lead to cardiac tamponade = fluid w/in pericardial sac (w/in 10 days post MI)
⟹ SSX = raised JVP + muffled heart sounds + pulsus paradoxus (= severe ↓ in BP during inspira’n)
→ Rupture of papillary muscle of mitral valve - acute mitral regurgita’n (24hrs later but in posterior STEMI only) → blood flows back into LA → pressure in LA ↑ → high pressure goes to pulm. circula’n → fluid transuda’n in lung interstitium + alveoli → pulm. edema → acute LV failure
→ Rupture of IV septum will cause acute heart failure
Long term complica’ns
- CHF
- Recurrent MI
- Chronic CHF
- Ventricular aneurysm → can lead to congestive cardiac failure, arrhythmia + dislodging of thrombus
- Dressler’s syndrome = autoimmune pericarditis, occurs 2-10 months after transmural MI
- Know for OSCE *
HTN + Kidney ✓
1- BP regula’n
2- Def, RFs, Eti, Pathophys, SSX, Diagnostic Criteria, Ddx, Ix, 1st line Mx, Complica’ns
1) How does our body detect + respond to BP Δs ? (Baroreceptor reflex through vagus nerve + RAAS)
- High BP baroreceptor reflex :
High BP = detected by baroreceptors in aortic arch + carotid sinus → high BP causes them to fire more ac’n ψs than usual → activates cardiac inhibitory center in medulla + inhibits cardiac acceleratory center → para = stimulated + sympa = inhibited ∴ HR + BP ↓ - a) Low BP baroreceptor reflex :
Low BP = detected by those same baroreceptors
→ low BP causes them to fire less ac’n ψs than usual → activates cardiac acceleratory center in medulla + inhibits cardiac inhibitory center → para = inhibited + sympa = activated ∴ HR + BP ↑
b) Low BP RAAS pathway :
Low BP = detected → juxtaglomerular cells of kidneys secrete renin
→ renin converts angiotensinogen (produced in liver) to angiotensin I
→ ACE converts angiotensin I to ATII (in kidneys)
→ ATII ↑ BP by vasoconstricting = by stimulating release of adrenergens + ↑ing blood volume = by stimulating adrenal glands to release aldosterone which ↑ Na reabsorp’n + since water follows salt, water reabsorp’n ↑ as well but inadvertently causes K to ↓ + stimulating posterior pituitary to release ADH which ↑ water reabsorp’n by causing vasoconstric’n via V1 receptor (will hence ↑ BP) + ↑ing express’n of aquaporin channels on luminal surface
2) Def
- 140-159 + 90-99 = Mild / Stage I
- 160-179 + 100-109 = Moderate / Stage II
≥180 + ≥110 = Severe / Hypertensive crisis
→ SSX of end organ damage = pulm. edema + SOB or dizziness / cardiac ischemia +/- chest pain / renal failure / neurological deficits such as vis’n Δs = Hypertensive Emergency !
⚠️ There must be ≥ 1 SSX of organ damage + severe BP in order to call it a hypertensive emergency otherwise it’s a hypertensive urgency !
RFs
> 60 y/o
- T2D
- obesity
- sleep apnea
- black ancestry
- metabolic syndrome
- aerobic exercise < 3x/wk
- moderate ~ high alcohol intake
- FHx of HTN or coronary artery disease
Eti for 1° / essential = RFs
Pathophys for 1° - high salt intake → ↑ in osmolality → ADH = secreted → we get water reabsorp’n aka water reten’n ↑ → CO ↑ → BP ↑
Eti for 2°
- Chronic renal disease
- chronic disease of the kidney
→ diabetic nephropathy
→ obstructive uropathy
→ chronic glomerulonephritis - reno-vascular disease such as renal artery stenosis → poor perfus’n to kidneys → activa’n of RAAS → TPR + CO ↑ → BP ↑
- acute glomerulonephritis
- acute polycystic kidney disease (APKD)
- autoimmune disease such as polyarteritis nodosa
- Coarcta’n of the aorta
- Endocrine disease
- Pheochromocytoma (↑ed adrenaline produc’n)
→ SSX = HA, sweating + palpita’ns
- Cushing’s syndrome
- Hyperaldosteronism (most common cause of 2° HTN)
⚠️Consider testing for hyperaldosteronism in pts w/ HTN who are younger, hypokalemic or fail to respond to Tx - Drugs
- steroids
- oral contraceptives
- NSAIDs → PGE2 blocked → afferent arteriole vasoconstricts → poor perfus’n → activa’n of RAAS → TPR + CO ↑ → BP ↑ - Pre-eclampsia
Complica’ns = end organ damage due to severe HTN
VASCULOPATHY = due to higher pressure exerted on vessels . . .
- aortic dissec’n
- aortic aneurysm
- endothelial dysfunc’n
- remodeling of arterial walls
- accelera’n of atherosclerosis → structural Δs in arterial wall → ↓ed transport of LDL particles from blood → ↑ed accumula’n of LDL in arterial wall → plaques aka fatty deposits form → stenosis
→ vascular injury → chronic inflamma’n = triggered + vessel compliance ↓
CEREBROVASCULAR DAMAGE
- acute hypertensive encephalopathy (due to cerebral edema)
- stroke (high BP can cause blood clots to form in arteries supplying brain ∴ blocking blood flow to brain + causing stroke)
- intracerebral hemorrhage (high BP can cause thin-walled arteries to rupture ∴ releasing blood into brain tissue)
RETINOPATHY → force of blood against artery walls = too high which causes vessels supplying retina to stretch, narrow + become damaged over time
HEART DISEASE
- aortic dissec’n due to aortic dilata’n
→ Type A involves ascending aorta = more serious than Type B + requires immediate surgical repair
> carotid dissec’n → can cause stroke
> coronary dissec’n → can cause MI
→ Type B ≠ involve ascending aorta
(Tx = medically control BP)
> celiac / mesenteric artery dissec’n
→ can lead to gut ischemia
> renal artery dissec’n → Ψ renal failure
> iliac artery dissec’n → can lead to lower limb ischemia
> external rupture → can lead to exsanginua’n i.e severe blood loss
- MI
- Afib
- CHD
- LVH due to pressure overload → Ψ heart
- accelerates coronary artery atherosclerosis which worsens ischemic heart disease
NEPHROPATHY
- micro-albuminuria
- proteinuria
- renal failure
- chronic renal insufficiency
Diagnosis
- Office visist
- ABMP if clinic BP = btw
140/90 - 180/120 mmHg
Tx for T2D OR < 55 + not black
- ACE-I or ARB (Angiotensin II receptor blocker)
- MOA of ACE-I : inhibits ACE ∴ Angiotensin I can’t be converted to ATII ∴ ATII can’t further ↑ BP
- side effects = dry cough, angio-edema + HyperK
- C/Is- African or Caribbean, renal failure, K-sparing diuretics, NSAIDs, pregnant, breastfeeding
→ ibuprofen can make it less effective
→ end in “PRIL”
- MOA of ARB : prevents ATII from binding to its receptor (AT1) ∴ inhibiting it
- side effect = HyperK, ↓ Li excre’n, so watch out for Li toxicity w/ ARBs, ibuprofen can make ARBs less effective
- C/Is : renal failure, K-sparing diuretics, NSAIDs, pregnant, breastfeeding
→ end in “ARTAN”
- Add dihydropiridine CCB or Thiazide-like diuretic
- MOA of dihydropiridine CCB : ↓ entry of Ca into vascular + cardiac cells which ↓ intracellular [Ca] ∴ relaxing arterial smooth muscles aka vasodila’n hence ↓ing BP
- side effects - flushing, ankle edema, HA, palpita’ns
- CI’s = unstable angina + severe aortic stenosis
- end in “PINE”
- MOA of Thiazide-like diuretic = inhibit Na/Cl co-transporter in proximal part of DCT ∴ ↓ing Na reabsor’n + subsequently water reabsorp’n as ∴ blood volume will ↓ + so will BP
- side effects = HypoNa, HypoK + impotence in men
- no C/Is
- end in “THIAZIDE”
- Add other from step 2
- 𝛼1 blocker/antagonist
- MOA : blocks 𝛼-adrenergic receptors found in smooth muscle of blood vessels + urinary tract
→ vasodila’n → ↓ in BP
- side effects = postural hypoTN, syncope + dizziness
- end in “OSIN”
Tx for > 55 and/or Black or Caribbean
- CCB
- Add ARB or Thiazide-like diuretic
- Add the other from step 2
- 𝛼 blocker
Emergency Tx i.e in hypertensive emergency = hydralazine
→ MOA - ↑ levels of cGMP
→ > smooth muscle relax’ in arterioles compared to veins
→ ↓ in BP
- Know for OSCE *
Afib ✓
Def - most common type of arrhythmia i.e irregular pulse
RFs
- HTN
- obesity
- advanced age
- cardiac / thoracic Sx
- obstructive sleep apnea
- congenital heart disease
- myocarditis / pericarditis
- excessive alcohol consump’n
- underlying heart / lung disease
- Hx of atrial arrhythmia, stroke or TIA
- endocrine disorders such as pheochromocytoma, diabetes, hyperthyroidism
Types
- 1st diagnosed = not diagnosed before, irrespective of dura’n or presence / severity of SSX
- Paroxysmal → terminates spontaneously +/- interven’n w/in 7 days of onset but can come back
- Persistent = continues beyond 7 days
- Long-standing persistent = present for > 12 months
- Permanent = Tx has been ended b/c all Tx op’ns failed
Eti = “SMITH”
- Sepsis
- Mitral valve pathology
- Ischemic heart disease
- Thyrotoxicosis
- HTN
Pathophys - RF / underlying heart disease causes dila’n of atria, fibrosis + inflamma’n
→ aberrant electrical activity from myocytes surrounding pulmonary veins overwhelms SA node, which causes re-entry circuits
→ propaga’n of irregular electrical activity of atria
SSX - often asymptomatic but can include . . .
- fatigue
- nausea
- palpita’ns
- chest pain
- tachycardia
- SOB / dyspnea
- polyuria (less common)
- dizziness (less common)
- diaphoresis / excessive sweating
Ddx
- atrial flutter
- atrial tachycardia
- hyperthyroidism
- WPW syndrome (ECG will show shortened PR interval)
Ix’s
- ECG → absence of distinct repeating P waves + variable/ irregularly irregular R-R intervals
- “CHA2 DS2 VAS” to assess pt’s need for anticoagulant
→ Congestive HF - give 1 point if pt has HF SSX
→ HTN - give 1 point if pt has resting BP > 140/90 mmHg on ≥ 2 occas’ns OR = on HTN medica’n
→ Age - give 2 points if pt ≥ 75 y/o
→ Diabetes - give 1 point if pt has fasting glucose > 125 mg/dL OR is on oral hyperglycemic agent
→ Stroke - give 2 points if pt ever had stroke or TIA
→ Vascular - give 1 point if pt ever had MI, aortic plaque or peripheral arterial disease
→ Sex - give 1 point if pt = female
⟹ Ttl of 0 points = no need for anticoagulant
⟹ Ttl of 1 point + female = no need for anticoagulant
⟹ Ttl of 1 point + male = consider anticoagulant
⟹ ≥ 2 points = give anticoagulant
- TSH to r/o hyperthyroidism
- U + E to r/o HypoMg / sepsis / dehydra’n
Emergency Tx i.e if pt is hemodynamically unstable = electrical DC cardiovers’n i.e defibrillator
Regular Tx
- DOAC if anticoagulant = indicated
+ β blocker for rate control
→ can also consider amiodarone
⟹ MOA of amiodarone = class 3 anti-arrhythmics ∴ prolongs plateau phase of myocardial ac’n Ψ / inhibits repolariza’n by slowing influx of Ca + efflux of K
⟹ side effects of chronic use = bradycardia, AV block, hepatitis, photosensitivity, pulmonary fibrosis, heartburn, dyspepsia
⟹ C/Is = WPW, 2nd or 3rd ° heart bock, prolonged QT interval
- Left atrial appendage occlus’n i.e Watchman device if there are absolute C/Is to anticoagulant use OR risk of bleeding outweighs benefits
- Abla’n + pacemaker
Complica’ns
- MI
- heart failure
- stroke b/c due to its rhythm irregularity blood flow through heart becomes turbulent + hence has high chance of forming thrombus (blood clot), which can dislodge to brain + cause stroke
- Know for OSCE *
AV Block ✓
Def - delayed or absent (in Type 3) conduc’n from atria to ventricles
RFs
- LVH
- HTN
- CHF
- sarcoidosis
- ↑ed vagal tone
- cardiomyopathy
- acid base or electrolyte disturbance
- recent cardiac Sx, interven’n or abla’n
- chronic stable coronary artery disease
- AV node blocking agents i.e β blockers, CCBs, digitalis / digoxin, adenosine
Eti
→ 1st ° or Mobitz I = usually due to high vagal tone or medica’n
→ Mobitz II + Type 3 i.e complete heart block = usually due to block in His-Purkinje system but can also be due to digoxin + anti-arrhythmics from all 4 classes
Pathophys - inappropriate conduc’n through AV node → SA node can’t do its job of controlling HR → CO can ↓ + pt can die
SSX = syncope + HR < 40
Ix = ECG
→ Type 1 = CONSISTENT prolonged PR interval i.e > 0.2 secs
→ Type 2 Mobitz I = PROGRESSIVE prolonging PR interval + loss of QRS complex
→ Type 2 Mobitz II = PROGRESSIVE prolonging PR interval W/O loss of QRS complex
→ Type 3 / complete heart block = inconsistent PR intervals
Emergency Tx = temporary pacing
Regular Tx
- 1st ° or Type 2 Mobitz I asymptomatic = monitor only
- 1st ° or Type 2 Mobitz I symptomatic = discontinue all AV node blocking medica’ns
- Type 2 Mobitz II or Type 3 = discontinue all AV node blocking medica’ns + then do cardiac resynchroniza’n therapy or place permanent pacemaker
Ventricular Tachycardia ✓
Types
- sustained → rhythm lasts > 30 secs OR hemodynamic instability occurs in < 30 secs
- non sustained → rhythm lasts < 30 secs + presents w/ tachyarrhythmia w/ > 3 beats of ventricular origin
RFs for both
- CAD
- long QT syndrome
- Brugada’s syndrome
- electrolyte imbalance
- left ventricular systolic dysfunc’n
- idiopathic dilated cardiomyopathy
- cardiomyopathies such as Chagas’ disease
- drugs that prolong QT interval such as macrolide Abx, chlorpromazine, haloperidol, anti-arrhythmic drugs such as digoxin, flecainide, sotalol, + dofetilide
- hypertrophic cardiomyopathy = genetic disorder resulting in myocardial cell disorganiza’n + asymmetrical thickening of ventricle
Eti for both
- IHD (most common cause)
- illicit drug use i.e cocaine/meth
- electrolyte imbalances such as HypoK, HypoCa or HypoMg
- infiltrative cardiomyopathy → can result from SLE, sarcoidosis, amyloidosis, RA + hemochromatosis
SSX for non sustained
- tachycardia
SSX for sustained
- tachycardia
- hypoTN
- weak pulse
- syncope due to cerebral hypoperfus’n from hypoTN
- dyspnea + chest discomfort due to inadequate coronary perfus’n
Ddx for non sustained
- electrical artifact
- supraventricular tachycardia w/ aberrant conduc’n
Ddx for sustained
- Panic
- Sepsis
- Electrical artefact
- Hyperthyroidism
- Acute hemorrhage
- Pheochromocytoma
- Supraventricular tachycardia w/ aberrancy
- Supraventricular tachycardia w/ pre-excita’n
Ix’s for both
- U + E
- cardiac markers to r/o MI
- previous Hx of IHD i.e MI / PCTA / CABG (MUST BE PRESENT TO DIAGNOSE VTach !)
- ECG → tachycardia + wide QRS complex + left axis devia’n (MUST BE PRESENT TO DIAGNOSE VTach !)
Emergency Tx i.e pt is hypotensive / in cardiac failure or has ischemia
= cardiovers’n
Tx for non sustained
- if due to electrolyte abnormality correct it
- if NOT due to electrolyte abnormality . . .
→ β blocker or CCB → catheter abla’n → anti-arrhythmic drug such as flecainide or propafenone
Tx for sustained
- hemodynamically unstable ventricular tachycardia w/ pulse = synchronized cardiovers’n + treat cause if present
- torsades de pointes = IV Mg SO4 → remove hurtful drugs + correct electrolyte abnormalities
- catecholaminergic polymorphic ventricular tachycardia = β blocker → implantable cardioverter defibrillator
- hemodynamically stable sustained ventricular tachycardia = IV anti-arrhythmic drug such as adenosine or procainamide + treat cause if present → synchronized cardiovers’n
⟹ MOA of adenosine - activates specific K channels → Ca influx = inhibited → AV node conduc’n = slowed
⟹ side effects - skin flushing, lightheadedness, nausea + sweating
⟹ C/Is = COPD, asthma + heart block
- ongoing = implantable cardioverter defibrillator → anti-arrhythmic monotherapy such as mexiletine (200 mg orally every 8 hrs) /
flecainide (100-150 mg orally bd) / propafenone (150-300 mg orally every 8 hrs) / sotalol (80-160 mg orally bd)
Complica’ns for non sustained
- Vfib
- sudden death
- cardiomyopathy
- ICD related infe’cn
Complica’ns for sustained
- Vfib
- cardiomyopathy
- sudden cardiac death
- amiodarone-induced thyroid dysfunc’n
- implantable cardioverter defibrillator-related infec’n or malfunc’n
Circula’n order ✓
- RA receives deO2ated blood from everything above chest from SVC + from everything below chest from IVC
- RA → RV via tricuspid valve
- RV → 2 pulm. arteries via pulm. valve
- Blood gets O2ated in lungs
- Lungs → LA via the 4 pulm. veins
- LA → LV via mitral valve
- LV → ascending aorta via aortic valve + then to rest of body
- If LV can’t efficiently pump blood we get pulm. fluid overload *
Cardiac conduc’n system ✓
- SA node generates ac’n Ψ
- Ac’n Ψ spreads to atria ∴ causing them to contract
- AV node delays conduc’n to give time for atria to empty before ventricles begin contracting (on ECG the delay is the horizontal line btw the 1st P wave + QRS complex)
- AV node sends signal via Bundle of His
- Bundle of His splits off into left + right bundle branch which send signal to left + right ventricle respectively ∴ causing them to contract
- Purkinje fibers of ventricles receive signal
→ they have the fastest conduc’n velocities in the heart
Ionotropic v.s Chronotropic v.s Dromotropic effect ✓
- Ionotropic = ↑ in contractility of ventricle myocytes which ↑ SV
- Chronotropic = ↑ in frequency of ac’n ψ of pacemaker cells in SA node which ↑ HR
⟹ para releases Ach → Ach binds to M2 receptors on cardiomyocytes + SA node
→ contractility + HR ↓ = -ve ionotropic + chronotropic effect
⟹ sympathetic system releases NA → NA binds to B1 receptors on cardiomyocytes + SA node → contractility + HR ↑ = +ve ionotropic + chronotropic effect
- Dromotropic = ↑ in conduc’n (AV node)
Aortic regurgita’n ✓
Def- diastolic leakage of blood from aorta into LV, acute AR = surgical emergency !
RFs
- aortitis (= inflamma’n of the aorta 2° to systemic diseases such as syphilis, Behcet’s, Takayasu’s, reactive arthritis + ankylosing spondylitis)
- endocarditis
- rheumatic fever
- Marfan’s syndrome
- bicuspid aortic valve
Eti
→ Acute causes . . .
- type A aortic dissec’n extending to aortic valve
- damage to leaflets from infective or non-infective endocarditis
→ Chronic causes . . .
- aortic stenosis
- calcific disease
- Marfan’s syndrome
- congenital bicuspid aortic valve
General Pathophys - retrograde flow of blood from aorta into LV → ↑ in left ventricular volume + dilata’n of the chamber → initially leads to ↑ in CO but that ↑ in CO leads to disten’n + ↑ed pressure in peripheral arteries ∴ causing ↑ in peripheral systolic pressure → eventually, this causes worsening of the regurgita’n, which can cause peripheral systolic pressure to rapidly↓+ in severe disease can cause cardiovascular collapse (this phenomenon causes the wide pulse pressure that’s characteristic in severe aortic regurgita’n)
Pathophys for Acute AR - end-diastolic pressure in LV ↑ sharply → heart tries to compensate by ↑ing HR + contractility to keep up w/ ↑ed preload, but = insufficient to maintain normal SV
Pathophys for Chronic AR - ↑ in left ventricular volume + pressure causes ↑ in wall tens’n → to compensate for ↑ed wall tens’n, heart wall undergoes hypertrophy (both concentric + eccentric hypertrophy can occur but most of the time is eccentric) → in eccentric hypertrophy, sarcomeres are laid down in SERIES + it results from VOLUME overload v.s in concentric hypertrophy, sarcomeres replicate in PARALLEL + it results from PRESSURE overload → systolic HTN occurs 2° to ↑ed SV → the volume overload, which is directly related to the severity of the leak, results in ↑ in left ventricular end-diastolic volume
⟹ In chronic AR, most pts remain asymptomatic for decades b/c LV maintains stroke volume w/ compensatory chamber enlarg’nt + hypertrophy
SSX
- soft S1
- orthopnea
- collapsing pulse
- diastolic murmur
- low diastolic pressure
- narrow pulse pressure
- cyanosis (sign of acute AR)
- Corrigan’s sign = forceful carotid pulse
- pallor (sign of cardiogenic shock)
- raised JVP (sign of cardiogenic shock + CHF)
- basal lung crepita’ns due to pulm. edema
- tachypnea (sign of acute AR w/ pulm. edema)
- dyspnea (caused by pulm. edema in acute AR)
- PND (sign of chronic AR due to progressive left ventricular dysfunc’n)
- fatigue (sign of chronic AR due to progressive left ventricular dysfunc’n)
- weakness (sign of chronic AR due to progressive left ventricular dysfunc’n)
Ddx
- Aortic stenosis
- Mitral stenosis
- Mitral regurgita’n
- Pulmonary regurgita’n
Ix’s
- ECG
- color flow doppler + pulse wave doppler
- CXR → may show cardiac enlarg’nt
Tx for Acute AR
- ionotropes such as dobutamine (0.5 micrograms/kg/min IV, max dose = 20 micrograms/kg/min) + vasodilators + urgent valve replac’nt / repair
Tx for Chronic AR
- aortic valve Sx if EF > 55% and/or LV end-systolic diameter < 50 mm
Complica’ns
- arrhythmias
- heart failure
- sudden death
- operative mortality
- myocardial ischemia
- infective endocarditis
- Know for OSCE *
What should all pts w/ mechanical valves be on long term ? ✓
Aspirin + warfarin
Where on kidneys do diuretics act on ? ✓
- Thiazide like diuretics = on DCT
- Loop diuretics = on Na K Cl co-transporter
Heart Failure ✓
1- Define cor pulmonale + recall common causes
2- Def, RFs, Eti, Pathophys, SSX, Diagnostic Criteria, Ddx, Ix, 1st line Mx, Complica’ns
- Cor pulmonale = right heart failure specifically b/c of lung disease such as a massive P.E (massive P.E involves proximal pulm. artery = only one that will cause ACUTE cor pulmonale)
→ Pathophys - lung disease → pulmonary HTN → cor pulmonale
→ CHRONIC causes of cor pulmonale
- pulmonary fibrosis
- COPD (most common chronic cause)
- recurrent small P.Es (will cause pulm. HTN but slowly)
- LHF = more common than RHF
RFs for Acute HF
> 70 y/o
- HTN
- smoking
- arrhythmias
- previous CVD
- previous chemo
- excessive alcohol intake
- previous episode of heart failure
- FHx of ischemic heart disease or cardiomyopathy
⚠️ NSAIDs + nondihydropyridine CCBs like diltiazem or verapamil can exacerbate heart failure !
Eti for LHF = CAD (most common cause) + HTN
Patophys for LHF based on Eti
- CAD → ischemic damage to myocardium
→ remodeling + scar forma’n
→ ↓ in contractility + CO - chronic / poorly controlled HTN → ↑ed afterload
→ ↑ed workload on heart → LVH as compensa’n measure
SSX for LHF
- SOB
- tachypnea
- cold + clammy in periphery
- peripheral / central cyanosis
- paroxysmal nocturnal dyspnea
- orthopnea (= SOB when lying down)
ETI for RHF
- most common cause = as a result of LHF + when this happens it’s called Chronic HF but can also happen acutely b/c of . . .
- pulm. HTN
- massive P.E
- circulatory collapse
- MI that involved RV but spared LV
- tricuspid or pulmonic valve insufficiency b/c will cause volume overload
- things that cause impaired filling such as constrictive pericarditis, tricuspid stenosis, systemic vasodilatory shock, cardiac tamponade, hypovolemia, SVC syndrome
- congenital heart disease such as pulmonic stenosis (b/c will cause chronic pressure overload) or ASD (b/c will cause volume overload)
PATHOPHYS for Chronic RHF :
- before it happens, RV will be slowly damaged over a period of time due to lung disease such as COPD / pulm. fibrosis / recurrent small pulmonary emboli
- in early stages, there’s enough time for RV to compensate so we get RVH but eventually RV will decompensate
SSX for Chronic RHF = “HEAP”, PND, cough, orthopnea + dyspnea
- Hepatomegaly
- Elevated JVP b/c jugular veins = congested
- Ascites
- Peripheral edema i.e pitting edema in lower extremities
Ddx for RHF
- MI
- PE
- CAP
- Cirrhosis
- Emphysema
- Respiratory failure
- Nephrotic syndrome
Ix’s for both
- BNP if echo not readily available → will be elevated = secreted from ventricular myocardium especially LV myocardium (can also be elevated in LVH, right ventricular overload, P.E, diabetes, cirrhosis, sepsis + GFR < 60)
→ can be falsely low in pt taking ARB + falsely high in pt w/ kidney failure - ECG + Troponin → to r/o MI
- LFTs → to r/o liver disease (in the case of hepatomegaly)
- CXR (“ABCDPE”)
→ Alveolar edema
→ kerley B lines (in stage 2 heart failure)
→ Cardiomegaly (no cardiomegaly in “MCM” i.e MI + constrictive pericarditis + mitral stenosis)
→ Dilated upper lobe vessels
→ Pleural Effus’n (in stage 3 heart failure)
→ Extra- previous CABG / prosthetic valve / pacemaker / defibrillator - perihilar pulmonary edema on CXR i.e bat-wing shape = indicative of CHF ! *
⚠️ Cardiomegaly DOES NOT ALWAYS mean heart failure !
→ could be pericardial effus’n or cardiomyopathy
HF Staging
I = no fatigue / palpita’ns / SOB w/ physical activity
II = slight “ “
III = SSX w/ light physical activity
IV = SSX @ rest or w/ any type of physical activity
Emergency Tx for Acute HF
- IV furosemide bolus if there’s pulm. edema + admit to CCU + stop NSAIDs / diltiazem / verapamil b/c can exacerbate heart failure !
→ MOA of furosemide = loop diuretic ∴ binds + inhibits Na-K-Cl co-transporter on thick ascending limb of loop of Henle ∴ inhibiting Na + Cl reabsorp’n + subsequently water reabsorp’n as well
→ side effects = dehydra’n + hypoTN
→ C/Is = anuria + severe electrolyte deple’n
→ end in “IDE”
⚠️ HF pts w/ renal disease might require higher doses of furosemide !
- ionotrope such as dobutamine if SBP < 100
- vasodila’n via nitrate infus’n if SBP > 100
Regular Tx for severe HF i.e w/ ↓ed EF
= ACE-I/ARB + β blocker
→ aldosterone antagonist → SGLT-2 inhibitor
⟹ aldosterone antagonists end in “ONE” i.e spironolactone / eplerenone) → act on collecting duct of kidney
⟹ side effects of aldosterone antagonists = HyperK (cause HyperK by interfering w/ K excre’n which is why they’re called “K sparing diuretics”), breast tissue growth
Indica’ns for CRT-D (Coronary Resynchroniza’n Therapy Device)
- EF ≤ 35%
- Stages 3 or 4
- Wide QRS i.e ≥ 150 ms + LBBB
Complica’ns for LHF
- RHF due to fluid overload
- arrhythmias (in acute heart failure)
- cardiogenic shock due to pump failure
- respiratory failure due to fluid overload → give pt CPAP in this case
- P.E, ACS, CVAs + rupture of myocardium = common causes of sudden death in pts w/ heart failure
- Know it for OSCE *
Aortic dissec’n ✓
Def - tear in tunica intima of aorta
RFs
- HTN
- smoking
- FHx of aneurysm or aortic dissec’n
- connective tissue disorders like Marfan’s or Ehlers-Danlos syndrome
Eti = RFs
Types
- Type A = involves ascending aorta
- Type B = ascending aorta ≠ involved
SSX
- sudden tearing/stabbing chest pain that might radiate to back
- blood pressure differential btw both arms or both legs (> 20 mmHg difference in SBP)
Ix’s
- ECG to r/o STEMI
- TTE or CT if TTE isn’t available → CT will show widened mediastinum
- Consider TOE for definitive diagnosis
Tx
1) β blocker or non-dihydropyridine CCB + IV opioid
2) EVAR or open air if pt = hemodynamically unstable OR it’s a confirmed type A OR a complicated type B
Complica’ns
- cardiac tamponade
- aortic incompetence
- Know for OSCE *
Mitral stenosis ✓
Def - narrowing of mitral valve orifice
RFs
- female
- streptococcal infec’n
Eti
- RA
- SLE
- carcinoid syndrome
- amyloid deposi’n in mitral valve
- degenerative calcifica’n (in the elderly)
- infective endocarditis w/ large vegeta’ns
- rheumatic heart disease due to rheumatic fever (= most common cause of mitral stenosis)
- congenital mitral stenosis (2° to parachute mitral valve or Lutembacher’s syndrome)
- inborn errors of metabolism such as Hurler-Scheie syndrome or Anderson-Fabry disease
Pathophys - filling of LV ↓ → pressure in LA ↑ → pulmonary congest’n + CO = limited b/c restricted orifice limits filling of LV
SSX
- dyspnea
- orthopnea
- diastolic murmur
- neck vein distens’n
- opening snap on ausculta’n
Ddx
- unexplained Afib
- left atrial myxoma = LA tumor that can obstruct mitral orifice + hence mimic SSX of mitral stenosis
Ix’s
- ECG → Afib / left atrial enlarg’nt / RVH
- trans-thoracic echocardiogram → hockey stick-shaped mitral deformity
- CXR → double right heart border indicating enlarged LA, prominent pulmonary artery + Kerley B lines
Tx
- diuretic such as furosemide
→ percutaneous balloon valvotomy → ivabradine if pt ≠ pregnant or β blocker such as atenolol
Complica’ns
- Afib
- stroke
- pulmonary HTN
- infective endocarditis
- warfarin induced hemorrhage
- Know for OSCE *
Mitral regurgita’n ✓
Def - retrograde flow from LV into LA
RFs
- Hx of MI
- Hx of IHD
- Hx of cardiac trauma
- elevated SBP
- infective endocarditis
- mitral valve prolapse
- Hx of rheumatic heart disease
- Hx of congenital heart disease
- hypertrophic cardiomyopathy
- left ventricular systolic dysfunc’n
- anorectic, dopaminergic drugs or serotonergic drugs such as ergotamine, pergolide + cabergoline
Eti
> ACUTE causes . . .
- infective endocarditis
- acute rheumatic fever
- ischemic papillary muscle dysfunc’n or rupture
- acute dilata’n of LV due to ischemia or myocarditis
> CHRONIC causes . . .
- infective endocarditis
- mitral valve prolapse
- acute rheumatic fever
- mitral annular enlarg’nt
- myxomatous degenera’n of mitral leaflets or chordae tendineae
- acute dilata’n of LV due to ischemia or myocarditis
- ischemic papillary muscle dysfunc’n or rupture
Pathophys - ↑ in blood volume w/in LA → ↑ed preload delivered to LV during diastole → left ventricular volume overload
> in chronic progressive MR, ventricular remodeling occurs so CO can be maintained
» initial ↑ in EF usually happens
SSX
- fatigue
- dyspnea on exer’n
- holosystolic murmur
- ↓ed exercise tolerance
- lower extremity edema
Ddx
- Atrial myxoma
- Aortic stenosis
- Mitral stenosis
- Infective endocarditis
- Acute coronary syndrome
- Aortic or pulmonic valve disease
Ix’s
- ECG → may show underlying arrhythmia or prior infarct
- trans-thoracic echo for presence + severity of MR + to check for structural + flow abnormalities
Tx = Surgical valve replac’nt
Complica’ns
- Afib
- post op stroke
- pulmonary HTN
- prosthesis stenosis
- post op endocarditis
- left ventricular dysfunc’n → CHF
- prosthesis dysfunc’n after valve replac’nt
- recurrent MR or peri-valvular regurgita’n after valve replac’nt
- Know for OSCE *
Congenital heart defects ✓
Left to R. shunt types
- ASD = hole btw L. + R. atria so extra blood flows into R. side of heart causing it to stretch + enlarge
→ SOB, difficulty feeding, poor weight gain, LRTIs
→ can cause stroke in pts w/ DVT
→ refer to pediatric cardiologist → if small + asymptomatic watch + wait → can be corrected surgically using a transvenous catheter closure (via femoral vein) or open heart surgery
→ in adults, anticoagulants (such as aspirin, warfarin) = used to ↓ risk of clots + stroke - VSD = most common one = hole btw L. + R. ventricle so extra blood flows into lungs ∴ causing high pressure in lungs, small VSD = asymptomatic, pansystolic murmur @ left sternal border
→ poor feeding, dyspnea, tachypnea, FTT
→ pts are at ↑ed risk of developing infective endocarditis
→ refer to pediatric cardiologist → if small + asymptomatic watch + wait → can be corrected surgically using a transvenous catheter closure (via femoral vein) or open heart surgery - PDA (prematurity = RF)
→ murmur on newborn exam
→ SOB, difficulty feeding, poor weight gain, LRTIs
→ pts = typically monitored until 1 y/o using echos + then after 1 y/o trans-catheter or surgical closure can be performed - Coarcta’n of the aorta = narrowing of aorta
→ weak femoral pulses, tachypnea, labored breathing, poor feeding, grey + floppy baby
→ Ix for immediate diagnosis = 4 limb BP
→ in cases of critical coarcta’n i.e risk of HF + death shortly, PGE such as alprostadil = given after after birth to keep ductus arteriosus open while waiting for Sx → Sx is then performed to correct coracta’n + ligate ductus arteriosus
Right to L. shunt types
- Tetralogy of Fallot = VSD + pulm. valve stenosis + RVH + overriding aorta (Rubella = RF)
→ cyanosis, clubbing, poor feeding, poor weight gain, ejec’n systolic murmur
→ in neonates, PG infus’n can be used to maintain ductus arteriosus but ttl surgical repair via open heart Sx = definitive Tx - Transposi’n of the great arteries = aorta + pulm. artery aren’t in their normal posi’n due to failure of aorticopulmonary septum to spiral during septa’n
→ often diagnosed during pregnancy on antenatal scans. If not detected during pregnancy will present w/ cyanosis, tachypnea + ‘egg-on-side’ appearance on CXR w/in a few days of birth
→ PG infus’n can be used to maintain ductus arteriosus but surgical repair = definitive Tx - Ebstein’s anomaly = when tricuspid valve doesn’t develop properly
→ gallop rhythm heard on ausculta’n, cyanosis, dyspnea, tachypnea, poor feeding
→ diagnosed w/ echo - Truncus arteriosus = pulm. artery + aorta are a single vessel ∴ there’s way too much blood flow to the lungs = FATAL so must be treated !
Features of innocent murmurs in kids ✓
” 5 S’s “
- soft i.e < grade 2/5 + no thrills
- short
- systolic
- symptomless
- situa’n dependent i.e quieter w/ standing or only appears when child = acutely ill
Aorta + its branches ✓
→ Ascending aorta gives rise to left + right coronary arteries which supply the heart hence they’re called the coronary vessels
→ Ascending aorta turns upwards + backwards to become aortic arch . . .
The 3 branches of the aortic arch =
- Brachiocephalic trunk → 2 branches
→ right subclavian supplies right arm + right common carotid right side of head and neck
→ right common carotid → 2 branches = right internal and right external
- Left common carotid artery → 2 branches = left internal carotid + left external carotid
- Left subclavian artery
Although left + right subclavian have diff origins, they both become axillary artery when they enter axilla
Axillary artery continues into arm as brachial artery which bifurcates @ cubital fossa into ulnar + radial artery
The aortic arch then turns downwards to become the descending / thoracic aorta (@ T4)
The thoracic / descending aorta then becomes the abdominal aorta (below the diaphragm i.e @ T12)
The abdominal aorta has 3 anterior branches =
- Celiac trunk → 3 branches = left gastric, splenic + common hepatic artery
- Superior mesenteric artery
- Inferior mesenteric artery
- abdominal aorta bifurcates @ L4 into its 2 terminal branches = right + left common iliac
→ each bifurcate into internal + external iliac
Each external iliac becomes femoral artery when enters thigh, its branch = deep artery of the thigh
- they become popliteal artery at the knee → 2 branches
→ anterior tibial → terminates into dorsalis pedis artery
→ posterior tibial → supplies posterior compart’nt of leg + plantar reg’n
Branches of descending abdominal aorta from diaphragm to iliacs ✓
” Inferior Prostitutes Cause Sad Swollen Red [Testicles In Men] Living In Sin “
- Inferior Phrenic artery
- Celiac (abdominal aorta)
- SMA (abdominal aorta)
- Suprarenal (middle)
- Renal (branches off abdominal aorta @ L2)
- Testicular
- Lumbars
- IMA (abdominal aorta)
- Sacral
AAA ✓
Def - localized, permanent, abnormal dilata’n of a blood vessel in this case AA by > 1.5x its normal diameter, ruptured aneurysm = surgical emergency !
- majority = below renal arteries
⚠️ All 3 blood vessel layers have to be involved for it to be a TRUE aneurysm !
RFs:
> 55 y/o
- FHx
- atherosclerosis
- hypercholesterolemia
- male (for occurrence)
- female (for risk of rupture)
- PMHx of connective tissue disorder
- HTN + current/previous smoking = strongest RFs
- other aneurysms such as iliac / femoral / popliteal so if pt has aneurysm in 1 of those 3 always check for AAA
Intact AAA = asymptomatic
SSX of RUPTURED AAA
- hypoTN
- abdo or back pain
- non-tender pulsatile abdominal mass
- blue toe syndrome bilaterally due to emboli
- flank ecchymosis / grey Turner sign → suggests retroperitoneal bleeding
Classifica’n
- Saccular = spherical shape + develops at 1 side of vessel wall = more likely to rupture b/c wall tens’n ≠ distributed equally
- Fusiform = spindle shape; involves all of vessel’s circumference
- False / Pseudo = expanding pulsatile hematoma that forms as a result of a leaking hole in an artery + stays in continuity w/ arterial lumen = false aneurysm b/c has no endothelial lining i.e doesn’t involve all 3 vessel layers
Ix for diagnosis = aortic U/S if ur not sure if it’s an aneurysm but if ur sure it’s an aneurysm do CT instead
Eti
- infec’n
- atherosclerosis
- inflammatory i.e CA, polyarteritis nodosa
- post dissec’n i.e after an accident
- congenital diseases such as tuberous sclerosis, Marfan’s, Ehlers-Danlos syndrome
Pathophys - enlarg’nt of atherosclerotic plaque → pressure / ischemic atrophy of media + loss of elastic fibers
→ weakening + dilata’n of aortic wall → aneurysm forms @ that weak spot
Ix’s
- U/S for SCREENING → don’t use in emergency setting b/c won’t necessarily catch rupture
- CT angiogram for diagnosing rupture
What to do based on diameter of AAA . . .
- if btw 3- 4.4 cm, do U/S every yr
- if btw 4.5 -5.4 cm, do U/S every 3 months
- if > 5.5 cm, refer to vascular Sx
Treat if aneurysm = ruptured OR pt is symptomatic OR asymptomatic but aneurysm > 5.5 cm OR asymptomatic but aneurysm > 4 cm + growing > 1cm/yr
Tx = Open repair or EVAR
→ open repair if pt < 70 y/o + EVAR if pt > 70 y/o
⟹ EVAR = through b/l femoral access, requires annual surveillance for endoleak + if there’s an endoleak, that will require Sx
→ open repair = longer recovery time but has longer durability
⟹ can use trans-abdominal approach or retroperitoneal approach which is good for obese pts or pts w/ multiple prior abdominal surgeries
Complica’ns of open repair
- incis’nal hernia
- spinal cord ischemia
- lower extremity ischemia
- graft infec’n → has very high mortality
- colon ischemia → pt will have bloody stools the day after
Complica’ns
- ileus
- post op AKI
- ischemic colitis
- intestinal obstruc’n
- abdominal compartment syndrome
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Cardiac Arrest ✓
Def - sudden circulatory failure as a result of a cardiac arrhythmia
RFs
- CAD
- HCM
- long QT syndrome
Eti
- Vifb = shockable
- Vtach = shockable
- pulseless electrical activity = non shockable
- asystole = nonshockable
SSX
- unresponsive
- lack of pulse
- abdonalr breathing
Ix = continuous cardiac monitoring to see if it’s a shockable rhythm or not
Tx
1. CPR
2. Defibrilla’n +/- epinephrine (if it’s a shockable rhythm) → can consider amiodarone or lidocaine if unresponsive to shock
Complica’ns
- death
- anoxic brain injury
- Know for OSCE *
Respiratory Arrest ✓
Eti
- asthma
- 2° to resp. arrest
- severe pneumonia
- acute on chronic respiratory failure
- plugged tracheostomy
- overdose of drug that causes respiratory depress’n such as morphine/barbiturates
Tx
1. A + B of ABCD
2. Ventila’n w/ 100% O2
3. Treat underlying cause
Cardioresp. arrest ✓
Def - cessa’n of adequate heart func’n + respira’n resulting in death
Eti
- P.E
- CAD (75% of cases = due to this)
- myocarditis
- tetralogy of Fallot
- valvular heart disease
- myocardial hypertrophy
- heart failure (if EF < 35%)
- inherited disorders like Brugada syndrome / short QT syndrome / long QT syndrome
- bronchospasm due to pneumonia / pulmonary edema / pulmonary hemorrhage
- severe asthma or COPD
- respiratory muscle weakness (for ex due to spinal cord injury)
Ddx
- Acidosis
- Hypoxia
- Hypothermia
- Hypovolemia
- Hypo or HyperK
- Cardiac tamponade
- Thrombus / acute MI
- Tens’n pneumothorax
- PE / Thromboembolism
- Toxic overdose of drugs
Emergency Tx = Basic Life Support → Defibrilla’n → Advanced Life Support → Post-resuscita’n care → Long-term Mx
PAD ✓
Def - narrowing or blockage of arteries that carry blood from heart to limbs = type of PVD
RFs
> 40 y/o
- T2D
- HTN
- HLD
- smoking
- sedentary lifestyle
Eti = atherosclerosis
SSX
- intermittent claudica’n i.e leg pain that starts when pt walks + stops when they rest
- “6 P’s” when it becomes limb ischemia i.e . . .
→ pain
→ pallor
→ paralysis
→ paresthesia
→ perishingly cold
→ pulselessness (late sign)
Ddx
- nerve root compress’n
- Baker’s cyst (pain will be present even at rest + area behind knee will be swollen + tender)
Order of Ix’s
- ABI
> 1.3 = calcified vessels
→ 0.8-1.3 = no PAD
→ 0.5-0.79 = mild~moderate PAD + claudica’n
< 0.5 = severe PAD i.e critical limb ischemia ∴ causing leg pain even @ rest - Duplex U/S
- CT angiography w/ contrast = gold std for diagnosis
Complica’n’s
- arterial ulcers
- acute limb ischemia = sudden ↓ in limb perfus’n that threatens viability of that limb hence = vascular emergency !
Emergency Tx i.e if there’s acute limb ischemia = surgical embolectomy + unfractionated heparin (if pt has Afib) → amputa’n if leg = non-viable
Regular Tx
- Smoking cessa’n + BP / glucose control
- Exercise training i.e structured + supervised program of regularly walking to point of near-maximal claudica’n pain, resting + repeating again
- Medical Tx i.e 80mg statin + 75mg clopidogrel daily + naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)
- Sx . . .
- endovascular angioplasty + stenting
- endarterectomy i.e cutting vessel open + removing atheromatous plaque
- bypass Sx = using graft to bypass blockage
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Carotid artery stenosis ✓
Def - narrowing of carotid artery lumen
RFs
- smoking
- older age
- Hx of CVD
Eti = atherosclerosis plaque
Classifica’n
- Mild stenosis = < 50% diameter reduc’n
- Moderate stenosis = 50 - 70% diameter reduc’n
- High grade stenosis = > 70% diameter reduc’n
- Near-occlus’n
- Occlus’n = completely occluded carotid artery
SSX = transient visual SSX i.e . . .
- homonymous hemianopia
- temporary vis’n loss in ipsilateral eye
Ix’s
1. duplex U/S
2. head/neck/chest CTA
Tx
- asymptomatic + stenosis < 70% = antiplatelet therapy + cardiovascular risk reduc’n i.e managing RFs
- asymptomatic + stenosis ≥ 70% + good surgical candidate = carotid endarterectomy + cardiovascular risk reduc’n i.e managing RFs
- asymptomatic + stenosis ≥ 70% + poor surgical candidate = carotid artery stenting + cardiovascular risk reduc’n i.e managing RFs
- symptomatic + ipsilateral carotid stenosis ≥ 50% = carotid endarterectomy or stenting + managing RFs + lipid-lowering therapy i.e statin
- symptomatic + ipsilateral carotid stenosis < 50% = antiplatelet therapy + managing RFs + lipid-lowering therapy i.e statin
Complica’n = ischemic stroke
Complica’n of carotid endarterectomy = hemorrhage that can cause airway compress’n
→ SSX = swollen neck, difficulty breathing, stridor
Varicose veins ✓
Def - distended superficial veins measuring > 3mm in diameter, usually in legs
RFs
- FHx
- DVT
- female
- obesity
- prolonged standing
- pregnancy b/c uterus causes compress’n of pelvic veins
Eti = venous valve incompetence
Pathophys - valve doesn’t func’n properly → blood pools → ↑ed pressure → veins distend
SSX = asymptomatic or . . .
- heavy / dragging sensa’n in legs
- edema
- itchy legs
- leg cramps
- restless legs
- leg fatigue or aching w/ prolonged standing
Ddx
- reticular veins = dilated blood vessels in the skin measuring 1-3mm in diameter
- telangiectasia/spider veins/thread veins = dilated blood vessels in the skin measuring < 1mm in diameter
Ix = duplex U/S
→ valve closure time > 0.5 second = indicative of reflux in superficial system
→ valve closure time > 1 second = indicative of reflux in deep system
Tx
- if due to pregnancy → usually improves after delivery
- symptomatic w/ no evidence of PVD or tributary insufficiency only = phlebectomy or foam sclerotherapy
- symptomatic superficial vein insufficiency w/ no evidence of PVD or truncal axial insufficiency only
= endovenous thermal abla’n (via radiofrequency or laser) → foam sclerotherapy if that doesn’t work →
open Sx (stripping + liga’n) - symptomatic w/no evidence of PVD w/ both truncal axial + tributary insufficiency = endovenous thermal abla’n + either phlebectomy or foam sclerotherapy → foam sclerotherapy of truncal + tributary veins if that doesn’t work → open Sx + phlebectomy
- symptomatic w/ no evidence of PVD + perforator veins w/ reflux = located near healed or active venous ulcers → either foam sclerotherapy or endovenous thermal abla’n + compress’n therapy (i.e bandage or stockings) → perforator Sx if that doesn’t work + compress’n therapy
- deep vein obstruc’n = stenting or reconstruc’n
Complica’ns
- DVT
- chronic venous insufficiency
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Ulcers ✓
Def - wounds or breaks in skin that heal slowly or not at all due to underlying pathology
Types
- arterial ulcer pathophys - PAD → insufficient blood supply to skin
- venous ulcer pathohys - venous insufficiency → pooling of blood + waste products in skin
Arterial v.s Venous ulcers
- well defined borders v.s irregular borders
- less likely to bleed v.s more likely to bleed
- more painful v.s less painful
- pain = worse w/ eleva’n v.s better w/ eleva’n
- arterial occurs on toes + heels, has deep punched-out appearance + leg might be cold w/ no palpable pulses
- venous ulcers have waxy texture
Ix’s = ABI to check if pt has PAD
Tx for arterial ulcer = like PAD
Tx for venous ulcer
- constant nurse wound care i.e clean → debride → dress
- analgesia
- Abx if infected
- compress’n stockings
Necrotizing Fasciitis ✓
Def - rare but life-threatening subcutaneous soft-tissue infec’n that progressively extends to deep soft tissues including muscle fascia + overlying fat, but not into underlying muscle = surgical emergency !
→ also known as flesh-eating bacteria due to the release of toxins
→ Fournier’s gangrene = necrotizing fasciitis of perineum + genital reg’n
RFs
- IV drug use
- Varicella zoster infec’n
- non-traumatic skin les’ns
- cutaneous injury / Sx / trauma
- contact w/ pt w/ group A strep infec’n
Types
Type I - polymicrobial infec’n caused by anaerobes such as Bacteroides, Clostridium or Peptostreptococcus + facultative anaerobes such as certain Enterobacterales (E. coli, Enterobacter, Klebsiella, Proteus)
Type II - monomicrobial infec’n caused by Streptococcus pyogenes i.e group A strep + sometimes Staph aureus or MRSA = usually seen in older pts w/ underlying illness
Pathophys - bacteria = introduced into skin + soft tissue due to minor trauma / Sx / puncture wound → infec’n extends through fascia but not into underlying muscle → release of bacterial toxins cause systemic SSX such as fever, tachycardia, hypoTN
SSX
- severe pain
- fever
- N + V
- hypoTN
- tachycardia
- lightheadedness
Ddx
- cellulitis
- impetigo
- erysipelas
Ix’s
- surgical explora’n
- blood + tissue cultures
- FBC, U + E, creatinine kinase, lactate
Emergency Tx
1. Emergency surgical debridement + supportive care + high dose broad spectrum Abx
2. Pathogen specific Abx
Complica’ns
- death
- skin loss + scarring
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Gangrene ✓
Def - decay of body tissue = complica’n of necrosis
RFs
- diabetes
- malignancy
- renal disease
- drug / alcohol abuse
- atherosclerosis (for ischemic)
- smoking (for ischemic gangrene)
- contaminated wound (for infectious
- trauma or abdominal Sx (for infectious gangrene)
Types
- infectious gangrene
- ischemic gangrene
Eti for infectious gangrene
- necrotizing fasciitis
- gas gangrene (usually caused by Clostridium perfringen or other clostridium species)
Eti for ischemic gangrene
- venous obstruc’n
- Atherosclerosis / PAD
- diabetes-associated microangiopathy
- hypercoagulable states such as IV drub abuse, vasculitis, malignancy, or antiphospholipid syndrome
SSX
- rotting appearance
- crepitus in gas gangrene
Ix’s
- FBC
- CMP
- LDH
- coagula’n panel
- blood culture to check for bacteremia
Tx
- necrotizing fasciitis + still waiting for culture + sensitivity results =
surgical debridement + intensive supportive care + empirical broadspectrum Abx - gas gangrene = intensive supportive care+ surgical debridement +/- amputa’n + IV Abx
- ischemic gangrene w/ viable extremity = IV heparin + thrombolytic therapy
- ischemic gangrene w/ threatened or non-viable extremity (limb expectancy > 2 yrs) = IV heparin +
surgical revasculariza’n +/- amputa’n - ischemic gangrene w/ threatened or non-viable extremity (limb expentancy ≤ 2 yrs = IV heparin + percutaneous transluminal angioplasty (PTA) +/- amputa’n
Complica’ns
- loss of limb
- sepsis → shock
- acute renal failure
- hemolysis b/c 𝛼 toxin= produced in gas gangrene = metallo-enzyme that causes lysis of erythrocytes, leukocytes, platelets, fibroblasts + muscle cells
Asthma ✓
Def - chronic inflammatory obstructive lung disease b/c “obstructs” air from exiting lungs by ↑ing airway resistance = reversible
⚠️ If FEVC1 measured over FVC measured < 0.7 or 70% = obstructive pb !
Eti
- Atopic / Extrinsic aka due to allergen exposure (pollen, pet, dust, etc)
- Nonatopic / Intrinsic aka due to irritant exposure (cold, smoking, exercise, aspirin induced)
→ less common than atopic
→ mainly neutrophils as opposed to eosinophils like in atopic - Hygiene hypothesis = ppl who are exposed to allergens early in life = less likely to develop asthma later in life as an adult *
Pathophys
1. Allergen/irritant = inhaled + transported by dendritic cell that has MHC-II molecule
2. Dendritic cell presents antigen aka allergen to Th-2 cell
3. On its membrane, Th-2 cell has CD4 molecule + T-cell receptor (specific to particular antigen)
4. CD4 molecule interacts w/ MHC-II molecule of dendritic cell + T-cell receptor interacts w/ allergen via binding
5. Interac’n triggers Th-2 to release IL-4 + IL-5
6. IL-4 activates plasma cells to produce IgE antibodies
7. IgE antibodies bind to mast cells which triggers mast cell to undergo degranula’n
8. When mast cells degranulate they produces histamines + leukotrienes
9. IL-5 activates eosinophils which will release leukotrienes + cytokines + proteases (chronically eventually damage respiratory system)
10. Histamines + Leukotrienes affect bronchioles → inflamma’n, broncho-constric’n + ↑ in mucus produc’n → airways narrow + resistance ↑
11. If this happens chronically, we can get fibrosis, which will cause PERMANENT airway narrowing instead of REVERSIBLE airway narrowing
SSX of poorly controlled asthma
- frequent breathing pbs
- use of reliever medica’n > 3x/wk
- cough + wheeze upon expira’n
- SSX wake pt up at night
Ix’s
- FeNO or spirometry w/ bronchodilator reversibility for diagnosis (FeNo preferably)
→ FeNO > 40 ppb = diagnostic
→ only use spirometry for pts > 5 y/o
⟹ reversibility i.e ↑ in FEV1 ≥12% = diagnostic
Tx for adults i.e > 12 y/o
- SABA (short acting β2 agonist)
= reliever inhaler ∴ should only be used when pt has attack (usually salbutamol aka ventolin)
- MOA = activate β2 receptors in bronchioles which causes relaxa’n of smooth muscles of bronchi i.e bronchodila’n
- side effects = HAs, palpita’ns, tachycardia, anxiety + tremors
- cau’ns = CVD such as angina
- end in “TAMOL” or “TEROL”
- Add Low dose ICS = preventer inhaler so must be taken everyday
- MOA = ↓ mucus secre’n + mucosal inflamma’n + widens airways
- side effects = oral thrush / candidiasis (fungal infec’n) + hoarse / raspy voice
→ if thrush happens change to large volume spacer - cau’ns = children
- end in “ONE”
- Add Leukotriene receptor antagonist (LTRA) to ICS + SABA
- MOA = competitively block leukotriene receptors ∴ ↓ bronchoconstric’n, vascular permeability + mucus secre’n
- side effects = liver toxicity
- CIs = liver impair’nt
- end in “LUKAST”
- Add LABA to low dose ICS + SABA
- end in “EROL”
⚠️ LABAs MUST ALWAYS BE USED W/ ICS !
- LAMA (anti-muscarinic drug / muscarinic receptor antagonist) or methylaxnthine derivative
- MOA of LAMA = competitively binds to M3 receptors in trachea / bronchioles so Ach can’t bind + activate them ∴ inhibiting para. system from broncho-constricting
- side effects = dry mouth
- C/Is = narrow angle glaucoma b/c inhibits para so instead of ciliary muscles constricting they will relax which will worsen humour drainage
- end in “TROPIUM”
- MOA of Meth. derivative = bronchodilates by inhibiting phospho-diesterase ∴ can no longer convert CAMP to 5-AMP which ↑ CAMP levels
- side effects = insomnia, N/V, seizure, arrhythmia, metabolized by cytochrome P-450 + blocks adenosine
- C/Is = arrhythmia or seizure disorder
- end in “PHYLLINE”
Tx for pts btw 5 + 12 y/o = same as adults but no leukotriene receptor antagonist + instead of LAMA = ↑ dose of ICS
1. SABA
2. ICS
3. LABA such as salmeterol
→ only continue LABA if pt has good response to it
4. Up titrate ICS to medium dose
5. ↑ dose of ICS to high dose
6. Specialist referral + asthma review every 3 months to consider ↓ing corticosteroid by 25-50%
Tx for pts < 5 y/o = same as adults but no LABA or LAMA
1. SABA
2. ICS or leukotriene antagonist
3. Add the other one you didn’t give in step 2
4. Specialist referral
Emergency Tx for adults
- O2 mask + nebulized SABA (2.5-5 mg) w/ SAMA + ICS
→ monitor vitals, O2sat, pCO2 + peak flow / PEFR
⚠️ Always do personalized asthma ac’n plan prior to discharge if pt = admitted for asthma exacerba’n !
Emergency Tx for children
1. Salbutamol inhaler via a spacer device → start w/ 10 puffs every 2 hrs
2. Nebulizer w/ salbutamol or ipratropium bromide
3. Oral prednisone
4. IV hydrocortisone
5. IV Mg SO4
6. IV salbutamol
7. IV aminophylline
8. ICU admiss’n for intuba’n + ventilator
Acute Complica’ns
MODERATE
- Peak Expiratory Flow Rate (PEF) 50-70% best or predicted → do measured / normal
- normal speech
- RR < 25/min
- HR < 110 bpm
SEVERE
- PEF 33-50% best or predicted
- can’t finish sentences
- RR ≥ 25/min
- HR ≥ 110 bpm
LIFE THREATENING (just 1 criteria = enough to make it life threatening !)
- PEF < 33% best or predicted
- O2sat < 92%
- Normal pCO2
- bradycardia / hypoTN / dysrhythmia
- exhaus’n / coma / confus’n
Chronic Complican’s
INTERMITTENT
- SSX < 1x/wk
- nocturnal SSX ≤ 2x/month
- PEF/FEV1 variability < 20%
- FEV1/PEF ≥ 80% predicted
MILD persistent
- PEF/FEV1 variability 20-30%
- FEV1/PEF ≥ 80% predicted
MODERATE persistent
- PEF/FEV1 variability ≥ 30%
- FEV1/PEF 60-80% predicted
- nocturnal SSX ≥ 1x/wk
SEVERE persistent
- PEF/FEV1 variability ≥ 30%
- FEV1/PEF ≤ 60% predicted
- frequent exacerba’ns
- frequent nocturnal SSX
- limited physical activity
Prognosis - improves after early childhood but can return in young adulthood
- Know for OSCE *
At which level does trachea bifurcate ? ✓
Trachea bifurcates into left + right main bronchi @ carina (T5)
Why are aspirated foreign bodies far more likely to enter + obstruct RIGHT bronchus ? ✓
B/c right main bronchus = wider, shorter + more vertical than left main bronchus
An object aspirated while standing or sitting upright will usually be found in the … ✓
Inferior por’n of right lower lobe
An object aspirated while supine will most often end up in the … ✓
Superior por’n of right lower lobe
How many lobes do the right + left lungs have ? ✓
Right = 3
→ upper/superior lobe
→ middle lobe
→ lower/inferior lobes
Left = 2
→ upper/superior lobe
→ lower/inferior lobe
How many fissures does each lung have ? ✓
Right lung has 2 fissures
→ Horizontal fissure btw superior + middle lobe
→ Oblique fissure btw middle + inferior lobe
Left lung has 1 fissure = Oblique fissure
Pleural Effus’n ✓
Def - when fluid collects in pleural space (space in btw parietal + visceral pleura)
→ empyema = infected pleural effus’n
⟹ pleural aspira’n will show pus, low pH, low glucose + high LDH = treated w/ chest drain + Abx
Types
- Exudative (has to have ≥ 1 of the following . . .)
→ Pleural protein : serum protein ratio > 0.5
→ Pleural LDH : serum LDH > 0.6
→ Pleural LDH > 2/3 of upper limit of normal serum LDH - Transudative → low protein content i.e < 30g/L
Exudative causes = inflamma’n causes protein to leak out of tissues + into pleural space i.e . . .
- TB
- RA
- pneumonia
- lung cancer
- mesothelioma
Transudative causes (fluid moves across or shifs into pleural space)
- congestive HF
- hypoTSH
- hypoalbuminemia
- Meigs syndrome = pleural effus’n + benign ovarian tumour + ascites
SSX
- cough
- chest pain
- u/l ↓ed breath sounds
- u/l dullness on percuss’n
- u/l ↓ed or absent tactile fremitus
- tracheal devia’n away from effus’n (in very large effus’n)
Ix’s
- CXR
→ blunting of costophrenic angle
→ fluid in lung fissures
- pleural U/S
- LDH + measure protein in serum + pleural fluid
- RBC of pleural fluid b/c >100,000 RBC/mm³ in PE / malignancy / trauma
- WBC of pleural fluid b/c lymphocyte > 90% = suggestive of either TB or lymphoma
- culture + pH of pleural fluid to check if it’s empyema
Tx
- if due to congestive HF = diuretic
- if empyema = empirical IV Abx → therapeutic thoracentesis (i.e drain) if pt gets worse
- if due to malignancy + pt has good performance status (i.e Karnofsky score > 30% or ECOG score of 0 or 1) = pleurodesis or intercostal drainage (pleural catheter drainage)
- if due to malignancy + pt has few yrs left to live or poor performance status (i.e Karnofsky score ≤ 30% or ECOG score ≥ 2) = therapeutic thoracentesis
Complica’ns
- atelectasis / lobar collapse
- pleural fibrosis (if was due to mesothelioma or TB)
Purpose of ciliated cells in trachea + bronchi ✓
To sweep mucus secre’ns + debris out of lungs + towards mouth
What are the func’ns of the 2 types of alveolar cells ? ✓
Type I Pneumocytes = to participate in gas exchange across alveolar-capillary membrane
Type II Pneumocytes
1) Regenerative cells of the lung i.e when lung damage occurs, they proliferate + have the ability to regenerate Type I cells
2) Contain foamy vesicles called lamellar bodies which continuously produce pulmonary surfactant that covers luminal surface of alveoli
Ventila’n v.s Diffus’n v.s Perfus’n ✓
- Ventil’an = process by which air moves in + out of lungs
- Diffus’n = spontaneous mov’nt of gases w/o the use of any E effort by the body btw alveoli + capillaries in lungs
- Perfus’n = process by which cardiovascular system pumps blood throughout lungs
Why does the trachea have rings of cartilage ? ✓
To prevent it from collapsing
Shape of Hgb - O2 dissocia’n curve ✓
Sigmoidal shape b/c of +ve cooperativity → when No O2 = bound, Hgb = in tense state aka hard for O2 to bind → but when 1st O2 binds it causes Hgb affinity for O2 to ↑ hence Hgb switches from tense to relaxed state + this continues until 4 O2 molecules = bound
Right + Left shifts in Hgb - O2 dissocia’n curve ✓
Right shift = RELEASE O2 to tissues
- ↓ pH i.e more acidic
- ↑ temp
- ↑ pCO2
- ↑ 2,3 DPG (crea’n of 2,3 DPG = favored in low pH)
Left shift = hold on to tissues
- ↑ pH
- ↓ temp
- ↓ pCO2
- ↓ 2,3 DPG
- CO b/c CO binding causes conforma’nal change that makes Hgb hold tightly to its O2; CO is also bad b/c it’s occupying binding spots that should have been for O2 so also ↓ O2-carrying capacity of Hgb
What is CarboxyHgb ? ✓
Hgb bound to CO
⚠️ Recall that Hgb binds to CO w/ 250x more affinity than it does O2 !
What is MetHgb ? ✓
Hgb w/ Fe3+ instead of Fe2+ ∴ can’t bind to O2 but has high affinity for CN- so pt can be given nitrates to treat CN- poisoning b/c MetHgb = caused by exposure to nitrates or dapsone
⚠️ Recall that Fe2+ is the only form of Fe that can bind to O2 !
Hypoxemia vs Hypoxia ✓
HYPOXEMIA = low O2 content in blood which can lead to HYPOXIA = when tissues are O2 starved
Shunt v.s dead space ✓
Both = mismatch btw ventila’n + perfus’n (V/Q) + hence gas exchange can’t take place
- Shunt = GOOD PERFUS’N but POOR VENTILA’N i.e lungs are doing their job but not enough air is coming in → paO2 ↓ + we get hypoxemia
⟹ ex’s : pneumonia, foreign body, food obstruc’n - Dead space = GOOD VENTILA’N but POOR PERFUS’N i.e air is coming in but lungs aren’t perfusing i.e P.E
⚠️ Dead spaces = normal in conducting zone but NOT in respiratory zone !
What are the 3 ways that CO2 is transported ? ✓
1- Bound directly to Hgb via N-terminus to form carbaminoHgb (makes up 5% of CO2 content in blood)
2- Dissolved in plasma (5%)
3- BICARBONATE BUFFER SYSTEM (90%)
a) CO2 produced by peripheral tissues enters erythrocytes through diffus’n where it combines w/ H2O to produce H2CO3 in a rxn catalyzed by carbonic anhydrase
b) H2CO3 instantaneously dissociates into H+ and HCO3- → generated H+ = buffered by deoxyHgb aka Hgb binds to free H+ ions
→ this buffering = important in maintaining pH in venous blood + RBCs w/in physiologic range
c) Finally, a large por’n of generated HCO3- moves outward from RBC into plasma in exchange for a chloride ion pumped inward (CHLORIDE SHIFT). Chloride shift happens in reverse when it’s time for CO2 to be expired through lungs
Neuron ac’n Ψ process ✓
- @ Rest = -70mV b/c of higher [Na ions] outside compared to inside (-ve means polarized); there’s more [K ions] inside than outside
- Stimulus causes voltage-gated Na channels in axon membrane to open → Na ions move down their [ ] gradient causing inside to become more +ve = DEPOLARIZA’N
- Depolariza’n travels along length of axon = Propaga’n *
- Na channels close + K channels open causing K ions to move out ∴ inside becomes -ve again
= REPOLARIZA’N - K channels open + close slowly so too many K ions diffuse out ∴ making inside way too -ve (aka more -ve than -70) = HYPERPOLARIZA’N / REFRACTORY PERIOD (no ac’n Ψ can occur during this period)
- K channels finally close → hyperpolariza’ n = corrected + inside goes back to initial resting Ψ
ABG Analysis ✓
- Hypoxemia = pO2 < 80 + O2sat < 95%
- Normal blood pH = 7.35-7.45
- Normal pCO2 = 35-45mmHg or 4.7-6.0 kPa
- Normal bicarb = 22-26mM
- pCO2 low = alkaline + high = acidic
- pH + pCO2 match = resp. acidosis / alkalosis
- pH + HCO3- match = meta. acidosis / alkalosis
- If the other value = normal then it’s UNCOMPENSATED, but if bicarb / pCO2 = abnormal as well, then we have RESP / RENAL COMPENSA’N *
- Know for OSCE *
Causes of metabolic acidosis + how to calculate anion gap ✓
⚠️ Lungs might compensate by HYPERventilating !
1) Keto-acidosis causes
- alcohol
- starva’n
- convuls’n
- high exercise
2) Excessive inges’n of toluene
3) Excessive loss of HCO3-
- diarrhea
- intestinal / biliary intuba’n
- addison’s disease
- fistula
4) Carbonic Anhydrase inhibitors
5) High anion gap causes (“MUDPILES”)
- MetOH
- Uremia i.e buildup of sulfates / nitrates / urates in blood that would normally be excreted in urine but aren’t b/c of renal insufficiency
- DKA
- Propylene glycol
- Isoniazid or Iron
- Lactic acidosis
- Ethylene glycol i.e antifreeze or EtOH
→ can cause uric acid crystals to precipitate in urine
- Salicylates (aspirin for ex)
⚠️ Anion gap = Na - (Chloride + Bicarb) = elevated if > 12
Causes of Metabolic Alkalosis ✓
⚠️ Lungs might compensate by HYPOventilating !
1) HCl loss
- vomiting
- NG suctioning
- intestinal fistulae
- antacid use
2) Excessive admin. of HCO3-
3) Hypovolemia
- thiazide diuretics
- loop diuretics
- dehydra’n
4) ↑ed renal acid secre’n
- K deple’n
- 2° HypoPTH
- diuretic therapy
- hyperaldosteronism
- exogenous mineralocorticoids
Causes of Resp. Acidosis ✓
ANYTHING CAUSING HYPOVENTILA’N !
- There could be renal compensa’n aka it attempts to ↑ bicarb *
1) Airway obstruc’n
- asthma
- COPD
- pneumonia
- bronchospasm
- laryngospasm
2) Resp. center depress’n
- anesthesia
- opioid / sedative / narcotic overdose
- brain tumor
3) Circulatory collapse
- cardiac arrest
- pulm. edema
4) Neurogenic
- MS
- myxedema
- cervical spine injury
- myasthenic crisis
- muscular dystrophy
- phrenic nerve injury
- paralytic agents / PO4’s
- Guillain Barré syndrome
5) Restrictive effects
- ARDS
- ascites
- obesity
- hydrothorax
- pneumothorax
Causes of Resp. Alkalosis ✓
ANYTHING CAUSING HYPERVENTILA’N !
- There could be renal compensa’n aka it attempts to ↓ bicarb *
1) Hypoxia
2) Lung Disease
- pneumonia
- P.E
3) CNS resp. stimula’n
- fever
- liver disease
- cerebral vascular accident or stroke
4) Anxiety / Panic attack / hyperventila’n syndrome
5) Pregnancy
6) Progesterone derivatives or salicylate intoxica’n
7) Hyperthyroidism
8) Delirium tremors
9) CHF
10) Sepsis
11) Peritonitis
12) Hepatic insufficiency
13) Mechanical ventila’n
CO poisoning ✓
- SSX = HA, confus’n, bright red cheeks
- Ix for diagnosis = ABG → will show low O2 satura’n + high carboxyHgb
The 3 fluid compartments ✓
2/3 ICF + 1/3 ECF (75% Interstitial Fluid + 25% Plasma)
The 3 types of dehydra’n ✓
- HYPOosmolal = losing LESS water aka more Na
→ ECF volume will ↓ in all 3 but especially in hypo b/c will get rid of water to make it more [ ]ed ∴ ICF volume will ↑
→ Plasma osmolarity will ↓ - HYPERosmolal = losing MORE water
→ ICF volume will ↓ b/c will try to give water to ECF
→ Plasma osmolarity will ↑ - ISOosmolal = losing both in same amts
→ ICF volume won’t change
Pathophys - ↓ in BP/ volume / hyperosmolarity
➔ ADH = secreted from posterior pituitary (thnx to hypothalamic osmo-receptors) ➔ water reabsorp’n ↑
➔ urine specific gravity + osmolality ↑ (urine will be more [ ]ed)
Tx = IV Hartmann’s solu’n
How does ORT work ? ✓
Uses SGLT-1= type of 1° active transport, specifically symport / co-transport of Na + glucose in jejunum
→ glucose uses E associated w/ Na to be uptaken against its [ ] gradient
Agonist vs Antagonist ✓
- Agonist = drug that binds to receptor to produce cellular response
→ Full Agonist = has full efficacy aka will produce 100% response ∴ = better for short term opioid Tx aka overdose but not for long term
→ Partial Agonist = less efficacy hence will never produce 100% response ∴ = better for long term opioid addic’n Tx
→ Inverse Agonist = binds to same receptor/binding site as endogenous agonist but produces “inverse” aka opposite effect as original - Antagonist = doesn’t directly produce a cellular response but instead BLOCKS effect of endogenous agonist
→ Surmountable Antagonism / Competitive = antagonist + endogenous agonist bind to same binding site so the one w/ the smaller kA will have > affinity + will win
→ will cause curve to shift to the right but W/O ↓ing max response
→ Insurmountable Antagonism = ↓ max response of endogenous agonist, doesn’t matter how much agonist is added, shifts curve to the right
⟹ Non-competitive = antagonist + endogenous agonist bind to diff sites
⟹ Irreversible = antagonist binds so strongly to binding site that it’s irreversible aka covalent binding (H2/ionic = reversible b/c = weak binding)
⚠️ Only agonists have efficacy b/c they produce a cellular response while antagonists don’t !
Sympathetic v.s Para (anatomy + chemical transmiss’n) ✓
SYMPATHETIC
- Neurotransmitter = Ach for pre + NE for all post except post that innervate sweat glands
- Effects . . .
→ dilate pupil, inhibit saliva produc’n, dilate bronchi, ↑ HR, inhibit GI organs (intestines / stomach / pancreas / gallbladder) + relax bladder i.e suppress bladder contrac’n + contract sphincters
PARASYMPATHETIC
- Neurotransmitter = Ach
- Effects . . .
→ constrict pupil, stimulate saliva produc’n, constrict bronchi, ↓ HR, stimulate GI organs, stimulate lacrima’n + contract bladder via contrac’n of detrusor muscle + relaxa’n of sphincters
What are the 4 receptor types ? ✓
- Inotropic/channel-linked = directly coupled to an ion channel
→ fast (millisecs) - G-protein coupled = single protein w/ 7 transmembrane domains
→ slower than ionotropic
→ most receptors fall w/in this category
a) Adenergic R’s = receptors that bind epinephrine / adrenaline + norepinephrine
- 𝛼1 = cause vascular smooth muscle contrac’n aka vasoconstric’n + pupillary dilator muscle contrac’n + intestinal / bladder sphincter muscle contrac’n (norepinephrine mainly binds to these)
- 𝛼2 = inhibit sympathetic aka inhibits insulin release/lipolysis/humour produc’n
- β1 = ↑ HR (on SA node) + contractility (on ventricular cardiomyocytes) + renin release + lipolysis
- β2 = activate smooth muscle relaxa’n in vessels + bronchi aka vasodila’n + bronchodila’n + lipolysis + cellular uptake of K + humour produc’n
- β3 = breakdown of fat aka lipolysis, thermogenesis in skeletal muscle + bladder relaxa’n
b) Choligernic R’s = receptors that bind Ach
→ Muscarinic (mainly activate para) = G-protein coupled, efflux of K + influx of Na/Ca
⟹ M1 = enteric NS
⟹ M2 = ↓ HR (on SA node) + ↓ contractility (on cardiomyocytes)
⟹ M3 = in bladder + trachea / bronchioles smooth muscle → cause broncho-constric’n
→ Nicotinic (both symp + para) = ligand ionotropic receptor
⟹ Nn (n = for “neuro” aka autonomic ganglia + adrenal medulla)
⟹ Nm (m = for “NMJ” of skeletal muscle)
- Tyrosine-kinase linked receptors, ex = insulin
→ slow response but not as slow as nuclear receptors - Nuclear receptors = intracellular while the others = transmembrane, ex = levothyroxine
→ ligands of these receptors have to be hydrophobic b/c are intracellular
→ regulate gene express’n
→ slowest response of the 4
Microcytic v.s Normocytic v.s Macrocytic Anemia ✓
Anemia = ↓ [ ] Hgb / Hematocrit / RBC count below normal range for age + sex
→ Men = Hgb < 13 g/dL
→ Non-pregnant women = Hgb < 12 g/dL
→ Pregnant women + Children ≤ 5 y/o = Hgb < 11 g/dL
Ψ SSX
- pale conjunctiva + mucous membranes
- brittle nails / koilonychia (spoon nails) / platonychia (flat nails)
- skin dryness
- brittle + dry hair
- weakness / fatigue
- SOB during exercise
- hypoTN / feeling faint
- angular cheilitis, painful glossitis, atrophic gastritis (in Fe deficiency anemia)
- Microcytic = MCV < 80 (causes = “TAIL”)
- Thalassemia = normal ferritin + the microcytic anemia is NOT new
- Anemia of chronic disease = high ferritin + the microcytic anemia is new
→ ex’s - RA, temporal arteritis, chronic infec’n / inflamma’n, rare causes like renal cell carcinoma, Hodgkin lymphoma, Castleman disease + myelofibrosis - Iron deficiency = low ferritin ➔ RBC shape will be normal, color will be pale b/c it’s hypochromic + like all microcytic anemias RBC size will be small
⚠️ Hgb should ↑ by > 20 after taking Fe supplement for > 3-4 wks so if that’s not the case suspect drug interac’n !
→ Causes of Fe deficiency:
⟹ ↓ed intake - poor diet or vegetarian diet
⟹ ↑ed demand - pregnancy / infants / puberty
⟹ Malabsorp’n - gastrectomy / celiac
⟹ Blood loss
a) Genitourinary tract
→ endometrial polyp = most frequent cause of Fe deficiency in pre-menopausal women
→ metrorrhagia = bleeding in btw periods (usually in puberty or close to menopause)
→ hematuria
b) GI tract = most frequent cause of Fe deficiency in adult men + post-menopausal women
→ esophageal varices
→ diaphragmatic hernia
→ gastric ulcer
→ chronic aspirin use
→ neoplasm / cancer
→ UC
→ diverticular disease
- Lead poisoning
- Normocytic = MCV w/in normal range aka 80-100
➔ Hemolytic / Hyperproliferative
= high reticulocyte count, ex: sickle cell, hem. anemia (can be inherited or acquired)
> Hemolysis = pre-mature peripheral RBC destruc’n , typically seen when life span ↓ from 120 days to < 30 days → doesn’t always cause anemia b/c bone marrow can compensate by ↑ing RBC produc’n (= known as compensated hemolytic disease)
→ can be intravascular (= pathological + usually acute + FATAL, happens in snake bites for ex) OR extravascular = excacerba’n of physiological process, usually chronic + NOT FATAL except if excess bilirubin crosses BBB
⟹ intravascular SSX = Schistocytes i.e fragmented RBCs w/ a helmet or triangular shape + Hbemia + Hburia b/c of ↓ed haptoglobin
⟹ causes of intravascular hemolysis . . .
a) Membrane pb i.e cytoskeleton defects = Coombs -ve
⟹ hereditary spherocytosis = ankyrin or spectrin deficiency or band 3 abnormality
⟹ hereditary ellipsocytosis = a + b spectrin defects
b) Hgb pb i.e abnormal structure like in SCD OR imbalance in globin chains synthesis like in thalassemia
c) Enzymopathies
→ pyruvate deficiency
→ glucose-6 PO4 dehydrogenase (G6PD) deficiency = X-linked
⚠️ G6PD = necessary b/c protects RBC from endo + exogenous oxidants ∴ w/o it, oxidizing agents convert Hgb to MetHgb (Fe3+ heme group) ∴ RBC = denatured + precipitates as Heinz bodies
⟹ extravascular hemolysis SSX = jaundice + hyperbilirubinemia + high LDH
⟹ causes of extravascular hemolysis . . .
a) Immune pb i.e antibody attack on RBC
> Autoimmune
→ AIHA = Coombs +ve (direct coombs) → Coombs = a type of direct antiglobulin test
⟹ RBC morphology = polychromasia, macrocytes, nucleated RBCs, spherocytes, agglutina’n + high reticulocyte count
⟹ warm reacts w/ RBC at 37°C + cold at 4°C, usually IgG antibodies for warm
⟹ Tx for warm AIHA = transfus’n
→ Cold AIHA gets worse in low temps ∴ Tx = treat underlying condi’n + avoid cold weather
→ CAD (Cold Agglutin Disease) = self-limiting usually (= IgM antibodies w/ complement activa’n)
→ PCH (Paroxysmal Cold Hburia) = severe + sometimes fatal (= IgG antibodies w/ complement activa’n)
> Alloimmune i.e transfus’n rxn / HDFN / marrow transplant → ex = pt w/ blood group A = transfused w/ incompatible blood of group B
b) Drug associated
c) RBC mechanical trauma (≠ immune i.e no antibody involv’nt) → will appear as fragmented cells or schistocytes on blood film (for MAHA)
d) Micro-angiopathic hemolysis (MAHA) i.e TTP (thrombotic thrombocytopenic purpura) / DIC (Disseminated intravascular coagula’n) / HELLP / HUS (Hemolytic uremic syndrome)
→ MAHA has 90% mortality, Tx = plasma exchange
e) Valve hemolysis = usually due to artificial heart valves, grafts or perivalvular leaks
f) March Hburia = RBC damage btw small feet bones due to prolonged marching / running
g) Infec’ns like malaria or clostridia
➔ Non-hemolytic / Hypo-proliferative
= low reticulocyte count
= aplastic anemia or anemia of chronic disease
- Macrocytic = MCV > 100
a) Megaloblastic → will show hyper-segmented neutrophils aka > 5 segments
= due B9 OR B12 deficiency OR drug
- Causes of B9 def
→ ↓ed intake i.e poor diet
→ ↑ed demand such as . . .
⟹ neonates
⟹ pregnancy (supplemental folic acid = given ≥ 1 month prior to concep’n + during early pregnancy to ↓ risk of neural tube defects)
→ Anti-folate drugs such as . . .
⟹ hydroxyurea
⟹ methotrexate
⟹ sulfonamides
⟹ anti-convulsants like phenytoin
→ Malabsorp’n such as . . .
⟹ chronic alcohol overuse
⟹ jejunum resec’n
⟹ jejunum pathologies like steatorrhea, celiac disease + tropical sprue
b) Non megaloblastic → will show NORMAL OR HYPO-segmented neutrophils on blood smear
→ NORMAL = due to alcoholism, liver disease, hypoTSH, hemolysis or drugs
→ HYPO = due to myelodysplastic syndromes
- Causes of B12 def
→ ↓ed Intake i.e poor diet
→ Malabsorp’n (achlorhydria i.e stomach can’t produce HCl, alcoholism, etc)
→ Intrinsic factor deficiency → Intrinsic Factor = secreted by parietal cells + forms complex w/ B12 to transport it to ileum for absopr’n + protect it from digest’n by GI enzymes
⟹ pernicious anemia = most common cause of B12 deficiency = autoimmune disease that causes destruc’n of parietal cells or IF via anti-parietal or anti-IF antibodies, only Tx = life long parenteral IM B12 injec’ns (1mg/wk + then monthly)
⟹ gastrectomy / gastric bypass Sx
⟹ congenital IF def
→ small intestine disease
⟹ small intestine resec’n (b/c of absence of terminal ileum)
⟹ Crohn’s (b/c of absence of terminal ileum just like surigcal resec’n)
⟹ tropical sprue
→ Small intestine parasites + bacteria
⟹ diphyllobothrium latum / fish tapeworm
⟹ blind loop syndrome = shorter small intestine due to bacteria overgrowth in intestine
⟹ diverticulosis
→ Drugs . . .
⟹ NO
⟹ PPI
⟹ Metformin
⟹ Colchicine
⟹ Neomycin
⚠️ Prolonged B12 deficiency will cause IRREVERSIBLE nerve damage !
SSX of B12 deficiency ✓
+ve Romberg’s
- numbness or tingling
- reduced vibra’n sense
- impaired jt posi’n sense up to ankles
- normal knee jerk reflex but ankle reflex = absent
- normal tone but both dorsiflex’n + plantar flex’n = weak
Blood smear terminology ✓
- Hypochromia = pale RBCs b/c contain less Hgb
➔ in microcytic anemia - Hyperchromia = presence of hyper-segmented neutrophils, bilirubin + LDH will be ↑ed
➔ in macrocyclic anemia - Anisocytosis = varia’n in RBC sizes, FBC will show ↑ed RDW
➔ in Hbopathies or myelodysplastic syndromes - Poikilocytosis = varia’n in RBC shapes = HAS TO BE THALASSEMIA
- Tear drop shape on blood smear means pb = bone marrow itself *
Central v.s peripheral type anemia ✓
- Central type = pb = bone marrow itself
→ ex’s = leukemia, aplastic anemia, myelofibrosis, myelodysplastic syndromes - Peripheral type = pb ≠ bone marrow itself but something else such as lack of nutrients in blood, kidney failure, EPO deficiency, ↑ed destruc’n due to hypersplenism / autoimmune / Hbopathy or blood loss i.e menstru’an / pathological bleeding
Structure of Fetal + Adult Hgb ✓
- Fetal Hgb = 2 𝛼 + 2 γ chains, can’t bind as well to 2,3 DPG ∴ has higher O2 affinity b/c 2,3 DPG can’t ↓ Hgb affinity for O2
- Adult Hgb = 2 𝛼 + 2 β chains, each chain = linked to heme group (Fe2+) that an O2 molecule can bind to, so 4 O2 molecules max can bind to 1 Hgb
4 types of hypersensitivity rxns ✓
ANTIBODY MEDIATED
- Type 1 = basically like acute inflamma’n w/ mast cells + IgE + Th2 cells = immediate response (= for allergic rxns i.e asthma / anaphylaxis)
- Type 2 = opsoniza’n + phagocytosis- w/ IgM or IgG
= for cell bound antigens
ex’s: organ rejec’n (via cytotoxic T cells), Grave’s, myasthenia gravis - Type 3 = complex mediated (complexes of IgM/IgG)
ex’s: RA, SLE, reactive arthritis, polyarteritis nodosa
T-CELL MEDIATED
- Type 4
ex: TB, MS, scabies, Guillain-Barre, Mantoux test
Anaphylaxis ✓
Def - most severe form of an immediate hypersensitivity rxn (= Type 1 rxn)
Eti = exposure to allergen i.e food (1/3 of cases), drugs, insect sting, latex
→ most common triggers = nuts, fish + shellfish, eggs + milk
→ kids that have milk + egg allergy usually outgrow them whereas fruit or seafood allergy tend to stay forever
→ bee sting leaves stinger whereas wasp sting DOES NOT leave stinger !
Pathophys - allergen = introduced into body by ingest’n / inhala’n / parenteral or skin contact → on 1st exposure, plasma cells of susceptible person make IgE antibodies specific to that antigen
→ IgE antibodies attach to high-affinity Fc receptors on basophils + mast cells
→ on subsequent exposure, binding of antigen to IgE antibodies leads to bridging + triggers degranula’n of mast cells
SSX
- SOB
- hypoTN
- pruritus
- urticaria
- erythema
- airway swelling
- angioedema i.e swelling of deeper tissues such as as eyelids, lips, mouth
⚠️ ≥ 1 of the ABC’s has to be affected for it to be anaphylaxis !
Ddx
- asthma
- septic shock
- panic disorder
- cardiogenic shock
- hypovolemic shock
- foreign body aspira’n
- acute COPD exacerba’n
Ix’s
- ABG to check for elevated lactate
- mast cell tryptase → will be high, normally = undetectable in healthy person who hasn’t had anaphylaxis in the past hrs
→ should be done NO LATER later than 4 hrs later ! - skin prick test
⚠️ Make sure pt hasn’t put lo’n or cream on inner forearm + that they didn’t take histamines or steroids
- Mark areas w/ pen or marker + include +ve + -ve control
→ +ve control = histamines + -ve control = water - Apply 1 drop of each allergen / control on their marked spot
- Prick each of those spots (use diff needle for each spot)
- Press entire forearm w/ paper towel
- Wait 15 mins + analyze results
→ +ve control should have rxn + -ve control should have NOTHING !
Emergency Tx = IM Adrenaline / Epinephrine (0.5 mg)
→ remove cap → stab needle in lateral thigh → count for 10 secs → Repeat after 5 mins if there’s no improv’nt
→ Epinephrine MOA - vaso-constric’n to maintain BP + divert blood away from skin, ↓ throat swelling which opens airways + prevents further release of histamine
Tx after stabiliza’n = oral antihistamines
- Know for OSCE *
COPD ✓
Def - PROGRESSIVE IRREVERSIBLE airway obstruc’n = usually due to cigarette smoking but interestingly, only a minority of smokers will actually develop COPD
RFs
- advanced age
- cigarette smoking → inactivates 𝛼1 antitrypsin in lungs, which leads to ↑ed ac’n of elastases → ↑ed breakdown of elastic tissue
- 𝛼1 antitrypsin deficiency (genetic) → causes lack of antiprotease
→ COPD, chronic bronchitis + emphysema have common clinical features b/c they all share the common trigger of SMOKING !
→ chronic bronchitis = productive cough for 3 consecutive months for 2 consecutive yrs
→ emphysema = permanent dilata’n of airways distal to terminal bronchiole
Pathophys in small airways - chronic inflamma’n → healing by fibrosis → airway stenosis
Pathophys in resp. bronchioles - destruc’n of walls w/ loss of elastic tissue but W/O sig fibrosis → airway dilata’n + emphysema
Pathophys in terminal bronchioles - irritant i.e smoking causes inflammatory response → neutrophils + macrophages = recruited to release inflammatory mediators such as oxidants + proteases → protease-mediated destruc’n of elastin → loss of elastic recoil → airway collapse during exhala’n → incomplete exhala’n → ↑ in CO2 + chest hyperinfla’n due to trapped air
SSX
- barrel chest
- SOB due to airway obstruc’n
- hyper-resonance on percuss’n
- coarse crackles + wheezing on ausculta’n
- sputum produc’n due to hyperplasia of mucus-producing glands in submucosa + of goblet cells on surface epithelium
→ productive cough = earliest SSX of COPD + if pt continues smoking . . .
⟹ sudden SOB upon exer’n
⟹ disease advances
⟹ SOB upon min. exer’n
⟹ disease advances
⟹ SOB at rest
⚠️ Cough + sputum present means LARGER airways = involved v.s SOB present means SMALLER airways = involved
Ddx
- TB
- CHF
- Asthma
- Lung cancer
- Bronchiectasis
Ix’s
- FBC → might show polycythemia = ↑ed hematocrit i.e > 55% due to ↑ed EPO produc’n
⟹ can cause myelofibrosis = when bone marrow becomes fibrotic therfoer liver + spleen have to take over RBC prodc’n + hence they become enlarged - O2 sat = 88-92% b/c they require hypoxic drive to breathe
- ABG to check for resp. failure
→ their ABG might show normal pH but bicarb will be really high - 𝛼1 antitrypsin level in pts w/ FHx of COPD or atypical COPD pts i.e young or non-smoker
- Spirometry for diagnosis → should show that there’s airflow obstruc’n
- CXR
→ CXR Findings (“FEBS”) . . .
- Flattened diaphragm i.e loss of sharp borders
- Eight anterior ribs (indicates hyperinfla’n b/c usually only up to 6 = visible)
- Barrel shaped on lateral view due to retrosternal air trapping
- Stretched out heart (heart looks like it was pulled vertically)
Emergency Tx = SABA
Regular Tx
- Smoking cessa’n therapy + both pneumococcal / influenza vaccina’ns + pulmonary rehab if they had an exacerba’n
- inhaled SABA or SAMA
- What to add if pt is still symptomatic . . .
→ if FEV1 >50% = inhaled LAMA or LABA
→ if FEV1 <50% = Inhaled LAMA or LABA+ICS - If still symptomatic add LABA+ICS or if already on LABA+ICS add LAMA
- Theophylline
Short Term Complica’ns
- respiratory failure
- acute exacerba’n = sustained worsening in pt’s SSX beyond normal day to day varia’n such as worsening of SOB or cough or ↑ed sputum produc’n = most commonly caused by infec’n but can also be caused by . . .
→ P.E
→ LVF
→ pneumothorax
→ lung carcinoma
⚠️ In an infective exacerba’n of COPD, focus of infec’n = airways v.s in pneumonia = alveoli
→ CXR in COPD = clear lung fields v.s in pneumonia = consolida’n
Long Term Complica’ns
- lung cancer
- cor pulmonale
→ initially RV will undergo hypertrophy to compensate, but eventually will decompensate - Know for OSCE *
Pneumonia ✓
Def - inflamma’n of lung parenchyma / alveolar space due to an infective agent
→ aspira’n pneumonia = when infec’n develops due to aspira’n of food or fluids = usually in pts w/ impaired swallowing i.e demented or after stroke = associated w/ anerobic bacteria
RFs
> 65 y/o
- COPD
- alcohol abuse
- poor oral hygiene
- contact w/ children
- use of acid-reducing drugs
- resides in healthcare facility
- exposure to cigarette smoke
Eti
- viral
- fungal
- bacterial = most common
→ hospital acquired pneumonia = when pt gets pneumonia ≥ 2 days after they’ve been admitted to hospital, 60% of cases of HAP = due to gram -ve bacteria such as . . .
- E.coli
- S.aureus
- Hemophilus (green sputum)
- Pseudomonas (green sputum)
- S. pneumoniae (rust colored sputum)
- Klebsiella (red currant jelly sputum)
→ causes aspira’n lobar pneumonia in pts w/ alcohol overuse + diabetes mellitus
→ CAP = when pt gets pneumonia outside of hospital i.e in everyday life
⟹ most common cause of community acquired pneumonia = streptococcus pneumonias / pneumococcus
⟹ can also be caused by atypical bacteria such as mycoplasma pneumoniae, chlamydophila pneumoniae, chlamydia psittaci + coxiella burnetii
Atypical pneumonia = pneumonia caused by organisms that can’t be detected via gram stain or cultured in the normal way
→ Eti = “ Legion of psittaci MCQs “
– Legionella pneumophila
– Chlamydia psittaci
– Mycoplasma pneumoniae
– Chlamydophila pneumoniae
– Q fever i.e coxiella burnetii
SSX
- SOB
- fever
- chills
- productive cough
- consolida’n on CXR
- coarse crackles + dullness on percuss’n due to lung tissue either collapsed or filled w/ sputum
Subtypes (can only classify on autopsy)
- Lobar pneumonia = characterized by diffuse inflamma’n affecting entire lobe(s)
→ may present w/ pleuritic chest pain that gets worse when pts cough + the regular pneumonia SSX - Bronchopneumonia = characterized by b/l (most of the time) widespread patchy inflamma’n = centered on airways
Ddx
- TB
- P.E
- CHF
- Covid
- Lung cancer
- Emphysema
- Pneumothorax
- Acute bronchitis
- COPD / Asthma / Bronchiectasis exacerba’n
Ix’s
- sputum culture
- CRP → will be high
- FBC → WCC will be high
- CXR → will show consolida’n
- CURB 65 score = used to asses severity of community acquired pneumonia
→ C = sudden onset of confus’n
→ U = Urea > 7 mmol/L
→ R = RR ≥ 30
→ B = BP < 90 (sys) or ≤ 60 (dia)
→ 65 = ≥ 65 y/o
→ give 1 point if pt has it + then tally the points
⟹ 0-1 point = outpt Tx at home
> 2 points = admit to medical ward
≥ 3 points = admit to ICU b/c risk of death ↑ as score ↑
Tx for CAP
- for low or moderate severity
= amoxicillin for 5 days
→ doxycycline or clarithromycin instead for atypical pneumonia or if pt has penicillin allergy - for high severity = co amoxiclav + clarithromycin / erythromycin
→ levofloxacin instead if pt has penicillin allergy
Complica’ns
- septic shock
- heart failure
- pleural effus’n
- acute respiratory distress syndrome (ARDS)
⚠️ Recall that consolida’n = when air in lungs = being replaced by something else i.e less black + in pneumonia that “something else” is acute inflammatory EXUDATE + in pulm. edema it’s TRANSUDATE !
⚠️ Be specific when describing consolida’n on CXR i.e right middle lobe consolida’n
- Know for OSCE *
What pts are at risk of aspira’n pneumonia ? ✓
- septic pts w/ ↓ed consciousness
- intoxicated pts i.e alcohol overuse
- acute stroke pts w/ impaired swallowing
Inspira’n v.s Expira’n ✓
Inspira’n v.s Expira’n
- Inspira’n = diaphragm contracts / pulls down + external intercostal muscles contract which moves ribs up + out → lung volume ↑ → pressure ↓ → air moves in (from high to low pressure)
- Expira’n = external intercostal muscles relax which moves ribs down + in, diaphragm relaxes/moves upward + internal intercostal muscles contract → lung volume ↓ → pressure ↑ → air moves out (from high to low pressure)
Resp. Failure ✓
Def - impaired gas exchange btw lungs + blood ∴ causing hypoxia (w/ or w/o hypercapnia)
Type 1 = Hypoxemia
Type 2 = Hypoxemia + Hypercapnia
RFs
- cardiac failure
- pneumothorax
- airway obstruc’n
- pulmonary infec’n
- cigarette smoking
- toxic fumes + gases
- chronic lung disease
- alveolar abnormalities
- perfus’n abnormalities
- hypercoagulable states
- opioid / sedative medicines
- traumatic spinal or thoracic injury
Eti
Resp. causes
- P.E
- Pneumonia
- Bronchiectasis
- Pneumothorax
- Acute epiglottitis
- Pulmonary edema
- Acute asthma exacerba’n
- ARDS including from Covid infec’n
- Alveolar abnormalities such as emphysema or Goodpasture’s syndrome
- Chronic lung disease such as COPD, CF, pulmonary fibrosis, chronic interstitial lung disease
Non resp causes
- Severe anemia
- Shock (septic and/or cardiogenic)
- Poisons such as chlorine gas or CO
- Drug overdose (opioids or sedative medicines)
- Hypovolemia (from hemorrhage or dehydra’n)
- Neuromuscular disorders such as Guillain-Barre, myasthenia gravis, muscular dystrophy, poliomyelitis
Traumatic causes
- Blood loss
- Spinal injury
- Direct thoracic injury
Ix’s = O2sat + ABG
Emergency Tx = mechanical ventila’n
- Know for OSCE *
1° Lung Cancers ✓
1) Def, RFs, Eti, Pathophys, SSX, Diagnostic Criteria, Ddx, Ix, 1st line Mx, Complica’ns
2) Lung nodule classifica’n
3) Define paraneoplastic syndrome + explain the pathophys of SIADH in small cell carcinoma
4) Describe the clinical presenta’n of Pancoast + Horner’s syndrome
5) Briefly outline the pathology of malignant mesothelioma, highlighting its associa’n w/ asbestos exposure + its dismal prognosis
- Epi
- lung cancer = 2nd most common cancer in the UK + peak incidence = 50-60 y/o
- 80-90% of cases can be attributed to cigarette smoking b/c contain carcinogenic compounds like benzopyrene
- asbestos alone ↑ risk of lung cancer + has synergistic RF effect when combined w/ smoking
Types of lung cancers
- majority = carcinomas
→ carcinoma of the lungs = most likely to metastasize to adrenal glands - 40% = adenocarcinoma = most common type of lung cancer in NON-SMOKERS !
→ tends to arise in peripheral smaller airways + mainly affects women
→ pre-malignant les’n for this = called atypical adenomatous hyperplasia = asymptomatic - 25% = SCC = strongly associated w/ smoking
→ tends to arise in larger airways near lung hilum
→ pathophys = metaplasia → dysplasia → carcinoma - 15% = small cell lung carcinoma
= highly aggressive tumor b/c of rapid growth rate + early spread
→ there’s no grading for this b/c = automatically high grade
→ unlike adenocarcinoma doesn’t have pre-malignant les’n
→ has the strongest associa’n w/ smoking out of all the types
→ usually arises in a central loca’n - 10% = large cell carcinoma
= undifferentiated carcinomas that can’t otherwise be categorized microscopically i.e lack morphological features of the other forms of lung cancer - the others = carcinoid / large cell neuroendocrine carcinoma
SSX
- cough
- SOB due to airway obstruc’n
- hemoptysis b/c of bleeding from tumor
- chest wall pain due to chest wall invol’vnt
- stridor / wheeze on insipra’n due to upper airway obstruc’n
- hoarse voice due to invas’n of left recurrent laryngeal nerve
- SVC obstruc’n b/c of pressure exerted by tumor → blood flow = obstructed → venous pressure ↑ + we get interstitial edema + retrograde collateral flow → collateral venous systems i.e azygous venous system / internal mammary venous system / long thoracic venous system try to pick up the slack but venous pressure still remains high = oncological emergency ! → give dexamethasone to ↓ tumor swelling
Staging = TNM
→ use CT scan for T + PET / PET-CT for N + M
Tx = small cell lung carcinoma v.s all the others
→ chemo for small cell b/c Sx = ineffective
→ chemo as well for the others but can use Sx if stage = low
- Lung nodules
- lung nodule > 20 mm = 81% chance it’s cancer
- lung nodule 8-20 mm = 15% chance it’s cancer
- lung nodule 4-7 mm = 1% chance it’s cancer
- lung nodule < 4 mm = 0% chance it’s cancer
- Paraneoplastic syndrome
= syndrome (i.e. collec’n of SSX) caused by substances produced by tumor cells that act remotely from the tumor itself
= common in lung cancers especially small cell lung carcinoma
→ ex 1- produc’n of PTH-related peptide by tumor cells → causes Ca to be released from bone into bloodstream hence SSX = HyperCa SSX
→ ex 2 - SIADH = produc’n of ADH by tumor cells
→ ex 3 - ACTH secre’n by tumor cells
→ will cause b/l adrenal cortical hyperplasia → cortisol produc’n will ↑ hence SSX = thirst + polyuria = features of cushing’s syndrome (pt usually dies before those manifesta’ns happen)
→ ex 4 - Lambert Eaton Myasthemic Syndrome (LEMS) = auto-antibodies block voltage gated Ca channels in presynaptic membrane ∴ blocking release of Ach
- Pancoast’s tumor = cancer in apex of lung involving 8th cervical nerve +
1st + 2nd thoracic nerves
→ can manifest as Pancoast’s syndrome = shoulder pain radiating in an ulnar distribu’n down the arm OR as Horner’s . . .
→ Signs of Horner’s = “PAME”
- PTOSIS (drooPY eyelid)
- ANHYDRIOSIS
- MIOSIS (constricted pupil)
- ENOPHTHALMOS (eyeball sinks inwards)
⚠️ Horner’s = ipsilateral
- Mesothelioma = malignant tumor of the pleura associated due to asbestos exposure
- has long latency period btw time of exposure + tumor develop’nt
- usually occurs in 60 y/o men
- SSX = SOB + chest pain +/- pleural effus’n
- diagnosis = made by cytological examina’n of pleural fluid OR histological examina’n of pleural Bx
- tumor spreads extensively w/in chest wall + eventually encases entire lung
- has no grade b/c by defini’n = highly aggressive
- prognosis = 18 months after diagnosis
- Know for OSCE *
Diffuse parenchymal lung diseases ✓
Def - large group of condi’ns characterized by inflamma’n centers on interstitium of alveolar walls
→ ex = asbestosis - diffuse fibrosis of lung parenchyma due to exposure to very high levels of asbestos
→ main SSX = gradually worsening SOB + eventual chronic respiratory failure
Eti
- idiopathic such as idiopathic pulmonary fibrosis
- pneumoconiosis i.e inhaling inorganic/mineral dusts like coal, silica or asbestos
- extrinsic allergic alveolitis or hypersensitivity pneumonitis
- side of effect of drugs like bleomycin or amiodarone or chest radia’n
- multi system diseases like sarcoidosis or SLE that can also involve lung
Pathophys - expans’n of interstitium by an inflammatory cell infiltrate i.e pneumonitis or alveolitis
→ gas exchange = impaired + we get SOB
⟹ episodes of alveolitis or pneumonitis might be followed by complete regenera’n i.e no residual damage to alveoli but in some instances, inflamma’n = followed by repair + scarring . . .
» release of fibrogenic cytokines by macrophages → collagen = secreted
→ scar tissue develops → over time scarring destroys func’nal units of lungs + as a result, lungs = converged into a mass of cystic air spaces separated by dense scarring = HONEYCOMB LUNGS
Ix = spirometry → will show restrictive effect
Complica’ns
- cor pulmonale
- fibrosis of lung tissue → oblitera’n of pulmonary arterioles + capillaries → gradual pulmonary HTN
What is interstitium ? ✓
Tissue that lies btw alveoli + contains pulm. artery capillaries = thin which is good b/c allows alveoli + capillaries to lie very close to one another ∴ ensuring optimal gas exchange
Pulmonary TB ✓
Def - infectious disease caused by Myobacterium TB = NOTIFIABLE DISEASE !
→ TB = small slow growing acid-fast rod-shaped bacillus w/ thick lipid-rich cell wall
→ = transmitted by air droplets i.e coughing / sneezing / talking + can only infect humans
→ can get reactivated after several months or yrs
→ even if sick person leaves room, room remains infectious for 30 mins
→ usually transmitted indoors + not outdoors b/c Myo TB = killed by UV light
RFs
- elderly
- HIV +ve
- alcohol
- silicosis
- apical fibrosis
- diabetes mellitus
- immunosuppressive medica’n
- born in endemic reg’n i.e Africa / Asia / Latin America
Pathophys - myo TB infects upper por’n of lower lobe of lung i.e apex → it gets engulfed by alveolar macrophages but doesn’t get destroyed thnx to cord factor which is a glycolipid in TB’s cell wall that’s directly cytotoxic to macrophages + prevents intracellular killing by phagocytic cells by preventing fus’n of vesicles containing the bacterium w/ lysosomes
→ over time fibrous scar develops around les’n which can be further calcified
→ les’n called Ghon focus = produced
→ Ghon focus + lymph node les’n form Ghon complex = calcified scar in lung parenchyma + hilar lymph node
→ cell mediated immune response (via Th1 cells) controls infec’n but leads to overproduc’n of TNF γ ∴ causing macrophages to damage healthy tissue
→ like in other chronic inflamma’ns we get forma’n of a granuloma = spherical collec’n of epitheloid macrophages w/ a small area of central necrosis
= formed to contain bacterium in an anoxic + acidic env’nt → that center undergoes liquefica’n + coagulate necrosis which produces caseous necrosis (also destroys healthy tissue)
→ caseous necrosis = unique to TB → if caseous necrotic material reaches lymph or bloodstream can cause miliary TB
→ can get ACTIVE TB if pt = immunosuppressed OR has inadequate T-cell immunity
⚠️ Latent TB can progress to active TB !
SSX
- chills
- fever
- anorexia
- no appetite
- hemoptysis
- night sweats
- uveitis sometimes
- weakness or fatigue
- persistent dry cough for ≥ 3wks
- cachexia (i.e weight loss + muscle wasting)
- asymptomatic in the case of latent TB
Ddx
- CAP
- Covid
- sarcoidosis
- lung cancer
- fungal infec’n
- non-tuberculous mycobacteria
Ix’s
- Interferon γ blood test
- 3 sputum samples for smear (i.e ZN stain) + culture or 3 gastric aspirates in children
→ smear will detect acid-fast bacillus
→ culture will tell us exactly what acid fast bacillus it is
1-3 wks for visible growth on liquid media
⟹ 3-8 wks for visible growth on lowenstein jensen solid media
⟹ Pts w/ +ve sputum smear = HIGHLY CONTAGIOUS
⟹ -ve sputum smear but +ve culture = CONTAGIOUS but not as much as above
⟹ -ve sputum + -ve culture = NON CONTAGIOUS - CXR Findings (“CREG”)
→ Cavities in lung apices (i.e upper lobe consolida’n)
→ Ranke complex (= calcified Ghon complex + calcified mediastinal lymph nodes = seen in healing TB infec’n)
→ Enlarged lymph nodes in left or right hilum of lung
→ Ghon’s complex (seen in UNTREATED TB infec’n)
Tx = “RIPE” i.e quadruple therapy of rifampicin, isoniazid, pyrazinamide + ethambutol (1st 3 = hepatotoxic)
→ RIPE for 2 months
→ R + I = for 4 addi’nal months
⟹ for 10 addin’al months instead if pt has CNS involv’nt
- rifampicin MOA = inhibits RNA synthesis
→ side effect = red/orange body fluids (not dangerous) - isoniazid side effect = peripheral neuropathy i.e numbness / tingling in hands + feet
⟹ pyridoxine (vit B6) = co-prescribed w/ it to ↓ risk of peripheral neuropathy - pyrazinamide side effects = muscle/bone pain + gout/kidney stones b/c causes hyperuricemia
- ethambutol side effects = color blindness or ↓ in visual acuity
TB notifica’n process (TB = notifiable disease so as soon as pt = diagnosed must do contact tracing w/o delay !)
1. Notify closest + most prolonged contacts (this will usually be household contacts)
2. Widen circle until there’s no evidence of transmiss’n
3. WGS (whole genome sequencing) for relatedness
4. Screening contacts for latent + active TB
5. Vaccinate those contacts if no C/I + treat those who are actively infected
- Know for OSCE *
What is DOT for TB ? ✓
DOT = Direct Observed Therapy = HCP provides undeserved groups like homeless ppl, prisoners, drug users + vulnerable migrants w/ TB Tx by watching them swallow to ensure compliance
Sarcoidosis ✓
Def - chronic non-caseating granulomatous disease that often affects lungs, if untreated can progress to pulm. fibrosis + restrictive lung physiology
→ r/o exposure to beryllium b/c berylliosis has same SSX as sarcoidosis
→ disappears in most pts after 2 yrs
RFs
20-50 y/o
- FHx
- black female
- of Scandinavian descent
SSX
- children will usually be asymptomatic
- in black female will present w/ SOB + dry cough
→ lung SSX (in 90% of cases lungs = affected)
- mediastinal lymphadenopathy
- pulm. fibrosis
- pulm. nodules
→ skin SSX
- erythema nodosum i.e b/l tender, red bruises on shins
- lupus pernio i.e raised purple les’ns on nose/cheeks
→ Lofgren’s syndrome = erythema nodosum + b/l hilar lymphadenopathy + polyarthralgia
→ systemic SSX
- fever
- fatigue
- weight loss
→ liver SSX
- liver nodules
- cirrhosis
- hepatosplenomegaly
→ eye SSX
- uveitis
- conjunctivitis
- optic neuritis
Ddx
- TB
- Berylliosis
- Lymphoma
Ix’s
- CXR
→ b/l perihilar and/or right paratracheal lymphadenopathy
→ b/l pulm. infiltrates (especially in upper lobes) - FBC → anemia, leukopenia
- HyperCa + low PTH sometimes b/c of ↑ed Vit D produc’n by macrophages in granulomas
- serum ACE → often elevated
- bronchoscopy → histology of mediastinal lymph nodes will show non-caseating granulomas w/ epitheloid cells
- U+E / LFTs / ECG / U/S to check if any other organs = affected
Tx = oral corticosteroids or IV if pt can’t tolerate PO + ventilatory support if pt = in acute resp. failure
→ co prescribe w/ bisphosphonates to protect against osteoporosis
Complica’ns
- pulm. fibrosis
- pulm. HTN
- corticosteroid related infec’n
- corticosteroid related osteoporosis
- corticosteroid related hyperglycemia
- Know for OSCE *
Idiopathic Pulmonary Fibrosis ✓
Def - rare chronic life-threatening fibrotic lung disease that progresses over the course of several yrs, usually presents in pts ≥ 60 y/o
→ characterized by forma’n of scar tissue w/in lungs
RFs
- FHx
- male
- smoking
No known Eti
- medica’ns such as amiodarone, bleomycin, biologics, long term nitrofurantoin use
SSX
- clubbing
- progressive dyspnea on exer’n
- chronic dry cough
- systemic SSX such as fatigue + cachexia
- b/l crackles in lower zone
Ix’s
- CXR → will show basilar, peripheral, b/l, asymmetrical, reticular opacities
- high resolu’n chest CT for diagnosis → will show honeycombing + ↑ed reticul’an
Tx for acute exacerba’n = admit to hosptial + give high dose corticosteroid
Regular Tx = anti fibrotic therapy i.e pirfenidone or nintedanib + smoking cessa’n + pulm. rehab + annual flu vaccine → lung transplant
Complica’n = acute exacerba’n → worsening in exercise tolerance
- Know for OSCE *
Bronchiectasis ✓
Def - abnormal dilata’n of bronchi due to destruc’n of elastic + muscular components of bronchial wall = obstructive pb → causes long term productive cough
RFs
- CF
- immunodeficiency
- 1°ciliary dyskinesia
- previous infec’n (especially H. influenza + pseudomonas aeruginosa)
Eti
- Post-infectious (18% of cases)
- COPD (15% of cases)
- Connective tissue disorders such as RA or Sjogren syndrome
- Asthma
- Immunodeficiency
- Allergic bronchopulmonary aspergillosis
- Aspira’n or inhala’n injury
Pathophys - micro-organisms colonize airways → chronic airway inflamma’n → bronchial wall edema + ↑ed mucus produc’n
→ neutrophils, T lymphocytes + other inflammatory cells = recruited to airways + subsequently release inflammatory cytokines, proteases + reactive oxygen mediators
→ progressive airway damage + recurrent infec’ns
SSX
- SOB
- cough
- fatigue
- hemoptysis
- A LOT of sputum produc’n
→ ≥ 3 of above had to have been present for ≥ 48hrs in order to diagnose
- weight loss
- recurrent chest infec’ns
- yellow nail syndrome = bronchiectasis + yellow nails + lymphedema
SSX on exam / ausculta’n
- clubbing
- SSX of cor pulmonale i.e raised JVP / peripheral edema
- crackles scattered throughout that change or clear when pt coughs
Ddx
- TB
- COPD
- Asthma
- Pneumonia
- Lung cancer
- Chronic sinusitis
- Pulmonary fibrosis
Ix’s
- high resolu’n chest CT for diagnosis → will show thickened bronchial dilata’n
- CXR → ring shadows + tram track opacities
- sputum culture
- FBC to r/o differentials
Regular Tx = Healthy diet + exercise + Vit D supplementa’n + airway clearance techniques such as active breathing / directed coughing for 15-30 mins (2-3x / day)
Tx for exacerba’n
1. sputum culture
2. Abx for 7-14 days
→ ciprofloxacin for P. aeruginosa
Complica’ns
- exacerba’ns
- cor pulmonale
- ischemic stroke
- respiratory failure
- severe hemoptysis
Cystic Fibrosis ✓
Def - autosomal recessive disease caused by defect of CFTR gene found on chromosome 7 (usually due to a dele’n of Phe508) = most common LETHAL genetic disease in pts of European descent
RFs
- FHx
- white ethnicity
- both parents being carriers of mutant CFTR alleles
Pathophys - CFTR gene codes for Cl channel that secretes Cl in lungs + GI tract + reabsorbs Cl in sweat glands
→ Phe508 dele’n → misfolded protein → protein absent from cell membrane → Cl + water secre’n ↓
→ intracellular [Cl] ↑
→ compensatory ↑ in Na reabsorp’n via ENac (epithelial Na channels) to ↑ water reabsorp’n
→ ↑ in Na reabsorp’n results in a more -ve transepithelial Ψ difference + secre’n of abnormally thick mucus into lungs, GI tract +
pancreas → in pancreas this leads to blockage of exocrine ducts, early activa’n of pancreatic enzymes + eventual auto-destruc’n of the exocrine pancreas which is why most pts require supplemental pancreatic enzymes
SSX
- failure to thrive
- chronic sinusitis
- child tasting salty
- voracious appetite
- hyperexpans’n on CXR
- thick sputum produc’n
- recurrent resp. infec’ns
- chronic wet-sounding cough
- genital abnormality (in males)
- steatorrhea due to fat malabsorp’n
- failure to pass meconium in neonate i.e meconium ileus
Ddx
- GERD
- Asthma
- Celiac disease
- Failure to thrive
- Chronic aspira’n
- 1° ciliary dyskinesia
- 1° immunodeficiency
- Protein-losing enteropathy
Ix’s
- newborn blood spot testing = performed on all children shortly after birth → will pick up most CF cases
- genetic testing
- pilocarpine-induced sweat test = gold std → will show ↑ed [Cl], > 60 = diagnostic
- newborn screening i.e IRT (immunoreactive trypsinogen) → will be ↑ed in newborn w/ CF due to clogging of pancreatic duct
- Regular sputum samples = sent for bacterial culture to check for infective exacerba’n
→ Pts infected w/ P. aeruginosa have a 2-3 fold ↑ed risk of death over 8 yrs
Tx
- chest physio bd (↑ frequency if they have infective exacerba’n)
- high calorie diet for children
- nebulized / inhaled dornase alfa (= DNase) → cleaves neutrophil-derived DNA in sputum to ↓ viscosity + ∴ help w/ sputum removal
→ mannitol dry powder (inhaled) for adult pts who can’t use DNase / whose lung func’n = rapidly ↓ing (i.e FEV1 ↓ > 2% / yr) or who can’t take any other type of osmotic agent - Prophylactic flucloxacillin tablets to ↓ risk of bacterial infec’ns (especially staph aureus infec’ns)
- nebulized hypertonic saline → facilitates mucus clearance
- Pancreatic enzyme replac’nt therapy i.e CREON tablets to replace missing pancreatic enzymes
- being up to date on vaccina’ns to prevent infec’ns (pneumococcal, influenza, varicella)
Complica’ns
- pancreatic insufficiency → in 90% of pts
- delayed puberty
- being underweight
- ↓ed female fertility
- deficient in fat soluble vitamins
- ↓ed bone mineral density → osteoporosis
- chronic liver disease (30% of adults w/ CF develop liver disease)
- CF related diabetes (uncommon in children < 10 y/o, 50% of adults w/ CF develop CF related diabetes + require Tx w/ insulin)
- upper airway complica’ns such as nasal polyps + sinusitis (prevalence ↑ w/ age)
- male infertility due to absent vas deferens (in 99% of males w/ CF hence most male CF pts = infertile)
- prone to staph. aureus + pseudomonas aeruginosa
→ = very difficult to get rid of b/c can become resistant to multiple Abx
→ ↑ morbidity + mortality in CF pts
→ can be treated w/ long term nebulized Abx such as tobramycin or oral ciprofloxacin
Causes of chest pain ✓
“CP4MT2A”
- Costochondritis
- P.E
- Pleural Effus’n
- Pneumothorax
- Pericarditis
- MI
- Cardiac Tamponade
- Aortic dissec’n
- Abdominal pb like GERD or hernia
Pneumothorax ✓
Def - air in pleural space = life threatening
→ traumatic = due to trauma - lung gets punctured → air leaks into pleural space = open pneumothorax i.e air can move in + out (= most common type of pneumothorax)
→ 1° spontaneous = happened w/o any underlying cause = common in tall, thin young men who smoke
→ 2° spontaneous = happened as a result of underlying lung disease such as CF / COPD / necrotizing lung infec’n / lung malignancy (1° or metastatic)
→ iatrogenic - as a result of thoracentesis, bronchospcy, etc
RFs
< 40 y/o
- TB
- CF
- FHx
- COPD
- chest trauma
- severe asthma
- cigarette smoking
- tall + slender body build
- recent invasive medical procedure
Pathophys - we need the -ve pressure inside lungs so air can move from high to low but due to accumula’n of air in pleural space, we have an ↑ in intrapleural pressure ∴ lung can’t reinflate
Tens’n v.s Closed pneumothorax
- tens’n pneumothorax = air can enter but can’t leave = most dangerous out of the 3 b/c air keeps on entering but has nowhere to leave ∴ amt of air in pleural space keeps ↑ing
- closed pneumothorax = air can leave but addi’nal air can’t enter
SSX of tens’n pneumothorax
- SOB
- hypoxia
- chest pain
- tachypnea
- tachycardia
- hypoTN
- tracheal devia’n away from side of pneumothorax due to ↑ in central venous pressure
- ↓ed breath sounds + hyper resonance on percuss’n + hyperinfla’n of hemithorax (on AFFECTED side for all 3)
Ddx
- MI
- P.E
- Pleural effus’n
- COPD exacerba’n
- Asthma exacerba’n
- Esophageal perfora’n
- Bronchopleural fistula
- Fibrosing lung disease
Ix’s
- erect CXR
- clotting profile b/c if INR ≥ 1.5 or platelets ≤ 50 x 10⁹/L, MUST BE CORRECTED BEFORE INSERTING CHEST DRAIN in pts who are NOT critically unwell !
- CT thorax b/c can detect small pneumothorax that CXR can’t
Emergency Tx (i.e for suspected tens’n pneumothorax)
- Immediate decompress’n by inserting large bore cannula in 4th/5th intercostal space in midclavicular line → hiss of air confirms diagnosis OR open thoracostomy if tens’n pneumothorax = 2° to trauma
- High flow O2
- Chest drain + hospital admiss’n
→ insert drain in triangle of safety i.e apex of axilla + 4th intercostal space mid clavicular line + anteriorly in 2nd intercostal space
⟹ after inserting drain do CXR to check posi’n of drain
Tx for large 1° spontaneous i.e > 2cm = aspirate + for any other 1° pneumothorax = discharge w/ written advise to come back to ED if SOB worsens + pulmonology f/u in 1-2 wks
Tx for large 2° spontaneous = chest drain + hospital admiss’n
Tx for moderate 2° spontaneous i.e 1-2 cm = percutaneous aspira’n +/-high flow O2
Tx for small 2° spontaneous i.e < 1 cm = high flow O2 + observa’n for 24 hrs + hospital admiss’n
Complica’ns of chest drain
- air leaks around drain site → indicated by persistent bubbling of fluid, particularly on coughing
- surgical / subq emphysema = when air collects in subq tissue
- Know for OSCE *
CXR analysis ✓
- Lungs should be black on CXR so if they’re white i.e instead of being sharp as they should be, lung borders = as if they’re blurry then that could mean . . .
→ no air getting in due to atelectasis / lung collapse
→ consolida’n i.e air is still getting in but something is replacing that air i.e . . .
⟹ a solid structure such as a tumor
⟹ pus (i.e in infec’n like pneumonia)
⟹ fluid such as . . .
- blood in trauma or vasculitis
- water in pulm. edema
⚠️ If u suspect that “something” is fluid do CT or U/S !
- In right lung collapse, left lung will be really dark = compensatory hyper-infla’n of left lung b/c it has to compensate for the collapsed right lung
Indica’ns for dialysis ✓
(“AEIOU”)
- Acidosis (pH < 7.1)
- Electrolyte pb i.e K > 6.5
- Ingest’n of SLIME toxins (Salicylates, Li, IsopropanOH, MetOH + Ethylene Glycol)
- Overload of fluid
- Uremia i.e High Urea : Cr ratio
- Know for OSCE *
AKI ✓
Def - acute but usually reversible ↓ in renal func’n, ≥ 1 of the following criteria has to be met for diagnosis . . .
→ ↑ in serum Cr by ≥ 0.3 mg/dL or 25 micromol/L w/in 48 hrs
→ ↑ in serum Cr to ≥ 1.5 times baseline w/in past 7 days
→ Urine volume < 0.5 mL/kg/hr for past 6 hrs
RFs
- Sx
- sepsis
- trauma
- pancreatitis
- cardiac arrest
- advanced age
- drug overdose
- nephrolithiasis
- malignant HTN
- diabetes mellitus
- iodinated contrast
- underlying kidney disease
- excessive fluid loss such as in hemorrhage
- myeloproliferative disorders such as multiple myeloma
- Na retaining states such as CHF, cirrhosis, nephrotic syndrome
- nephrotoxins like vancomycin, penicillin, cancer Tx, NSAIDs, ACE-I’s, diuretics
Eti
1) Pre-renal = most common of the 3 = due to ↓ed renal perfus’n → ischemia
Causes
→ pre renal azotemia = most common cause of AKI in hospitalized pts
→ renal artery stenosis
→ renal artery hypoperfus’n due to sepsis
→ low blood volume
⟹ severe burn
⟹ heart failure
⟹ hypovolemic shock
⟹ dehydra’n, vomiting, diarrhea
⟹ major blood loss i.e hemorrhage
⟹ rhabdo b/c they’ve been lying on the floor for a long time w/o water (their CK will be >10K)
→ drugs (“DAMN”)
⟹ Diuretics
⟹ ACE-I’s/ARBs
⟹ Metformin
⟹ NSAIDs → vasoconstrict afferent arteriole
Diagnosis = high Urea : Cr ratio (i.e > 20) + urine output improves w/ fluids
2) Intrinsic / Renal = direct injury to kidney parenchyma i.e pb = nephrons themselves
Causes
- contrast
- glomerulonephritis
- acute interstitial nephritis (AIN)
→ will cause eosinophils in urine
→ pt will also have fever, rash + flank pain
- acute tubular necrosis (ATN) → will cause granular brown casts in urine
→ can be caused by nephrotoxic drugs like vancomycin, amino-glycosides, contrast media, cisplatin, heavy metals like lead, heme pigments in rhabdomyolysis, ethylene glycol
Diagnosis = low Urea : Cr ratio (i.e < 15)
3) Post-renal = ureter or renal vein obstruc’n (ureters usually) → obstruc’n HAS TO BE B/L b/c if it’s u/l the other can do the work for both of them
Causes
- BPH
- lymphoma
- urinary reten’n
- renal calculi / kidney stones
- stricture of ureter/urethra (= most common @ renal calyces + renal pelvis)
⚠️ All 3 types of AKI will cause low GFR (w/in a few days), low urine output + high Cr !
⚠️ Obstruc’n of renal tract must always be excluded in anuric pt !
Ddx
- CKD
- iatrogenic
Ix’s
- FENa
→ < 1% = pre-renal
→ > 2 % = ATN
Emergency Tx - rehydrate w/ NS (0.9%) if volume depleted → stop all nephrotoxic drugs after doing the following Ix’s . . .
⟹ urine dipstick + urine microscopy + culture
⟹ U+E, FBC, LFTs, ABG, Ca, myeloma screen
⟹ U/S of kidneys, ureters + bladder
→ treat HyperK if present
→ dialysis IFF pt has ≥ 1 of “AEIOU” life-threatening or intractable pulmonary edema / uncontrollably rising K / severe (i.e pH < 7.2) or worsening acidosis
Complica’ns
- uremia → pericarditis, encephalopathy
- HyperK
- HyperPhos
- metabolic acidosis
⚠️ Kidneys have 30 mins w/o blood supply before they start to shut down !
- Know for OSCE *
CKD ✓
Def in adults - abnormalities in kidney structure or func’n for ≥ 3 months
Def in children - GFR < 60 for > 3 months + ≥ 1 of the following . . .
- proteinuria
- albuminuria
- pathologic abnormalities on histology or imaging
RFs
> 50 y/o
- HTN
- diabetes
- kidney disease
- chronic use of nephrotoxic drugs such as NSAIDs
Eti
1. Diabetic nephropathy
2. HTN
3. Other causes i.e . . .
- amyloidosis
- lupus nephritis
- obstructive uropathy
- membranous nephropathy
- rapidly progressive glomerulonephritis
- cystic disorders of the kidney such as PCKD
Pathophys - Eti → renal injury → ↑ in intraglomerular pressure w/ glomerular hypertrophy b/c kidney has to compensate for nephron loss in order to maintain normal GFR
→ ↑ in glomerular permeability + ↑ in ATII produc’n due to renal injury
→ renal scarring w/in glomerulus
SSX
- asymptomatic or . . .
- anemia SSX once GFR ↓ to < 50 due to ↓ in EPO produc’n
- uremia due to kidney failure
- N/V due to uremia
- anorexia due to uremia
- restless legs due to uremia
- pruritus due to uremia + scratch marks due to the pruritus
- edema b/c ↓ in GFR causes ↑ in salt + water reten’n
- foamy urine due to proteinuria b/c kidneys are leaking protein
Ddx
- glomerulonephritis
- nephrotic syndrome
- obstructive uropathy
- diabetic nephropathy
- ischemic nephropathy
- hypertensive nephrosclerosis
Ix’s
- for diagnosis → GFR < 60 mL/min/1.73 m^2 over 3 months OR ≥ 1 indicators of kidney damage i.e proteinuria / microscopic OR Urine albumin : Cr ratio (ACR) consistently > 3 mg/mmol
- urinalysis → Ψ hematuria or proteinuria (quantified by urine albumin : Cr ratio)
- U+E → elevated urea + Cr + electrolyte abnormalities
- renal U/S → kidney atrophy (can diagnose CKD if kidney atrophy = present w/ obstruc’n, hydro-nephrosis or bladder reten’n)
- BP/ lipid profile / A1c to identify RFs
Staging
- G1 = GFR ≥ 90
- G2 = GFR from 60-89
- G3a = GFR from 45-69
- G3b = GFR from 30-44
- G4 = GFR from 15-29
- G5/ESRD = GFR ≤ 15 OR pt is already on dialysis (these pts require long-term dialysis or transplant)
Criteria for nephrology referral (only 1 = needed)
- GFR < 30
- ACR > 70 (ACR = Albumin : Cr Ratio)
- accelerated progress’n i.e ↓ in GFR of 25% in past yr
- 5 yr risk of requiring dialysis > 5%
- uncontrolled HTN despite being on ≥ 4 antihypertensives
Tx
- Statin 20mg to ↓ risk of CVD
- BP + glucose control
→ BP target for ACR > 70 = < 130/80
→ BP target for ACR <70 = < 140/90
a) ACE-I/ARB titrated to highest dose if pt has ACR > 70 OR HTN + ACR > 30 OR diabetes + ACR > 3
⚠️ Monitor their K while they’re under Tx !
b) Dapagliflozin (SGLT-2 inhibitor) if pt has diabetes + ACR > 30
- G5 stage or pt has uremia = dialysis + then kidney transplant hopefully
→ peritoneal dialysis can be done at home
⟹ catheter = inserted into abdomen + dialysis fluid = instilled → fluid + toxic waste products = removed + drained from body on a daily basis
→ hemodialysis = pt has to come in 3x/wk + each sess’n lasts 3-4hrs
⟹ pt’s blood = removed from body through AV fistula / AV graft / dialysis catheter + is then returned after traversing dialysis membrane + dialysis solu’n
- Renal Diet i.e low Na, low protein, low K + low PO4
Complica’ns
- anemia → treat w/ IV iron +/- EPO
- CVD
- pulmonary edema due to fluid overload
- HyperK due to kidney’s inability to excrete K
- metabolic acidosis due to kidney’s inability to excrete acid (happens when GFR is < 50) → treat w/ oral Na bicarb
- renal osteodystrophy / CKD mineral + bone disorder (CKD-MBD) in advanced CKD b/c kidney can’t activate Vit D → HypoCa
→ HyperPTH + HyperPhos to compensate → bone mineral imbalance → bone weakening
→ bone pain + fractures
→ gait + limb weakness
⟹ treat w/ PO4 binders such as Ca acetate + calcitriol b/c it ↓ PTH
⚠️ Stop metformin prior to imaging w/ contrast + give CKD pts prophylactic IV NS to prevent contrast-induced nephropathy !
- Know for OSCE *
Kidney stones (nephrolithiasis) ✓
= most common at renal calyces + renal pelvis
→ can also occur at trigone b/c that’s where ureters join together before emptying their urine into bladder
→ larger stones tend to remain confined to kidney but smaller stones can pass into ureter + cause ureteric colic (VERY SEVERE PAIN !)
SSX
- vomiting
- hematuria
- renal colic i.e u/l descending groin pain i.e from top to bottom (due to stone moving)
→ DON’T use X-ray b/c might show Ca stones b/c they’re white but won’t show uric acid stones → use U/S instead → only pb w/ U/S = won’t show stones < 5 mm ∴ use CT KUB instead
Ix = non-contrast CT KUB which is basically a CT scan of renal tract
Complica’ns
- obstruc’n
- hydronephrosis
- infected stone → sepsis
Complica’ns of obstruc’n
- HTN
- AKI
- Hydroureter + hydronephrosis due to ↑ in pressure proximal to stone
- u/l obstructive uropathy i.e loss of kidney func’n on affected side
- UTI → ascends to kidney + becomes pyelonephritis → rapid destruc’n of kidney → sepsis (immediate complica’n)
Tx for non obstructed stone
- if stone < 7 mm = likely to pass on its own so just hydra’n + analgesia w/ NSAIDs
Emergency Tx i.e for obstructed stone causing sepsis = nephrostomy = inser’n of tube through abdominal wall into renal pelvis through which urine can drain freely
- Know for OSCE *
Urethral stricture ✓
Def - narrowing of urethra
Eti
- BPH
- prior urethral inflamma’n (infec’n usually)
SSX
- difficulty in passing urine
- slow stream
- feeling like bladder isn’t completely emptied
- straining due to attempt to “completely empty bladder”
Nephrotic v.s Nephritic syndrome ✓
NEPHROTIC
- severe PROteinuria (≥ 3.5 g/L/day, urine might have frothy appearance)
- hypoalbuminemia (≤ 30 g/L)
- edema + HLD + hypercoagulability
→ Eti . . .
- SLE
- amyloidosis
- diabetic nephropathy
- minimal change disease = most common cause of nephrotic syndrome in children
- membranous nephropathy = most common cause of nephrotic syndrome in adults
→ involves deposits of immune complexes in glomerular basement membrane ∴ histology will show IgG + complement deposits on basement membrane
→ can occur 2° to malignancy, SLE or drugs such as NSAIDs
→ Do Renal Bx for all adult pts w/ nephrotic syndrome !
→ Tx = furosemide
→ Complica’ns . . .
- HTN
- HLD
- thrombosis
NEPHRITIC
- hematuria
- oliguria
- minor proteinuria
- red cell casts in urine
→ Eti . . .
- vasculitis
- lupus nephritis
- post-streptococcal glomerulonephritis
→ presents 1-3 wks after strep infec’n such as tonsillitis or impetigo ⟹ usually affects pts < 30 y/o + pts usually make full recovery
- Know for OSCE *
Polycystic kidney disease (PCKD) ✓
Def - genetic disorder where healthy kidney tissue = replaced by cysts
RFs
- HTN
- male
- proteinuria
Types
- autosomal dominant
- autosomal recessive
Eti based on type
- autosomal dominant
→ muta’n of PKD1 gene on chromosome 16 (most of the time)
→ muta’n on PKD2 gene on chromosome 4 - autosomal recessive = due to mutat’n of PKHD1 gene on chromosome 6 = more rare but more severe
→ often picked up on antenatal scan → scan will show oligohydramnios
SSX
- flank pain
- mitral regurgita’n
- colonic diverticula
- hematuria if cyst ruptures
- underdeveloped ear cartilage, low-set ears + flat nasal bridge for recessive
Ix’s = U/S of renal tract + genetic testing
→ diagnostic criteria . . .
- ≥ 3 renal cysts (u/l or b/l) if ≤ 39 y/o
- ≥ 2 cysts in each kidney if 40-59 y/o
- ≥ 4 cysts in each kidney if ≥ 60 y/o
Tx
- Antihypertensives for HTN
- Analgesia for acute pain
- Abx for infec’ns
- Drainage of symptomatic cysts
- Dialysis / transplant for end-stage renal failure
- Tolvaptan in autosomal dominant PCKD to slow disease progress’n
Complica’ns
- kidney stones
- recurrent UTIs
- cerebral aneurysms
- hepatic, splenic, pancreatic, ovarian, prostatic cysts
- subarachnoid hemorrhage hence these pts might need a LP
- end stage renal failure (usually occurs around 50 y/o for dominant + before adulthood for recessive)
- Know for OSCE *
SIADH ✓
Eti
- post op
- chest infec’n
- drugs i.e TCAs, SSRIs, carbamazepine, sulfonylureas
- CNS disturbance such as traumatic brain injury
- ADH secreting tumor such as in small lung cancer
Pathophys - ↑ in ADH secre’n by posterior pituitary
→ ↑ in water reabsorp’n
→ diluted blood + [ ]ed urine
SSX = HypoNa SSX
Ddx = other causes of HypoNa
Ix’s
- U + E → HypoNa
- serum osmolality → will be low
- urine osmolality + urine Na → will both be high
- CT thorax, abdomen + pelvis + head MRI to check for malignancy
Tx
- admit if HypoNa = severe i.e < 125
- treat underlying cause
- fluid restrict pt to 750-1000 mL/day
- tolvaptan = vasopressin receptor antagonist so blocks ADH receptors
→ can only be initiated by endocrinologist + requires close Na monitoring i.e every 6 hrs
- Know for OSCE *
HypoNa ✓
= most common electrolyte abnormality
→ serum osmolality must be low i.e < 280 mOsm/kg for it to be true HypoNa !
RFs
- old age
- SSRI use
- ecstasy use
- hospitaliza’n
- thiazide diuretic use (especially if pt also takes PPIs)
Eti
- Hypovolemic HypoNa = ↓ in blood volume for whatever reason i.e severe diarrhea or vomiting, pancreatitis, severe hypo-albuminemia, mineralo-corticoid deficiency
→ in this type of HypoNa we expect to see hypovolemia SSX i.e pallor, ↓ed skin turgor, tachycardia, orthostatic hypoTN - Hypervolemic HypoNa = due to fluid overload i.e CHF, pulmonary edema, AKI, CKD, cirrhosis, nephrotic syndrome
→ in this type of HypoNa we expect to see SSX of fluid overload - Euvolemic HypoNa causes . . .
→ high fluid intake
→ medica’ns such as vasopressin, thiazide diuretics, antidepressants + opioids
→ syndrome of inappropriate ADH secre’n
→ psychogenic polydipsia = when pt compulsively drinks >10 L of water/day
SSX of SEVERE HypoNa i.e cerebral edema maybe
- progressive HA
- N/V
- AMS / Δ in level of consciousness
Ix’s
- U + E → Na will be < 135 mmol/L
- Serum glucose (random or fasting) to r/o hyperglycemia-associated HypoNa
- Serum osmolality → must be < 280 mmol/kg or mOsm/kg for it to be true HypoNa
→ if normal check for hyperproteinuria or hyperlipidemia
→ if > 280 check for hyperglycemia/mannitol or sorbitol use/recent contrast - Physical Exam
- If there are fluid overload SSX = Hypervolemic
a) Urinary Na < 20 = due to CHF / cirrhosis / hypoalbuminemia
b) Urinary Na > 20 = due to renal failure
- If there are dehydra’n SSX = Hypovolemic
a) Urinary Na < 20 = due to EXTRArenal loss i.e vomiting, diarrhea, bowel obstruc’n
b) Urinary Na > 20 = RENAL loss i.e diuretic use, mineralocorticoid deficiency
- No SSX of hypo or hypervolemia = Euvolemia
a) Urine osmolality < 100 = 1° polydipsia or beer potomania
b) Urine osmolality > 100 = SIADH, hypoTSH or adrenal insufficiency
Tx
- for hypervolemic HypoNa = fluid + Na restric’n + treat underlying cause
- for hypovolemic HypoNa = 0.9% saline (= isotonic saline)
- for euvolemic HypoNa = calculate electrolyte free water clearance = (Urine Na + K) / Serum Na
→ if < 0.5 then Tx = 1L fluid restric’n
→ if btw 0.5-1 then Tx = 0.5L fluid restric’n
→ if > 1 give tolvaptan → monitor Na every 6hrs (goal = Na of 130)
Complica’ns
- osteoporosis
- ↑ed risk of falls
- cerebral edema in severe HypoNa (Tx = IV mannitol) → brain hernia’n → death
- osmotic demyelina’n syndrome if u correct HypoNa too quickly
→ Na [ ] should not change > 10 mmol/L in 24 hrs !
→ SSX usually occur after 2 days . . . - dysarthria
- dysphagia
- paraparesis or quadriparesis
- seizures
- confus’n
- coma
- Know for OSCE *
HyperNa ✓
RFs
- Li use
- 1° hypodipsia
- large salt intake
- renal [ ]ing defect
- limited access to water
- ↓ in ability to [ ] urine (in old age for ex)
- GI disorders such as prolonged vomiting or severe watery diarrhea like in viral gastroenteritis
Eti
- free water loss causes (most common)
- Na overload such as in mineralocorticoid excess
- pure free water intake deficit i.e impaired thirst mechanism or not consuming enough water
SSX
- ↓ed JVP
- oliguria
- weight loss
- impaired thirst
- orthostatic hypoTN
- diarrhea or vomiting
Ix’s = urine + plasma osmolality
→ urine osmolality ≤ plasma osmolality suggests diabetes insipidus
→ urine osmolality ≥ plasma osmolality suggests pure volume deple’n NOT due to diabetes insipidus
→ urine osmolality ≈ plasma osmolality suggests renal [ ]ing defect (usually due to renal failure, osmotic diuresis or diuretic use)
Tx - treat underlying cause if possible
→ correct dehydra’n by replacing free water losses → correct hypovolemia if present by giving electrolytes + free water
Complica’ns
- CPM
- cardiac toxicity
- Tx related brain edema
- Tx related hyperglycemia
- rhabdomyolysis (not common)
- Know for OSCE *
HypoK ✓
RF = psychiatric pts due to their medica’ns
Eti
- ↑ed entry of K from blood to tissues / cells
→ chloroquine intoxica’n
→ ↑ed β adrenergic activity such as in Cushing’s syndrome b/c catecholamines (adrenaline, cortisol) promote K ENTRY into cells by ↑ing Na K ATPase activity which is why excess admin of β agonists can cause HypoK
→ alkalosis b/c H+ ions will LEAVE cells to enter blood to correct pH which will cause K to leave blood + ENTER cells
→ ↑ed availability of insulin b/c insulin ↓ serum K by stimulating Na/K ATPase pump
- K loss from upper GI tract i.e prolonged vomiting
- K loss from lower GI tract
→ villous adenoma → will cause diarrhea + rectal secre’ns = rich in K
→ vasoactive intestinal peptide secreting tumor (VIPoma) - K loss from urine
→ loop + thiazide diuretics
→ hypomagnesemia
→ mineralocorticoid excess such as in 1° aldosteronism/Conn’s syndrome
Asymptomatic for mild-moderate
SSX for severe
- constipa’n
- generalized weakness
- muscle pain
Ix = ECG → ≥ 1 of the following signs . . .
- T wave invers’n
- long PR interval
- flat T waves in almost all leads (flat = shaped like P wave)
Tx
1) Oral K + plenty of fluids (w/ or after meals)
2) IV KCl in pts w/ severe N/V or abdominal distress
→ 0.9% NaCl = preferred infus’n fluid as 5% glucose may cause trans-cellular shift of K into cells + hence make the HypoK worse
Complica’ns
- flaccid paralysis
- rhabdomyolysis
- muscle weakness
- hepatic encephalopathy in pts w/ cirrhosis
- cardiac arrhythmias + sudden cardiac death
→ pts w/ CHF, on digoxin or aggressive therapy for hyperglycemia such as in DKA = most @ risk of this
- Know for OSCE *
HyperK ✓
= MEDICAL EMERGENCY b/c can cause paralysis, arrhythmias + cardiac arrest
Eti
- ↓ed renal excre’n . . .
→ NSAIDs
→ mineralocorticoid deficiency
→ acute or chronic renal insufficiency such as in AKI or CKD (stage 4 or 5)
→ ACE-Is / ARBs b/c cause a state of hypoaldosteronism - ↓ed entry of K into cells i.e metabolic acidosis b/c MORE H+ ions will leave blood to ENTER cells to correct pH ∴ LESS K will ENTER cells
- ↑ed exit of K out of cells
→ TLS
→ rhabdo
→ admin of mannitol b/c will cause ↑ in osmolality i.e plasma becomes more [ ]ed b/c more solutes leave cells to enter blood (K included)
SSX
- diarrhea
- vomiting
Ix = ECG → will show ≥ 1 of the following signs . . .
- long PR interval
- flat or completely absent P waves
- broad/wide QRS complexes aka broad + short instead of tall + pointy (i.e looks more like a T wave)
- tall tented T waves in almost all leads aka tall + pty instead of broad (i.e looks more like QRS complex)
Emergency Tx i.e HyperK ECG signs OR K > 6.5 = IV Ca gluconate b/c stabilizes cardiac muscle cells hence ↓ing risk of arrhythmia (asystole specifically)
→ insulin dextrose b/c insulin drives K from extracellular to intracellular space by stimulating Na K ATPase pump + dextrose = to prevent hypoglycemia
- Know for OSCE *
Should you treat asymptomatic bacteriuria ? ✓
NO unless pt = pregnant !
UTIs (in adults + kids) ✓
Def - infec’n of kidneys, bladder or urethra that are more common in women
→ usually caused by E. coli + 2nd by Klebsiella pneumoniae
→ most common UTI = infectious cystitis (bladder infec’n)
RFs in kids
< 1 y/o
- female
- previous UTI
- sexually active
- urinary obstruc’n
- uncircumcised boys in 1st yr of life
RFs in men
> 50
- BPH
- previous UTI
- catheteriza’n
- urological Sx
- urethral stricture
- ureter or kidney stones
RFs in women
- sexual activity
- spermicide use
- post menopause
- Hx of recurrent UTIs
SSX
- nocturia
- confus’n (in older pts)
- suprapubic pain/tenderness
- cloudy or foul smelling urine
- urinary frequency and/ or urgency
- macroscopic hematuria i.e visible hematuria
- dysuria i.e pain/burning/stinging during urina’n
- CVA tenderness = in btw 12th rib + spine (on their back, on each side for each kidney)
Ddx
- urethritis
- prostatitis
- epididymitis
- renal cancer
- bladder cancer
- prostate cancer
- pyelonephritis
- ureter or kidney stones
- vaginitis, overactive bladder
- urethral syndrome / abacterial cystitis = UTI SSX w/o infec’n
Ix’s
- gram stain
- MSU for urine microscopy + culture
- urine dipstick → only diagnostic if shows +ve nitrites or +ve leukocytes w/ RBCs
Tx in adults = nitrofurantoin (narrow spectrum Abx) OR trimethoprim
→ C/Is of nitrofurantoin = 3rd trimester of pregnancy + GFR < 45
→ MOA of trimethoprim = inhibits folic acid forma’n by preventing bacterial convers’n of tetrahydrofolate to its active form
→ side effects = rash, photosensitivity + folate deficiency
→ C/Is = 1st trimester, liver or renal failure + hematological disorder
a) if they’re < 65 y/o + NOT pregnant treat if pt has ≥ 2/3 of the following . . .
- cloudy urine
- dysuria
- nocturia
OR has ≥ 1 of those 3 + relevant dipstick
b) if they’re ≥ 65 y/o treat if pt has new onset dysuria OR ≥ 2 of the following . . .
- temp is 1.5ºC above normal in last 12 hrs
- new frequency or urgency
- new incontinence
- new or worsening delirium
- new suprapubic pain
- visible hematuria
c) If they’re pregnant just treat
Preven’n for women
- hydrating + urinating after intercourse
- taking prophylactic Abx if she has Hx of recurrent UTIs
Dura’n of Abx Tx for aduts
- 3 days for non pregnant woman that is otherwise healthy (regardless of age)
- 5-10 days for immunosuppressed women or pts w/ abnormal anatomy or impaired kidney func’n
- 7 days for men, pregnant women or catheter-related UTIs
Tx in children
a) ≤ 2 months = ampicillin for 7-14 days
b) > 2 months = cefixime for 7-14 days
⚠️ Recurrent UTIs in children requires f/u U/S in 6 wks + DMSA scan in 4-6 months !
Complica’ns
- sepsis
- prostatitis (in men)
- renal func’n impairment
- pyelonephritis (especially in pregnant women)
- PROM / pre term labor (in pregnant women)
- Know for OSCE *
Atypical UTIs in children ✓
SSX
- child = seriously ill
- poor urine flow
- abdominal / bladder mass
- ↑ed Cr
- septicemia
Ix’s if pt < 6 months . . .
- urgent USS during infec’n
- MCUG scan once infec’n resolves
- routine DMSA 4 months later
- Know for OSCE *
Mx of fever in pt < 3 months old ✓
- Urgent referral for peds assess’nt in hospital
- Ix’s
- FBC
- CRP
- blood culture
- urinanalysis
- stool culture if baby has diarreha
- CXR if baby has resp SSX
- Know for OSCE *
Acute Pyelonephritis ✓
Def - severe infectious inflammatory disease of renal parenchyma, renal calices + renal pelvis
RFs
- UTI
- diabetes
- pregnancy
- stress incontince
- frequent sexual intercourse
- foreign body in urinary tract i.e calculus / catether
- immunosuppressive state i.e HIV / transplanta’n / chemo/ long term or high dose corticosteroid use
Eti - usually E. coli just like UTIs
SSX = fever + N/V + loin/back pain + UTI SSX (especially CVA tenderness)
Ddx
- UTI
- PID
- urethritis
- acute prostatitis
- lower lobe pneumonia → do CXR to rule it out
Ix’s
- urinanalysis → might show . . .
⟹ +ve nitrites
⟹ +ve leukocytes
⟹ WBC casts → indicates UTI of renal origin - urine culture + sensitivity
Tx = oral Cefalexin for 7-10 days while waiting for culture
→ IV CTX or co-amoxiclav instead if pt = vomiting
Complica’ns
- renal failure
- sepsis (do Sepsis 6 immediately if pt = septic)
- lack of response to Tx (usually happens in pts w/ kidney stone or renal abscess)
- Know for OSCE *
Tx for salicylate overdose ✓
- Activated charcoal
- IV Na Bicarb to enhance elimina’n of aspirin in urine
Indica’ns for dialysis in salicylate overdose ✓
- coma
- seizures
- acute renal failure
- pulmonary edema
- serum [salicylate] > 700mg/L
Insulin v.s Glucagon ✓
- Insulin = secreted by β cells of pancreatic islets of Langerhans to ↓ blood glucose
- Glucagon = secreted by 𝛼 cells of pancreatic islets of Langerhans to ↑ blood glucose
Tx op’ns for neuropathic pain ✓
- amitriptyline
- gabapentin
- pregabalin
- duloxetine
Type 1 + 2 Diabetes Mellitus ✓
Def - diabetes mellitus = group of metabolic diseases where pt has high blood glucose either b/c pancreas isn’t PRODUCING insulin at all (i.e Type 1 → usually occurs in young ppl) OR b/c tissues aren’t RESPONDING to insulin (i.e Type 2 / insulin resistance → usually occurs in older ppl)
⟹ Idiopathic Type 1 = no identifiable antibody
⟹ Auto-immune Type 1 = identifiable antibody = attacking β cells + hence preventing them from making insulin
RFs for T2D
> 40 y/o
- FHx
- HTN
- CVD
- PCOS
- stress
- dyslpidemia
- gesta’nal diabetes
- non white ancestry
- overweight or obese
SSX
- unexplained weight loss / ↑ in appetite for T1D
- polydipsia due to loss of water in urine
- polyuria due to glucose in tubules drawing water in
- glucose in urine (= abnormal in non-diabetic pt)
- acanthosis nigricans in T2D (rare tho) = usually in neck, armpits or groin area
⚠️ High glucose can also cause blurry vis’n !
⚠️ Polyuria = greater urine output i.e > 3L / day v.s urinary frequency = peeing more OFTEN than usual !
Ddx
- diabetes insipidus
- psychogenic polydipsia
- T2D for T1D + vice-versa
- gesta’nal diabetes if pt = pregnant
Diagnostic Criteria for T2D
- SSX + Fasting glucose > 7mmol OR any other glucose > 11.1 mmol OR HbA1c > 6.5% (CANNOT R/O diabetes just b/c HbA1c = normal !)
→ DON’T use HbA1c in . . .
⟹ pts who had diabetic SSX for < 2 months
⟹ pancreatic Sx / damage
⟹ pts suspected of having T1D
⟹ pts who require hospital admiss’n
⟹ children b/c they have higher RBC turnover rate
⟹ pts on medica’ns that can quickly ↑ blood glucose such as steroids or anti-psychotics
⟹ presence of genetic / hematologic / illness-related factors that influence HbA1c + its measur’nt such as pregnancy
Tx for T1D
- Detemir basal bolus insulin injec’n bd (= rapid acting insulin) + oral aspirin od IF pt = pregnant b/c = at risk of developing pre-eclampsia
→ fixed dose insulin (in NON-PREGNANT adults only !)
⚠️ Prescribe these pts amitriptyline if they have burning pain in feet / difficulty sleeping or ↓ed GFR
Tx for T2D
- Lifestyle Δs + after 3-6 months check if pt reached target HbA1c, if not . . .
- Metformin OR DPP-4 inhibitor / pioglitazone / sulfonylurea if metformin = contraindicated OR SGLT-2 inhibitor if the other 3 aren’t appropriate for pt
- Add SGLT-2 inhibitor if pt has chronic heart failure or established atherosclerotic CVD
→ if pt = at high risk of DKA i.e already had DKA / is unwell w/ intercurrent illness or is on very low carb diet such as keto diet, fix modifiable risks before starting them on SGLT-2 inhibitor - ↑ dose of metformin
- Triple therapy i.e metformin + 2 of the other op’ns
→ Metformin
⟹ MOA - oral biguanide that ↓ glycogenolysis + gluconeogenesis
⟹ C/Is - advanced heart pb or renal pb hence must stop it if GFR < 30
⟹ Side effects
- nausea
- diarrhea
- abdominal discomfort
- ↑ed [lactic acid] → lactic acidosis (very rare but can be fatal)
- B12 deficiency in chronic use of metformin (= due to ↓ed B12 absorp’n)
⟹ monitoring → U+E before prescribing + then yrly (STOP IT IF GFR < 30 !)
⟹ don’t take before or after contrast
⟹ stop it temporarily if sick + restart it after 24-48 hrs
→ SGLT-2 inhibitors : (end in “GLIFLOZIN”)
⟹ MOA - inhibits SGLT 2’s which are proteins expressed in PCT of kidneys that reabsorb filtered glucose from tubular lumen + also co- transport Na along w/ glucose → glucose + Na reabsorp’n ↓ → urinary excre’n of glucose ↑
⟹ C/I = dialysis
⟹ Side effects
- euglycemic DKA
- urinary urgency
- genital fungal infec’ns
- hypoTN due to fluid deple’n b/c of the ↓ in Na reabsorp’n
→ DPP-4 inhibitors - (end in “LIPTIN”)
⟹ MOA - DPP-4 enzyme degrades incretin hormones such as GLP-1 + GIP which ↑ insulin secre’n + ↓ glucagon secre’n ∴ by inhibiting DPP-4 we have ↑ed insulin secre’n by GLP-1 + GIP
⟹ C/I = T1D, DKA + Hx of pancreatitis
⟹ Side effects
- HA
- UTI
- URTI
- arthralgia
- nasopharyngitis
→ Sulfonylureas : (begin in “GLI” + end in “IDE”)
⟹ MOA - bind to + inhibit ATP sensitive K channels on pancreatic β cells → ↓ in K efflux
→ β cell membrane depolarizes
→ Ca channels open → influx of Ca
→ ↑ in intracellular [Ca] stimulates pancreatic β cells to release insulin regardless of blood glucose levels
⟹ C/Is = none
⟹ Side effects
- weight gain hence should be avoided in obese pts
- hypoglycemia (especially after a missed meal, exercise or taking high dose of sulfonylurea),
Acute complica’ns
- DKA (more in Type 1) → urinalysis will show ketones in urine + ABG will show metabolic acidosis
- HHS (more in Type 2)
- Hypoglycemia b/c of . . .
→ sulphonylurea use
→ not eating enough
→ over-exercising
→ injecting too much insulin / excessive alcohol consump’n
RFs for chronic complica’ns
- FHx
- HTN
- smoking
- dyslipidemia
- excess weight
- long disease dura’n b/c the more the disease progresses, the more glucose there is + high glucose = directly toxic to β cells
Chronic complica’ns
- Microvascular
→ UTIs
⟹ urinalysis might show +ve leukocytes or nitrites but only give Abx in pregnant pt
→ Nephropathy (NOT the same as diabetic kidney disease)
⟹ screen via microalbuminuria 1st + then Urea / Cr b/c Urea / Cr happens later + then via GFR
⟹ in end stage kidneys can no longer activate Vit D so we get HypoCa + hence 2° HyperPTH
→ Retinopathy i.e cotton wool spots (due to retinal ischemia or retinal infarct as a result of diabetes) + even blindness
⟹ screen via fundoscopy, retinal photography + fluorescein angiography where indicated
⟹ classifica’n . . .
- maculopathy = more common in T2D
- proliferative retinopathy (PDR) =
more common in T1D
→ 50% of these pts = blind in 5 yrs
- non-proliferative diabetic retinopathy (NPDR)
→ Peripheral Neuropathy → diabetic foot ulcers due to poor wound healing + loss of sens’an so pt doesn’t realize foot is injured + neuropathic pain
⟹ complica’n of diabetic foot ulcer = osteomyelitis
⟹ screen via peripheral vascular exam + motor / sensory neuro exam
⟹ treat neuropathic pain w/ drug for neuropathic pain
→ Autonomic Neuropathy . . .
⟹ ED
⟹ diabetic gastroparesis i.e delayed gastric emptying → SSX = vomiting, early satiety, postprandial fullness + pt feels bloated
- Macrovascular
→ HTN
→ stroke
→ heart disease
→ recurrent skin infec’ns
→ peripheral vascular disease
⚠️ Exogenous v.s Insulinoma i.e endogenous insulin overproduc’n v.s Sulphonylurea
- Insulin = ↑ in all 3
- C-peptide = undetectable in exo + ↑ in other 2
- Sulphonylurea = only detectable in sulphonylurea
- Know for OSCE *
DKA ✓
Def - acute complica’n of diabetes (Type 1 usually) = fatal if left untreated = leading cause of morbidity + mortality in children w/ T1D
Precipitating factors
- MI
- infec’n
- missed insulin doses
- alcohol excess (acutely)
SSX
- N/V
- dehydra’n
- hyperventila’n
- acetone breath
- abdominal pain
- ↓ed consciousness
- polyuria + polydipsia
Pathophys - dehydra’n → uncontrolled lipolysis → excess of free fatty acids → they get converted into ketone bodies
Ix’s
- dipstick + ABG → will show ketosis + metabolic acidosis
- U + E → might show HypoK
- glucose → mild-moderate hyperglycemia ( > 200 mg/dL or 11 mmol/L)
- FBC → leukocytosis = common in DKA
Diagnostic criteria (all must be met)
- Glucose > 11 mmol/l or known diabetes mellitus
- blood pH < 7.3
- Bicarb < 15 mmol/l
- Ketones > 3 mmol/l or urine ketones ++ on dipstick
Tx in adults
1. 500 ml 0.9% NS for 10 mins
2. Fixed-rate infus’n of fast acting insulin until acidosis resolves
3. Correct K w/ KCl
4. Heparin if pt = immobile or unconscious (for DVT ppx)
Tx in children
- Correct dehydra’n evenly over 48 hrs via bolus fluid followed by maintenance fluid in order to dilute ketones + hyperglycemia
⚠️ Don’t correct any faster or else u might cause demyelina’n syndrome ! - Fixed rate insulin infus’n → allows cells to start using glucose again hence switching off ketone produc’n
Complica’ns
- HypoK due to high dose insulin
- cerebral edema in children b/c rapid correc’n of dehydra’n + hyperglycemia causes rapid shift in water from extracellular space to intracellular space in brain cells hence causing brain to swell which can lead to brain cell destruc’n + death
HHS ✓
Def - life threatening complica’n of T2D
Eti - usually due to acute infec’n or inadequate insulin therapy
3 Hallmark SSX = HypoTN + Hyperosmolality + Severe Hyperglycemia
Other SSX
- N/V
- confus’n
- tachycardia
- diabetes SSX
- dehydra’n SSX i.e ↓ed skin turgor / dry oral mucosa
Ix’s
- dipstick + ABG to r/o DKA → absent ketosis + minimal acidosis unlike DKA
- glucose → severe hyperglycemia i.e > 600 mg/dL or 33.3 mmol/L
- serum osmolality → will be > 320 mOsm/kg
- FBC → leukocytosis = common in HHS
Tx = same as DKA . . .
- Fluid replac’nt w/ NS
- Insulin infus’n
- Subq Heparin for VTE Ppx
Pre-diabetes v.s diabetes ✓
Ix = A1c
→ btw 39-47 mmol/L = pre-diabetes
→ > 48 = diabetes
Mx for pre-diabetes = refer to diabetes preven’n program for diet + lifestyle modifica’ns to prevent them from actually getting diabetes
Causes of poor wound healing ✓
“DID NOT HEAL”
Diabetes
Infec’n / Irradia’n
Drugs i.e chemo / steroids
Neoplasia + Nutri’nal deficiencies (Zinc / Vit A / Vit C)
Object i.e foreign material
Tissue necrosis
Hypoxia
Excess tens’n on wound
Another wound
Low temp / Liver pb
Hypoglycemia ✓
Def - blood glucose < 4 mmol/L
RFs for newborns
- preterm
- SGA
- LGA
- infants of mothers w/ gesta’nal diabetes
Eti in adults - uncommon in pts who don’t have diabetes but can be due to . . .
- alcohol ingest’n
- adrenal insufficiency
Eti in newborns
- physiological → newborn blood glucose ↓ in first 1-2 hrs after delivery due to transi’n from continuous supply from placenta to intermittent supply via milk feeds but stabilizes w/in 1st 48 hrs of life
- low glycogen reserves due to prematurity or fetal growth restric’n
- disorders that cause excess insulin secre’n such as meconium aspira’n syndrome or polycythemia
- ↑ed glucose utiliza’n such as in infec’n
SSX for diagnosis in adults = Whipple’s triad . . .
- hypoglycemia SSX i.e . . .
→ confus’n
→ seizures
→ LOC
→ visual Δs
→ hunger
→ tremor
→ weakness
→ sweating
→ palpita’ns
→ tachycardia
→ paresthesias - low plasma glucose [ ] when above SSX = present
- SSX disappear after glucose level is returned to normal
SSX in newborns (can be asymptomatic)
- pallor
- seizures
- sweating
- irritability
- tachypnea
- jitteriness/tremors
- poor feeding
- weak or high-pitched cry
- Δ in level of consciousness
Classifica’n for adults
- mild = pt conscious + able to swallow + doesn’t have neuro SSX
- moderate = pt conscious + able to swallow but has neuro SSX i.e difficulty speaking or concentrating / confus’n / HA / weakness / drowsiness
- severe = pt unconscious
Tx for mild OR moderate but pt = cooperative = 15-20g fast-acting glucose such as via . . .
- 4 Gluco tabs (1 tab contains 4g of glucose)
- 200ml of fruit juice
Tx for moderate + pt ≠ cooperative = 2 tubes of GlucoGel
⚠️ Check that pt’s gag reflex = present prior to giving them this
Tx for severe
1. ABC
2. place pt in recovery posi’n
3. if pt is on insulin infus’n STOP IT !
4. If pt already has an IV give 100mls of 10% Glucose or 1mg of IM Glucagon
- Know for OSCE *
Diabetes Insipidus ✓
Def - metabolic disorder characterized by absolute or relative inability to [ ] urine
RFs
- pituitary Sx
- les’n in pituitary stalk
- traumatic brain injury
- congenital pituitary abnormalities
- craniopharyngioma (= intracranial tumor)
- genetic muta’n such as muta’n in AVPR2 receptor = X linked recessive
Eti
→ Central / Cranial = ↓ in synthesis or release of ADH
- idiopathic
- pituitary Sx
- brain tumor
- brain injury
- genetic muta’n in ADH gene
- brain infec’n such as meningitis or encephalitis
→ Nephrogenic = collecting ducts of kidneys aren’t responding appropriately to ADH
- idiopathic
- HypoK
- HyperCa
- kidney diseases such as PCKD
- long term Li therapy b/c Li ↓ collecting duct response to ADH
SSX
- polyuria
- postural hypoTN
- dehydra’n b/c of polyuria
- hypotonic urine i.e VERY dilute urine
- polydipsia b/c of dehydra’n + polyuria
Ddx
- HyperCa
- diuretic use
- diabetes mellitus
- psychogenic polydipsia
Ix’s
- urine osmolality → will be very low
- serum glucose to r/o diabetes
- serum corrected Ca to r/o HyperCa
⚠️ MUST DO THIS BEFORE PROCEEDING W/ WATER DEPRIVA’N TEST TO R/O HYPER-PTH ! - urine dipstick to r/o diabetes or underlying renal disease
- 24 hr urine collec’n for volume → will be > 3L/ 24hr
- water depriva’n / desmopressin stimula’n test (diagnostic Ix)
1. pt avoids all fluids for up to 8 hrs before test
2. after that water depriva’n, urine osmolality measured
3. if urine osmolality = high, DI = ruled out
4. urine osmolality < 300 = enough to diagnose DI b/c means that pt ≠ able to [ ] urine
5. give synthetic desmopressin to figure out if eti = cranial or nephrogenic
6. urine osmolality = measured over the 2-4 hrs following desmopressin admin
7. if after desmospressin is given, urine osmality ↑, that means pb = central but if it remains low that means pb = kidneys
→ should not be performed in pts w/ renal insufficiency / hypovolemia or uncontrolled diabetes mellitus - MRI of pituitary gland if eti = cranial
Tx for Central = desmopressin
→ pt shouldn’t take too much in order to avoid HypoNa
⟹ b/c of that HypoNa risk, serum Na should be checked every 1-3 months
Tx for Nephrogenic
1. Treat underlying cause, stop nephrotoxic drugs + maintain adequate fluid intake
2. Low Na diet + thiazide diuretics or indomethacin to ↓ urine output
Complica’ns
- bladder dysfunc’n due to excess urine produc’n (in nephrogenic)
- iatrogenic HypoNa (in central)
Obesity ✓
Def - chronic adverse condi’n where pt has an excessive amt of body fat
RFs
- hypoTSH
- hypercortisolism
- corticosteroid therapy
Eti (mainly in Western world)
- large por’ns
- mental illness
- eating disorders
- sedentary lifestyle
- poor dietary habits
Ddx
- HypoTSH
- Cushing’s syndrome
BMI ≥ 30 = obesity
→ 30-34.9 = Grade I obesity
→ 35-39.9 = Grade II obesity
→ ≥ 40 = Grade III obesity i.e morbidly obese
Obesity + hormones
- ghrelin = high b/c ↑ appetite
- leptin = low b/c ↓ appetite + ↑ satiety so when there isn’t enough of it ur constantly hungry + never feel full ∴ will end up eating more
Tx
- Dietary Δs + ↑ in physical activity
- BMI ≥ 30 OR BMI ≥ 28 + comorbidity = treat w/ medica’n i.e orlistat
→ orlistat = lipase inhibitor ∴ ↓ absorp’n of dietary fat - BMI ≥ 40 OR BMI ≥ 35 + comorbidity such as HTN / diabetes / GERD / sleep apnea = refer for Bariatric Sx
Complica’ns
- T2D
- HTN
- HLD
- metabolic syndrome
- non alcoholic fatty liver disease
- Know for OSCE *
Diagnostic criteria for metabolic syndrome ✓
≥ 3/4 of the following . . .
- HTN
- BMI > 30
- Impaired glucose tolerance
- Dyslipidemia i.e ↓ed LDL or triglycerides >150 mg/dL
- Know for OSCE *
HypoTSH in adults ✓
Types
- 1° = thyroid gland is the pb
→ TFT will show high TSH + low T3/T4
- 2° = pituitary gland is the pb
→ TFT will show low TSH + low T3/T4
RFs
- female
- Turner’s
- 30-50 y/o
- Down syndrome
- radiotherapy to head + neck
- Li use b/c inhibits T3/T4 synthesis + their release
- iodine deficiency b/c iodine = needed to produce T3/T4
- FHx of autoimmune thyroiditis i.e Hashimoto’s
→ pts w/ Hashimoto’s will have antithyroid peroxidase (TPO) or antithyroglobulin (Tg) antibodies
Eti for 1°
- Hashimoto’s = most common cause in iodine sufficient areas / developed world
- Tx for hyperthyroidism i.e carbimazole / propylthiouracil
radioactive iodine / thyroid Sx
- Li use b/c inhibits produc’n of thyroid hormones in + thyroid gland
- amiodarone b/c interferes w/ thyroid hormone produc’n + metabolism
Eti for 2° (less common)
- Sx to pituitary
- radiotherapy
- pituitary adenomas
- Sheehan’s syndrome = avascular necrosis of pituitary gland due to PPH
Pathophys
- thyroid gland mainly produces T4
→ T4 gets converted to T3 which has metabolic roles (stimula’n of cellular O2 consump’n / E genera’n)
→ for whatever reason thyroid gland isn’t producing enough T4 (in 1°)
→ not enough T3 as well consequentially
→ pituitary ↑ produc’n of TSH to compensate (-ve feedback)
SSX = ↓ in metabolism so . . .
- constipa’n
- weight gain
- hair thinning
- ↓ed appetite
- depressed mood
- ↓ in temp so pt feels colder i.e cold intolerance
- hoarse voice
- in addi’n to having the same metabolic SSX as any other hypoTSH, Hashimoto’s also has ↑ed anti-TPO antibodies, anti-thyroglobulin + non-pitting myxedema
Ddx
- 1° v.s 2°
- anemia
- depress’n
Ix’s
- T4 + serum TSH
- FBC to r/o anemia
- anti TPO + anti-Tg to check for Hashimoto’s if eti = 1°
Tx = oral levothyroxine = synthetic vers’n of T4
→ Check for SSX improv’nt + measure TSH after 2-3 months of Tx
⟹ if TSH is still high that means dose is too low so ↑ it
⟹ if TSH is now low that means dose is too high so ↓ it
⚠️ Advise pts to avoid Ca + Fe supplements b/c they can ↓ levothyroxine absorp’n !
Complica’ns
- Afib
- angina
- osteoporosis
- pregnancy complica’ns
→ miscarriage
→ fetal neurological
maldevelop’nt
⟹ this is why women of childbearing age = encouraged to wait until they’re euthyroid before they try to conceive
- myxoedema coma = hypoTSH + multi organ failure
→ usually in older untreated pts w/ multiple comorbidities = medical emergency !
- Know for OSCE *
HypoTSH in children ✓
Eti
- Congenital = child is BORN w/ an underactive thyroid gland
→ screened for during newborn blood spot screening test
⟹ SSX (assuming it got missed at birth) . . .
- poor feeding
- prolonged neonatal jaundice
- constipa’n / sleeping more than expected / ↓ed activity
- slow growth + develop’nt
- Acquired = child or adolescent suddenly develops an underactive thyroid gland although it was previously working normally . . .
→ most common cause = Hashimoto’s
→ T1D + celiac don’t cause it but are associated w/ it
→ same SSX as adults i.e fatigue, low E, poor growth, weight gain, constipa’n, dry skin, hair loss as well as poor school performance
SSX = ↓ in metabolism so . . .
- constipa’n
- weight gain
- hair thinning
- ↓ed appetite
- depressed mood
- ↓ in temp so pt feels colder i.e cold intolerance
- in addi’n to having the same metabolic SSX as any other hypoTSH, Hashimoto’s also has ↑ed anti-TPO antibodies, anti-thyroglobulin + non-pitting myxedema
Ix’s
- T4 + serum TSH
- thyroid U/S
- anti TPO + anti-Tg to check for Hashimoto’s if eti = acquired
Tx = oral levothyroxine
- Know for OSCE *
Thyrotoxicosis ✓
Def - clinical syndrome of hyper-metabolism due to ↑ed free thyroxine (T4) and / or free triiodothyronine (T3) serum levels regardless of etiology
→ hyperthyroidism = when it’s specifically due to excessive endogenous thyroid hormone produc’n
Types
- 1° = thyroid gland is the pb
→ TFT will show low TSH + high T3/T4 - 2° = pituitary gland is the pb
→ TFT will show high TSH + high T3/T4
RFs :
- female
- tobacco use
- FHx of Grave’s
- high iodine intake
Eti for 1° (“GIST”)
- Grave’s = autoimmune hyperthyroidism = most common cause of thyrotoxicosis
→ Grave specific SSX in addi’n to regular hyperthyroidism SSX =
- exophthalmos
- diffuse goiter W/O nodules
- thyroid acropachy = hand swelling + finger clubbing
- pretibial myxedema = deposits of glycosaminoglycans under the skin on anterior aspect of leg as a rxn to TSH receptor antibodies → that area of skin will have a discolored, waxy, + edematous appearance = SPECIFIC TO GRAVE’S !
→ pathophys of Grave’s - immune system produces TSH receptor antibodies that stimulate TSH receptors on thyroid
- inflamma’n i.e thyroiditis (De Quervain’s thyroiditis, post partum thyroiditis, drug induced thyroiditis)
- solitary toxic thyroid nodule
- toxic multinodular goiter
- Eti for 2° = TSH secreting pituitary adenoma
SSX = ↑ in metabolism so . . .
- diarrhea
- weight loss
- ↑ed appetite
- ↑ed sweating
- anxious mood
- ↑ in temp so pt feels warmer i.e heat intolerance
Ix’s
- serum T4 + TSH
- TSH receptor antibodies (TRAb) for Grave’s
* Subclinical hyperthyroidism = low TSH but NORMAL normal T3/T4 + little to no SSX *
→ for subclinical always repeat TFT !
Tx = thyroid drugs
1. carbimazole for 12-18 months
→ side effect = neutropenia + agranulocytosis ∴ pt should tell u if they notice any infective SSX, especially a sore throat
2. propylthiouracil (PTU) which ↓ convers’n of T4 to T3
3. β blocker (propanolol) for adrenergic SSX i.e tachycardia/sweating + for thyroid storm
4. ttl thyroidectomy if all else fails
→ these pts will require life long levothyroxine
Complica’n = thyroid storm / thyrotoxic crisis = only in thyrotoxicosis due to hyperthyroidism
→ SSX = fever, tachycardia + delirium
- Know for OSCE *
The 5 cancers that metastasize to bone ✓
“BLT KP”
- breast (#2)
- lung (#3)
- thyroid
- kidney
- prostate (#1)
⚠️ All = osteoLYTIC metastases except prostate = osteoSCLEROTIC metastasis !
- Know for OSCE *
Common malignancies that metastasize to the liver ✓
“CS yr PBL”
- Colon
- Stomach
- Pancreas
- Breast
- Lung
Liver metastases = common b/c of its rich vasculature i.e portal venous system
Thyroid Cancer ✓
RFs
- female
- head + neck irradi’an
- FHx of thyroid cancer
Types
- papillary carcinoma (most common type) = well differentiated
→ spreads through lymph nodes - Hürthle cell carcinoma
- follicular = spreads directly through blood
SSX
- voice hoarseness
- cervical lymphadenopathy
Ddx = benign thyroid nodule
Ix’s
- TSH
- neck U/S to get dimens’ns of nodule + see if it’s solid or cystic
→ micro calcifica’ns, marked hypoechogenicity + irregular margins = U/S features that should make u suspect malignancy - FNA for diagnosis
Tx
- newly diagnosed papillary, follicular, or Hürthle = active surveillance or Sx
- anaplastic = Sx + chemoradia’n
- offer ttl thyroidectomy to pts/ w/ ≥ 1 of the following . . .
→ T3 or higher stage primary tumor
→ reg’nal lymph node involvement i.e N1
→ distant metastatic disease i.e M1
Complica’ns
- airway obstruc’n
- post op HypoPTH
- post op recurrent laryngeal nerve nerve damage
- Know for OSCE *
Thyroid eye disease ✓
Def - autoimmune inflammatory disease of the orbit = most common cause of exophthalmos in adults
RFs
- female
- current smoking
- african american
- autoimmune diseases like pernicious anemia, SLE, Addison’s, vitiligo, celiac, RA
Eti = Grave’s usually
SSX
- lid lag
- eye dryness
- eye redness
- watery eyes
- pain behind eyes
- mild photophobia
- proptosis/exophthalmos i.e eye bulging
- lagophthalmos i.e incomplete eyelid closure
- upper eyelid retrac’n especially in lateral aspect of eyelid = lateral flare
- restrictive myopathy i.e restrictive eye mov’nts due to swollen tissues
- blurry or double vis’n requires PROMPT INTERVEN’N b/c it means sight = threatened !
Ddx = allergic conjunctivitis but if there’s SSX like lid retrac’n or blurry vis’n u can rule it out
Tx
→ moderate to severe = corticosteroid therapy
→ sight threatening = urgent orbital decompress’n Sx + IV corticosteroid
- Know for OSCE *
HLD ✓
Modifiable RFs
- diet
- high BP
- smoking
- diabetes
- low HDL
- high LDL
- high BMI
- lack of exercise
Non-modifiable RFs
- male sex
- advanced age
- African American or South Asian ethnicity
- FHx of premature CVD or sudden death (i.e before 55 in men + 65 in women)
Eti
→ 1° = genetic
→ 2° = hypoTSH, diabetes, renal disease, liver disease, alcohol
SSX = corneal arcus = lipid deposits in cornea
Ix’s
- TFTs
- U + E
- Fasting glucose
- LFTs (ALT, AST, ALP) + GGT (gamma)
- full fasting lipid profile i.e ttl cholesterol, LDL, HDL, triglycerides
Tx = statin, cholestyramine
- statin MOA → ↓ hepatic cholesterol synthesis by targeting rate limiting enzyme in cholesterol synthesis → upregula’n of LDL receptors + ↑ed hepatic uptake of LDL cholesterol from circula’n i.e less LDL in blood
- statin monitoring → LFTs before prescribing, then again @ 3 months, then again @ 12 months
- side effects = muscle pain, abdo pain, nausea + diarrhea
- C/I = pregnancy
- don’t take w/ grapefruit
- cholestyramine MOA → bile acid sequestrant ∴ ↓ bile acid reabsorp’n in small intestine
→ side effects = abdominal cramps + constipa’n, ↓ed absorp’n of fat soluble vitamins, bleeding/bruising due to ↓ed Vit K absorp’n, cholesterol gallstones
→ if rhabdo = suspected (severe muscle ache / prolonged ie / crush Injury), measure CK
⟹ stop statin if CK > 5x upper limit of normal
⟹ ↓ statin lose if CK < 5x upper limit of normal
Complica’n = CVD
- Know for OSCE *
Addison’s disease / Autoimmune 1° adrenal insufficiency ✓
Def - autoimmune disease where adrenal glands don’t produce enough steroid hormones (cortisol + aldosterone in particular) = rare but is life threatening if pt goes in addisionian crisis
→ 2° adrenal insufficiency = pituitary gland is the pb → it’s not adequately releasing ACTH which is necessary to stimulate adrenal glands
⟹ could be due to hypoplasia (congenital underdevelop’nt) of pituitary / pituitary Sx / surgery / radiotherapy
RFs
- female
- adrenal hemorrhage
- adrenocortical auto-antibodies
- auto-immune disease, especially celiac
Pathophys - destruc’n of adrenal cortex → impaired synthesis + secre’n of all steroids from all 3 cortical layers (90% of adrenal cortex has to be destroyed to cause SSX) → pt has deficiency in cortisol + aldosterone → ↑ in ACTH due to inhibited -ve feedback
Pathophys of addisonian crisis due to abruptly stopping long term corticosteroid medica’n (type of 3° adrenal insufficiency) - long term steroid use i.e > 3 wks
→ hypothalamus = suppressed during that time b/c there were steroids from another source
→ exogenous steroid = suddenly w/drwan → hypothalamus doesn’t “wake up” fast enough
→ endogenous steroids don’t get adequately produced
SSX
- anorexia
- depress’n
- weight loss
- muscle cramps
- muscle weakness
- fatigue + ↓ed libido
- bronze hyperpigmenta’n (especially on skin creases)
SSX of Addisonian crisis
- N/V
- dizziness
- abdominal pain
- confus’n + weakness
- hypoTN (especially postural hypoTN)
- hypoNa
- hyperK
→ Tx = 100 mg IV Hydrocortisone stat
Ddx
- hyperthyroidism
- anorexia nervosa
- hemochromatosis
- occult malignancy
Ix’s
- morning serum cortisol → will be low
⟹ we take it in the morning b/c that’s when cortisol levels = at their peak so if they’re low during that time that’s suspicious - Synacthen / ACTH stimula’n test for diagnosis (ideally performed in the morning)
- Give pt Synacthen (synthetic ACTH)
- Check blood cortisol 30 mins before + 60 mins after dose
→ synthetic ACTH will stimulate adrenal glands to produce cortisol → cortisol level should at least double in healthy adrenal glands
→ if it doesn’t it means there’s adrenal insufficiency - Plasma ACTH to distinguish btw 1° + 2°
→ high = 1° b/c when glucocorticoid levels are normal that causes -ve feedback loop that inhibits ACTH release but since glucoortioid levels = low, that -ve feedback is now inhibited
→ low = 2°
Ongoing Tx = LIFELONG hydrocortisone (a glucocorticoid) to replace cortisol + fludrocortisone (a mineralocorticoid) to replace aldosterone if also deficient
→ pts = given steroid card, ID tag + emergency letter to alert emergency services that they depend on steroids for life
⚠️ Doses should not be missed, as they are essential to life + dose should be doubled during acute illness to match normal steroid response to illness !
→ Pt + their close contacts = taught how to give IM hydrocortisone in an emergency
Complica’ns
- Cushing syndrome 2° to over-replac’nt of glucocorticoids
- osteopenia / osteoporosis due to over-replac’nt of glucocorticoids b/c excessive bone exposure to glucocorticoids causes ↓ in osteoblast activity + ↑ in osteoclast activity
- Know for OSCE *
Things to remember about long term corticosteroid use ✓
” C STOP “
- Can worsen glycemic control in diabetes, cause immunosupress’n, neutrophilia, high WBC count + ↑ risk of mania
- S = double pt’s dose when they’re Sick to prevent adrenal crisis
- T = pt should carry steroid Tx card to alert others that they’re steroid dependent
- O = Osteoporosis preven’n w/ bisphosphonates / Ca / Vit D
- P = PPIs for gastroprotec’n
- Know for OSCE *
Cushing’s syndrome ✓
Def - persistent excess of circulating glucocorticoids (specifically cortisol)
RFs
- adrenal adenoma
- pituitary adenoma
- adrenal carcinoma
- exogenous glucocorticoid use
Eti
> ACTH dependent = excessive cortisol secre’n by adrenal glands due to high ACTH levels
- Pituitary ACTH-secreting adenoma (most common cause)
→ in this case ONLY it’s called Cushing’s disease
→ will cause adrenal cortex hyperplasia - Ectopic ACTH-secreting tumors such ACTH-producing small cell lung cancer cells → results in excess cortisol secre’n by adrenal gland
> ACTH independent = excessive cortisol secre’n by adrenal glands despite suppressed ACTH
- adrenal adenomas
- b/l adrenal hyperplasia
- adrenal carcinomas (very rare)
- exogenous admin of glucocorticoids in the Tx of another disease (most common cause)
SSX
- tan skin
- weight gain
- purple striae
- easy bruising
- muscle weakness
- peripheral vis’n loss
- hirsutism (in women)
- buffalo hump
- moon face i.e face = rounder
- pigmenta’n (in ACTH-dependent causes)
- truncal / abdominal / central obesity
- menstrual irregularities in women + libido loss in men due to gonadal dysfunc’n
Ddx
- obesity
- metabolic syndrome
Ix’s
- pregnancy test in women of childbearing age to r/o pregnancy
- glucose levels → might be high b/c cortisol promotes produc’n of free glucose in the body + ↑ insulin resistance
- Either 1a or 1b for diagnosis . . .
1a) late-night salivary cortisol → will be high
1b) low dose dexamethasone suppress’n test (preferred in pts w/ renal failure) or 24 hr urinary free cortisol in pregnant pt
- Serum ACTH to figure out if it’s ACTH independent or dependent
→ will be high in dependent + low in independent
Tx depends on cause
→ for ex if due to adrenocortical adenoma remove it surgically via adrenalectomy + treat peri-operatively w/ IV hydrocortisone
Complica’ns
- HTN
- osteoporosis
- metabolic syndrome
- T2D due to insulin resistance
- CVD (most common cause of death)
- nephrolithiasis b/c excess cortisol interferes w/ how kidneys handle Ca ∴ can cause Ca kidney stones
- Nelson’s syndrome - b/l adrenal gland removal → no more steroid hormones → no more -ve feedback on pituitary → pituitary tumor can expand + produce excess ACTH
- Know for OSCE *
Hyperaldosteronism ✓
Def - excess aldosterone
→ 1° = adrenal glands are the pb i.e they’re producing too much aldosterone
→ 2° = something is causing too much renin to be released hence too much aldosterone is being secreted
RFs
- HTN
- FHx of hyperaldosteronism
- FHx of early onset of HTN and/or stroke
Eti for 1°
- b/c adrenal hyperplasia (most common cause)
- aldosterone secreting adenoma (usually a u/l adrenal adenoma)
→ in this case it’s called Conn’s syndrome
- familial hyperaldosteronism (very rare)
Eti for 2°
- heart failure
- renal artery stenosis
- liver cirrhosis + ascites
Ix’s
- aldosterone : renin ratio (ARR)
→ will be high in 1°
→ will be low in 2 °
- U + E → will show high Na + low K b/c ↑ in Na reabsorp’n means ↑ in K excre’n in urine
- CT or MRI to check for both adrenal tumor + adrenal hyperplasia
Tx
- dietary Na restrict’n
- surgical adrenalectomy for pts w/ u/l Conn’s syndrome
- lifelong MRA (eplerenone /spironolactone) in pts w/ b/l Conn’s syndrome or in ptw w/ u/l who Conn’s who can’t / don’t want to undergo Sx
Complica’ns
- MI
- HTN
- stroke
- heart failure
- impaired renal func’n
- Know for OSCE *
Pituitary tumors ✓
- Pituitary adenomas = most common disease of the anterior pituitary = BENIGN tumors
Types
- Func’nal
→ Prolactinomas → secrete excess prolactin = most common type of func’nal adenoma
⟹ SSX . . .
- osteoporosis
- ↓ in libido in both sexes
- amenorrhea / oligomenorrhea i.e 4-9 periods / yr instead of 12
- galactorrhea in women
- ED / gynecomastia in men
⟹ Ix’s = prolactin level + brain MRI to check for pituitary tumor
⟹ Tx = Cabergoline = dopamine agonist b/c dopamine inhibits prolactin
→ GH secreting adenomas - will cause HAs / visual pbs (usually in men or post-menopausal women) + ACROMEGALY i.e thick hands + feet, protruding lower jaw, coarse facial appearance, larger tongue, excessive sweating, oily skin + ↑ in collar size
⟹ mortality rate = 2x that of normal popula’n b/c of LVH + CVD as a result of insulin resistance
→ TSH secreting adenomas - produce excess TSH ∴ cause hyperthyroidism SSX
⟹ mortality rate = 2x that of normal popula’n b/c of LVH + CVD as a result of insulin resistance
NON-FUNC’NAL = don’t secret any hormones
- Know for OSCE *
Ca distribu’n in our body ✓
- 98.9% = skeleton
- 1% = intracellular
- 0.1% = extracellular (45% bound to albumin, 10% unbound as a free ion)
Vit D + Ca ✓
- Vit D synthesis = cholesterol → 25 hydroxyla’n (in liver) → 1 hydroxyla’n (in kidneys)
- HIGH Ca INHIBITS parathyroid glands from releasing PTH
- LOW Ca STIMULATES parathyroid glands to release PTH + PTH ↑ Ca by . . .
→ stimulating kidneys to convert inert form of Vit D to its active form which helps ↑ Ca b/c active form of Vit D = necessary for Ca absorp’n in small intestine
→ ↑ing osteoClast activity ∴ Ca + PO4 will be released from hydroxyapatite
→ ↓ing serum PO4 by inhibiting tubular reabsorp’n of PO4 i.e promoting urine excre’n of PO4 + since PO4 binds to Ca, if there’s less PO4 to bind to it, there’s more free Ca
- Mg = required for PTH secre’n + sensitivity ∴ low Mg will cause low PTH hence causing HypoCa
- Calcitonin = released by C cells of thyroid gland → ↓ Ca + PO4 by inhibiting osteoclasts
⚠️ Blood pH affects Ca level b/c lower pH = more H+ ions to bind to albumin → higher [Ca] b/c less albumin = available to bind to Ca
1° HyperPTH ✓
Def - ↑ in PTH due to pb in parathyroid gland itself
Eti - parathyroid adenoma usually
RFs
- FHx
- 50-60 y/o
- female sex
- Past or current Li Tx
SSX
- anxiety
- myalgia
- depress’n
- poor sleep
- memory loss
Ddx
- sarcoidosis
- multiple myeloma
Ix’s = serum Ca + PTH
Tx = remove tumor surgically
Complica’n = calciphylaxis = calcifica’n of tunica media of small vessels
- Know for OSCE *
2° HyperPTH ✓
Def - ↑ in PTH as a response to HypoCa b/c of . . .
- CKD
- aging
- Vit D def (could be due to inadequate sunlight exposure, malbasorp’n, etc)
Ddx = 1°
Ix’s = serum Ca, ALP + PTH
Complica’n = nephrolithiasis b/c excess Ca can precipitate + cause kidney stones
- Know for OSCE *
HypoPTH ✓
Def - low PTH
RFs
- parathyroid Sx
- hypomagnesemia
- thyroid gland Sx b/c parathyroid glands might have been removed accidentally
SSX = complica’ns of HypoCa b/c of consequential ↓ in Ca i.e dry hair + brittle nails
Ddx
- hypomagnesemia
- hypoalbuminemia
- CKD / renal failure
Ix’s = Ca, Albumin, Mg + PTH
Tx
- for symptomatic acute = IV Ca
- for asymptomatic acute = oral Ca
- for chronic = oral Ca + calcitriol
Complica’ns = cataracts = after long term HypoCa !
- Know for OSCE *
HyperCa ✓
Def - high Ca
Eti
- 1° HyperPTH
- Medica’ns i.e Li / Thiazide diuretics
- High bone turnover
- Cancers that produce excess Ca or peptides that mimic PTH such as breast cancer / lung squamous cell / bone metastasis
- Multiple myeloma
- HYPER Vit D (due to excessive intake OR overactiva’n)
→ ex of overactiva’n of Vit D = by epithelioid macrophages in granulomatous diseases such as TB or sarcoidosis
SSX
- nausea
- fatigue
- lethargy
- confus’n
- polyuria
- polydipsia
- constipa’n
Ix’s
- PTH
- Vit D
- CXR
- TFTs
- Albumin
- Ca, PO4, U+E
- Myeloma Screen
- Urinary Ca excre’n
- ECG → short QT interval
Tx = 0.9% NaCI to make pt euvolemic
Complica’ns
- pancreatitis
- renal failure
- kidney stones
- Know for OSCE *
HypoCa ✓
Def - low Ca
Eti
- Cancer
- HypoPTH
- PTH resistance
- Acute pancreatitis
- Toxic shock syndrome
- Acute rhabdomyolysis (crash injuries)
- Ca chelators (ex : citrate in blood transfus’n)
- VitD deficiency (PTH will be high to compensate)
- Bone breaking inhibitors like bisphosphonates or calcitonin
SSX
- seizures
- muscle cramps
- muscle fascicula’ns
- finger or periroral paresthesia
- tetany i.e involuntary muscle contrac’ns
+ve Trousseau sign and/or +ve Chvostek sign = twitching of facial muscles when facial nerve = tapped
Ix’s
- Mg
- PTH
- Vit D
- Ca, PO4, U+E
- corrected Ca if albumin = low
- B12 / Folate / Ferritin / Celiac screen (b/c pb could be malabsorp’n)
Tx = IFF Ca < 1.8 mmol/L OR pt has tetany / seizures / +ve Trousseau or Chovstek sign = oral CaCO3 or IV Ca gluconate
Complica’ns
- dry hair
- brittle nails
- life threatening arrhythmia
- Know for OSCE *
The 3 categories of jaundice ✓
- Pre hepatic - excessive RBC breakdown i.e hemolysis → too much bilirubin for liver to conjugate
→ unconjugated bilirubinemia
→ normal urine color b/c only conjugated bilirubin is water soluble + normal stool color b/c flow of bile to duodenum isn’t impaired
⟹ ex’s = SCD or other hemolytic condi’ns - Intra-hepatic - ↓ed hepatocyte func’n for whatever reason
→ liver = able to conjugate bile but not fully
→ mix of conjugated + unconjugated bilirubin in blood → dark urine b/c of conjugated bilirubin + normal stool color b/c flow of bile to duodenum isn’t impaired
⟹ ex’s = cirrhosis, hepatitis, hepatic tumors b/c directly affect hepatocytes - Post-hepatic - drainage of bile = obstructed but b/c liver doesn’t have a pb it’s able to conjugate bilirubin → conjugated bilirubinemia → dark urine b/c of conjugated bilirubin + pale stool b/c bilirubin gives stool it’s brown color so when there’s something obstructing flow of bile to small intestine, stool ends up pale b/c it doesn’t contain any bilirubin
⟹ ex’s = gallstones, stricture, pancreatitis
LFT analysis ✓
- High ALT + AST = liver pb
- High Gamma + ALP = bile flow pb
Why does zone 1 of liver regenerate 1st + not zone 2 or 3 ? ✓
B/c zone 1 = closer to portal vessels
Liver v.s Vit K v.s Inhibitors pb (in bleeding / coagula’n issue) ✓
- Liver hepatocytes = produce all coagula’n factors except 8 (made by hepatic sinusoidal endothelial cells) + secrete TPO = necessary for platelet produc’n ∴ liver pb can affect both coagula’n time + platelet count
→ can also affect spleen b/c . . .
liver disease → portal HTN → splenomegaly → hyper-splenism → ↑ platelet sequestra’n
→ thrombocytopenia - Vit K = necessary for factor 2, 7, 9, 10 + Protein C + S so can affect COAGULA’N TIME but NOT PLATELET COUNT !
→ Causes of low Vit K . . .
- chronic diarrhea
- anti Vit K medica’n such as warfarin
- fat malabsorp’n b/c Vit K = fat soluble
- biliary duct obstruc’n(b/c Vit K = fat soluble
- parenteral nutri’n i.e receiving nutrients via IV
- new born b/c don’t have gut flora yet to make Vit K
- broad spectrum ABs → might kill gut flora that produce Vit K
⟹ What test can help you differentiate btw liver pb + Vit K deficiency ?
→ Factor 5 + Factor 7 activity assay b/c if only factor 7 = ↓ then it’s a Vit K pb but if both = ↓ then it’s a liver pb b/c liver produces both + 7 whereas Vit K is only needed for 7
- Inhibitors = antibodies circulating in blood that inhibit coagula’n factors
→ most common = inhibitors to factor 8
→ cause acquired Hemophilia A
Scenario 1: pt has ↑ed PT but no liver or Vit K pb
→ do mixing test of their blood w/ normal plasma . . .
a) if PT = corrected = factor 7 deficiency
b) If PT ≠ corrected = inhibitor pb
Scenario 2 : pt has ↑ed aPTT but no liver or Vit K pb
→ do mixing test of their blood w/ normal plasma . . .
a) if aPTT = corrected = factor 8 / 9 / 10 / vWF deficiency
b) If aPTT ≠ corrected = inhibitor pb
→ factor 7 = shortest half life out of all the Vit K dependent clotting factors, hence will be the 1st whose levels start to ↓ if the pt is deficient in Vit K
Acute liver failure ✓
Def - rapid ↓ in hepatic func’n = jaundice + coagulopathy i.e INR > 1.5 + hepatic encephalopathy in pts w/ no prior Hx of liver disease
2 most common causes = paracetamol overdose + viral hepatitis (in that order)
RFs
- female
- pregnancy
- chronic Hep B
- fasting / malnutri’n
- chronic paracetamol use
- chronic alcohol misuse → alcohol = bad for liver b/c alcohol dehydrogenase converts it to acetylaldehyde which generates ROS
SSX
- tenderness on right side
- pruritus due to elevated bilirubin
- fetor hepaticus = rotten egg / garlic breath
- hepatic encephalopathy SSX i.e confus’n, agita’n, irritability
Ix’s
- INR > 1.5
- LFTs → hyperbilirubinemia + elevated ALT + AST
- U + E → elevated urea + creatinine (due to renal failure)
Complica’ns
- GI bleed
- renal failure
- cerebral edema
- hepatic encephalopathy
⚠️ Safe dose of paracetamol in 24hrs = 4g !
→ gets conjugated into NAPQI by glutathione which is safe but when there’s too much paracetamol, glutathione gets depleted + we get oxidized free radicals which damage hepatocytes via the peroxida’n of lipids in cell membranes
→ paracetamol overdose Tx = IV N-acetylcysteine b/c it replenishes glutathione
Addi’nal Mx
- check salicylate levels
- psych assess’nt
- Know for OSCE *
Drugs that can precipitate hepatic encephalopathy in pts w/ chronic liver disease ✓
- drugs w/ constipating effects i.e opioids
- drugs that ↓ K i.e loop + thiazide diuretics b/c HypoK ↑ renal ammonium produc’n
- drugs w/ sedative effects i.e benzos / antihistamines such as chlorphenamine
Drinking recommenda’ns ✓
Max of 14 units / wk spread evenly over ≥ 3 days + max of 5 units in a single day
Equivalent of 1 unit
- 1/2 a pint of cider or weak beer
- 1/2 a small glass of wine
Larger/stronger vers’ns of the above = 3 units
What is Binge drinking ? ✓
- For men = > 8 units of alcohol in a single sess’n
- For women = > 6 units of alcohol in a single sess’n
Pathophys of alcohol + brain ✓
Alcohol = depressant so stimulates GABA receptors in brain → relaxing effect on rest of brain
→ alcohol also inhibits NMDA / glutamate receptors → further relaxing effect b/c glutamate = excitatory neurotransmitter → so in chronic drinkers, body’s way of compensating is to down regulate GABA system + up regulate glutamate system
NAFLD ✓
Def - excessive fat in liver cells, specifically triglycerides
RFs
- HTN
- obesity
- smoking
- diabetes
- dyslipidemia
- sedentary lifestyle
- metabolic syndrome
Pathophys - fat deposits interfere w/ normal func’ning of liver cells
Progress’n - NAFLD → NASH (Non-alcoholic steatohepatitis) → fibrosis → cirrhosis
SSX = asymptomatic
Ix’s
- LFTs → raised ALT
- Liver Bx = gold std → will tell you if it’s in hepatitis stage or cirrhosis stage
- Liver U/S to see if it has progressed to hepatic steatosis → will see ↑ed echogenicity if that’s the case
- ELF (enhanced liver fibrosis) blood test to see if progressed to fibrosis
→ measures HA, PIIINP + TIMP-1)
⟹ < 10.51 means advanced fibrosis = unlikely (check this every 3 yrs in NAFLD pts)
⟹ > 10.51 means there’s advanced fibrosis - Transient elastography / FibroScan to check if fibrosis has progressed to cirrhosis
Tx
- exercise
- weight loss
- Mediterranean diet
- alcohol + smoking cessa’n
- controlling diabetes, HTN + HLD
- refer to liver specialist if there’s fibrosis → might give vitamin E, pioglitazone
- liver transplanta’n in end stage liver disease
Complica’n = cirrhosis
SSX of alcohol intoxica’n ✓
- tremor
- slurred speech
- bloodshot eyes
- smelling of alcohol
- telangiectasia i.e dilated capillaries on the face
Diagnostic criteria for alcohol dependence ✓
≥ 1 of the following SSX . . . (“CT WPOC”)
- Compul’sn to drink
- Tolerance
- W/drawal SSX
- Primacy
- Ongoing use
- Control loss
Alcohol w/drawal ✓
Ix’s
- FBC
- U + E
- LFTs
- B12
- folate
- Mg
- lipase
- glucose
- CRP
- CK
- head CT if head injury = suspected
SSX of alcohol w/drawal i.e 6-12 hrs later . . .
- tremors
- anxiety
- agita’n
- irritability
- loss of appetite
- N/ V
- sweating
→ 24-72 hrs after stopping = window for delirium tremens
⟹ SSX of delirium tremens = above + tachycardia, pyrexia + visual hallucina’ns = medical emergency !
Tx for DT = ABCDE if pt has seizure + high flow O2 + IV lorazepam or IM Haloperidol
Tx for regular w/drawal SSX = chlordiazepoxide HCl (Librium) or diazepam
Wernicke’s Encephalopathy ✓
Def - neurological emergency caused by thiamine deficiency
→ usually due to chronic alcohol overconsump’n b/c alcohol ↓ thiamine absorp’n
RFs
- AIDS
- chemo
- malnutri’n
- previous GI Sx
- alcohol dependence
SSX
- mental slowing
- confus’n
- impaired [ ]
- ataxia i.e difficulty w/ coordinated mov’nts
- ocular motor findings i.e gaze palsies, CN 6 palsies, impaired vestibulo-ocular reflexes
Ix’s
- therapeutic trial of parenteral thiamine → diagnosis = clinical improv’nt after admin of thiamine
- LFTs to see if due to alcohol related liver disease
- serum ammonia to r/o metabolic encephalopathy 2° to hyperammonemia
Emergency Tx = IV Pabrinex(thiamine) for 5-7 days
→ oral thiamine
→ multivitamin to replenish deficient vitamins
Complica’ns
- seizures
- hearing loss
- Korsakoff syndrome
→ Korsakoff syndrome = amnestic disorder caused by chronic alcohol overuse
⟹ SSX = confabula’n, personality Δs + permanent memory loss i.e pt can’t form new memories
Alcohol related liver disease ✓
Eti = long term excessive alcohol consump’n
RFs
- hep C
- female
Pathophys - excess drinking causes buildup of fat in liver (this is reversible w/ abstinence from alcohol) → alcohol related hepatitis (usually reversible w/ permanent abstinence from alcohol if it’s mild) → alcohol induced cirrhosis
Ix’s
- AST + ALT = elevated
- AST : ALT ratio > 2
Tx
- alcohol w/drawal Mx via oxazepam PO or IV diazepam → lorazepam PO
- weight loss + smoking cessa’n
- nutri’nal supplementa’n
- influenza + pneumococcal vaccines
- corticosteroids in severe alcoholic hepatitis
Complica’ns
- portal HTN
- coagulopathy
- renal failure
- hepatocellular carcinoma
- Wernicke-Korsakoff Syndrome (WKS) = Wernicke encephalopathy + Korsakoff syndrome
How to screen for harmful alcohol use ? ✓
“CAGE”
C = Cut down → ask pt if they ever think they should cut down ?
A = Annoyed → do they get annoyed when others comment on their drinking ?
G = Guilty → do they ever feel guilty about drinking ?
E = Eye opener → do they ever drink in the morning to help hangover or nerves ?
Cirrhosis ✓
Def - end stage of chronic liver disease = characterized by fibrosis + regenerative nodules b/c of liver trying to regenerate itself
→ 5 yr survival = 50% once it has developed
RFs
- obesity
- IV drug use
- alcohol misuse
- unprotected sex
Eti
- Hep B / Hep C
- NAFLD
- autoimmune hepatitis
- alcohol related liver disease
SSX
- melena
- hematemesis
- telangiectasia
- jaundice + pruritus
- spider nevi (> 5 = pathological)
- bruising due to abnormal clotting
- leukonychia due to hypo-albuminemia
- portal HTN b/c cirrhosis ↑ resistance to blood flow livers ∴ causing ↑ed back pressure on portal system
- thrombocytopenia b/c portal HTN → splenomegaly → ↑ed plt destruc’n
- ascites due to portal HTN
- esophageal varices / caput medusa due to portal HTN b/c back pressure in portal system causes swollen + tortuous vessels @ sites where collaterals form btw portal + systemic venous systems
Ix’s
- Liver Bx to confirm it’s cirrhosis
→ Mallory bodies = sign of irreversible liver cell injury - albumin → will be low
- U + E → HypoNa + HyperK
- clotting profile → prolonged prothrombin time
- LFTs → hyperbilirubinemia + elevated ALT + AST
- U/S to screen for hepatocellular carcinoma
Mx
- MELD score every 6 months for estimated 3 month mortality chance → uses Cr, bilirubin, INR + Na
- U/S + AFP every 6 months for hepatocellular carcinoma screening
- Endoscopy every 3 yrs to check for esophageal varices = asymptomatic until they start bleeding
→ due to the high blood flow, bleeding from varices can cause patients bleed out very quickly - Child-Pugh score to assess severity of cirrhosis + prognosis
→ give score of 1-3 for each
→ “ABCDE” mnemonic . . .
A = Albumin
B = Bilirubin
C = Clotting i.e INR
D = Dila’n i.e ascites
E = Encephalopathy
→ score of 5-6 = class A → 1yr survival = 100%
→ score of 7-9 = class B → 1yr survival = 80%
→ score of > 10 = class C →1yr survival = 45%
Tx
- Treat underlying cause i.e . . .
- lifestyle Δs for NAFLD
- antiviral drugs for hep C
- immunosuppressants for autoimmune hepatitis - Liver transplant if they have features of decompensated liver disease i.e “AHOY” . . .
A = Ascites
H = Hepatic encephalopathy
O = Oesophageal varices
Y = Yellow (jaundice)
Complica’ns
- bleeding + thrombosis
- ascites due to portal HTN
- hepatocellular carcinoma
- spontaneous bacterial peritonitis due to ascites
- malnutri’n b/c cirrhosis ↓ amt of protein liver produces + disrupts ability of liver to store glucose as glycogen / release glucose from glycogen
- cachexia b/c less protein = available to maintain muscle tissue + muscle tissue = broken down for fuel since liver isn’t releasing glucose when needed
- hepatorenal syndrome b/c portal HTN causes portal vessels to release vasodilators → vasodila’n leads to ↓ in BP → kidneys respond by activating RAAS → renal vasoconstric’n results in kidneys being starved of blood
- hepatic encephalopathy b/c liver cells can no longer metabolize ammonia + collateral vessels btw portal + systemic circula’n means ammonia can bypass liver + directly enter systemic system
→ main SSX = asterixis
→ Tx = lactulose → PO4 enemas → stop diuretics if Na < 130mmol/L → avoid sedatives → consider IV broad spectrum ABs such as rifaximin (can only be initiated by hepatology consultant !) - Know for OSCE *
⚠️ Liver enzymes = poor indicators of liver func’n b/c are usually low in end-stage cirrhosis
→ albumin + INR/PT = better
⟹ PT = even better than albumin due to shorter half life
Viral Hepatitis ✓
ALL 5 ARE NOTIFIABLE DISEASES !
- Hep A = RNA virus, can get vaccinated for it before travelling to endemic area such as S. Asia
→ incuba’n period = 2-4 wks
→ most common viral hepatitis worldwide is but rare in the UK
→ Tx = supportive b/c resolves on its own - Hep B = reverse transcriptase DNA virus, has vaccine, incuba’n period = around 10 wks
→ Tx = nothing b/c is
self limiting but can often give anti viral therapy to slow progress’n
⟹ 2 consecutive tests conducted ≥ 3 months apart = needed before starting antiviral therapy - Hep C = RNA virus, no vaccine
→ Tx = direct-acting antivirals - HepD = RNA virus, no vaccine
→ Tx = pegylated interferon 𝛼 - HepE = RNA virus, no vaccine, incuba’n period = 1-2 months
→ Tx = supportive
→ A+E = fecal oral route i.e via ingest’n of contaminated food/water or direct contact w/ infected person
→ B+C = blood or other bodily fluids i.e sex (B can also transfer perinatally i.e vertical transmiss’n), RFs = needles + unsafe sex
→ D = have to get B first
Hep B
Def- most common liver infec’n worldwide = caused by HBV i.e Hep B virus
RFs
- IV drug use
- incarcera’n
- sex workers
- unprotected sex
- men who have sex w/ men
- mom w/ Hep B during pregnancy
- endemic reg’n such as Asia or Africa
Eti
- chronic viral hepatitis
- alcohol related liver disease
- non alcoholic fatty liver disease (NAFLD)
- less common causes = hemochromatosis, CF, autoimmune hepatitis
Asymptomatic
Ix’s
- LFTs → elevated ALT + AST + maybe hyperbilirubinemia
- albumin → will be low
- U + E → HypoNa
- Hep B surface antigen (HBsAg)
→ +ve means ACTIVE infec’n (will be detected 4 wks after exposure to virus) - Hep B surface antibody (HbsAb)
→ +ve means past infec’n / current infec’n / vaccinated - IgM/IgG core antibodies
→ useful b/c will appear after window for HBsAg has passed + before HbsAb appears
→ +ve IgM w/ high titre = ACTIVE ACUTE INFEC’N
→ + ve IgM w/ low titre = ACTIVE CHRONIC INFEC’N
→ +ve IgG = PAST INFEC’N - e antigen → +ve means ACTIVE infec’n + that’s it’s very early in infec’n ∴ pt is the MOST CONTAGIOUS they can be
- serum HBV DNA = direct count of viral load (used to monitor response to Tx) ∴ might initially be high but should then be 0 if Tx is working
Who should get nucleoside analogue Tx i.e antiviral therapy ?
a) ≥ 30 y/o + HBV DNA > 2000 + abnormal ALT
b) < 30 y/o + HBV DNA > 2000 + abnormal ALT + evidence of fibrosis
c) HBV DNA > 20,000 + abnormal ALT
d) Detectable HBV DNA + cirrhosis
Complica’ns
- cirrhosis
- Hep B reactiva’n
- fulminant liver failure
- hepatocellular carcinoma
- Hep B associated glomerulonephritis
Hep C (= more chronic)
RFs
- incarcera’n
- sex workers
- unprotected sex
- IV/intranasal drug use
- men who have sex w/ men
- needle injury in healthcare
- HIV (these pts = less likely to clear Hep C)
Eti
- chronic viral hepatitis
- alcohol related liver disease
- non alcoholic fatty liver disease (NAFLD)
- less common causes = hemochromatosis, CF, autoimmune hepatitis
No SSX b/c = asymptomatic
Ix’s
- HCV antibody enzyme immunoassay (EIA) for screening
→ +ve means ACTIVE OR PAST infec’n - HCV RNA PCR for diagnosis
→ +ve means ACTIVE INFEC’N - LFTs → ALT might be high
Tx = Direct-Acting Antivirals (DAAs) i.e sofosbuvir / daclatasvir
Complica’ns
- cirrhosis
- skin complica’ns
- hepatocellular carcinoma
- cryoglobulins in skin / kidneys (@ low temps)
- Know for OSCE *
Autoimmune Hepatitis ✓
Def - chronic inflammatory disease of the liver of unknown etiology
RFs
- immune dysregula’n
- HLA genetic pre disposi’n
- female sex (just like most auto immune condi’ns)
Types
- Type 1 → typically affects women in their late 40s/50s
→ presents around or after menopause
→ SSX = fatigue + features of liver disease = more chronic progress’n than type 2
→ auto antibodies = ANA, anti-actin + anti SLA/LP - Type 2 → usually affects young girls
→ presents w/ acute hepatitis , jaundice + high transaminases (i.e ALT + AST)
→ auto antibodies = anti-LKM1 + anti-LC1
Ix’s
- albumin → will be low
- INR → PT will be prolonged
- γ globulins → will be high
- LFTs → hyperbilirubinemia + elevated ALT + AST
- Liver Bx → will show interface hepatitis + plasma cell infiltra’n
Tx = high dose corticosteroid i.e prednisolone + immuno-suppressants such as azathioprine to control disease
Complica’ns = side effects of long term corticosteroid use
- Know for OSCE *
Liver cancer ✓
→ 1° liver cancer = cancer originates from liver
⟹ main type = hepatocellular carcinoma
→ 2° = cancer metastasized to liver but originates from somewhere else
RF = cirrhosis
SSX = weight loss + liver disease SSX
Ix’s
- liver U/S = 1st line
- 𝛼 fetoprotein (AFP) = tumor marker for hepatocellular carcinoma
- CT + MRI for staging
- Bx for histology
Barcelona Staging
- Stage 0 = single tumor < 2cm + liver is working normally
- Stage A = up to 3 tumors that are all < 3 cm + liver is working well
- Stage B = > 3 tumors in liver but liver is still working well
- Stage C = cancer has spread elsewhere or pt doesn’t feel well / is less active
- Stage D = severe liver damage
Tx
- Stage 0 or A + good surgical candidate = resec’n or thermal abla’n
- Stage 0 or A but NOT good surgical candidate = RFA → TACE (transarterial chemo-emboliza’n) = IR procedure
- Stage B = TACE or TARE
- Stage C = monoclonal antibody → TARE after trying 2 monoclonal antibodies
- Stage D = hospice +/- liver transplant
- Know for OSCE *
Upper GI bleed ✓
Def - bleeding from esophagus, stomach or duodenum
→ blood loss originates proximal to ligament of Treitz (= @ duodojejunal junc’n)
→ source of bleeding = gastroduodenal artery usually
Eti
- peptic ulcers = most common cause → should definitely suspect this as cause of upper GI bleed in pt w/ Hx of chronic NSAID use
- esophageal varices → usually 2° to portal HTN in pts w/ Hx of alcohol misuse
- gastric carcinoma → will be accompanied w/ unwanted weight loss + usually seen in “high risk” pts i.e male smokers > 55 y/o who maybe have past Hx of H. pylori infec’n
- Mallory-Weiss tear = tear of esophageal mucosa
SSX (1 is enough)
- melena
- hematemesis
- bright red blood on NG tube
- coffee ground emesis (looks like coffee ground due to exposure to stomach acid)
Ix - Glasgow Blatchford score or Rockall’s score if after an endoscopy
→ w/ Glasgow-Blatchford Bleeding Score, score > 0 means pt = @ high risk for upper GI bleed
U + E → elevated urea
Emergency Tx = “ABATED”
A = ABCDE
B = Bloods i.e . . .
→ FBC for Hgb + platelets
→ U+E for urea
→ INR
→ LFTs to check if due to liver disease
→ crossmatch 2 units of blood
A = Access (ideally 2 large bore cannulas)
T = Transfus’n
→ FPP (contains blood, platelets + clotting factors (fresh frozen plasma) for pts w/ MASSIVE bleed
→ Platelets in pts w/ active bleed + platelet count < 50
→ Prothrombin complex concentrate in pts on warfarin
E = Endoscopy (must be done w/in 24 hrs)
D = Drugs → stop anticoagulants + NSAIDs + give terlipressin +
broad spectrum Abx if due to esophageal varices
⚠️ In hypovolemic shock tachycardia comes BEFORE hypoTN, hypoTN comes after loss of > 15% of blood volume !
- Know for OSCE *
Lower GI bleed ✓
Def - GI blood loss originating after duodojejunal junc’n
Eti
- Crohn’s
- anal fissure
- colon polyps
- ischemic colitis
- infectious colitis
- rectal cancer
- diverticular disease
- internal hemorrhoids
- Meckel’s diverticulum (occurs @ around age 2)
→ SSX = abdo pain + tenderness in RIF + bloody stool
→ Littre’s hernia = protrus’n of meckel’s diverticulum through an abdominal weakness
SSX = hematochezia i.e bright red blood per rectum
Emergency Tx i.e if theres’s hypoTN + tachycardia = IV fluids + transfus’n if there’s sig. active blood loss
- Know for OSCE *
Gastric cancer ✓
Def - stomach cancer
→ 2 most common types = intestinal type adenocarcinoma + diffuse type adenocarcinoma
RFs
- smoking
- High Na diet
- gastrectomy
- pernicious anemia
- H. pylori infec’n (strongest RF)
- polyp w/ medium grade dysplasia
- intestinal metaplasia of columnar type @ gastric cardia
- nitrate consump’n b/c bacteria in mouth can convert nitrate to nitrite (is an additive in cured meats)
SSX
- N + V
- dysphagia
- abdominal pain
- unwanted weight loss
- Trosier’s sign (indicates metastasis)
Ddx = peptic ulcer disease
Ix’s
- metabolic panel
- FBC → might show anemia
- upper GI endoscopy + Bx → signet ring cells will show prominent invasive growth w/in all layers of gastric wall
Tx
- localized = Sx or chemo-radiotherapy if pt ≠ suitable for Sx
- metastasized = chemo
- Know for OSCE *
Metaplasia v.s Dysplasia ✓
- Metaplasia = cell changes into another cell type but that other cell type is a normal cell type
→ can be pathological like in GERD or physiological like the cervix during puberty
= reversible if agent that caused the change = removed but if progresses into dysplasia = irreversible - Dysplasia or carcinoma in situ = normal cell becomes an abnormal cell = pre-malignant i.e can lead to cancer
→ ≠ cancer b/c base’nt membrane hasn’t been invaded + has no metastatic Ψ due to lack of access to lymph or blood
GERD ✓
In adults
RFs
- FHx
- male
- obesity
- older age
- alcohol + smoking
- hiatus hernia = hernia’n of stomach up through diaphragm
SSX = “DOAC”
- Dysphagia + Dyspepsia
→ dypepsia = pain after eating /
bloating / hoarse voice
- Odynophagia
- Acid regurgita’n i.e heartburn
- Chest pain (epigastric pain) = made worse by lying down or bending forward, @ night or after eating spicy foods
Ddx = peptic ulcer disease
Ix’s
- 1st line = PPI trial i.e put them on PPI + see if SSX improve
- gold std = 24hr ambulatory pH monitoring
→ pH of esophagus will be < 4 which is abnormal (only do if diagnosis = uncertain) - EGD → will show erosive esophagitis or Barrett’s esophagus
Tx
- Lifestyle Δs i.e weight loss, smoking cessa’n + avoiding known precipitants such as alcohol / coffee / fatty foods / citric foods
- Full dose PPI for 1-2 months (lasoprazole)
⟹ MOA - irreversibly inhibits H+/ K ATPase in parietal cells ∴ can’t export H+ into gastric lumen, so no HCl produc’n
⟹ side effects = loose stools + ↓ed Fe absorp’n b/c gastric acid ↑ iron absorp’n + these medica’ns ↓ gastric acid
⟹ end in “PRAZOLE”
→ H2 receptor antagonist such as ranitidine if PPI doesn’t work
⟹ MOA - ↓ gastric acid secre’n by reversibly binding to histamine H2 receptors on parietal cells
⟹ side effect = gynecomastia
⟹ end in “DINE”
Complica’ns
- erosive esophagitis (most common complica’n) → can cause ulcers, bleeding + stricture
- Barrett’s esophagus = stratified squamous epithelia of esophagus is becoming like epithelium of stomach i.e non ciliated columnar w/ goblet cells = ex of metaplasia → can lead to esophageal adenocarcinoma
In Children - usually occurs in children < 2 months old
SSX
- NBNB emesis
- chronic cough
- hoarse cry
- poor weight gain
- unexplained reluctance to feed
- distress after feeding
- faltering growth
Ddx of vomiting in children
- overfeeding
- appendicitis
- gastroenteritis
- Intestinal obstruc’n
- pyloric stenosis (NBNB emesis as well)
- infec’ns such as UTI / tonsillitis / meningitis
Ix = clinical but refer them to pediatrician if it persists after pt is 1 y/o or if pt is not responding to Tx
Tx
- Trial alginate therapy if baby = breastfed or thickened formula feeds if baby = bottle fed
- PPI trial if pt has ≥ 1 of the following . . .
- unexplained feeding difficulties
- distressed behavior
- growth faltering
Advice to give to parents
- don’t overfeed baby
- small, frequent meals
- keep baby upright after feeding
- regular burping to help milk settle
- Know for OSCE *
Alarm GERD SSX that require urgent endoscopy referral (i.e < 2 wk wait) to check for Barrett’s ✓
- N + V
- anemia
- GI bleed
- weight loss
- raised platelet count
- dysphagia regardless of age
- new dyspepsia + pt > 55 y/o
- FHx of GI cancer in 1st ° relative
- upper abdominal mass on palpa’n
H. pylori ✓
Def - spiral shaped gram -ve bacteria associated w/ chronic gastritis + peptic ulcers (especially duodenal ulcers) = RF for peptic ulcer disease, gastric adenocarcinoma + MALT lymphoma
→ produces ammonium OH which creates alkaline env’nt that helps it survive in acidic mucosa of stomach antrum but that in turn causes gastric mucosal damage
→ test all pts who present w/ dyspepsia for H. pylori
⟹ pt had to have been 2 wks PPI free for test to be accurate
Ix’s
- stool antigen test
- urea breath test (uses radiolabeled carbon 13)
- H. pylori antibody test (blood)
- rapid urease test during endoscopy (also known as CLO test) → involves taking a small Bx of stomach mucosa → sample = added to liquid medium that contains urea → ↑ in pH means pt = H. pylori +ve
Tx = Triple therapy for 7 days i.e 2 Abx (amoxicillin + clarithromycin) + 1 PPI
→ amoxicillin MOA = penicillin i.e β lactam AB → inhibits bacterial cell wall forma’n by inhibiting cross-linking of peptidoglycan in bacterial cell wall (but some bacterial strains such a E. coli are resistant to β lactam Abx b/c produce β lactamase = enzyme that breaks down β lactam rings)
⚠️ Use metronidazole instead if pt has penicillin allergy
= nitroimidazole Abx that damages bacterial DNA
→ clarithromycin MOA = macrolide → inhibit 50S subunit of bacterial ribosomes = bacteriostatic AB b/c inhibits bacterial protein synthesis
→ side effects = prolonged QT interval + diarrhea b/c also kills guts flora
→ C/Is = pregnancy, prolonged QT interval
→ end in “OMYCIN” (vancomycin ≠ macrolide)
- Know for OSCE *
Peptic ulcer disease ✓
Def - break in mucosal lining of stomach or duodenum > 5mm in diameter all the way down to submucosa ( < 5mm or w/o depth = EROS’N NOT ULCER !)
RFs
- ↑ing age
- smoking
- FHx of peptic ulcer disease
- Past Hx of peptic ulcer disease
- H. pylori infec’n + chronic NSAID use = strongest RFs
Eti = H. pylori infec’n or NSAID use
Pathophys
→ duodenal ulcers = usually due to hypersecre’n of gastric acid in H. pylori infec’n = more common
→ gastric ulcers = due to longstanding H.pylori infec’n + severe inflamma’n → gastric mucin degrada’n (mucin = viscous gel-like bicarb protective layer secreted by surface mucus cells)
SSX
- N + V
- dyspepsia
- upper GI bleed SSX
- epigastric / abdominal pain (radiating to back for duodenal ulcer)
→ gastric ulcer pain = worse after eating hence these pts tend to LOSE weight
→ duodenal ulcer pain = worse @ night + w/ stress but better after eating hence these pts tend to GAIN weight
Ix’s
- upper GI endoscopy for diagnosis
- H. pylori C-13 urea breath test or stool antigen test to check for H. pylori
- Lipase might be elevated
Tx = stop NSAIDs + full dose PPI therapy for 4-8 wks (even if pt = H.pylori -ve)
Complica’ns
- upper GI bleed from ulcer (most common complica’n)
- scarring + stricture
- gastric outlet obstruc’n = narrowing of exit of stomach due to scarring + stricture → SSX = early fullness after eating, upper abdominal discomfort, abdominal disten’n + vomiting (particularly after eating)
→ can be treated w/ balloon dila’n during an endoscopy or in OR - perfora’n (= life threatening so must be urgently treated w/ surgical repair) → can cause peritonitis
⟹ SSX of peritonitis = pyrexia, tachycardia
⟹ SSX on exam . . . - rigidity
- guarding = involuntary tensing of abdominal wall muscles on palpa’n to protect painful area below
- rebound tenderness = when rapidly releasing pressure on abdomen creates worse pain than the palpa’n itself
- Know for OSCE *
The various MOAs of NSAIDs ✓
- anti inflammatory via ↓ vasodila’n hence ↓ blood flow hence less inflammatory mediators can come
- anti pyretic via inhibi’n of PG synthesis in hypothalamus
- analgesic via ↓ PG synthesis which control nociceptors
→ COX 1 = affects GI ∴ ONLY non selective NSAIDs will cause GI SSX b/c will bind to both COX-1 + COX-2
→ COX 2 selective = NO GI SSX !
⚠️ NSAIDs can ↓ the anti-hypertensive effects of ACE-Is !
Gastritis ✓
Def - inflamma’n of gastric mucosa
RFs
- alcohol
- NSAID use
- H. pylori infec’n
- auto immune disease
Eti
- NSAIDs / alcohol
- chronic H. pylori infec’n → induces inflamma’n w/ gastric mucin degrada’n + ↑ed mucosal permeability
- auto immune atrophic gastritis → anti-parietal cell antibodies stimulate a chronic inflammatory, mononuclear + lymphocytic infiltrate involving oxyntic mucosa ∴ leading to loss of parietal + chief cells in gastric corpus
SSX
- N/V
- anorexia
- dyspepsia
Ddx
- GERD
- peptic ulcer disease
Ix = H. pylori C-13 urea breath test or stool antigen test → might test +ve for H. pylori
Tx = treat cause
Complica’ns
- achlorhydria
- B12 deficiency
- gastric carcinoma
- gastric lymphoma
- Know for OSCE *
Esophageal cancer ✓
Def - cancer of the esophagus
→ 2 main types = SCC + adenocarcinoma
RFs
- FHx (SCC)
- male (both)
- alcohol (SCC)
- smoking (both)
- older age (both)
- GERD (adenocarcinoma)
- hiatal hernia (adenocarcinoma)
- Barrett’s esophagus (adenocarcinoma)
SSX
- dysphagia
- odynophagia
- unwanted weight loss
Ddx = achalasia
Ix’s
- EGD + Bx
- CT thorax + abdomen → for metastasis
- FDG PET scan → for metastasis that CT might not have identified
Tx = Sx → chemoradiotherapy
- Know for OSCE *
Achalasia ✓
Def - esophageal motility disorder due to impaired relaxa’n of lower esophageal sphincter i.e LES fails to open during swallowing
SSX
- dysphagia
- regurgita’n
- weight loss
- substernal chest pain
Ix’s
- EGD → bird beak appearance
- Upper GI swallow
- Manometry
Tx
- CCB or sublingual isosorbide dinitrate while waiting for definitive Tx
- botulinum toxin → gastostomy if needed (for poor surgical candidates)
- Heller’s cardiomyotomy = indicated for. . .
→ pts < 40 y/o who will require lifelong dila’ns or botulinum toxin injec’ns
→ pts w/ recurrent or persistent SSX after multiple medical Tx
→ pts who choose Sx initially
→ pts at high risk for perfora’n w/ pneumatic dila’n i.e pts who had prior Sx in esophagogastric junc’n
Complica’ns
- GERD
- esophagitis
- esophageal perfora’n
- aspira’n pneumonia
- esophageal cancer
Eosinophilic Esophagitis ✓
Def - chronic, immune / allergen mediated condi’n where eosinophils build up in esophagus
RFs
- male
- FHx
- children / young adults
- white
- Hx of atopy
Pathophys - eosinophil build up in esophagus → damage + inflamma’n of esophagus
SSX
- heartburn
- chest pain
- dysphagia
Ix’s
- EGD
→ can be normal or can show . . . - fixed esophageal rings
- focal esophageal strictures
- diffuse esophageal narrowing
- crêpe-paper mucosa
- Bx for diagnosis
→ peak eosinophilic count ≥15 +/- eosinophil micro abscesses, layering, degranula’n + subepithelial sclerosis
Tx
1. Topical corticosteroid (budesonide) or PPI for 8-12 wks
2. Repeat EGD + Bx
3. Maintenance therapy or ↑ dose
Complica’ns
- FTT
- esophageal stricture
- esophageal perfora’n
IBD ✓
Crohn’s
Def - autoimmune condi’n that causes transmural i.e full-thickness inflamma’n of the entire GI tract, extends from mouth to anus, TI = linked to genetic defect in NOD-2 gene
RFs
- FHx
- white ethnicity
- 15-40 y/o or 50-60 y/o
- smoking (= protective factor for UC)
SSX
- RIF pain
- weight loss
- mouth ulcers
- prolonged diarrhea
- perianal les’ns i.e skin tags / fistulae / abscesses / anal fissure
- NO PR BLEEDING !
Ddx
- UC
- IBS
- appendicitis
- ectopic pregnancy
Ix’s
- FBC → might show anemia
- B12 → might be low
- Fe study → b/c IBD pts = @ risk of malnutri’n
- ESR / CRP → will be elevated
- OGD + Bx for diagnosis
Tx = oral corticosteroids such as prednisolone → immuno-modulators such as methotrexate / infliximab / dalimumab if SSX = poorly controlled
Complica’ns
- gallstones
- anal fissure
- colorectal cancer
- intestinal obstruc’n
- fistulae / abscesses
- anemia / B12 deficiency
UC
Def - inflamma’n confined to mucosal + submucosal layer of colon, rectum = almost always involved
RFs
- infec’n
- FHx of IBD
- human leukocyte antigen B-27
SSX
- rectal bleeding
- painless red eye
- bloody / mucus diarrhea
- SSX of severe UC = > 6 bloody stools / day + ≥ 1 of the following …
→ fever > 37.8°C
→ tachycardia > 90 bpm
→ Hgb < 10.5g/dl
→ ESR > 30mm/hr
Ddx
- IBS
- Crohn’s
- diverticulitis
Ix’s
- stool microscopy + culture to r/o infec’n
- fecal calprotectin → will be elevated
- EGD + Bx for diagnosis
- FBC → might slow high platelet b/c of inflamma’n + in UC might show anemia
- CRP → will be elevated
- albumin b/c in severe disease might be low
Acute Tx for severe = IV hydrocortisone
Acute Tx for mild-moderate = aminosalicylate → corticosteroid
Regular Tx = oral aminosalicylate (end in “SALAZINE”)
Complica’ns
- stricture
- perfora’n
- colorectal cancer
- massive lower GI bleed
- 1° sclerosing cholangitis (PSC)
→ = diagnosed w/ MRCP → will show beaded appearance of CBD
- toxic megacolon = atonic colon w/ dilata’n = @ risk of perforating ∴ = surgical emergency !
→ presenta’n = rigid abdomen + dilated loops of colon on AXR
→ Tx = subttl colectomy w/ end ileostomy
- Know for OSCE *
UC v.s Crohn’s Histology ✓
→ Crohn’s . . .
- cobblestone
- patchy (skip les’ns)
- transmural so isn’t just limited to 1 area
- wall thickening
- stricture
- deep knife-like / fissuring ulcers
- epitheloid i.e non-caseating granulomas
- goblet cells
→ UC
- mucosal inflamma’n w/ broad + superficial mucosal ulcers
- pseudopolyps
- diffuse
- extends proximally from rectum continuously
- wall thinning
- crypt abscess
Celiac Disease ✓
Def - autoimmune disease triggered by eating gluten
RFs
- FHx
- T1D
- Down’s
- IgA deficiency
- auto immune thyroid disease
Eti = exposure to gluten (even in trace amts)
→ must carry either HLA-DQ2 (in 95% of pts) or HLA-DQ8 to have Celiac !
SSX
- anemia
- bloating
- weight loss
- steatorrhea
- IgA deficiency
- FTT in children
- chronic diarrhea
- abdominal pain / discomfort
- dermatitis herpetiformis = pruritic les’ns over buttocks + arms / legs / trunk due to IgA deposi’n
Ix’s
- IgA + Anti TTG IgA antibodies = 1st line
→ antibodies will be normal or elevated (normal doesn’t exclude diagnosis !)
OR Anti TTG IgG or anti EMA antibodies if pt = IgA deficient → elevated
- Endoscopy + duodenal Bx = gold std → will show subttl villus atrophy, crypt hypertrophy + intra epithelial lymphocytes
Tx = lifelong gluten free diet
Complica’ns
- dermatitis herpetiformis
- osteoporosis / osteopenia
- iron /B9 / B12 deficiencies
- hyposplenism b/c of excessive loss of lymphocytes
- Know for OSCE *
Who should be tested for Celiac ? ✓
Adult w/ new diagnosis of T1D OR child w/ FHx of celiac, autoimmune thyroiditis, T1D, juvenile chronic arthritis, Down, Turners’ or selective IgA deficiency OR child w/ any of the following SSX . . .
- FTT
- chronic constipa’n
- persistent diarrhea
- dermatitis herpetiformis
- recurrent abdominal pain
⚠️ Don’t start pt on gluten free diet w/o having an official diagnosis of Celiac !
- Know for OSCE *
Cow’s milk protein allergy ✓
Def - condi’n in children < 1 y/o where their body doesn’t react well to cow’s milk (≠ the same as lactose intolerance !)
→ can present in breastfed babies if mom consumes dairy products
→ in IgE mediated rxn occurs w/in 2 hrs of consuming milk v.s in non-IgE mediated can occur over several days
RFs
- being formula-fed
- personal or FHx of other atopic condi’ns
SSX
- vomiting
- weight loss / FTT
- watery stools
- atopic dermatitis
- distended non-tender abdomen
- allergic rxn SSX such as hives, angioedema, watery eyes, sneezing
Tx = mom has to exclude dairy from her diet + can use hydrolyzed formula instead
- Know for OSCE *
IBS ✓
Def - chronic abdominal pain + bowel dysfunc’n
RFs
> 50 y/o
- FHx
- PTSD
- female
- physical / sexual abuse
- previous enteric infec’n
SSX =”ABC”
→ consider IBS if pt has had the following SSX for ≥ 6 months . . .
- abdominal pain (often relieved w/ defeca’n)
- bloating
- Δ in bowel habit
Ddx
- IBD
- Celiac
- infec’n
Ix = FBC to r/o infec’n
Tx
- exercise
- laxatives for SSX relief
- eliminating precipitating substances such as caffeine, lactose or fructose
Complica’n = diverticulosis
- Know for OSCE *
Anorexia nervosa ✓
Def - eating disorder characterized by low body weight due to restric’n of calorie intake + intense fear of gaining weight + distorted self-percep’n of body image
RFs
- female
- teenage / puberty
Diagnostic criteria
- restric’n of E intake that leads to a low body weight given pt’s age, sex, physical health + develop’ntal trajectory in the case of children
- intense fear of gaining weight / becoming fat or persistent behavior that prevents weight gain despite being underweight
- distorted percep’n of body weight + shape / disproportionate influence of weight + shape on self-worth or denial of seriousness of one’s low body weight
SSX
- bradycardia
- postural ↓ in BP
- cool peripheries
- significantly low body weight
- amenorrhea in women
Ddx
- depress’n
- bulimia nervosa
- hyperthyroidism
- avoidant restrictive food intake disorder = no distorted self image
Tx (goal = for pt to reach a healthy body weight)
1. Structured eating plan + psychotherapy (family therapy instead for pediatric pts)
2. Inpt admiss’n if their weight < 75% of where they should be
Bulimia nervosa ✓
Def - eating disorder characterized by recurrent episodes of binge eating followed by purging i.e compensatory behaviors such as self-induced vomiting, fasting, excessive exercise, misuse of laxatives / diuretics /enemas
RFs
- female sex
- personality disorder
- Hx of sexual abuse
- FHx of depress’n
- FHx of eating disorder
- FHx of alcohol use disorder
- childhood overweight or obesity
Diagnostic criteria
- Episodes of binge eating i.e pts feel that they can’t control their eating
- Inappropriate compensatory behavior to prevent weight gain
- Above behaviors must occur ≥ once/wk for a period of 3 months
- disproportionate influence of weight + shape on self-worth
- disturbance doesn’t occur exclusively during episodes of anorexia nervosa
SSX
- normal weight
- dental eros’n
- alkalosis on ABG
- parotid gland hypertrophy
- Russel’s sign = calluses on knuckles where they have been scraped across teeth → indicative of self-induced vomiting
Ddx
- MDD
- anorexia nervosa
- binge eating disorder = NO compensatory behaviors after episodes of binge eating
Tx = CBT for adults + family therapy for children → SSRI or SNRI
Transfus’n rxns ✓
RFs
- IgA deficiency
- prior pregnancy
- Hx of tranfus’n rxn
- Hx of transplanta’n
- previous transfus’n
- immuncompromised
Types
- Allergic / anaphylactic rxn = Type I hypersensitivity rxn against plasma proteins in transfused blood
→ minutes to 2-3 hrs due to release of pre-formed inflammatory mediators in degranulating mast cells
→ SSX = urticaria, pruritus, wheezing (anaphylaxis), hypoTN (anaphylaxis), respiratory arrest (anaphylaxis) + shock (anaphylaxis)
- Acute hemolytic transfus’n rxn = Type II hypersensitivity rxn caused by RBC destruction by IgM-type antibodies
→ during transfus’n or w/in 24 hrs due to pre-formed antibodies
→ SSX = fever, hypoTN, tachypnea, tachycardia, flank pain, hemoglobinuria (in intravascular hemolysis) + jaundice (in extravascular hemolysis)
- Febrile non-hemolytic transfus’n rxn = accumula’n of cytokines created by donor WBCs during storage of blood products, more common in children
→ SSX = fever, HAs, chills + flushing
- Transfus’n-related acute lung injury (TRALI)
→ occurs 6 hrs later
→ SSX = fever, cough, hypoTN, dyspnea/ tachypnea - Delayed hemolytic transfus’n rxn
= anamnestic response to foreign antigen on donor RBC previously encountered by recipient such as Rh D or other minor blood group antigens, typically causes extravascular hemolysis + is usually self-limiting
→ onset = over 24 hrs but usually presents w/in 1-2 wks due to slow destruc’n by reticulo-endothelial system
→ SSX = usually asymptomatic but pt can present w/ mild fever + hyperbilirubinemia
⚠️ Furosemide = safe Tx to give w/o having to worry about tranfus’n rxn
- Know for OSCE *
When should u transfuse ✓
When pt’s Hgb < 7
Anticoagulant vs Antiplatelet v.s Thrombolytic drugs ✓
- Anticoagulant = doesn’t prevent new clots from forming but prevents EXISTING clots from growing by inhibiting coagula’n cascade
- Antiplatelet = INHIBITS CLOT FORM’AN by preventing platelets from sticking together
- Thrombolytic drug = PROMOTES CLOT BREAKDOWN by activating thrombolysis / fibrinolysis
DIC (Disseminated Intravascular Coagula’n) ✓
Def - too much bleeding + clotting @ the same time
RFs
- organ destruc’n
- hematological malignancies
- major trauma such as burn or severe infec’n
Eti
- acute DIC = subacute bleeding + diffuse thrombosis
- chronic DIC = rapid onset bleeding + thrombosis → results in hypoperfus’n + infarc’n + end organ damage
Pathophys - continuous GENERA’N of intravascular fibrin + DEPLE’N of procoagulants + platelets → too much clotting + not enough clotting at the same time
SSX
- oliguria + hypoTN + tachycardia (when progresses to shock)
- SSX of thrombosis i.e purpura fulminant, gangrene, aural cyanosis
- SSX of bleeding i.e petechiae, ecchymosis (bruising), oozing, hematuria
Ix’s
- PT → will be prolonged
- FBC → thrombocytopenia
- fibrinogen → will be low
- D dimer → might be elevated
Emergency Tx = platelet transfus’n + coagula’n factors + coagula’n inhibitors
Complica’ns
- hemothorax
- hemorrhage
- acute renal failure
- cardiac tamponade
- intracerebral hematoma
- thrombosis → ischemia → gangrene → loss of digits
- Know for OSCE *
Coagula’n Panel ✓
- INR = ratio of pt PT to mean PT (PT= how much time it takes for blood to clot)
→ ↑ed INR = pt takes too long to clot
→ ↓ed INR = pt clots too quickly i.e likely to have DVT - PTT = used to see if heparin is working
P.E + DVT ✓
Embolism = occlus’n of a vessel by undissolved material that is transported via the circula’n such as a blood clot / air / fat
→ clinical effects of embolism depend on what vessel = occluded + what tissue that vessel supplied
RFs for PE (provoked = caused by identifiable RF)
- obesity
- smoking
- OCP use
- FHx of VTE
- pregnancy
- active malignancy
- recent VTE (vessel wall damage)
- immobility i.e Sx / long travel / bed rest for > 5 days (stasis)
→ can prevent it during Sx w/ intra-operative compress’n socks
- major physical trauma w/in past 2 months (vessel wall damage)
- genetic thrombophilias i.e protein C / protein S deficiency or antiphospholipid syndrome (hypercoagubility)
Eti for P.E = DVT 90% of the time + PVT 10% of the time (pelvis)
→ DVT Eti = Virchow’s triad . . .
a) Vessel wall damage - endothelial cell damage promotes thrombus forma’n, usually at venous valves
b) Venous stasis - poor blood flow aka stasis promotes thrombi forma’n
c) Hypercoagubility aka more prone to clot (usually genetic)
Pathophys of Clotting
- Thromboxane (TXA2) binds to platelets + makes platelets aggregate at site of injury
→ forms loose platelet plug (platelets adhere to plug via vWF) - Coagula’n cascade
→ Extrinsic pathway (= faster than intrinsic) : 12 activates 11 → 11 activates 9 → 9 forms complex w/ 8 → complex activates 10
→ Intrinsic pathway - 3 activates 7 → 7 activates both 9 + 10
⟹ both intrinsic + extrinsic result in activa’n of factor 10
→ Common pathway - 10 forms complex w/ 5 + Ca
→ that complex activates prothrombin activator
→ prothrombin activator activates 2
→ 2 goes from prothrombin to thrombin
→ 2 polymerizes / links w/ 1 (fibrinogen) to now become fibrin + activates 13 via Ca
→ 13 turns fibrin into fibrin mesh + now we have stable plug that shouldn’t easily dislodge
* Vit K = necessary b/c Vit K epoxide reductase needs to make Protein C + S func’nal + carboxylate 2, 7, 9, 10 so they can be active *
- Fibrinolysis aka getting rid of clot - Tissue plasminogen activator (tPA) = secreted by endothelial cells + converts plasminogen to plasmin → plasmin breaks down fibrin mesh → D-dimer = produced
→ Complex of Protein C + S degrade 5 + 8
P.E Pathophys - medium-sized embolus → occlus’n of a segmental pulm. artery b/c clot in vessel creates dead space / shunt where gas exchange can’t occur → mismatch btw perfus’n + ventila’n, (NO perfus’n b/c blood is able to reach lungs but isn’t getting O2ated in those lungs)
→ pulm. infarc’n +/- pleuritis + effus’n
SSX
- SOB
- tachypnea
- pain on 1 side of chest
- hypoxemia (i.e O2 sat < 95%)
- hemoptysis i.e coughing blood
- sinus tachy on ECG
- calf pain + erythema + swelling + warmth + Ψ loss of func’n (for VTE)
Ix’s
Do CXR 1st to r/o other causes !
- CTPA to diagnose P.E but V/Q scan instead if pt has kidney pb or is allergic to contrast dye
- Wells score to figure out if DVT = cause of P.E (Well’s score > 4 = DVT likely)
- If Wells score = +ve do proximal leg vein U/S + if -ve do D-dimer + follow steps 4 + 5
- If U/S = +ve start Tx + if it’s unprovoked DVT do CT scan of abdomen + pelvis to r/o malignancy + if -ve do D-dimer test
- If D-dimer = +ve repeat U/S + if -ve it’s NOT DVT !
- If repeat U/S = +ve start Tx + if -ve it’s NOT DVT !
Tx = anticoagulants for 3 months if provoked + for 6 months if unprovoked
- DOAC (Direct Oral Anti-Coagulant)
- MOA = Direct Factor 2 or 10 inhibitor
- side effects = hemorrhage, rash, nausea
- C/Is = high risk of bleeding
- Factor 10 inhibitors end in “XABAN” - Warfarin → must monitor via INR (we expect it to ↑ to 2-3 but if it ↑ above 5 STOP it immediately + give IV Vit K + Prothrombin Complex Concentrate to reverse effects of warfarin)
- MOA : inhibits Vit K epoxide reductase ∴ blocks γ-carboxyla’n of the Vit K dependent clotting factors i.e 2, 7, 9, 10, C + S
- side effects = warfarin-induced skin necrosis, bleeding, bruising, diarrhea, jaundice, N/V, teratogenic
- C/Is : pregnancy b/c = teratogenic, liver disease, active bleed
- Cau’ns : drug interac’ns can either ↑ or ↓ anticoagula’n effect
- avoid contact sports due to risk of bleed + don’t take w/ alcohol b/c can ↓ anticoagula’n effect
- don’t stop it w/o consulta’n, do not double missed dose
→ drugs that ↑ it i.e lower INR = PPIs, SSRIs, quinolones, grapefruit, cranberry juice
→ drugs that ↓ it i.e raise INR = alcohol, rifampicin, carbamazepine
- Heparin → MUST monitor PTT !
- MOA : binds + activates antithrombin ∴ inhibiting thrombin
→ LMWH for cancer pts or stable pts w/ normal renal func’n
→ Unfractionated hep for pts who may still require thrombolysis or have renal pb
- side effects = bleeding + HITT (Heparin Induced Thrombo-cytopenia Thrombosis = auto-immune rxn)
- C/Is = active bleed, Hx of HITT, platelet count ≤ 100,000/mm
Tx for pregnant pt = Dalteparin
- Know for OSCE *
PE ECG Findings ✓
- sinus tachy (most common finding)
- T wave invers’n in anterior leads
- S1Q3T3 i.e S wave in lead 1, Q wave in lead 3 + T wave invers’n in lead 3
Post op DVT ppx ✓
- LMWH for ortho Sx (unfractionated heparin instead if pt has renal failure)
- Fondaparinux Na for abdominal / bariatric / cardiothoracic Sx OR for pts w/ LE immobiliza’n / fragility fractures of pelvis, hip or proximal femur
- Know for OSCE *
ASA Classifica’n ✓
ASA I = normal healthy pt
ASA II = mild systemic disease (controlled asthma for ex)
ASA III = severe systemic disease (asthma w/ frequent inhaler use for ex)
ASA IV = pt w/ severe systemic disease that’s a constant threat to their life
ASA V = moribund pt that is not expected to survive w/o opera’n
ASA VI = brain dead pt whose organs are being removed for dona’n purposes
Fasting requirements for Sx ✓
- Water + other clear liquids = up to 2 hrs before induc’n of anesthesia
- Food + milk-containing drinks = up to 6 hrs before induc’n of anesthesia
Suxamethonium / succinylcholine MOA ✓
Short-acting depolarizing muscle relaxant ∴ can cause malignant hyperthermia in pt w/ any RFs
What do we monitor in anesthesia induc’n ? ✓
Vitals + ECG
Causes of post-op confus’n ✓
- PE
- infec’n
- electrolyte abnormality i.e hypoglycemia / HypoNa
Colloids v.s Crystalloids ? ✓
- Colloids = large molecule solu’ns ∴ stay in bloodstream longer
- Crystalloids = solu’ns w/ small molecules, move rapidly throughout body
→ NS, dextrose, LR i.e Hartmann’s
Effects of propofol after injec’n ✓
- ↓ in BP
- resp. depress’n
- painful sensa’n on injec’n
- hypnosis
Ddx of post op fever ✓
” 4 W’s”
Post op day 1-2 = “WIND” i.e lungs . . .
- atelectasis
- pneumonia
Post op day 3-5 = “WATER” i.e UTI / CAUTI
Post op day 5-7 = “WALK” i.e PE/DVT, abscess
Post op day 10 = “WOUND”
→ inspect wound for redness, swelling, drainage of pus or blood
When do cardiac complica’ns in non-cardiac opera’ns most frequently occur ? ✓
W/in the first 72 hrs after Sx
What is parity ? ✓
Amt of times woman has given birth to fetus that was ≥ 20 wks gesta’n
Pregnancy + VTE ✓
RFs for VTE in pregnancy
- advanced maternal age
- BMI > 30
- parity > 3
- smoker
- varicose veins
- pre-eclampsia
- immobility
- FHx of unprovoked VTE
- low risk thrombophilia
- multiple pregnancy
- IVF pregnancy
Pregnant woman w/ 3 RFs should be started on LMWH from 28 wks gesta’n – 6 wks postnatal + those w/ > 3 RFs should begin LMWH immediately till 6 wks postnatal !
Thrombotic thrombocytopenic purpura (TTP) ✓
Def - deficiency of ADAMTS 13 either due to gene muta’n on chromosome 9q34 or develop’nt of neutralizing antibodies
= characterized by mechanical RBC destruc’n in microcircula’n + thrombocytopenia due to consump’n + tissue ischemia + infarct b/c of microcircula’n obstruc’n
RFs
- black
- female
- obesity
- cancer therapy
- pregnancy (especially end of term or post partum)
Eti
- pregnancy
- post infec’n
- drugs i.e ciclosporin, OCP, penicillin, clopidogrel, aciclovir
- tumors
- SLE
- HIV
Pathophys - deficiency of ADAMTS-13 → ↑ in vWF → aggrega’n of circulating platelets → thrombi forma’n in microvasculature / microcircula’n
Diagnostic criteria
- fever
- renal insufficiency
- thrombocytopenic purpura
- microangiopathic hemolytic anemia (only visible on blood film)
- neuro SSX i.e HA / confus’n / blurry vis’n / tinnitus / lethargy / seizures
⚠️ Need ≥ 3/5 to diagnose !
Ix’s
- FBC → will show thrombocytopenia + anemia
- haptoglobin (= produced by liver) → will be low b/c so many RBCs are being destroyed so it’s busy binding to released Hgb
- blood smear → will show microangiopathic hemolytic anemia w/ schistocytes
- urinalysis → might show proteinuria due to renal insufficiency
- U + E → urea + creatine might be elevated due to renal insufficiency
- direct coombs test → to r/o AIHA
Tx = plasma exchange w/in 24 hrs + corticosteroids → immuno- suppressants → splenectomy
Complica’ns
- MI
- ischemic stroke
- renal dysfunc’n
- Know for OSCE *
1° v.s 2° hemostasis ✓
1° hemostasis = forma’n of weak platelet plug = mediated by interac’n btw platelets + vessel wall
→ disorders of 1° hemostasis = usually due to platelet or vWF abnormality
⟹ Thrombasthenia Glanzmann
= genetic GPIIb / IIIa deficiency ∴ causes impaired platelet aggrega’n
→ main SSX = gingival bleeding + epistaxis (uncontrolled nose bleed) + heavy periods
⟹ Bernard Soulier
= genetic GPIb deficiency ∴ causes impaired platelet adhes’n
→ main SSX = bleeding + enlarged platelets + mild thrombocytopenia on blood smear
⟹ Von Willebrand’s disease
2° hemostasis = stabliza’n of platelet plug = mediated by coagula’n factors
→ disorders of 2° hemostasis = usually due to inherited or acquired coagula’n factor(s) abnormality such as Hemophilia
Von Willebrand Disease ✓
Def - bleeding disorder where pt = deficient qualitatively or quantitatively in vWF ∴ platelet adhes’n = impaired + we get excessive bleeding
= most common inherited bleeding disorder
→ severity depends on type
→ usually detected accidentally b/c of metrorrhagia, pre-op lab exam (pt has prolonged bleeding time) or after tonsillectomy / abor’n b/c pt had mucocutaneous bleeding
RFs
- FHx
- incest
Eti
- Type 1= quantitative partial deficiency
= autosomal dominant = most common of the 3 but isn’t severe - Type 2 = func’nal abnormality = autosomal dominant + is rare
- Type 3 = complete deficiency = autosomal recessive + rare but is the most severe of the 3
SSX
- post op bleeding
- getting bruised easily
- excessive bleeding from minor wounds
- menorrhagia i.e extremely heavy periods
Ix’s
- PT → will be normal
- vWF antigen (for diagnosis) → will be low
- APTT → will only be prolonged if factor 8 activity < 35% of its normal activity ∴ can’t exclude vWF even if APTT = normal
Emergency Tx i.e in severe blood loss = platelet transfu’n
Regular Tx = vWF containing concentrate
Inherited Hemophilia ✓
Def - X linked recessive disorder where pt = deficient in either factor 8 or 9
RFs
- FHx
- male
Eti
- Hemophilia A = factor 8 deficiency
- Hemophilia B = factor 9 deficiency
SSX
- bleeding into muscles
- hemarthrosis (bleeding into a jt) → causes fixed jts
- mucocutaneous bleeding i.e epistaxis / gum bleeding
Ix’s
- PT → will be normal
- APTT → will be prolonged
- X ray to check for hemarthrosis
- plasma vWF to r/o vW disease
- LFTs to make sure it’s not a liver pb
- plasma factor 8 or 9 assay → will be ↓ed or absent
Tx = factor 8 or 9 replac’nt depending on type of hemophilia pt has
Complica’ns
- hemorrhage
- jt / muscle damage such as synovitis, arthropathy, muscle atrophy
- Know for OSCE *
SCD ✓
Def - AR disorder where pt has sickle-cell shaped RBCs instead of normal RBCs
→ SSX start @ age 1 b/c prior to that pt = protected by fetal Hgb
→ if heterozygous = sickle cell TRAIT NOT SCD !
RFs = African American or Mediterranean
Eti - missense mutat’n in β chain of Hgb gene → causes new codon which codes for valine instead of glutamic acid → valine = hydrophobic → mutated Hgb polymerizes under deO2ated condi’ns → RBCs have sickle cell shape
→ RBCs = reversibly sickled INITIALLY IF reO2ated but after multiple cycles become IRREVERSIBLY SICKLED via Gardos pathway (Ca-activated K channel where Ca enters cell + activates K channel → causes K efflux along w/ water → cell becomes dehydrated → HbS precipitates + polymerizes)
Pathophys
- VASO-OCCLUSIVE CRISIS :
→ sickled RBCs = more adhesive than normal RBCs so stick to one another + to walls of vessel + have shorter lifespan (20 days instead of 120) → poor blood supply to tissue → hypoxia
= most common crisis in sickle cell
= triggered by O2 condi’ns such as stress / infec’n / dehydra’n / cold weather - SEQUESTRA’N CRISIS :
→ pt has overactive spleen (hypersplenia) b/c spleen = “sequestering” more RBCs than normal to destroy sickled RBCs → can cause splenomegaly - APLASTIC CRISIS :
= sudden ↓ in Hgb w/ reticulocytopenia
→ can happen b/c of hydroxyurea use or streptococcal infec’n but most often happens b/c of Parvovirus B19 = virus that replicates in erythroblasts + causes red rash covering cheeks that spares nasolabial folds (“slapped cheek syndrome”) → causes reticulocytopenia + severe ↓ in Hgb b/c suppresses bone marrow’s ability to make RBCs ∴ making the anemia worse - HEMOLYTIC CRISIS = ↑in hemolysis rate to destroy sickled RBCs ∴ causing sudden ↓ in Hgb + reticulocytosis + hyperbilirubinemia
SSX + Complica’ns
- Due to vaso-occlusive crisis :
→ bone pain, dactylitis (swollen digits), silent cerebral infarct, limp in children
→ acute chest syndrome (b/c of lung infarct) = when vessels supplying lungs become clogged w/ RBCs = medical emergency w/ high mortality !
⟹ SSX = fever, SOB, shortness of breath, chest pain, cough + hypoxia → CXR will show pulmonary infiltrates - Due to hypersplenia / asplenia :
→ splenomegaly, ↑ed risk of infec’n from encapsulated bacteria (i.e streptococcus pneumoniae /meningococcus such as neisseria meningitides / Hemophilus influenza Type B which often cause septicemia + salmonella typhi / staph. aureus / E.coli which often cause osteomyelitis) - Due to hemolytic crisis :
→ kidney damage b/c of free floating Hgb after RBC destruc’n
→ vasospasm / abdo pain / pulm.HTN b/c of less NO due to arginase release + NO = required for smooth muscle relaxa’n / vasodila’n
- Due to the anemia itself :
→ pale palmar creases / mucous membranes, fatigue + Fe overload from transfus’n
Ix’s
- Electrophoresis
> 75-95% = SCD, 43-45% = SCT - Peripheral Blood Smear
→ smear will show sickle-shaped cells + nucleated RBCs + purple Howell-Jolly bodies aka remnants of RBC nuclei due to destruc’n by spleen
Emergency Tx for acute painful sickle cell crisis = subq morphine
Regular Tx
- prophylactic vaccina’n against encapsulated bacteria i.e pneumococcus, hemophilus influenza B + meningococcus
- paracetamol / ibuprofen for in vaso-occlusive crisis
⟹ paracetamol MOA - acetaminophen → inhibits COX but doesn’t bind to COX1/COX2 like NSAIDs which is why it’s an anti-pyretic + analgesic but NOT an anti-inflammatory
⟹ side effect = non itchy skin rash
⟹ C/Is = liver disease, < 3 months old (same for ibuprofen) - frequent transfus’ns (when severe i.e pt has sequestra’n crisis / B19 infec’n / hyperhemolytic crisis)
- Ψ bone marrow transplant
- Know for OSCE *
Thalassemia Major ✓
Def - complete absence of both β chains = most severe form of β thalassemia (AR)
→ pts = transfus’n dependent + like SCD, infants = protected by fetal Hgb
→ thalassemia minor = heterozygous muta’n aka muta’n in only 1/2 of genes so instead of LACK of β chain we get UNDERPRODUC’N of β chain
- β = 2 genes v.s 𝛼 = 4 genes *
- 𝛼 thalassemia = due to gene DELE’N NOT muta’n like in β *
→ 1 gene deleted = asymptomatic
→ 2 genes deleted = 𝛼 thalassemia minor aka trait / carrier = mild hypochromic (pale RBC b/c they have less Hgb than they should) microcytic anemia
→ 3 genes deleted = 𝛼 thalassemia intermediate / HbH disease = severe hypochromic microcytic anemia
⟹ transfus’n only needed in old age or pregnancy
→ 4 genes deleted = hydrops fetalis
= 4 γ chains will form tetramer Hgb called Hgb Bart’s in newborn = fatal
RF = Mediterranean
Pathophys - produc’n of β-globin chains = deficient or absent → imbalance btw 𝛼 + β chains → precipita’n of excess 𝛼 chains in erythroid precursors + maturing RBCs → membrane damage + cell destru’n → cells can’t survive → ineffective erythropoiesis → anemia
SSX + Complica’ns
- fatigue, pale skin, stunted growth / delayed puberty due to anemia
- jaundice (due to hyperbilirubinemia as a result of intravascular hemolysis)
- chronic Fe deposi’n due to multiple transfus’ns
→ can result in bronze skin, arrhythmia, precipita’n, hepatosplenomegaly
Ix’s
- Fe study → will show low ferritin
- Reticulocyte count → will be high
- FBC → will show microcytic anemia
- Hgb electrophoresis → will show larger %age of HbF + HbA2 + absent or very low HbA
Tx = life long transfus’ns + Fe chela’n (drugs that remove excess Fe from body)
- Know for OSCE *
Pancytopenia ✓
Def - ↓ in all 3 blood cells i.e RBCs, WBCs + platelets
Eti = central or peripheral
→ Central = ↓ed PRODUC’N by bone marrow
⟹ ex - aplastic anemia = due to aplasia or hypoplasia of bone marrow
→ Peripheral = ↑ed peripheral DESTRUC’N
SSX
- infec’n
- anemia
- purpura
- petechiae
- easy bruising
- gum bleeding
Splenomegaly + Lymphadenopathy ✓
1) Splenomegaly = palpable spleen i.e speen has enlarged ≥ 2x its normal size
Eti
- portal HTN
- inflammatory diseases like RA or SLE
- chronic bacterial infec’ns such as TB or brucellosis
- chronic parasitic infec’ns such as leishmaniasis or malaria
- hematological condi’ns such as hemolytic anemia or leukemia
- acute infec’ns such as septic shock, typhoid or infective endocarditis
2) Causes of lymphadenopathy (“CHICAGO”) :
- Cancer i.e hematological malignancies like Hodgkin lymphoma, Non-Hodgkin lymphoma, Acute Leukemia, Myelofibrosis, CML in blastic crisis or metastasis
- Hypersensitivity such as after vaccin’an
- Infec’ns
> VIRAL
→ Infectious Mono / Epstein Barr Virus
→ CMV
→ HSV 1/2
→ Rubella
→ Herpes Zoster
→ HIV
→ Human Herpes Virus 6 (HHV-6)
→ Parvovirus Β19
→ Hepatitis Viruses
> BACTERIAL
→ streptococcal infec’ns
→ salmonella
→ brucella
> FUNGAL = in immunosuppressed pts
> PARASITIC
→ toxoplasma
→ leishmania
- Connective tissue disorders like RA, SLE, Sjogren syndrome, dermato-myosiitis
- Atypical lymphoproliferative disorders like Castleman disease or Wegener’s granulomatosis
- Granulomatous disorders like TB or sarcoidosis
- Others like Kikuchi lymphadenitis or immunodeficiency
Leukemia ✓
Def - malignant transforma’n of hematopoietic precursor cells in bone marrow = most common cancer in children
→ ALL = most common form of acute leukemia in children, peak prevalence = 2-5 y/o
→ AML peak prevalence = < 2 y/o
→ CML = caused by Philadelphia chromosome ∴ ALL CML pts will be Philadelphia +ve !
⚠️ Philadelphia chromosome DOESN’T CAUSE ALL but DOES ↑ RISK !
RFs
- Down syndrome
- Kleinfelter syndrome
Types
- Acute Myeloid Leukemia
- Chronic Myeloid Leukemia
- Acute Lymphoid Leukemia
- Chronic Lymphoid Leukemia
→ acute = immature so can’t perform their func’n @ all, blasts rapidly ↑ in # ∴ disease progresses very quickly
→ chronic = mature-ish so can perform some of their func’ns, blasts ↑ in # slowly ∴ disease progresses slowly + gradually
→ myeloid = precursor to all WBCs (except lymphocytes) + RBCs + platelets
⟹ myeloid = larger blasts, more cytoplasm + cytoplasm might contain granules
→ lymphoid = precursor to lymphocytes
⟹ lymphoid = smaller blasts + cytoplasm lacks granules
Myeloid v.s Lymphoid Classficia’n :
- Myeloid = M0-M7
→ M0 = minimally differentiated
→ M1 = no matur’an
→ M2 = w/ matura’n
→ M3 = hyper granular promyelocytic (has favorable prognosis so NO transplant for M3 pt)
→ M4 = myelomonocytic
→ M5a = monoblastic
→ M5b = monocytes
→ M6 = erythroleukemia
→ M7 = megakaryoblastic
- Lymphoid = L1-L3
→ L1 = small + monomorphic
→ L2 = large + heterogeneous
→ L3 = Burkitt cell type
SSX = “ N- BLAST “
- Neutropenia → will make child more prone to infec’ns hence they’ll often be febrile
- Bone pain → child might have difficulty walking
- Lymphadenopathy
- Anemia + weight loss → will cause pallor + lethargy
- Splenomegaly
- Thrombocytopenia → will cause bleeding / petechial rash / purpura
→ petechial rash means pt has SEVERELY LOW PLT COUNT i.e < 20K
⚠️ Suspect leukemia if child has the following SSX (“CHILD CANCER “) . . .
→ Continual unexplained weight loss
→ HAs accompanied by early morning vomiting
→ ↑ed swelling or persistent bone / jt pain
→ Lump or mass (especially in abdomen, neck, chest, pelvis, armpits)
→ Develop’nt of excessive bruising / bleeding or rash
→ Constant or recurrent infec’ns
→ A whitish color behind pupil
→ Nausea that persists or vomiting +/- seizures
→ Constant tiredness or noticeable paleness
→ Eye / vis’n Δs suddenly + persistently
→ Recurrent or persistent fevers of unknown origin
AML ✓
RFs
> 65 y/o
- previous chemo TX
- radian or benzene exposure
- previous hematological disoder
Ix’s
- FBC → anemia, leukocytosis, neutropenia, thrombocytopenia
- Blood smear / film → will show blast cells → ≥ 20% blast cells confirms AML diagnosis
Tx = chemo
Complica’ns
- DIC
- infec’ns
- pancytopenia
- tumor lysis syndrome = oncological emergency !
CML ✓
RF = > 65 y/o
Ix’s
- blood smear/ film → will show mature myeloid cells
- FBC → anemia, leukocytosis, thrombocytopenia or normal platelet count
- bone marrow bx (required to confirm phase of disease) → will show granulocytic hyperplasia
Tx = tyrosine kinase inhibitor
Complica’n = pancytopenia
ALL ✓
RF = < 5 y/o
Ix’s
- blood smear/ film → will show lymphoblasts
- FBC → anemia, leukocytosis, thrombocytopenia
- bone marrow aspirate + bx →
≥ 20% lymphoid blast cells confirms diagnosis
Tx = chemo + CNS Ppx to prevent CNS disease
Complica’ns
- pancytopenia
- tumor lysis syndrome
CLL ✓
RF = > 60 y/o
Ix’s
- blood smear/ film → will show smudge cells (not diagnostic tho)
- FBC → anemia + leukocytosis (specifically lymphocytosis)
Tx = tyrosine kinase inhibitor IFF pt = symptomatic
Lymphoma ✓
- Hodgkin’s Lymphoma
Def - hematological malignancy arising from mature B cells = characterized by presence of Hodgkin’s cells + Reed-Sternberg cells
RFs
- FHx
- Hx of EBV infec’n
- young adult < 35 y/o or > 55 y/o
SSX
- fever
- weight loss
- night sweats
- cervical +/- supraclavicular lymphadenopathy
Ix’s
- FBC → anemia + thrombocytopenia
- CXR → will show bulky mediastinal lymphadenopathy
- PET / CT for staging
Tx = chemo
- Non-Hodgkin’s Lymphoma = B or T cell lymphoma
Types
- Lymphoblastic
- Anaplastic Large Cell
- Burkitt’s = starry-sky appearance of intermediate-sized lymphoid cells interspersed w/ macrophages surrounded by clear spaces on Trephine Bx = associated w/ c-MYC oncogene
RFs
> 50 y/o
- HIV
- male
- Hep C
- celiac disease
- H.pylori infec’n
- Hx of EBV infec’n
- Sjogren syndrome
- human herpes virus 8
SSX
- fever
- fatigue
- weight loss
- night sweats
- splenomegaly
- lymphadenopathy
Ix’s
- lymph node Bx → will be +ve
- bone marrow Bx → will be +ve
- PET / CT for staging
- LFTs → will be elevated if spread to liver
- blood smear → will show nucleated RBCs
- FBC → will show pancytopenia + lymphocytosis
- LDH → will be elevated (indicates rate @ which lymphoma = spreading)
Tx = chemo → excis’n or radiotherapy
Multiple Myeloma ✓
Def - B cell neoplasia characterized by prolifera’n of abnormal plasma cells in bone marrow that produce excessive light chains (usually kappa) → results in abnormal monoclonal antibody called paraprotein (usually abnormal IgG)
Pathophys - cytokines such as IL-1 + TNFs → osteoblast progenitor cells = inhibited from becoming osteoblasts → osteoblast activity ↓ + osteoclast activity ↑ so bone breaking ↑ b/c there aren’t osteoblasts to inhibit them
SSX
- HyperCa SSX
- Bence Jones protein
- hepatosplenomegaly occas’nally
- ↑ed risk of infec’n due to ↓ in Ig produc’n
- bone pain + ↑ed risk of fractures due to lytic les’ns
- anemia b/c bone marrow crowding suppresses erythropoiesis
- thrombocytopenia due to bone marrow crowding → ↑ed risk of bruising + bleeding
- Rouleaux forma’n → indicates hyperviscosity (causes blurry vis’n, dizziness + HAs)
- lytic les’ns on X ray due to bone marrow infiltra’n by plasma cells + cytokine-mediated osteoclast overactivity
Ix’s
- peripheral blood film → will show Rouleaux forma’n
- serum protein electrophoresis → will show elevated M protein in blood/urine
- bone marrow aspira’n + Bx for diagnosis → ≥10% plasma cells in bone marrow = enough to diagnose
- serum free light chain → will show Bence Jones protein = diagnostic
Tx = chemo
Complica’ns
→ leukopenia
→ recurrent infec’ns
→ fracture of vertebral bodies
→ renal failure b/c light chains = directly toxic to kidney + also b/c Bence Jones protein produces casts that obstruct tubular lumen hence causing tubular / renal inflamma’n
SVC obstruc’n (cancer complica’n) ✓
Def - oncological emergency where SVC = obstructed due to tumor compress’n
Eti = lung cancers or lymphomas that grow so big that they start to compress SVC
Pathophys - cancer grows so big that it starts to compress SVC → venous return from head, thorax + upper extremities to RA = interrupted → ↑ in venous pressure
SSX
- SOB
- pulseless JVD
- visual disturbance
- swelling of face, neck + arms
- distended neck + chest veins
Ix’s
- CXR
- chest CT for diagnosis
- Emergency Tx = secure airway via intuba’n + IV dexamethasone +/- endovenous stent if pt has stridor
Tumor Lysis Syndrome (cancer complica’n) ✓
Def - oncological emergency where tumor cells release their contents into bloodstream after chemo
→ HyperK
→ HyperPhos
→ Hyperuricemia b/c of released nucleic acids
→ HypoCa b/c Phos binds to Ca so the more Phos = released the less freely floating Ca there is
⚠️ ≥ 2 of the above must be present for diagnosis !
Eti = Cancer Tx
Pathophys - high tumor burden so when chemo / radia’n = initiated there’s a rapid lysis of tumor cells
SSX
- lethargy
- arrhythmia
- N/V due to HyperK
- diarrhea due to HyperK
- seizures / muscle cramps / tetany due to HypoCa
Ix = U + E + serum urate / uric acid
Emergency Tx = Ca gluconate for HyperK
→ intense IV fluid resucita’n +/- loop diuretic
→ rasburicase for hyperuricemia
Complica’ns
- uric acid precipita’n + CaPO4 deposi’n in renal tubules can cause renal vasoconstric’n → ↓ in renal blood flow → pre-renal AKI
Neutropenic sepsis ✓
Eti = recently started chemo
Tx = broad spectrum IV Abx
Myelodysplastic syndrome ✓
Def - ineffective + dysplastic hematopoiesis = step right before AML
RF = > 70 y/o
SSX
- pallor
- fatigue
- exercise intolerance
- petechiae / purpura
Ix’s
- FBC → anemia, leukopenia, thrombocytopenia
- reticulocyte count → inappropriately low or normal i.e not what it should be when u look @ ° of anemia
- bone marrow aspira’n w/ Fe stain → blasts < 20%
- bone marrow core Bx → hypercellular marrow
- bone marrow cytogenetic analysis to check for chromosomal abnormalities that could be causing the MDS
Tx for symptomatic = hematopoietic GFs → DNA methyltransferase inhibitors
Complica’ns
- AML
- infec’ns
- bleeding
Essential thrombocythemia ✓
Def - ↑ in size + # of circulating platelets due to prolifera’n of abnormal megakaryocytes in bone marrow
SSX
- bleeding
- splenomegaly
- livedo reticularis
- erythromelalgia = burning redness + pain in limbs
Ix’s
- FBC → thrombocytosis
- blood smear → thrombocytosis w/ varying °s of platelet anisocytosis (varia’n in SIZE)
Tx = anti platelet therapy such as aspirin or clopidogrel
→ omeprazole ↓ effect of clopidogrel ∴ pts taking both should be switched to diff PPI
Complica’ns
- AML
- bleeding
- arterial / venous thrombosis
- intrauterine death / spontaneous abor’n if occurs during pregnancy
Func’ns of white + red pulp of spleen ✓
Funcn’s of White pulp
- antigen presenting cells can enter which activates residing T cells who in turn activate B cells so they can become plasma cells
- pathogen enters follicles directly = where B cells are + they present antigen to T cells which activates T cells who then activate B cells = co stimula’n
- B cells fight off encapsulated bacteria
Func’ns of Red pulp
- platelet sequestra’n
- destruc’n of old or damaged RBCs
- phagocytosis of opsonized bacteria by macrophages
- storage of RBCs in case of severe blood loss
Anemia of chronic disease ✓
Def - anemia due to underlying disease
Eti
- RA
- SLE
- HIV
- GCA
- malaria
- liver disease
- renal failure
- cancers like lymphoma or myeloma
Cancer ✓
1- Compare + contrast benign + malignant tumors
2- Define tumor grade + stage + explain how they differ from one another
3- Give ex’s of the diff terminology used for pre-malignancy in diff anatomical sites
4- Tumor markers
1) Neoplasm or tumor = abnormal tissue mass w/ uncontrolled growth
→ can be benign or malignant + it’s when it’s malignant that we call a tumor cancer
⟹ Benign =
- slower growing
- well circumscribed
- often encapsulated
- NOT locally invasive
- NO metastatic Ψ
- very well differentiated cells i.e cells closely resemble cells of origin
- cellular uniformity throughout tumor i.e tumor cells look exactly or roughly the same
- few mitoses
- normal nuclear : cytoplasmic ratio
⟹ Malignant =
- faster growing
- poorly circumscribed
- non-encapsulated
- invasive growth
- has metastatic Ψ
- variable differentia’n (can range from well to poorly differentiated)
- cellular pleomorphism (i.e of variable size + shape)
- plenty of mitoses
- high nuclear: cytoplasmic ratio
- nuclear hyperchromatism (chromatin condensa’n)
2) Staging = for malignant tumors + grading = for pre + malignant tumors
→ grading for malignant = how aggressive tumor is
→ grading for pre-malignant = how LIKELY it is to become malignant
→ staging = extent of spread, helps for prognosis
3) Tumor w/ “epithelium” in it’s name means that it’s a tumor that affects lining of a body surface i.e squamous epithelium for skin / esophagus + glandular epithelium for resp / GI tract
→ carcinoma = malignant tumor of an epithelium = most common type of malignant tumor, usually metastasizes via lymph
⟹ SCC = keratin form’an + intercellular bridges btw cells
⟹ adenocarcinoma = glandular / acinus forma’n + mucin produc’n
→ “sarcoma” = malignant, usually metastasizes via bloodstream
⟹ osteosarcoma (bone)
⟹ liposarcoma (adipose)
⟹ chondrosarcoma (cartilage)
⟹ angiosarcoma (blood vessel)
⟹ leiomyosarcoma (smooth muscle)
⟹ rhabdomyosarcoma (striated muscle)
→ melanoma / mesothelioma / lymphoma or leukemia / glioma = malignant as well
→ melanomas can mimic almost all tumors ∴ must perform immuno-histochem
→ “oma” = benign tumor
ex’s- squamous cell papilloma, hemangioma, leiomyoma, osteoma
→ “adenoma” = benign tumor of glandular epithelium except in GI where it refers to pre-malignant
4)
- AFP for liver cancer
- CEA for colon cancer
- Ca 15-3 breast cancer
- Ca 19-9 for pancreatic cancer
- Ca 125 for ovarian cancer
- PSA for prostate cancer
- β hCG for testicular cancer
Hemochromatosis / Fe Overload ✓
Def - autosomal recessive disorder where too much Fe = released from macrophages
RFs
- FHx
- male
- white
- 40-50 y/o
- supplemental Fe
SSX
- fatigue
- weakness
- arthralgia
- bronze skin
- hepatomegaly
Ix’s
- serum transferrin satura’n → will be > 45%
- serum ferritin → will be elevated
Tx = low Fe diet → Fe chela’n therapy
⚠️ These pts should avoid Vit C b/c Vit C ↑ Fe absorp’n !
Complica’ns
- T2D
- CHF
- cirrhosis
- bone loss
- hepatocellular carcinoma (HCC)
- hypogonadism → loss of libido + impotence in men
- Know for OSCE *
Neonatal Jaundice ✓
Def - when neonate has serum bilirubin > 5 mg/dL or > 85.5 micromol/L
→ physiological jaundice = after first 24hrs of life + resolves spontaneously w/in 10 days = b/c of fetal hepatic + immaturity + their RBCs have a higher hemolysis rate than our RBCs
→ pathological jaundice = W/IN first 24hrs of life !
RFs
- breastfeeding
- low birth weight
- maternal diabetes
Eti for pathological jaundice based on timing
→ < 24 hrs = RBC pb i.e . . .
- rhesus hemolytic disease
- ABO hemolytic disease
- G6PD deficiency
- hereditary spherocytosis
→ > 14 days = non-RBC pb i.e. . .
- prematurity
- biliary atresia
- hypoTSH
- UTI / TORCH infec’n
- breast milk jaundice b/c components of breast milk inhibit the liver’s + inadequate breastfeeding may lead to slow passage of stools hence ↑ing absorp’n of bilirubin in intestines
Ix’s
- transcutaneous bilirubin (TcB) = screening that all newborns get 24-48 hrs after birth (for newborns that are visibly jaundiced it has to be w/in 24 hrs of birth !)
- ttl serum bilirubin for diagnosis
- FBC + blood film to r/o polycythemia
- conjugated bilirubin b/c elevated levels indicate hepatobiliary cause
- blood type testing of mother + baby to r/o ABO or rhesus incompatibility
- direct Coombs Test to see if mom has ABO or Rh antibodies
- G6PD levels to r/o G6PD deficiency
- TFTs to rule out hypothyrodisim as cause
- blood + urine cultures if infec’n = suspected
Tx = plot ttl bilirubin levels on Tx threshold charts
→ Tx op’ns = phototherapy or exchange transfus’n which involve removing blood from baby + replacing it w/ donor blood
⟹ phototherapy converts unconjugated bilirubin into soluble isomers that can be excreted in urine w/o requiring liver conjuga’n
1. remove baby’s clothing down to diaper to expose skin + eye patches to protect eyes
2. light-box shines blue light on baby’s skin (little or no UV light = used)
3. once phototherapy = complete, rebound bilirubin = measured 12-18 hrs later
→ side effect = bronze baby syndrome
Complica’n = kernicterus = brain damage due to high bilirubin levels b/c bilirubin can cross BBB → leads to permanent damage i.e cerebral palsy, deafness + learning disability
Hemolytic Disease of the Fetus + Newborn (HDFN) ✓
Def - when Rh -ve pregnant woman carries Rh +ve baby for the 2nd time OR she was transfused w/ RhD antigen
Pathophys - memory B lymphocytes await reappearance of RBCs containing RhD antigen i.e subsequent pregnancy of Rh +ve baby
→ when challenged by those RBCs, the B lymphocytes differentiate into plasma cells + produce IgG
→ maternal IgG crosses placenta + attaches to fetal RBCs that have expressed RhD antigen
→ those RBCs are then sequestered by macrophages of the fetus’ spleen
→ extravascular hemolysis occurs → splenomegaly → portal HTN → can lead to hydrops fetalis
⟹ antibodies aginst RhD antigen usually develop after 28th wk of gesta’n or postpartum
Ix’s
- maternal blood type b/c we need to know if she’s Rh -ve
- maternal serum Rh antibody screen (in 2nd pregnancy) → will be elevated (assuming previous pregnancy was Rh + ve baby or she was transfused w/ Rh +ve blood)
Tx = prophylactic 500 IU anti-D @ 28 + 34 wks gesta’n for pregnant Rh -ve women
Hemorrhagic disease of the newborn ✓
Def - bleeding in 1st days of life
Pahtophys - Vit K deficiency b/c their guts don’t have bacteria to make Vit K yet → defective γ-carboxyla’n of glutamate residues of clotting factors 2, 7, 9 + 10 → elevated PT → hemorrhagic disease of the newborn
Neonatal Immune thrombocytopenia ✓
= diagnosis of exclus’n
SSX
- sudden appearance of petechial rash
- sudden appearance of bruising and / or bleeding but child is otherwise healthy
→ 60% of children w/ ITP have previous Hx of viral illness
→ most children w/ ITP recover spontaneously after 3-6 months but 20% will develop chronic ITP
Sjogren syndrome ✓
Def - chronic inflammatory autoimmune disorder characterized by ↓ in lacrimal + salivary gland secre’n
RFs
- RA
- SLE
- middle age women
- scleroderma / systemic sclerosis
Eti
→ 1° = occurs spontaneously
→ 2° = due to RA or SLE
SSX
- dry eyes
- xerostomia i.e dry mouth
- jt pain + stiffness
Ix’s
- Schrimer’s test → insert folded filter paper under lower eyelid w/ end hanging out
⟹ +ve if if < 5 mm of paper is wet after 5 mins
- salivary gland Bx
- anti Ro / SSA + anti La / SSB → will be +ve
- rheumatoid factor might be +ve but obviously it’s not RA
Tx = based on SSX
- dry eyes = artificial tears → ciclosporin drops → cholinergic drug such as pilocarpine
- dry mouth = salivary substitute such as fluoride gels, saliva-stimulating lozenges or chewing gums
- MSK SSX = NSAIDs for pain → DMARD → oral corticosteroid
- vasculitis = corticosteroid → Iv Ig → rituximab
Complica’ns
- oral thrush
- dental cavities
- blepharitis
- corneal ulcers
- keratoconjunctivitis sicca
- Know for OSCE *
Polymyositis / Dermatomyositis ✓
Def - idiopathic autoimmune disorder that causes muscle inflamma’n
RFs
- female
- black
- children or > 40 y/o
Eti
- cancer
- viral infec’ns such as Coxsackie or HIV
Diagnostic criteria
- Progressive, symmetrical, proximal muscle weakness
- Muscle Bx shows necrosis / phagocytosis / regenera’n / inflamma’n
- Elevated CK or Aldolase
- Electromyography typical findings
- One of the following skin Δs . . .
- Gottron les’ns / papules = purple papules on knuckls, elbows or knees
- heliotrope rash on face / eyelids
- periorbital edema
- photosensitive erythematous rash on back, shoulders + neck
→ SSX 1-4 present = polymyositis
→ SSX 1-5 present = dermatomyositis
Ddx = other things that cause elevated creatine kinase
- MI
- AKI
- rhabdomyolysis (in rhabdo CK will be ≥ 10,000)
- statin use
- strenuous exercise
Ix’s
- muscle Bx
- creatinine kinase + aldolase → ≥ 1 of the 2 will be elevated b/c = released by inflamed muscle tissue
- ANA → often +ve but not always
- Jo 1 antibody → will be +ve
Tx = corticosteroid + photoprotec’n if there’s skin involv’nt
Antiphospholipid syndrome ✓
Def - when pt persistently has elevated antiphospholid antibodies
→ can be lupus anticoagulant, anti cardiolipin antibody and/or anti β2 glycoprotein 1 so test all 3 antibodies !
RFs
- SLE
- auto immune disease
- auto immune + rheumatological disease
Eti = 1° or 2° to SLE
SSX
- migraine
- livedo reticularis (usually in young white women)
- pregnancy morbidity i.e loss of ≥ 3 embryos before 10th wk of gesta’n
Complica’ns
- stroke
- MI
- P.E / DVT
- pre eclampsia
- pregnancy loss
- placental abrup’n
- TIA / ischemic stroke
Tx = long term warfarin to prevent thrombosis or LMWH + aspirin instead if pt = pregnant
SLE ✓
Def - chronic multisystem autoimmune disorder
RFs
> 30 y/o
- female
- African descent but living in Europe / U.S
Eti
- regular lupus
- neonatal lupus = SLE in pregnant woman + anti SSA / Rho = +ve
→ SSX = cytopenia + transaminitis + heart block + diffuse or peri-orbital rash - drug induced lupus (“SHIPP MT”)
→ Sulfonamides
→ Hydralazine
→ Isoniazid
→ Procainamide
→ Phenytoin
→ Minocycline
→ TNF 𝛼 inhibitors
SSX (need ≥ 4)
- oral ulcers
- leukopenia
- lymphopenia
- renal dysfunc’n
- photosensitive rash
- malar butterfly rash
- non erosive polyarthritis
- discoid rash (on head + neck)
+ve anti dsDNA / anti smith / anti phospholipid antibodies
Ix’s
- ANA (most SENSITIVE but NOT specific for lupus i.e by itself can’t diagnose lupus but should definitely make us suspect lupus especially if pt has SSX b/c it’s the antibody that’s most commonly +ve in lupus)
→ = Ix that we use to r/o lupus since it’s the most sensitive
→ can also be +ve in RA, EBV, TB, Hep C or even in perfectly healthy person - anti dsDNA → if +ve it means there’s renal involv’nt i.e lupus nephritis = most SPECIFIC for lupus hence is used for diagnosis
- C3/C4 → both will be low
- anti-smith → if +ve u can diagnose lupus but very few lupus pts will have a +ve anti-smith
- anti histone → if +ve it means it’s drug induced lupus
- anti cardiolipin antibody or some other anti phospholipid antibody → could be +ve if pt also has antiphospholipid syndrome
- APTT → might be prolonged if pt also has antiphospholipid syndrome
- U + E → elevated urea + Cr due to renal dysfunc’n
Tx = hydroxychloroquine + lifestyle Δs → add corticosteroids if there’s skin manifesta’ns or lupus nephritis → add immunosuppressant if there’s hematological manifesta’ns
Lifestyle Δs
- sunscreen use
- smoking cessa’n
- contraceptive pill use
- cardio-protective diet i.e high fish oil + low saturated fat
Complica’ns
- anemia of chronic disease
- leukopenia
- thrombocytopenia
- lupus nephritis
- anti phospholipid syndrome = ↑ in coagulability → ↑ in risk of DVT, thrombotic events, pregnancy loss, pre-mature birth
- Know for OSCE *
Vasculitis ✓
Def - chronic blood vessel inflamma’n
RFs = white + > 50 y/o
Eti = large, medium or small vessel vasculitis
Systemic SSX
- fever
- malaise
- myalgia
- arthralgia
Small vessel SSX
- hematuria
- palpable purpura
- otorrhea / ear pain / muffled sensa’n in ears
- nasal discharge / epistaxis / nasally ulcers / sinus pain / wheeze
Medium vessel SSX
- abdominal pain
- cutaneous ulcers
- foot and/or wrist drop
Large vessel SSX
- vis’n loss
- carotid bruits
- asymmetric brachical pusles
- upper extremity or jaw claudica’n
Ix’s
- ESR / CRP → will be elevated
- ANCA auto antibody → will be +ve
- urinalysis to check for hematuria
- Bx of affected tissue → will show vessel wall necrosis, fibrinoid necrosis, RBC extravasa’n + karyorrhexis i.e fragmenta’n of nucleus + break up of chromatin into unstructured granules
Tx = corticosteroid
Complica’n = aortic aneurysm
Raynaud’s phenomenon ✓
Def - painful physical response to cold temps
RFs
- female
- FHx
- connective tissue disorder
Eti
1° = not due to underlying disorder
2° = due to underlying disorder such as SLE or scleroderma
Pathophys - cold temp → vasospasm → digits initially turn pale due to vasoconstric’n → then turn blue due to cyanosis → then turn red once reperfused
Tx = keeping hands warm + CCB such as nifedipine
⚠️ These pts should avoid β blockers b/c can make their SSX worse !
Complica’n = ischemic digit
Systemic sclerosis / Scleroderma ✓
Def - autoimmune condi’n involving inflamma’n + fibrosis of connective tissues, skin + internal organs
→ has high morbidity + mortality
SSX = (“CREST”)
- Calcinosis → Ca deposits under skin (usually on fingertips)
- Raynaud’s → MUST BE PRESENT TO DIAGNOSE !
- Esophageal dysmotility i.e GERD
- Sclerodactyly i.e hardening of skin on hand that causes hand to have claw shape
- Telangectiasia i.e broken blood vessels on skin
⚠️ If pt has scleroderma SSX but all antibodies = -ve suspect paraneoplastic scleroderma = malignancy !
Types
- Limited cutaneous systemic sclerosis → SSX = CREST
- Diffuse cutaneous systemic sclerosis = CREST SSX + internal organ involv’nt such as CAD / HTN / pulm. fibrosis / scleroderma renal crisis (= medical emergency that presents w/ severe HTN + renal failure)
Ix’s
- serum auto antibodies → +ve ANA in 90% of pts
- anti-centromere antibodies → most often associated w/ limited cutaneous systemic sclerosis
- anti-Scl-70 antibodies → most often associated w/ diffuse cutaneous systemic sclerosis
Emergency Tx for scleroderma renal crisis = ACE-Is → any addi’nal anti-hypertensive → renal dialysis or transplant
Regular Tx
- DMARDs + rituximab
- avoiding smoking
- gentle skin stretching to maintain ROM
- regular emollients
- avoiding cold triggers (for Raynaud’s)
Complica’ns
- skin ulcers
- hypoTSH
- heart / lung / kidney involv’nt
- Know for OSCE *
Erythema Nodosum ✓
Def - delayed-type hypersensitivity rxn that presents w/ erythematous, tender nodules on shins due to inflamma’n of subq fat
→ overtime nodules settle + become bruises
Triggers
- TB
- gastroenteritis
- streptococcal throat infec’ns
- drugs such as NSAIDS or OCP
- pregnancy
- malignancy
- inflammatory condi’ns such as IBD or sarcoidosis
SSX = red, inflamed, subcutaneous nodules across both shins
Ix’s to see if idiopathic or due to underlying disease
- throat swab for strep
- CXR to r/o TB + sarcoidosis
- stool microscopy + culture to r/o campylobacter + salmonella
- fecal calprotectin for IBD
Tx = supportive b/c usually resolves spontaneously w/in 6 wks
- rest
- leg eleva’n
- NSAIDs → K iodide → intrales’nal cortisteroid injec’n
Erythema Multiforme ✓
Def - mild, self-limiting, Ψly recurring mucocutaneous inflammatory condi’n = hypersensitivity rxn
RFs
- herpes simplex virus
- mycoplasma pneumonia
Eti
- viral infec’n
- drugs
SSX
- widespread itchy les’ns that resemble a bull’s eye
→ erupt over 24 - 48 hrs + last 1-2 wks
Ix = clinical diagnosis
Tx = topical emollient → topical or oral corticosteroid
1° immune deficiency ✓
1- Def, RFs, Eti, Pathophys, SSX, Diagnostic Criteria, Ddx, Ix, 1st line Mx, Complica’ns
2- What features of a clinical Hx might lead you to suspect 1° immune deficiency
1)
Types
- Antibody deficiencies = 50% of cases
→ pts = more susceptible to . . . - C. fetus
- S. aureus
- M. hominis
- H. influenzae
- P. aeruginosa
- enteroviruses
- U. ureolyticum
- N. meningitidis
- S. pneumoniae
- G. lamblia protozoa
a) Selective IgA deficiency (= asymptomatic)
→ lack of serum + mucosal IgA but normal IgG + IgM
→ most pts = asymptomatic but are at ↑ed risk of mucosal infec’ns especially viral ones + at ↑ed risk of having anaphylactic rxn to blood products
b) X linked agammaglobulinemia
→ B cells + ALL Igs = completely absent OR very low
→ age of onset = 6-12 months (affects males mainly)
→ Tx = IVIG therapy to prevent infec’ns + bronchiectasis
c) CVID (common variable immunodeficiency)
→ onset = any age
→ pts might have auto-antibodies + SLE
→ pts will have recurrent sino-pulmonary infec’ns + consequentially bronchiectasis
→ serum IgG + IgA = low in ALL pts + serum IgM = low in 50% of pts
→ Tx = IVIG therapy + prophylactic Abx
- B cell deficiencies
→ cause ↑ed susceptibility to enterovirus + encapsulated bacteria infec’ns - Cellular / T cell deficiencies
→ pts = more susceptible to . . . - S. typhi bacteria
- Non tuberculous mycobacterium including BCG
- C. albicans, H. capsulatum, A. fumigatus + C. immitis fungi
a) DiGeorge syndrome (AD) = contiguous gene dele’n involving 22q11.2 reg’n on 1 copy of chromosome 22
→ causes defects in 3rd + 4th pharyngeal arches
→ pt will have almost completely absent T cells due to thymic hypoplasia
→ SSX (“CATH”):
- Congenital Cardiac defects
- Abnormal / dysmorphic facial features i.e narrow palpebral features, hypertelorism (↑ed distance btw eyes), micrognathia (smaller than normal jaw), cleft palate, low set ears, fish shaped mouth
- Thymic hypoplasia
- HypoCa due to no parathyroid glands → may present as neonatal seizures
> Wiskott Aldrich syndrome (X-linked) → causes “ERT” i.e severe Eczema, Recurrent bacterial infec’ns + Thrombocytopenia (pt will have petechiae)
b) Ataxia-Telangiectasia → SSX . . .
- progressive cerebellar ataxia that starts at early age
- telangiectasia in ear lobes + conjunctivae
(“ spider veins “ i.e broken blood vessels) → develops after 2 y/o
- SCID (Severe Combined Immunodeficiency) = only 20% of immunodeficiency cases but are the most severe
→ disturbs develop’nt + func’n of BOTH T cells + B cells + can lead to early death in the 1st yr of life
→ 50% = X-linked + the ones that are autosomal recessive are due to muta’ns in the genes for T cell receptor signaling such as JAK3 (Janus kinase 3), ADA (Adenosine Deaminase) + ZAP70 kinase (zeta-chain protein kinase 70)
→ pts will have the following SSX :
- weight loss
- chronic diarrhea
- persistent candidiasis
- low ttl lymphocyte count
- recurrent SEVERE infec’ns
- absent thymic shadow on X-ray
- failure to thrive due to hypermetabolism
⚠️ Present thymic shadow doesn’t r/o SCID !
→ pts = more susceptible to . . .
- ALL viruses
- P. carinii + T. gondii protozoa
- L. monocytogenes, S. typhi + enteric flora bacteria
- same bacteria as antibody deficiency + same myobacterium + fungi as cellular deficiency
→ these pts have to be isolated in +ve pressure to eliminate risk of infec’n
→ Tx = early diagnosis obviously + bone marrow transplant before they start school
- Phagocyte deficiencies = 18% of cases
→ pts often present w/ infec’ns of the skin + reticuloendothelial system
→ pts = more susceptible to . . . - P. carinii protozoa
- A. fumigatus + C. albicans fungi
- Non tuberculous mycobacterium including BCG
- S. aureus, P. aeruginosa, S. typhi, N. asteroides + enteric flora bateria
- Complement deficiencies
→ pts often present w/ blood borne infec’ns caused by encapsulated bacteria such as bacteremia + meningitis
→ pts = more susceptible to same bacteria as antibody deficiency ESPECIALLY N. meningitidis
a) C1 esterase inhibitor deficiency → AD disorder that will cause recurrent episodes of well-demarcated angioedema w/o urticaria (most commonly affects skin or mucosal tissues of upper resp. + Gl tracts
→ pathophys → inhibits classical pathway + bradykinin inflammatory pathway ∴ resulting in agnioedema b/c of excess produc’n of bradykinin which is a potent vasodilatory mediator
⟹ can be precipitated by trauma-dental work, opera’ns or infec’ns
b) Hereditary Angioedema (HAE) → AD disorder caused by defective gene on chromosome 11
→ leads to non-painful, non-pruritic + non-pitting edema
⟹ edema in the larynx can lead to asphyxia’n + abdominal anigoedema attacks require Sx
⟹ Tx = purified C1 inhibitor by slow IV infus’n, FFP (fresh frozen plasma) in case of emergency, tracheostomy in sig laryngeal edema + selective bradykinin B2 receptor antagonist for acute HAE in adults
→ Type 1 = low C1 inhibitor + low C4 + C2
→ Type 2 = dysfunc’nal C1 but normal or elevated in level + low C4 + C2
→ Type 3 = mutat’n of clotting factor 12
→ disinhibits bradykinin pathway → C4 + C1 inhibitor levels will be normal
2) SSX that should make u suspect 1° immunodeficiency . . .
- pt needs IV Abx to clear infec’ns
- FHx of 1° immunodeficiency
- recurrent deep skin or organ abscesses
- persistent mouth thrush or fungal skin infec’n
- infant fails to gain weight or grow normally
> 4 new ear infec’ns w/in 1 yr
> 2 pneumonias w/in 1 yr
> 2 months on Abx w/ little effect
> 2 serious sinus infec’ns w/in 1 yr
> 2 deep-seated infec’ns including septicemia
COVID ✓
Def - acute infectious respiratory disease caused by SARS-Cov2
RFs
- T2D
- CVD
- CKD
- HTN
- male
- obesity
- smoking
- older age
- pregnancy
- immunosuppres’n
- respiratory disease
- residing in long term facility
- contact w/ possible or confirmed case
SSX
- fever
- cough
- dyspnea
- altered sense of taste / smell
Ix’s
- RT PCR → will be +ve
- rapid antigen test → will be +ve
Tx = self limiting but treat SSX as needed i.e anti pyretics, analgesics
Complica’ns
- AKI
- DIC
- thrombosis
- resp. failure
- cardiac arrest
- Know for OSCE *
Influenza ✓
Def - self-limiting acute respiratory tract infec’n caused by ssRNA viruses influenza A or B
→ transmitted through respiratory droplets i.e coughing / sneezing / talking
→ goes away in 10 days
RFs
≥ 65 y/o
- T2D
- CKD
- pregnancy
- immunosuppres’n
- healthcare worker
SSX
- fever
- dry cough
- fatigue
- HA
- sore throat
- jt / muscle ache
⚠️ Flu SSX v.s common cold SSX
- abrupt SSX onset v.s gradual onset
- fever v.s no fever
- pt feels wiped out v.s pt feels fine
Ix = rapid throat or nasal swab or PCR (most accurate)
Regular Tx = vaccine for Ppx but is self limiting
Tx for pts at risk of influenza complica’ns = Oral oseltamivir OR inhaled zanamivir (both are bd for 5 days)
→ Tx should be started w/in 48 hrs of onset of SSX
Complica’ns
- otitis media
- sinusitis
- bronchitis
- encephalitis
- viral pneumonia
- febrile convuls’ns (in young children)
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HIV / AIDS ✓
Def - infec’n caused by retrovirus = retrovirus b/c encodes reverse transcriptase enzyme
→ inherently error-prone ∴ has high rate of muta’n which is why there’s often the pb of resistance
→ can be transmitted through bodily fluids i.e blood, sperm + breast milk
→ 10-20% of ppl w/ HIV in the UK = undiagnosed
RFs
- needle stick injury
- high maternal viral load
- IV drug use + needle sharing
- unprotected receptive anal sex
- unprotected receptive vaginal sex
Pathophys - virus gains entry into cells by attaching to CD4 receptor + co-receptor (CCR5 or CXCR4) via its envelope glycoproteins
→ once integrated into host DNA, virus resides in nucleus of infected cells + can remain quiescent for extended periods of time OR can become transcriptionally active + use human host cell machinery to replicate itself
→ viral RNA + proteases take over hence we see ↓ in CD4 T cells
SSX
- fever
- diarrhea
- weight loss
- skin rashes
- night sweats
- uveitis sometimes
- oral ulcers / angular chelitis / oral thrush
Ix’s
- serum HIV ELISA → will be +ve
- serum HIV rapid test → will be +ve
- CD4 count = monitored every 3-6 months in early disease + every 2-3 months in late disease
> 500 = asymptomatic
< 350 = immunosuppressed
< 200 = AIDS - HIV RNA / viral load to monitor if Tx is working
Tx for everyone
- antiretroviral therapy (ART) = triple therapy i.e 2 nucleotide reverse transcriptase inhibitors / NRTIs (tenofovir + emtricitabine) + third agent such as (bictegravir = protease inhibitors that target HIV’s protein processing)
- pre exposure ppx for high risk adults = emtricitabine + tenofovir disoproxil = taken before + after sex in . . .
→ men or transgender individuals who have sex w/ men
→ HIV -ve sexual partners of HIV +ve individuals w/ detectable or unknown viral load unless the partner has been on ART for ≥ 6 months + viral load is < 200
⟹ if taken as prescribed chance of being infected wi/ HIV via sexual intercourse by up to 99%
- post exposure ppx for 28 days
- yrly cervical cancer screening
- avoiding live vaccines but being up to date on all vaccines that they can get
- moms should avoid breastfeeding
Addi’nal Tx / Mx
- pt w/ AIDS = given co-trimoxazole to protect against PCP (pneumocystis jirovecii pneumonia)
Complica’ns :
- Kaposi sarcoma = neoplasm of vascular endothelial cells due to herpes virus 8 (usually occurs in immuno-compromised pts or pts w/ poorly controlled HIV but can also occur spontaneously in men of Eastern European descent + Sub-Saharan Africans)
→ progresses from patch to erythematous (red or purple) cutaneous plaques in lower extremities / face / oral mucosa / genitalia
→ on Bx we’ll see proliferating spindle cells forming slit-like spaces filled w/ blood
→ can affect GI + pulm. systems ∴ should do screening for occult GI bleed via occult blood test + for pulm. les’ns via CXR - AIDS opportunistic infec’ns
→ Cryptosporidium = genus of protozoal pathogens that cause watery diarrhea + abdo. cramps
⟹ other SSX include . . .
- N/V, fever, weight loss, SSX of dehydra’n i.e ↓ed skin turgor + dry mucous membranes, orthostasis
= mild + self-limiting in immuno-competent pts but severe + life-threatening if immunocompromised
⟹ diagnosis = made by stool antigen test or by detec’n of luminal oocysts via acid-fast staining
⟹ Bx of colon + then light microscopy on acid-fast stain will show cryptosporidiosis i.e small, round oocysts on colonic epithelial surface
⟹ Tx = supportive i.e fluids, electrolytes + anti-parasitic therapy
→ Candida albicans
⟹ causes oral thrush + esophagitis
⟹ staining w/ Gomori methenamine Ag or periodic acid-Schiff will show pseudohyphae + budding yeasts
→ Cryptococcus neoformans
⟹ can cause meningitis in AIDS pts
⟹ staining w/ India ink or mucicarmine will show encapsulated yeast w/ narrow-based budding
→ CMV (= herpes virus 5)
⟹ can cause esophagitis, pneumonia + retinitis in AIDS pts
⟹ diagnosis = made w/ ELISA to detect anti-CMV Ig + PCR amplifica’n of viral DNA
⟹ light microscopy might show intracellular inclus’n bodies known as Cowdry bodies
→ MAC (Myobacterium avium complex)
⟹ causes atypical pneumonia + GI infec’ns in AIDS pts
⟹ light microscopy will show acid-fast, periodic acid-Schiff +ve bacilli
⟹ pts w/ AIDS = given azithromycin for MAC Ppx
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General STI Mx ✓
- Tx
- full screening for other STIs
- contact tracing
- advice about avoiding sexual activity until STI = treated
- educa’n on importance of practicing safe sex
Chlamydia ✓
Def - most common STI in the UK
RFs
- previous STI
- unprotected sex
< 25 y/o + sexually active
- having sex w/ infected partner
- new sex partner
- multiple sex partners
Eti - Chlamydia trachomatis = gram -ve intracellular bacterium ∴ enters + replicates w/in cells before rupturing cell
→ it’s due to this unique life cycle that it can’t be cultured on artificial media
SSX in women
- asymptomatic
- dysuria
- pelvic pain
- cervical inflamma’n
- abnormal vaginal bleeding
- yellow, cloudy vaginal discharge
SSX in men
- dysuria
- penile discharge
Ix = nucleic acid amplifica’n test (NAAT) for diagnosis → will be +ve
⟹ sample can be collected via . . .
- vulvovaginal swab
- endocervical swab
- 1st catch urine sample
- urethral swab (in men)
- rectal swab (after anal sex)
- pharyngeal swab (after oral sex)
Tx = doxycycline OR erythromycin instead if pt = pregnant or breastfeeding
→ MOA of doxycycline = tetracycline AB - inhibit 30S subunit ∴ inhibit bacterial protein synthesis ∴ is a bacteriostatic AB
⟹ side effects - GI distress, abd. discomfort, photosensitive rash
⟹ C/I = pregnancy b/c of risk of hepatotoxicity to mother, children < 8 y/o due to permanent yellow / brown discolora’n of fetal teeth + impairment of long bone growth
⟹ should not be taken w/ Fe, Ca or Mg b/c they chelate w/ tetracyclines ∴ preventing adequate absorp’n
⟹ end in “CYCLINE”
Tx of chalmydial salpingitis = doxy + metronidazole
Complica’ns
- LGV
- cervical cancer
- reactive arthritis
- PID if left untreated + infec’n ascends
- ectopic pregnancy (as a result of the PID)
- infertility in women if infec’n ascends (as a result of the PID)
- epididymitis + prostatitis in men if infec’n ascends
Complica’ns in pregnancy
- infants born to women w/ untreated chlamydia = @ risk of neonatal conjunctivitis + pneumonia
- PROM
- Low birth weight
- Preterm delivery
Who gets chlamydia screening ?
- every sexually active person < 25 y/o annually OR when they change sexual partner
→ everyone that tests +ve gets re-tested 3 months after Tx
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Gonorrhea ✓
Def - STI caused by Neisseria gonorrhea = gram -ve diplococcus bacterium
→ infects mucous membranes w/ columnar epithelium i.e endocervix urethra, rectum, conjunctiva + pharynx
→ spreads via contact w/ mucous secre’ns from infected area
→ due to unique life cycle can’t be cultured on artificial media
RFs
- black
- 20-29 y/o
- unprotected sex
- having another STI
- men who have sex w/ men
- multiple recent sex partners
SSX in men
- dysuria
- epididymo-orchitis
- odorless green / yellow penile discharge
SSX in women = often asymptomatic but can sometimes present w/ . . .
- dysuria
- pelvic pain
- green / yellow vaginal discharge
Ix’s
- NAAT → will be +ve for gonorrhea DNA or RNA
- culture = definitive diagnosis test → will show +ve chocolate agar culture
- charcoal endocervical swab should be taken for microscopy, culture + AB sensitivities before initiating AB Tx = important due to high rates of AB resistance
Tx
1) Single dose of IM CTX if sensitivities aren’t known OR single dose of oral ciprofloxacin if sensitivities = known
2) F/u test of cure w/ NAAT testing if pt = asymptomatic + w/ culture instead if pt = symptomatic
→ do culture 3 days after Tx
→ do RNA NAAT 7 days after Tx
→ do DNA NAAT 14 days after Tx
Complica’ns
- PID if left untreated + infec’n ascends
- ectopic pregnancy (as a result of the PID)
- chronic pelvic pain (as a result of the PID)
- infertility in women if infec’n ascends (as a result of the PID)
- Disseminated gonococcal infec’n (DGI) → SSX = tenosynovitis, migratory polyarthritis + dermatitis
→ can lead to Fitz Hugh Curtis syndrome
Pregnancy complica’n = gonococcal conjunctivitis in neonate = contracted from mother during birth
→ neonatal conjunctivitis i.e ophthalmia neonatorum
= medical emergency characterized by sepsis, eye perfora’n + blindness !
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Syphilis ✓
Def - STI caused by Treponema pallidu bacterium = spiral shaped bacteria
→ transmitted by contact w/ infected area whether through oral, anal or vaginal sex
→ incuba’n period = 21 days on avg
RFs
- sex worker
- illicit drug use
- HIV or other STI
- unprotected sex
- multiple sex partners
- having syphilis during pregnancy
- sexual contact w/ infected person
Eti
- congenital syphilis = pregnant pt w/ syphilis gives it to baby during pregnancy
- 1° syphilis = single painless chancer @ original site of infec’n + local lymphadenopathy → heals spontaneously
- 2° syphilis = 4-8 wks after 1° syphilis infec’n = when it spreads via blood → leads to wide spread vasculitis → SSX = condylomata lata (grey wart-like les’ns around genitals + anus), low-grade fever + lymphadenopathy → SSX resolve 3-12 wks later but pt can enter latent syphilis stage = when pt becomes asymptomatic despite still being infected
- 3° syphilis = latest stage
→ gummatous les’ns + neuro + cardio SSX → can occur yrs after initial infec’n
Neurosyphilis - can occur @ any stage if infec’n reaches CNS + presents w/ . . .
- HA
- paralysis
- altered behavior
- ocular syphilis (affecting the eyes)
- tabes dorsalis = demyelina’n affecting posterior columns of spinal cord
SSX
- uveitis
- fatigue
- diffuse rash
- lymphadenopathy
- rhinitis + hepatosplenomegaly in congenital syphilis
- painless ulcer (chancer) in anogenital reg’n = hallmark sign of 1° syphilis
Ix’s
- antibody test for screening
- PCR or dark field microscopy of swab from les’n for diagnosis
→ will show coiled spirochaete bacterium w/ a corkscrew appearance + motility - treponemal serology tests = +ve for life ∴ could be past or active infec’n
- non treponemal serology tests → +ve means active infec’n
- rapid plasma reagin (RPR) + VDRL test = SENSITIVE but not specific = used to assess if pt has active syphilis infec’n
→ higher # = > chance that pt has active disease
Tx = single dose of IM benzathine benzylpenicillin
→ MOA - inhibits bacterial cell wall synthesis
Complica’ns
- HIV
- Jarisch Herxheimer rxn = rxn that occurs w/in first 24 hrs of AB therapy due to rapid killing of treponemes
→ SSX = HA, acute fever + myalgia
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HPV / Genital warts ✓
Def - STI caused by HPV 6 + 11
→ peak incidence = 16-25 y/o
RF = intercourse @ an early age
Eti - HPV = non enveloped dsDNA
Ix = clinical diagnosis
Tx = Podophyllotoxin gel to affected areas or cryotherapy / acetic acid / surgical excis’n (in non pregnant + non immunocompromised pt !)
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Trichomoniasis ✓
Def - STI caused by protozoan trichomonas vaginalis, most common nonviral STI worldwide, affects females more than males
→ requires genitourinary medicine referral
SSX (50% of cases = asymptomatic) . . .
- itching
- dysuria
- vaginal discharge
- dyspareunia
Diagnostic Ix = charcoal swab w/ microscopy
→ in women swab should be taken from posterior fornix of vagina i.e behind cervix
→ in men use urethral swab or first catch urine
Tx = metronidazole + contact tracing
Complica’n = can ↑ risk of . . .
- BV
- PID
- cervical cancer
- contracting HIV by damaging vaginal mucosa
- pregnancy-related complica’ns such as preterm delivery
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PID ✓
Def - acute ascending polymicrobial infec’n of female gynecological tract frequently associated w/ Neisseria gonorrheae or Chlamydia trachomatis
→ begins in cervix + if untreated can ascend to upper genital tract
Subtypes
- endometritis = inflamma’n of endometrium
- salpingitis = inflamma’n of fallopian tubes
- oophoritis = inflamma’n of ovaries
- parametritis = inflamma’n of parametrium = connective tissue around uterus
- peritonitis i.e inflamma’n of peritoneal membrane
Eti
- Neisseria gonorrhea → tends to produce more severe PID
- Chlamydia trachomatis
- Mycoplasma genitalium
RFs
- IUD use
- prior history of PID
- onset of intercourse at young age
- prior chlamydia or gonnorhea infec’n
- unprotected intercourse w/ multiple sexual partners
SSX
- Pelvic or lower abdominal pain
- abnormal vaginal discharge
- abnormal bleeding
- dyspareunia
- fever
- dysuria
SSX on exam
- pelvic tenderness
- inflamed cervix
- cervical excita’n / mo’n tenderness
Ix’s
- NAAT swabs for gonorrhea + chlamydia
- NAAT swabs for Mycoplasma genitalium if available
- HIV test
- syphilis test
- high vaginal swab to look for BV, candidiasis + trichomoniasis
- microscopy → absence of pus cells = can r/o PID
- pregnancy test to r/o ectopic pregnancy
- CRP + EST → will be elevated
Tx for mild to moderate = CTX + doxycycline + metronidazole + treat sexual contacts as well (don’t wait for swab to start Tx)
Tx for severe = admit for IV Abx + then switch to oral Abx once pt can tolerate PO
Complica’ns
- sepsis
- infertility
- tubo ovarian abscess
- chronic pelvic pain
- ectopic pregnancy
- Fitz Hugh Curtis syndrome = adhes’ns btw liver + peritoneum due to infec’n + inflamma’n of Glisson’s capsule (liver capsule)
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Bacterial Vaginosis ✓
Def - overgrowth of anaerobic bacteria in vagina + loss of lactobacilli bacteria
→ NOT sexually transmitted
RFs
- Cu coil
- smoking
- recent Abx use
- multiple sexual partners
- excessive vaginal cleaning such as douching or using vaginal cleaning products
Eti = anaerobic bacteria
→ Gardnerella vaginalis (most common)
→ Mycoplasma hominis
→ Prevotella species
Pathophys - lactobacilli bacteria produce lactic acid in vagina → keeps vaginal pH < 4.5 → BV causes loss of these good bacteria → vaginal pH ↑ → alkaline env’nt enables anaerobic bacteria to multiply
SSX = watery grey / white vaginal discharge w/ fishy smell
→ usually more noticeable after menses or intercourse
Ix = vaginal swab for pH + microscopy
→ normal vaginal pH = 3.5-4.5 so pH > 4.5 = suggestive of BV
→ microscopy will show clue cells
No Tx for asymptomatic BV
Tx for symptomatic = metronidazole orally or by vaginal gel
→ MOA - nitroimidazole Abx that damages bacterial DNA
⚠️ pts should not drink alcohol while on this medica’n b/c can cause disulfiram-like rxn w/ N+V, flushing + sometimes more severe SSX such as shock + angioedema
Complica’n = can ↑ susceptibility to chlamydia, gonorrhea + HIV
Complica’ns during pregnancy
- PROM
- miscarriage
- preterm delivery
- chorioamnionitis
- low birth weight
- postpartum endometritis
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Vaginal thrush / Vulvovaginal candidiasis ✓
Def - symptomatic inflamma’n of vagina and/or vulva
Eti - Candida albicans usually
SSX
- thick, white vaginal discharge
- itchiness around vagina
- soreness / pain during sex or urina’n
Ix = clinical diagnosis
Tx = PO fluconazole or clotrimazole pessary in pregnancy
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Herpes simplex virus ✓
Def - virus that causes cold sores / oral herpes (herpes labialis) + genital herpes (STI)
→ oral herpes / cold sores = caused by HSV-1
→ genital herpes = caused by HSV-1 or HSV-2
RFs
- HIV infec’n (RF for clinical disease)
- immunosuppressive drugs (RF for clinical disease)
- high risk sexual behavior (RF for seropostitivity)
Eti - virus spreads through direct contact w/ affected mucous membranes or via viral shedding in mucous secre’ns
→ virus can be shed even pt is asymptomatic
Pathophys - after initial infec’n virus becomes latent in associated sensory nerve ganglia → pt can develop SSC months or yrs after initial infec’n when latent virus = reactivated
⟹ trigeminal nerve ganglion in oral herpes
⟹ sacral nerve ganglia in genital herpes
SSX chronology of oral herpes
1. tingling sensa’n
2. vesicular throat + mouth ulcers
3. ulcerative throat + mouth ulcers
SSX genital herpes (appear w/in 2 wks)
- genital ulcerative / blistering les’ns but can also cause mouth les’ns
- neuropathic type pain i.e tingling / burning / shooting pain
- fatigue
- HAs
- dysuria
- inguinal lymphadenopathy
→ if first time SSX can last 3 wks whereas in recurrent episodes, SSX = milder + resolve more quickly
Ix’s
- diagnosis can be made clinically but HSV PCR swab from les’n can confirm diagnosis + causative organism
- viral culture if les’ns = present → virus will be detected
Tx = aciclovir
→ MOA - inhibits DNA synthesis + viral replica’n
SSX Mx
- paracetamol
- topical vaseline or lidocaine 2% gel
- cleaning w/ warm salt water
- wearing loose clothing
- avoiding intercourse w/ SSX
Genital herpes + pregnancy → after an initial infec’n w/ genital herpes mom will develop antibodies to the virus → during pregnancy these antibodies can cross placenta → fetus has passive immunity + is protected during labor + delivery
Complica’n of genital herpes during pregnancy = baby contracting neonatal herpes simplex infec’n during labor + delivery
→ has high morbidity + mortality
⟹ Tx for 1st time genital herpes + pregnant = aciclovir + continue it from 36 wks onwards to ↓ risk of genital les’ns during labor + delivery
→ C-sec’n if pt = symptomatic
→ vaginal delivery if pt = asymptomatic + > 6 wks have passed since initial infec’n
⟹ Tx for recurrent genital herpes = prophylactic aciclovir from 36 wks onwards to ↓ risk of genital les’ns during labor + delivery
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Chicken Pox ✓
→ highly contagious + usually occurs during childhood
→ incuba’n period ≈ 14 days (can range from 9-21 days)
RFs
- exposure to varicella
- 1-9 y/o
- non immunized
- occupa’nal exposure such as military recruits or ppl who work w/ children
Eti = Varicella zoster virus
Pathophys - susceptible person = exposed to virus either by direct contact w/ les’ns or through infected droplets i.e through coughing or sneezing
→ after contact, virus spreads to reg’nal lymph nodes = 1° phase
→ on days 4-6 infec’n spreads to liver, spleen + other cells w/in reticuloendothelial system
→ day 9 = 2° phase where mononuclear cells transport virus to skin + mucous membranes hence causing rash
→ virus = detectable in nasopharynx 1-2 days before onset of rash + pt is infectious @ this time
→ once ALL les’ns have crusted over pt is no longer infectious !
SSX
- fever (usually 1st SSX)
- malaise
- wide spread pruritic, vesicular rash that starts on trunk or face + spreads outwards
Ix = clinical diagnosis
Pts @ risk for moderate complica’ns
≥ 13 y/o
- pts w/ chronic skin disease such as atopic dermatitis
- pts w/ underlying pulmonary disease
- pts on long term salicylate therapy
- pts receiving short course or intermittent oral corticosteroids
Pts @ risk for severe complica’ns
- neonates
- pregnant women
- immunosuppressed pts
Tx for pts w/ moderate risk = oral aciclovir
Tx for pts w/ severe risk = IV aciclovir
Addi’nal Mx
- pts should not go to school for 5 days or until all les’ns are crusted over + should avoid high risk ppl during that time
- pts should trim nails, keep cool + use calamine lotion for itchiness
Complica’ns
- death
- pneumonia
- encephalitis
- hepatitis
- 2° bacterial infec’n
- can lie dormant + reactivate later in life as shingles or Ramsay Hunt syndrome
→ SSX of Ramsay Hunt syndrome = acute ipsilateral facial paralysis, Δ in taste, ear pain + hearing loss
→ Tx = oral aciclovir + corticosteroids
- chickenpox in mother around time of delivery can lead to life threatening neonatal infec’n
→ Tx = varicella zoster Igs + aciclovir
Complica’ns in pregnancy
- varicella pneumonitis
- hepatitis
- encephalitis
- fetal varicella syndrome
- severe neonatal varicella infec’n if mom = infected around delivery
- congenital varicella syndrome if mom = infected in first 28 wks of gesta’n
→ fetal growth restric’n
→ microcephaly
→ cataracts + inflamma’n in eye (chorioretinitis)
→ hydrocephalus
→ learning disability
→ limb hypoplasia / underdeveloped limbs
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Impetigo ✓
Def - contagious bacterial skin infec’n
→ usually occurs in children 2-5 y/o but can also occur in older children + even adults
→ Ix = clinical diagnosis but can do swab + culture if disease = extensive
Eti - usually caused by staph. aureus but can also be caused by strep pyogenes
Classifica’n
- Non Bullous impetigo (more common form) → typically occurs around nose or mouth
→ SSX = vesicles → gold / honey colored crust
→ Tx = hydrogen peroxide 1% cream / fusinic acid if localized + oral flucloxacillin if severe or wide spread
- Bullous impetigo = always caused by staph aureus
→ more common in children < 2 y/o but can also occur in older children + even adults
→ in severe infec’ns when les’ns are widespread = called staphylococcus scalded skin syndrome
→ SSX . . .
- itchy + painful bullae → grow + form golden / honey crust when they burst → eventually heal w/o scarring
- fever + general malaise.
→ Tx = flucloxacillin
Mx
- tell pts to not touch or scratch les’ns - good hand hygiene
- avoiding sharing face towels + cutlery
- pts need to be off school until all les’ns have healed or they have been treated w/ Abx for ≥ 48 hrs
Complica’ns
- cellulitis if infec’n gets deeper in skin
- sepsis
- scarlet fever
- post streptococcal glomerulonephritis
- staphylococcus scalded skin syndrome
- Know for OSCE *
Cellulitis (usually in legs) + Erysipelas ✓
→ erysipelas = superficial skin infec’n i.e only involves upper dermis but also has lymphatic involv’nt
→ cellulitis = infec’n of deep dermis + subq tissue
RFs
- diabetes
- venous insufficiency
- eczema
- edema
- lymphedema
- obesity
- previous episodes of cellulitis
Eti
- #1 = strep pyogenes = part of Group A strep
- #2 = strep dysgalactiase = part of Group C strep
SSX
- u/l pain, swelling, redness, warmth
- golden / yellow crust indicates staph. aureus infec’n
- fever + tachycardia → means it’s severe so treat w/ IV flucloxacillin
Ddx
- vasculitis
- insect bite
- gout attack
- lymphedema
- herpes zoster
- septic bursitis
- osteomyelitis
- septic arthritis
- contact dermatitis
- erythema migrans
Eron Classifica’n
- Class 1 = no systemic toxicity or comorbidity
- Class 2 = mild systemic toxicity or comorbidity
- Class 3 = significant systemic toxicity i.e confus’n / tachycardia / tachypne / hypoTN OR a significant comorbidity such as PAD or morbid obesity
- Class 4 = sepsis or life threatening such as necrotizing fasciitis
Ix’s
- clinical diagnosis
- always check blood glucose in pt w/ recurrent skin infec’n to check for diabetes
Tx for Class 1 or 2 = oral flucloxacillin → clarithromycin instead if pt has penicillin allergy + erythromycin instead if pt has penicillin allergy + is also pregnant
Tx for Class 3-4 or if pt is frail / immuno-compromised / has significant lymphedema = admit for IV flucloxacillin
→ IV co-amoxiclav instead it pt has facial or orbital cellulitis
Complica’ns
- sepsis
- endocarditis
- osteomyelitis
- septic arthritis
- bacteremia i.e bacteria in blood stream
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Candidiasis / Oral Thrush ✓
Def - oral yeast infec’n caused mainly by Candida albicans
RFs
- T2D
- HIV
- dry mouth
- malignancy
- chemo / radiotherapy
- malabsorp’n / malnutri’n
- poor oral hygiene (especially in older pts who wear dentures)
SSX
- burning mouth pain
- unpleasant taste in mouth
- spotty red areas on buccal mucosa
- white or yellowish plaques in oral mucosa
- cracks / ulcers / crusted fissures radiating from angles of mouth
Ix = superficial smear of les’n for microscopy → will be +ve for Candida hyphae
⚠️ Test for diabetes if pt has recurrent candidiasis !
Tx = clotrimazole or miconazole dissolved in mouth
→ MOA - antifungal that prevents forma’n of ergosterol (part of fungal cell membrane) by inhibiting cytochrome P450-dependent demethyla’n rxn
→ end in “NAZOLE”
⚠️ Order LFTs before prescribing antifungals b/c they’re hepatotoxic !
Complica’n = esophageal candidiasis (usually happens in severely immunocompromised pts)
→ SSX = dysphagia + odynophagia
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LGV ✓
Def - LGV (lymphogranuloma venereum) = penile or vulvar inflamma’n + ulcera’n caused by Chlamydia trachomatis = endemic to the tropics i.e Africa / India / Southeast asia
RFs
- 20-40 y/o
- having other STIs
- HIV sero +ve
- MSM
SSX chronology
- 1 ° stage → single painless ulcer on penis, vaginal wall or on rectum if pt had anal sex
- 2 ° stage → lymphadenitis i.e swelling, inflamma’n + pain in inguinal or femoral lymph nodes
- 3 ° stage → proctitis i.e inflamma’n of rectum + anus (occurswks later)
⟹ will cause anal pain, tenesmus + Δ in bowel habit
Ix’s
- NAAT on genital or lymph node specimen
→ will test +ve for Chlamydia trachomatis - anoscopy swab for gram staining
- RT-PCR = only way to confirm diagnosis → will be +ve for LGV
- test pt for other STIs as well
Tx = doxycycline for 21 days
→ erythromycin instead if pt = pregnant, breastfeeding or = allergic to tetracyclines
Complica’ns
- reactive arthritis
- ↑ed susceptibility to HIV + other STIs
- chronic inflamma’n can lead to scaring, fibrosis + lymphedema of genitals or to stricture + fistulae forma’n if there’s anorectal involv’nt
- Know for OSCE *
Tropical STI - Chancroid ✓
Def - STI that mainly occurs in poor countries
= caused by gram -ve bacteria coccobacillus Hemophilus ducreyi = co factor in HIV transmiss’n so always check these pts’ HIV status
→ sexual partners w/in 10 days prior to onset of SSX must be traced + treated even if asymptomatic !
RFs
- male
- unprotected sex
- substance abuse
- multiple sex partners
- not being circumcised
- sexual contact w/ sex worker
Eti - infec’n occurs through contact w/ mucous membranes such as during sex or via abras’ns in skin of genital reg’n
SSX
- bubo forma’n / lymphadenitis
- painful genital papules → in later stages will pustulate + then ulcerate + we now have painful genital ulcers
Ix’s
- bubo aspirate + gram stain of ulcer swabs → will be +ve for gram -ve cocobacilllus
- culture of the above → will specifically identify Hemophilus ducreyi
- Hemophilus ducreyi PCR → will be +ve
- RPR rest to check for syphilis co-infec’n (usually -ve)
- HSV PCR + viral culture to make sure it’s not herpes
- HIV testing
Tx = azithromycin or CTX
Complica’ns
- inguinal abscess
- urethral and/or rectovaginal fistula
- Know for OSCE *
Pyrexia of unknown origin (PUO) ✓
Eti
INFECTIOUS CAUSES
- TB
- abdo. infec’ns
- Infective endocarditis
- viral infec’ns like HIV, EBV, CMV
→ consider geography . . .
⟹ for ex in Mediterranean pt consider Brucella / Leishmaniasis + in returning traveler consider Dengue fever, malaria, enteric fever from typhoidal salmonella
CONNECTIVE TISSUE DISEASES
- RA
- Still’s disease
- SLE → mainly in young adults
- Temporal arteritis + polymyalgia rheumatica (elderly pts usually)
MALIGNANCY b/c some neoplasms produce pyrogenic cytokines
→ accounts for 18% of FUO + includes lymphomas, hyper-nephromas, colorectal + CNS cancers
Classifica’n
- Classic FUO
- fever > 38.3°C
- dura’n of > 3wks
- no diagnosis after > 2 outpt visits or 3 days of hospital Ix - Nosocomial /Health-care associated) = fever > 38.3°C on several occas’ns
- Neutropenic (immune-deficient)
- fever > 38.3°C
- neutrophil count < 500
- no diagnosis after 3 days of hospital Ix - HIV-related FUO
- fever > 38.3°C
- dura’n of > 3 wks for outpts + > 3 days for inpts
- Know for OSCE *
Why pts taking broad spectrum Abx might get diarrhea ✓
B/c Abx killed healthy gut flora as well
→ if diarrhea = smelly ≠ due to Abx → if diarrhea ≠ smelly = due to Abx
Abx that most commonly cause C. diff + Tx ✓
” 4 C’s”
- cipro
- cephalosporins i.e CTX
- clindamycin
- co-amoxiclav
Tx = oral vancomycin
Traveller’s Diarrhea ✓
Def - ≥ 3 unformed stools in past 24 hrs during trip to 3rd world country + ≥ 1 of the following SSX . . .
- fever
- N/V
- bloody stools
- abdominal cramps
- tenesmus → feeling that you still need to empty bowels even after having BM
RFs
< 30 y/o
- immunocompromised
- travelling when it’s hot + wet season in that country
Eti = Campylobacter jejuni usually, spread by . . .
- raw or improperly cooked poultry
- untreated water
- unpasteurized milk
Incuba’n period = 2-5 days + SSX usually resolve after 3-6 days
Ix’s
- stool culture + sensitivity to identify causative bacteria / pathogen
- stool occult blood
- stool ova + parasite in case causative pathogen = parasite + ≠ bacteria
Tx = loperamide + azithromycin
- Know for OSCE *
Malaria ✓
Def - parasitic infec’n caused by protozoa of the genusPlasmodium
= transmitted to humans by being bitten by infected female Anophelesmosquito but can also be transmitted by blood transfus’n or organ transplanta’n
RF = travelling to endemic area i.e India / West or Central Africa
Eti
- Plasmodium malariae
- Plasmodium knowlesi
- Plasmodium vivax (dormant liver stage but can reactivate)
- Plasmodium ovale (dormant liver stage but can reactivate)
- Plasmodium falciparum = most severe
Pathophys - during a blood meal infected femaleAnophelesmosquito injects sporozoites in victim
→ sporozoites rapidly enter hepatocytes + reproduce by asexual fiss’n (tissue schizogony) to form pre-erythrocytic schizont (this part of the life-cycle produces no SSX)
→ after a period of time merozoites = released into bloodstream to penetrate erythrocytes after attaching via receptors
→ most merozoites undergo blood schizogony to form trophozoites which evolve into schizonts which rupture to release new merozoites
→ disrupts RBC membrane integrity + causes RBC lysis
→ rupture of erythrocytes releases toxins that induce release of cytokines from macrophages ∴ resulting in malaria SSX
SSX
- fever that spikes very high every 48 hrs
- chills
- sweats
- myalgia
- diarrhea
- anorexia
- HA
- jaundice
- pallor due to anemia
- hepatosplenomegaly
Ix’s
- Glemsa stained thick + thin blood film → will show plasmodium thropozoites inside RBCs
⟹ 3 -ve samples taken over 3 consecutive days = required to exclude malaria ! - RDT → but can only detect falciparum + vivax
- LFTs → unconjugated hyperbilirubinemia
- FBC → might show anemia
Tx for pts w/ falciparum malaria = admit for IV artesuntate
Tx for all others = riamet
Malaria ppx before travelling to endemic area
- mosquito spray
- using mosquito nets in sleeping areas
- antimalarial medica’n such as . . .
→ malarone
→ doxycycline
→ mefloquine
Complica’ns
- AKI
- cerebral malaria → can lead to seizures, ↓ed consciousness + even coma
- Know for OSCE *
Lyme Disease ✓
Def - infectious disease transmitted to humans through the bite of an Ixodes scapularis tick that was infected w/ Borrelia burgdorferi bacteria
RF = outdoor activities
SSX
- fatigue
- at early stage presents w/ flu-like SSX + erythema migrans i.e spreading target symbol rash @ site of tick bite (rythema migrans develops w/in 1-2 wks)
- late stage manifesta’ns = arthritis, heart block + facial nerve palsy (bilaterally usually)
Ix = enzyme immunoassay or immunofluorescence assay → will be +ve
Tx = doxycycline
- Know for OSCE *
Scabies ✓
Def - highly contagious skin infesta’n caused by mite Sarcoptes scabiei
→ can take up to 8 wks after initial infesta’n for SSX to appear
RFs
< 15 y/o or > 65 y/o
- overcrowded living condi’ns
- immunocompromised
- living in close quarters w/ others who are infected
Eti - transmitted through direct + prolonged skin-to-skin contact
Pathophys - mite burrows into skin + lays its eggs in stratum corneum
→ delayed-type IV hypersensitivity rxn to mites/eggs occurs ≈ 30 days after initial infec’n
SSX
- widespread itching sparing that’s worse @ night
- incredibly itchy small red spots, btw finger webs but can spread to whole body
- track marks where mites burrowed
- other household members w/ similar SSX
- crusted scabies = seen in immunosuppressed pts such as HIV pts → isolate these pts + treat them w/ single dose oral Ivermectin
Ix = clinical diagnosis but can microscopy to detect eggs or scyballa (fecal pellets)
Tx - permethrin 5% cream → malathion 0.5% cream
⟹ permethrin cream should be applied on whole body when skin is cool + should be left on for 8 -12 hrs before you wash it off + repeat the whole process for 1 more wk to kill hatched eggs that survived 1st round
- Know for OSCE *
Head lice ✓
Def - scalp infesta’n caused by Pediculus humanus capitis parasite
→ usually occurs in school aged children
→ = transmitted by head to head contact or by sharing equipment that touches head such as combs or towels
SSX = itchy scalp
Tx = Dimeticone 4% lotion on hair
→ should be left on hair for 8 hours i.e overnight + then washed off
⟹ do this for 8 days to kill any head lice that have hatched
Mx = detec’n combing to check if Tx was successful
- Know for OSCE *
Folliculitis ✓
Def - inflamma’n of hair follicle
→ most common cause of superficial folliculitis = Staph. aureus
RFs
- shaving
- diabetes
- immunosuppress’n
Eti
- gram -ve bacteria (i.e Klebsiella, Enterobacter, Proteus)
- viral
- fungal
- parasitic
- eosinophilic pustular in infants (= on scalp)
- drug induced i.e Li, isoniazid, corticosteroids
SSX = erythematous papules or pustules in areas w/ terminal hair growth such as head, neck, axilla, groin + buttocks
Ix’s
- bacterial skin swab for PCR if there is a definite pustule that can be unroofed w/ a 15 blade
- viral skin swab for PCR if Hx + exam = suggestive of Herpes simplex infec’n
Tx for uncomplicated folliculitis = nothing b/c = self-limiting
Tx for recurrent / deep folliculitis due to methicillin susceptible stap. aureus (MSSA) = cefalexin = cephalosporin
Tx for recurrent / deep folliculitis due to MRSA = clindamycin
Tx for gram -ve folliculitis = topical benzyl peroxide
- Know for OSCE *
Delirium ✓
Def - acute state of confus’n
Causes (“VVITAMEN Double D’s”) . . .
- Vitamin deficiencies - thiamine, B12
- Vascular disorders - cerebrovascular hemorrhage or infarc’n / vasculitis
- Infec’n - UTI, pneumonia, sepsis, meningitis, encephalitis, malaria
- Toxins - CO, heavy metals, barbiturate / benzo / SSRI w/drawal
- Alcohol intoxica’n or w/drawal
- Metabolic - hypoxia, electrolyte abnormalities such as HypoNa or HyperCa, hypo or hyperglycemia, uremia, liver failure, thyrotoxicosis
- Epilepsy
- Neoplasm
- Drugs - benzos, analgesics such as morphine, anti-cholinergics, anti-convulsants, anti-parkinsonism medica’ns, steroids
- Dehydra’n
- Sleep depriva’n
Immediate “stabilizing” Tx i.e if delirious pt = aggressive + agitated = low dose haloperidol
→ MOA = dopamine receptor antagonist
- Know for OSCE *
Dementia ✓
Def - > 3 months of GRADUAL confus’n
RFs
- FHx
- HTN
- female
- old age
- diabetes
- head trauma
- hypoTSH
Eti
1) Alzheimer (50-60%) (MMSE typically ↓ 3 points / yr)
→ SSX = 8 A’s
- Aphasia
- Altered percep’n
- Apathy i.e lack of drive to do things
- Amnesia → pt will lose their short term memory 1st + then they’ll lose their long term memory
- Amyloid-β plaques extracellularly + hyperphosphorylated Tau intra- cellularly
- Anosognosia = not realizing that something is wrong i.e not realizing that ur forgetting stuff
- Agnosia = loss of ability to recognize things via senses i.e objects, ppl,smells, sounds, tastes although the sense itself isn’t defective
- Apraxia = loss of ability to execute or carry out learned purposeful mov’nts despite having desire + physical ability to perform those mov’nts
- Vascular dementia (15-20%)
→ SSX = stepwise ↓ in cognitive ability w/ late onset memory impair’nt + pt has RFs such as HTN / T2D - Lewy body dementia (10-15%)
→ SSX = Parkinsonism, progressive cognitive decline, visual hallucina’ns, delus’ns, fluctuating levels of alertness + REM sleep disorders
⚠️ Regular Parkinson’s can also have Lewy bodies !
- Fronto temporal dementia / Pick’s disease
→ SSX = early Δs in personality / behavior +/- aphasia
Ddx
- depress’n
- normal aging
- temporal lobe seizure
- intracranial space occupying les’n i.e tumor
Ix’s
- 6 part MMSE test → tests orienta’n, ability to repeat, calcula’n, recall, language + copying
→ 27-30 = normal
→ 25-26 = cognitively impaired
→ 21-24 = mild dementia
→ 10-20 = moderate dementia
→ 0-9 = severe dementia
- brain MRI → In early Alzheimer’s, might see atrophy of temporal lobe, particularly hippocampus
Tx for mild ~ moderate = Achesterase inhibitor
→ MOA - inhibits Achesterase from breaking down Ach
→ side effects = too much para b/c Ach is it’s neurotransmitter
⟹ hypersaliva’n, hyperlacrima’n, urinary reten’n, diaphoresis, GI hypermotility, emesis
→ C/Is = bradycardia, urinary reten’n, gastric ulcers
→ end in “MINE”
- Tx for for moderate ~ severe = add NMDA receptor antagonist such as memantine
→ side effects = constipa’n, HA, drowsiness, HTN, hallucina’ns, balance pbs - Know for OSCE *
Delirium v.s Dementia ✓
- fluctuates v.s progresses
- days ~ wks v.s permanent
- reversible v.s NOT reversible
Pressure sores / Pressure ulcers ✓
Def - localized damage to skin + underlying soft tissue over a bony prominence b/c of prolonged immobiliza’n
RFs
- Sx / immobility
- older age
- ICU stay
- sensory impairment
Ix = clinical diagnosis
Ppx for pressure ulcers = pressure reducing aids + frequent repositioning
Regular Tx = wound dressing, analgesia + diet optimiza’n
Tx for deep ulcers i.e stage 3 or stage 4 = debridement of necrotic tissue + flap reconstruc’n
Complica’ns
- sepsis
- cellulitis
- osteomyelitis
- Know for OSCE *
Eczema / Atopic Dermatitis ✓
Def - chronic inflammatory skin condi’n characterized by dry + itchy skin
→ usually diagnosed before 5 y/o
→ these pts tend to have more food allergies than the avg popula’n
RFs
< 5 y/o
- muta’ns in filaggrin gene
- personal or FHx of eczema or other atopic diseases such as asthma or allergic rhinitis
SSX = dry, red itchy paches of skin on flexor surfaces i.e knee / elbow
Ddx
- irritant contact dermatitis
- allergic contact dermatitis
Ix = clinical diagnosis
Tx = emollients → hydrocortisone → eumovate → betnovate → dermovat
Complica’ns
- flares
- breakdown of skin’s protective barrier gives an easy entry for infective organisms (staph. aureus usually)
- eczema herpeticum = viral skin infec’n in eczema pts → = caused by HSV or VZV
→ SSX = widespread, painful, vesicular rash + systemic SSX such as fever, lethargy, lymphadenopathy, irritability + ↓ed oral intake
→ Tx = aciclovir
- Know for OSCE *
Allergic contact v.s Irritant contact dermatitis ✓
Allergic contact dermatitis = T cell mediated, delayed-type hypersensitivity response to exogenous agent
Irritant contact dermatitis = localized, inflammatory skin response to a chemical or physical agent
→ not immune mediated unlike allergic contact dermatitis
RFs
- infants for irritant contact
- Hx of atopic dermatitis
- working w/ chemicals i.e hairdresser, HCPs
SSX = erythematous, indurated, scaly plaques localized to areas that came into contact w/ allergen or chemical
Ddx = each other
Tx = identifying + avoiding causative agent
- Know for OSCE *
Diaper rash ✓
Def - contact dermatitis in diaper area due to fric’n btw skin + diaper
RFs
- delayed diaper changing
- irritant soap products
- vigorous cleaning
- poorly absorbent diapers
- diarrhea
SSX = sore, red, inflamed skin in diaper area sparing creases
Tx
- switching to highly absorbent diapers
- prompt diaper changing
- using water or gentle alcohol free products to clean diaper area
- not wearing diaper all the time
- nystatin if it’s fungal infec’n
Complica’ns
- eros’n
- ulcera’n
- candida infec’n
- cellulitis
Erthryoderma ✓
Def - severe + Ψly life-threatening condi’n that presents w/ diffuse erythema + scaling, involves ≥ 90% of skin surface area = dermatological emergency !
Eti = psoriasis
SSX
- warm psoriatic les’ns
- fever
- malaise
- tachycardia
- lymphadenopathy
- peripheral oedema
Ix = clinical diagnosis
Emergency Tx = ciclosporin + infliximab
Mx
- bed rest in a warm room (30-32°C)
- emollients + cool, wet dressings
- treating complica’ns
- nutri’nal support
Complica’ns
- dehydra’n
- hypothermia
- cardiac failure
- sepsis
- protein loss
- death
- Know for OSCE *
How to use the Rule of 9’s to calculate %age of TBSA lost after burn ✓
- head + neck = 9%
- each arm = 9%
- torso = 18%
- back = 18%
- each leg = 18%
- groin area = 1%
- Know for OSCE *
Classifying burns ✓
1st ° / superficial burn
→ depth = epidermis
→ SSX = pain, redness + mild swelling
2nd ° / superficial partial burn
→ depth = papillary reg’n of dermis
→ SSX = pain, blisters, splotchy skin + severe swelling
3rd ° / deep partial burn
→ depth = reticular reg’n of dermis
→ SSX = white, leathery + relatively painless
Full thickness burn
→ depth = hypodermis / subq
→ SSX = charred, no sensa’n, w/ eschar
- Know for OSCE *
Parkland formula to determine how much to fluid resucitate burn pt in the 1st 24 hrs ✓
For children = 3 ml x % TBSA burned x pt’s weight in kg
For adults = 4 ml x % TBSA burned x pt’s weight in kg
Emergency Tx for thoracic burn ✓
Aggressive IV fluid resucita’n using Parkland formula → escharotomy
→ urgent transfer to burn center
Indica’ns for transfer to burn center ✓
- burns ≥ 2% TBSA in children or ≥ 3% in adults
- full thickness burns
- circumferential burns
- any burn that hasn’t healed after 2 wks
- suspici’n that burn = due to non-accidental injury (must be done w/in 24 hrs)
Inhala’n injury ✓
Def - injury caused by inhaling lots of smoke (after house fire for ex)
SSX
- harsh cough
- hoarse voice
- burns to face
- singed hair / eyebrows / eyelashes
- soot around face, mouth + nose
Initial Tx = intuba’n
What is flap reconstruc’n ? ✓
Technique in plastic + reconstructive Sx where any type of tissue = lifted from donor site + moved w/ its intact blood supply to recipient site
→ used when extensive areas of tissue = lost such as in mastectomy
→ TRAM (transverse rectus abdominis) = often used for flap
⚠️ Unlike a flap, a graft DOES NOT have an intact blood supply !
Develop’ntal Milestones ✓
1 MONTH
Social behavior
- can follow parents w/ eyes
Language
- quiets or turns to parents’ voice
Gross Motor
- holds chin up when on stomach
Fine Motor
- can slightly open fingers
2 MONTHS
Social behavior
- smile responsively
- make sounds that show that they’re happy or upset
Language
- can make short cooing sounds
Gross Motor
- lift head + chest when on stomach
- keep head steady when held in sitting posi’n
Fine Motor
- can open + shut hands
- can briefly bring hands together
4 MONTHS
Social behavior
- laugh
- look for parent / caregiver when they’re upset
Language
- turn to voices
Gross Motor
- roll over from stomach to back
Fine Motor
- keep hands unfisted
- can grasp objects
6 MONTHS
Social behavior
- smile at own reflec’n
- look when their name is called
Language
- start babbling i.e sounds like ma / ba / ga
Gross Motor
- roll over from back to stomach
- can sit briefly w/o any support
Fine Motor
- can pass objects from one hand to the other
- bang small objects
9 MONTHS
Social behavior
- can do basic gestures such as waving
- look for dropped objects
- play games like peekaboo
Language
- can say mama or dada
- copy sounds parents make
Gross Motor
- can sit w/o support
- pull to stand
- crawl
Fine Motor
- can pick up food or objects
12 MONTHS
Social behavior
- look for hidden objects
- imitate new gestures
Language
- can use one word other than mama or dada
- can follow direc’ns w/ gestures
Gross Motor
- 1st steps
- can stand w/o support
Fine Motor
- can drop object in cup
- can pick up small object w/ 2 finger pincer grasp
15 MONTHS
Social behavior
- can imitate scribbling
- can drink from regular cup w/ little spill
- points to ask for something
Language
- can use 3 words other than names
- can follow direc’ns w/o gestures
Gross Motor
- run
- squat to pick up objects
Fine Motor
- can take object in + out of container
18 MONTHS
Social behavior
- help to dress + undress themselves
- begin to scoop w/ spoon
- can use words to ask for help
Language
- can name ≥ 5 familiar objects
- can identify ≥ 2 body parts
Gross Motor
- can sit in small chair
- carry toys while walking
Fine Motor
- scribble spontaneously
- can throw ball while standing
2 y/o
Social behavior
- parallel play i.e playing alongside other children
Language
- have ≥ 50 words in vocabulary
- can follow 2 step commands
- can name ≥ 5 body parts
Gross Motor
- can kick ball + jump off the ground w/ both feet
Fine Motor
- can stack objects
- can turn book pages/ knobs / lids
- can draw lines
2.5 y/o
Social behavior
- can pee in potty or toilet
- can spear food w/ fork
- can wash + dry hands
- imaginary play
Language
- use pronouns correctly
Gross Motor
- can walk up steps
- can run w/o falling
Fine Motor
- grasp crayon w/ thumbs + fingers instead of fist
- can catch large ball
3 y/o
Social behavior
- can enter bathroom + pee by themselves
- can put on upper clothes by themselves
- can eat independently
- sharing / cooperative play
Language
- can use 3 word sentences
- can tell a story from TV or a book
Gross Motor
- can ride tricycle
- can climb
- can jump forward
Fine Motor
- can draw circle
- can cut w/ child scissors
⚠️ Global develop’ntal delay = delay in all 4 categories !
Urticaria / Hives ✓
Types
- acute = allergic rxn
- chronic = idiopathic autoimmune rxn
Eti for acute
- allergy to food, medica’n or animal
- contact w/ chemicals or latex
- viral infec’n
- insect bites
- dermatographism
Triggers for chronic inducible urticaria
- sunlight
- temperature change
- exercise
- strong emo’ns
- extreme heat or cold
SSX
- small itchy lumps on skin associated w/ a patchy erythematous rash
- might be accompanied w/ flushing + angioedema
Tx = antihistamines (end in “AMINE” or “ADINE”)
→ fexofenadine specifically for chronic urticaria
→ side effect = dry mouth
- Know for OSCE *
Henoch-Schoenlein Purpura / IgA vasculitis ✓
Def - vasculitis that commonly presents in children < 10 y/o, occurs due to IgA deposits in blood vessels = most common childhood vasculitis
Eti - often triggered by upper airway infec’n or gastroenteritis
SSX = “PAAK”
- Purpura rash on buttocks + lower limbs
- Arthralgia
- Abdominal pain
- Kidney disease
Diagnostic criteria = palpable purpura + ≥ 1 of the following . . .
- diffuse abdominal pain
- arthritis or arthralgia
- Bx showing IgA deposits
- proteinuria or hematuria
Ddx
- meningococcal septicemia
- leukemia
- idiopathic thrombocytopenic purpura
- hemolytic uremic syndrome whose SSX =
→ diarrhea
→ elevated reticulocyte count
→ low haptoglobin levels
→ thrombocytopenia
→ abnormal stool studies
Ix’s
- FBC to check for thrombocytopenia, sepsis + leukemia
- GFR + U + E to check for renal involv’nt
- serum albumin to check for nephrotic syndrome
- BP to check for HTN
- urine dipstick to check for proteinuria
- Urine protein : Cr ratio to quantify proteinuria
Tx = supportive i.e analgesia, rest + hydra’n
Mx
- repeated urine dipstick monitoring
- repeated BP monitoring
Prognosis
- abdominal pain usually settles w/in a few days
- pts w/o renal involv’nt fully recover w/in 4-6 wks
- 1/3 of pts have a recurrence w/in 6 months
- only a small propor’n of pts will develop end stage renal failure
Steven Johnson Syndrome + Toxic Epidermal Necrolysis ✓
Def - severe cutaneous T cell mediated rxn characterized by extensive necrosis + detach’nt of epidermis = medical emergency !
→ SJS = < 10% of body surface area detached
→ TEN = > 30% of body surface area detached
RFs
≥ 65 y/o
- HIV
- malignancy
- black + asian ethnicity
- connective tissue disorder
Eti = medica’n or infec’n
→ medica’n usually → 40% of medica’n induced SJS cases = due to Abx
→ medica’n
- Abx
- NSAIDs
- allopurinol
- anti-epileptics
→ infec’n
- HIV
- HSV
- CMV
- Mycoplasma pneumonia
SSX chronology
- non-specific SSX of fever, cough, sore throat, sore mouth, sore eyes + itchy skin
- Pt develop purple or red rash that spreads across skin + starts to blister
- A few days after blistering starts, skin starts to break away + shed ∴ leaving raw tissue underneath
→ pain, erythema, blistering + shedding can also happen to lips + mucous membranes
→ eyes can also become inflamed + ulcerated
→ can also affect lungs + urinary tract
Definitive Ix for diagnosis = skin Bx
→ will show keratinocyte apoptosis w/ detach’nt of epidermis from dermis
Emergency Tx
- Admit to burn unit / specialized wound care or derm ICU
- Order FBC, U+E, LFTs, glucose, Mg, PO4, bicarb, mycoplasma serology, CXR, skin Bx + BL body weight
- Establish peripheral venous access
- Insert NG tube if pt ≠ able to take PO
- Insert urinary catheter if urogenital involv’nt is causing significant dysuria / urinary reten’n
- Identify causative agent + stop it immediately
- Clean wounds + intact skin regularly by gently irrigating w/ sterile water, saline or antimicrobial such as chlorhexidine
- apply a greasy emollient over whole epidermis (including denuded areas)
- apply non-adherent dressings to denuded dermis
- 2° foam or burn dressing should be used to collect exudate (suitable dressings include
- remove necrotic / infected epidermis w/ topical antimicrobial agent
(betadine or chlorhexidine) + under general anesthesia - daily ophthalmological during acute illness
→ ocular lubricant every 2 hrs - daily review of mouth during acute illness
→ white soft paraffin ointment to lips every 2 hrs
→ clean mouth daily w/ warm saline mouthwash or oral sponge
→ anti-inflammatory oral rinse w/ benzydamine hydrochloride every 3 hrs (especially before before eating)
→ anti-septic oral rinse w/ chlorhexidine 2x / day
Complica’ns
- sepsis
- dehydra’n
- blindness
- permanent skin damage
- 2° bacterial infec’n / cellulitis
- lung injury / pneumonia / pulm. edema / atelectasis
- Know for OSCE *
Melanoma ✓
Def - malignant skin tumor arising from melanocytes
→ most common cause of skin cancer related death
RFs
- FHx
- previous Hx of skin cancer
- white skin
- light eye color
- sun exposure
- red or blonde hair
- high freckle density
- use of tanning bed
- immunosuppression
SSX = “ABCDE “
- Asymmetry i.e if les’n were cut in half, the 2 halves wouldn’t be identical
- Borders that are irregular
- Color varia’n i.e presence of multiple shades of color
- Diameter ≥ 6 mm
- Evolu’n i.e les’n is changing in size, shape or color
Ix’s
- skin Bx for diagnosis → will show abnormal melanocytic prolifera’n in epidermis
- immunhistochemistry to check for presence of melanocytic markers associated w/ melanoma
- Breslow tumor thickness = best indicator of prognosis
→ < 1 mm = little chance of cancer spreading
Staging
- Stage 1 = ≤ 1mm in thickness or
1-2 mm thick but skin overmelanoma has not broken - Stage 2 = ≥ 2 mm in thickness or 1-2mm thick but outer layer of melanoma = broken / ulcerated
- Stage 3 = has spread to lymph nodes
- Stage 4 = has metastasized
Tx for stage 1 or 2 = surgical excis’n → repeat surgical excisn but w/ wider margin
⟹ < 1mm = 1 cm margin
⟹ 1-2 mm = 1-2 cm margin
⟹ > 2 mm = 2-4 cm margin
Tx for resectable stage 3 or 4 = pembrolizumab + Sx
Tx for non-resectable stage 3 or 4 = nivolumab + ipilimumab or talimogene laherparepvec
Ppx = ↓ing UV exposure
- Know for OSCE *
SCC of skin ✓
Def - skin cancer that occurs in keratinocytes
RFs
- UV exposure
- immunosuppress’n
- white
- male
- older age
- actinic keratosis
- previous skin cancer
Types
- Actinic keratosis = pre-cancerous les’n
- Bowen’s disease = confined to outer layer of skin i.e SCC in situ
- Invasive SCC = had spread into deeper layers of skin
- Metastatic SCC
SSX = erythematous, well-demarcated, scaly patches or plaques located in sun-exposed areas such as head, neck + extremities
Ix’s
- skin Bx for diagnosis → in Bowen’s disease will see full thickness atypia w/ intact basement membrane that is confined to epidermis
- urgent referral on skin referral pathway
Tx for Bowen’s disease = 5-fluorouracil cream (Efudix)
Tx for invasive / metastatic < 2 cm in diameter = surgical excis’n
Tx for invasive / metastatic > 2 cm in diameter = Mohs micrographic Sx
Tx for immunocompromised pts = oral retinoid
- Know for OSCE *
Basal cell carcinoma ✓
Def - common skin cancer arising from basal layer of epidermis = locally invasive ∴ rarely metastasizes
→ most common histological subtype = nodular
RFs
- fair skin
- blue eyes
- previous BCC
- exposure to UV radia’n such as too much sun / tanning beds / phototherapy
SSX = slow growing pearly white / pink papulo-nodules varying in size
→ can ulcerate / spontaneously bleed
Ix = skin Bx → will show dermal masses w/ diff sizes + shapes composed of basophilic cells w/ uniform nuclei + scant cytoplasm
Regular Tx = Moh’s Sx
Tx for nodal disease = Sx
Tx for advanced disease = neoadjuvant vismodegib or cemiplimab + Sx
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Melanocytic nevi ✓
Def - benign clonal prolifera’ns of melanocytes that develops @ birth (congenital) or after birth (acquired)
RFs
- fair skin
- sun exposure
- being immunocompromised
How les’ns can look like . . .
- brown, flat macules
- raised dome-shaped papules
- bluish-grey macules
Ddx = melanoma
Ix = clinical diagnosis + can do Bx if unsure if it’s melanoma
Tx = observa’n → surgical removal if suspicious for melanoma
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Pemphigus ✓
Def - life-threatening autoimmune bullous diseases characterized by blistering + eros’n of skin and/or mucous membranes
→ pemphigus foliaceus = confined to skin
→ pemphigus vulgaris = skin + mucosa
RF for pemphigus vulgaris = HLA DR4 + HLA DQ1
SSX
- chronic erosive ulcering of skin + mucosa (mouth especially)
- pain
- impaired sleep
- impaired swallowing if esophagus = involved
Ix’s
- clinical diagnosis
- direct immunofluorescence staining of biopsied skin → will show Ig + C3 deposits on keratinocyte surface + histology will show keratinocyte acantholysis
Regular Tx = long term rituximab
Tx for severe = IV Ig or IV corticosteroid
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Bullous Pemphigoid ✓
Def - chronic, acquired autoimmune sub epidermal blistering disease
RF = 60-90 y/o
Eti - auto-antibodies against hemidesmosomal antigens
SSX = blisters typically on the flexor surfaces of arm, legs, axillae, abdomen + groin
Ix’s
- Bx of entire newly formed blister
→ will show sub-epidermal blister w/ infiltrate rich in eosinophils - Skin Bx for direct immunofluorescence testing = best Ix → +ve result = linear band of IgG and/or C3 along basement membrane zone
⟹ indirect immunofluorescence testing after +ve result → will be +ve fo bullous pemphigoid antibodies
Tx for localized les’ns = topical corticosteroid such as clobetasol or topical tacrolimus
Tx for widespread = oral prednisolone
→ side effect of prednisolone = dyspepsia
Complica’ns
- 2° infec’n
- corticosteroid side effects
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Polymyalgia rheumatica ✓
Def - inflammatory rheumatological condi’n in pts > 50 y/o that causes pain + stiffness in shoulders, pelvic girdle + neck
RFs
- old + white
- GCA
SSX must be present for > 2 wks . . .
- raised IL-6
- difficulty rising up when seated
- pain + morning stiffness involving neck, shoulder, hip girdle + proximal limb muscles
→ pain = worse after rest / inactivity
Ddx
- GCA
- early RA
- fibromyalgia
- polymyositis
Ix
- ESR / CRP → will elevated
- must do the following Ix’s before starting steroid Tx
→ FBC
→ U + E
→ LFTs
→ TFTs
→ Ca
→ Serum protein electrophoresis for myeloma
→ CK to r/o myositis
→ rheumatoid factor to r/o RA
→ urine dipstick
Tx = corticosteroid i.e oral prednisolone for 1-2 yrs
→ f/u w/ pt 1 wk later b/c if they haven’t improved at all by then, then u probably have the wrong diagnosis
Complica’ns
- relapse
- side of effects of long term corticosteroid use
Temporal arteritis / Giant cell arteritis (GCA) ✓
Def - type of large + medium vessel vasculitis of extracranial branches of carotid arteries, if occurs in pts > 50 y/o = medical emergency !
RFs
- female
- old + white
SSX
- PMR SSX
- scalp tenderness
- auditory SSX such as tinnitus or hearing loss
- temporal artery tenderness
- u/l HA around temple or forehead
- vis’n pbs such as blurry vis’n / diplopia due to involv’nt of ciliary arteries
- jaw + limb claudica’n i.e pain on chewing + exer’n respectively = relieved by rest
Ix’s
- ESR / CRP → will be elevated
- temporal artery duplex U/S → will show stenosis of artery + wall thickening i.e hypoechoic halo sign
= diagnostic of GCA - temporal artery Bx for diagnosis but -ve Bx ≠ enough to r/o GCA !
→ will show granulomatous vasculitis i.e intima thickening, elastic lamina fragmenta’n
→ in 50% of cases will show multinucleate giant cells = diagnostic of GCA
Emergency Tx i.e if pt has visual SSX or jaw claudica’n = IV methylprednisolone
Regular Tx = prednisolone
Complica’ns
- stroke
- aneurysm
- irreversible blindness due to optic nerve ischemia
RA ✓
Def - chronic inflamma’n of lining of synovial jts
RF = FHx
Ddx
- PA
- OA
- SLE
- gout
Ix’s
- RF → might be +ve
- anti CCP → might be +ve
- X ray → X ray findings = “LESS”
→ Loss of jt space
→ Eros’n (peri-articular)
→ Soft tissue swelling
→ Soft bone i.e osteopenia / juxta-articular osteoporosis - DAS-28 to monitor response to Tx → points = given based on swollen jts, tender jts + ESR/CRP
Tx = Disease-Modifying Anti-Rheumatic Drugs (DMARDs)
- Methotrexate normally but hydroxychloroquine instead if pt = pregnant
- Add other DMARD
- Methotrexate MOA → ↓ dTMP (deoxythymidine monoPO4) + prevents convers’n of folic acid to its active form FH4 by inhibiting dihydrofolate reductase ∴ must co-prescribe w/ wkly folic acid supplements to ↓ risk of myelosuppress’n
→ folate has to be taken ≥ 24hrs after methotrexate
→ side effects - teratogenic ∴ pts must avoid unprotected sex during Tx + 3-6 months after Tx, hepatotoxic, bone marrow suppress’n which can lead to infec’ns or unexplained bruising, methotrexate pneumonitis (can lead to pulmonary fibrosis)
⟹ b/c of all these side effects, FBC, LFTs + renal func’n tests = required before initiating Tx + every 1-2 wks until dosage = stabilized - Hydroxycholoroquine MOA → inhibits phospholipase A2, ↑ pH of lysosomes + ↓ secre’n of immunological proteins
→ side effects = corneal edema or retinopathy, blue-grey skin pigmenta’n + hair bleaching = least toxic DMARD - Sulfasalazine MOA - inhibits dihydropteroate synthase hence inhibiting folic acid form’an = anti-inflammatory + immunosuppressant effect
→ side effects = orange urine + male infertility b/c ↓ sperm count - Leflunomide MOA → inhibits dihydro-orotate dehydrogenase ∴ inhibits pyrimidine synthesis
→ side effects = HTN + peripheral neuropathy
- Biologic if pt has tried methotrexate + other DMARD for ≥ 6 months + they haven’t worked
→ main side effect = TB reactiva’n ∴ MUST do CXR / interferon γ before prescribing it !
- TNF 𝛼 inhibitors MOA → neutralize TNF 𝛼 ∴ ↓ inflamma’n rxn
- B cell Inhibitor MOA → induce B cell death
- IL 1 + 6 Inhibitor MOA → ↓ inflamma’n
- Selective co-stimula’n modulators MOA → prevent T cell activa’n + prolifera’n
⚠️ Juvenile RA / Juvenile idiopathic arthritis SSX = pain + inflamma’n in jts + uveitis + lymphadenopathy + rash
→ SSX must occur before 16 y/o in order to diagnose !
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OA ✓
Def - progressive degenera’n / wear + tear of articular cartilage of bone
RFs
- FHx
- female
- obesity
- trauma / injury
- knee malalign’nt
- occupa’n (manual work / physically demanding sport)
Pathophys - overexpress’n of MMPs synthesized by chrondrocytes = matrix-degrading enzymes → loss of cartilage
SSX
- u/l jt involv’nt
- bone pain + stiffness that improves w/ rest + worsens w/ activity
- mild morning stiffness < 30 mins
- Heberden’s nodes (= in DIP)
- Bouchard’s nodes (= in PIP)
Jts affected
- DIP + PIP
- CMC of thumb
- weight-bearing joints i.e hip + knee
Ddx
- RA
- PA
- gout
X ray findings (“LOSS”)
- Loss of joint space
- Osteophyte forma’n
- Subchondral cyst
- Subchondral sclerosis
Tx
1) Paracetamol
2) Oral NSAIDs such as ibuprofen or naproxen
→ side effect of naproxen = ankle edema
→ C/I of ibuprofen = 3rd trimester of pregnancy b/c can cause premature closure of ductus arteriosus
3) Opioids
4) IA Corticosteroids for flares
5) Hyaluronic acid
6) Jt replac’nt Sx
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Gout ✓
Def - type of crystal arthropathy associated w/ chronically high uric acid levels
RFs
- male + old
- FHx
- obesity
- menopausal
- high purine diet i.e meat, seafood, alcohol
- diuretic use
- pyrazinamide use
- kidney disease
Pathophys - urate crystals deposit in jt ∴ causing it to become inflamed
SSX
- gouty tophi on hands / ears / elbows
- usually presents w/ a single acute hot, swollen + painful jt such as . . .
→ big toe MTP jt
→ thumb CMC jt
→ wrist
Ddx
- septic arthritis
- pseudogout → rhomboid-shaped CaPO4 crystals w/ +ve birefringent under polarized light
- RA
- OA
- reactive arthritis
Ix’s
- serum uric acid levels → will be elevated
- arthrocentesis w/ synovial fluid aspira’n → needle-shaped urate crystals w/ -ve birefringent under polarized light
X ray findings = “LPE”
- Lytic les’ns
- Punched out eros’ns
- Eros’ns that have sclerotic borders w/ overhanding edges
Acute Tx i.e for acute gout attack = NSAID like Naproxen OR oral prednisolone if pt has kidney pb
Long term Tx = NSAID + PPI for gastroprotec’n → colchicine
→ allopurinol or febuxostat for long term Ppx = xanthine oxidase inhibitors
⟹ allopurinol can only be started 3-4 wks after gout attack has completely resolved !
Lifestyle Δs
- weight loss
-↓ing alcohol intake
- avoiding diuretics
Complica’n = kidney stones
- Know for OSCE *
Pseudogout ✓
Def - crystal arthropathy caused by Ca pyroPO4 crystals collecting in jt
SSX = asymptomatic or gout SSX
Ddx
- gout
- septic arthritis
Ix to confirm diagnosis = jt aspira’n → will show rhomboid shaped crystals that are +vely birefringent under polarized light
X ray findings → same as OA + chondrocalcinosis (white line in middle of jt space) = due to Ca deposits in jt cartilage
Tx
1. NSAID + PPI
2. Colchicine
3. IA steroid injec’ns (r/o septic arthritis first !)
4. Oral steroids
- Know for OSCE *
Types of skin les’ns ✓
- Vesicle = fluid filled les’n < 0.5 cm that accumulates w/in or below epidermis
- Bullae = vesicle > 0.5 cm
- Macule = local color / texture skin Δ < 0.5 cm
- Patch = Macule > 0.5 cm
- Papule = small solid eleva’n of the skin < 0.5 cm
- Nodule = papule > 0.5 cm
- Plaque = palpable plateau-like skin eleva’n > 2cm
Psoriasis / Psoriatic Arthritis ✓
Def - chronic autoimmune condi’n that causes recurrent SSX of psoriatic skin les’ns i.e erythematous, scaly, silvery plaques
→ usually on extensor surfaces i.e scalp, elbow, knees + lumbosacral reg’n
→ genetic predisposi’n = HLA-CW6 + PSOR 1-9
→ stress can trigger flares
RF = FHx
Types of psoriasis
- Guttate = scaly, raindrop shaped plaques on the trunk / limbs, commonly occurs after strep URTI
- Pustular = white pustules
- Chronic plaque = well demarcated, erythematous plaques covered by silvery scales
- Flexural = on flexor surfaces
- Erythrodermic = fire-red scales, affects > 90% of body surface
Pathophys - disordered matura’n of keratinocytes + epidermal transit time ↓ from 30 days to 3-4 days
→ epithelial hyperprolofer’an, thickened epidermis + ↑ed vascularity in upper dermis
SSX
a) Derm SSX (“DAWK”) :
- Dactylitis
- Auspitz sign i.e pinpoint bleeding under skin’s surface
- Well-demarcated, erythematous plaques covered by silvery white scales
- Koebneriza’n = scale forma’n @ sites of minor skin injuries, such as scratches or insect bites when injury = healing
→ scaling can persist for several wks or months
→ vitiligo pts can also get this
b) Nail SSX (“SOOT”) :
- Subungual hyperkeratosis i.e accumulated keratin beneath nail
- Oil spots
- Onycholysis i.e lifting of nail bed
- Thickening of nail plate
c) Psoriatic arthritis SSX
- HLA B27 (FHx in 1st ° relative)
- Pencil in cup deformity on x-ray
- DIPs / wrists / fingers / toes affected
d) Psychological SSX = low mood / depressive state
Ddx
- RA
- gout
- reactive arthritis
Ix’s
- Clinical diagnosis
- Psoriasis Area + Severity Index (PASI) score
- histology → will show neutrophil infiltra’n of stratum corneum
Tx
- 1st 4 wks: lifestyle advice, emollients, topical corticosteroids for localized areas + Vit D analogue (arrange for review after 4 wks)
- Wk 4-8 + good response = continue topical Tx until skin clears
- Wk 4-8 + poor response → potent corticosteroid + Vit D analogue for another month
- Wk 8-12 : derm referral + consider coal tar prepara’n / short term dithranol
→ narrow band UVB phototherapy or biologic such as ciclosporin
Psoriasis drugs + their side effects
- Vit D analogs : HyperCa SSX i.e fatigue, weakness, N/V, abdominal pain, constipa’n + dry mouth
- Topical steroids : acne, HTN + closed-angle glaucoma
- UV radia’n + psoralens : redness, dry skin + blisters
- Retinoids : teratogenic ∴ contraindicated in pregnancy, HAs, weakness + fever
- Ciclosporin : gingival hyperplasia + hirsutism
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RA v.s OA v.s PA v.s Gout ✓
Affected Jts
RA - MCP, PIP, wrist + cervical spine
OA - PIP, DIP, CMC of thumb + hip, knee, spine i.e weight bearing jts
PA - DIP, Spine
Gout - Big toe (MTP), thumb (MCP)
Inflammatory ?
RA - Yes
OA - No
PA - Yes
Gout - Yes
M/F ?
RA - women more (Age 20-40)
OA - women more (Age > 50)
PA - both
Gout - men more
Symmetrical ?
RA - Yes
OA - No in general but Yes if polyarthritis
PA - Yes in general but No if oligoarticular
Gout - No
Jt quality
RA - soft + warm, swan neck +/- boutonniere deformity
OA - bony + tender
PA - pencil in cup deformity on X-ray
Gout - warm / red / painful
Systemic SSX
RA - fatigue, fever, morning stiffness > 1 hr, worst in the morning, gets better w/ activity
OA - morning stiffness < 30 min, worst throughout the day, gets better w/ rest + worse w/ activity
PA - dactillytis + Nail SSX, worst in the morning, gets better w/ activity
Gout - gouty tophi (subcutaneous uric acid)
Rosacea ✓
Def - chronic skin condi’n that presents w/ a variety of cutaneous or ocular manifesta’ns
RFs
- white
- female
- FHx
- hot baths / showers
- sunlight
- emo’nal stress
Exacerbating factors
- alcohol
- exercise
- hot drinks
- spicy foods
- sun exposure
- extreme temps
- certain drugs such as nicotinic acid + vasodilators
Cutaneous SSX (mainly on face)
- flushing
- persistent facial erythema
- dilated prominent telangiectasias
Ocular SSX
- ocular irrita’n
- lid margin telangiectasias
Ix = clinical diagnosis
Tx
- identifying + avoiding triggers
- sunscreen w/ Zinc oxide or TiO2
- advise pts to avoid midday sun + to wear wide-brimmed hat when out in the sun
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Acne vulgaris ✓
Def - chronic skin condi’n that peaks during adolescence
RFs
- 12-24 y/o
- oily skin
Pathophys - pilosebaceous units = tiny dimples in skin that contain hair follicles + sebaceous glands
→ ↑ in androgenic hormones during puberty ↑ in sebum produc’n → dead skin = trapped + pilosebaceous unit = blocked → swelling + inflamma’n in pilosebaceous unit i.e pimple
SSX for inflammatory acne
- papules
- pustule
- nodules
- cysts
SSX for non inflammatory acne
- blackheads
- comedones / whiteheads
Classifica’n
- mild = most of les’ns = comedones + pt has < 10 inflammatory les’ns
- moderate = 10-40 inflammatory les’ns
- moderately severe = > 40 inflammatory les’ns
- very severe = many large, painful nodular / cystic les’ns
Ix = clinical diagnosis
Tx
- Topical adapalene w/ benzoyl peroxide, or topical tretinoin w/ clindamycin
- For mild - moderate =
topical benzoyl peroxide w/ clindamycin - For moderate - severe = topical adapalene w/ benzoyl peroxide w/ doxycycline
Complica’ns
- scarring
- hyperpigmenta’n
- self image issues
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Osteoporosis ✓
Def - skeletal disease characterized by low bone density + hence thinned trabeculae, → affects women more b/c women have a lower peak bone mass to begin w/
RFs (“L-SHATTERED”) :
- Low Ca / Vit D
- Steroid / glucocorticoid use
- Hyperthyroidism or HyperPTH
- Alcohol + smoking
- Thin i.e BMI < 22
- Testosterone deficiency
- Early menopause b/c after menopause bone mineral density ↓ more rapidly
- Renal or liver failure
- Erosive or inflammatory disease
- Diabetes
Pathophys - osteoclast activity > > osteoblast activity
SSX = bone breaking easily but NO PAIN
Ix’s
- Normal serum Ca, normal serum PO4, normal ALP + normal PTH
Diagnostic Ix = DEXA scan (T score compares pt to an avg healthy young adult but Z score adjusts for age, gender + ethnic factors)
→ T score > -1 = normal
→ - 2.5 < T score < -1 = osteopenia
→ T score < -2.5 = osteoporosis
⚠️ Can only diagnose osteoporosis w/ DEXA scan !
Tx
1) Bisphosphonates for pre-menopausal + raloxifene for post menopausal
→ MOA of bisphosphonates - inhibit osteoclasts
→ side effects = jaw osteonecrosis (hence pts should have regular dental checkups), diarrhea + esophageal pbs i.e heartburn / esophagitis / indigest’n
→ end in “DRONIC ACID” or “DRONATE”
⚠️ Not Zoledronic acid b/c it’s only given IV !
→ MOA of raloxifene - selective estrogen receptor modulator (SERM)
2) Subq Denosumab (start w/ this if pt already has ulcer or gastritis to not give them more GI pbs !)
→ MOA - monoclonal antibody RANK-L inhibitor
→ monoclonal antibodies end in “MAB” or “NIB”
Complica’n = Wedge fracture
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Paget’s disease of the bone ✓
Def - chronic bone disordered characterized by ↑ed bone remodeling
RFs
> 50 y/o
- FHx
- male
Eti
- Monostotic = involves only 1 bone (most common site = femur) occurs in 25% of pts
- Polyostotic = involves > 1 bone (usually femur, pelvis, skull, tibia, or vertebrae), occurs in 75% of pts
Pathophys - osteolytic Δs in early stages + sclerotic Δs in later stages
SSX (most pts = asymptomatic)
- bone pain
- bony deformities
Ddx = osteomalacia
Ix’s
- X ray
- ALP → elevated due to ↑ed osteoblast activity
- normal Ca + PO4
X ray findings = “VBOC”
- V-shaped osteolytic defects in long bones
- Bone enlargement + deformity
- Osteoporosis circumscripta = well-defined osteolytic les’ns that are less dense than normal bone
- Cotton wool appearance of skull
Tx = bisphosphonate
→ either oral risedronate or IV zoledronate
⚠️ Only treat symptomatic pts !
Complica’ns
- fractures
- spinal stenosis (diagnosed w/ MRI)
- skull thickening
- spinal cord compress’n
- hearing loss if ear bone = affected
- heart failure
- osteosarcoma = rare bone cancer, but has poor prognosis
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Rickets / Osteomalacia ✓
- Rickets = Vit D deficiency in children
- Osteomalacia = Vit D deficiency in adults
RFs
- poor diet
- darker skin
- malabsorp’n
- pre-mature birth
- low sun exposure
- HypoPhos = low ALP
- FHx of Rickets (for Rickets)
- renal failure such as in CKD
- liver failure / advanced liver disease
- anticonvulsants → ↑ Vit D catabolism
Pathophys - normally, osteoblasts lay osteoid so that it can be mineralized by Ca + PO4 to form bone but in osteomalacia / Rickets pt has low Vit D → low Ca + low PO4 → poor osteoid mineraliza’n in adults + defective mineraliza’n of epiphyseal growth plate cartilage in children
SSX
- waddling gait
- looser zones on x-ray
- bone pain + tenderness (usually in back and/or pelvis)
- Low Ca
- Low PO4
- Low Vit D
- High PTH (= compensatory mechanism in response to low Ca)
- High ALP (due to ↑ed osteoblast activity i.e trying to reBuild bone)
- Do U + E to check if it’s b/c of renal failure
Addi’nal SSX for Rickets
- Genu varum / Bowing of the legs i.e exaggerated arqué
- Frontal bossing = enlarged forehead due to osteoid deposi’n on skull
- Pigeon-breast deformity = inward bending of ribs w/ anterior protrus’n of sternum
- Rachitic rosary = visible rib cage due to osteoid deposi’n at costochondral junc’n
Ddx for osteomalacia
- osteoporosis
- Paget’s disease of the bone
Tx = colecalciferol (Vit D₃)
→ check serum Ca w/in 1 month of loading regime
Complica’ns
- 2° HyperPTH
- tetany due to HypoCa
- ↑ed risk of fractures due to fragile bones
- skeletal deformities + growth retarda’n (in Ricket’s)
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Septic arthritis ✓
Def - jt infec’n, pt has 6hrs to live ∴ = medical emergency !
→ commonly occurs in children < 4 y/o
→ usually affects knee
→ can occur @ same time as osteomyelitis of adjacent bone
RFs
> 80 y/o
- T2D
- cirrhosis
- endocarditis
- immunosuppress’n i.e HIV
- procedures causing transient bacteria such as injec’n drug use, indwelling catheters
- trauma to jt b/c allows transloca’n of cutaneous organisms i.e pre-existing jt disease like RA / recent jt Sx / skin or soft tissue infec’n
Eti - usually due to staph aureus infec’n but can also be caused by gonorrhea
SSX
- 1 hot, red, swollen jt (usually knee or hip in children)
- stiffness + severe ↓ inROM (usually ↓ed internal rota’n when leg = in flex’n)
- fever, lethargy + chills
Ix’s
- FBC → leukocytosis
- ESR + CRP → will be high
- Arthrocentesis i.e synovial fluid jt aspira’n → gram staining → crystal microscopy , culture + sensitivity
- blood culture + sensitivity to check for septicemia
⚠️ Do both cultures + sensitivities before starting Abx unless you absolutely can’t afford to delay Abx
Ddx
- gout
- viral synovitis = when viral infec’n causes inflamma’n in synovium of a jt
→ usually affects hip jt
→ commonly occurs in children
→ like in septic arthritis ESR + CRP will be high but there WON’T BE leukocytosis !
Emergency Tx
1. Immobilize inflamed jt
2. NSAID for analgesia
3. AB
→ for pts > 3 y/o = flucloxacillin or IV vancomycin instead if pt has penicillin allergy b/c will cover staph. aureus + other gram +ve cocci)
⟹ switch to specific Abx once cultures come back
→ for pts < 3 y/o = amoxicillin or a cephalosporin such as cefotaxime or CTX b/c will cover H. influenzae
- Rehab once SSX resolve
Complica’ns
- osteomyeltis
- destruc’n of that jt
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Osteomyelitis ✓
Def - bone inflamma’n caused by infective organism
→ can be acute or chronic
→ usually involves a single bone
RFs
- penetrating injury
- IV drug use
- diabetes
- HIV
- recent Sx
- sickle cell
- RA
- CKD
- immunocompromised
- chickenpox or URTI (in children)
Eti - staph. aureus usually
SSX
- pain (especially in acute), warmth, redness + swelling @ site of infec’n
- fever (in acute)
- limp or reluctance to bear weight on limb (especially in children)
Ix’s
- MRI for diagnosis in acute + X ray for diagnosis in chronic
- FBC
- ESR / CRP → will be elevated in acute
- blood culture (wait for culture to come back before starting AB therapy unless you can’t afford to wait)
Tx = extensive surgical debridement + Abx i.e . . .
→ fucloxacillin OR clidamycin insteead if pt has penicillin allergy
→ vancomycin if MRSA = suspected
⟹ in addi’n, consider adding fusidic acid or rifampicin for the 1st 2 wks of Tx
Dura’n of Tx
- 6 wks for acute
- 3-6 months for chronic
Complica’ns
- bone abscess
- bacteremia
- bone fracture
- septic arthritis
- cellulitis of overlying soft tissue
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What are the 4 Sero-ve spondyloarthopathies caused by the HLA-B27 gene ? ✓
“PAIR”
- Psoriatic Arthritis
- Ankylosing Spondylitis = anterior uveitis (i.e red painful inflamed eye + photophobia + blurry vis’n) + bamboo spine + shoulder/ back pain / stiffness (spine / sacroiliac jts = involved) + enthesitis of Achilles tendon / plantar fascia
→ stiffness = usually worse in morning + improves w/ exercise
→ pt might experience pain @ night which improves when they get up
→ more common in young males i.e < 30 y/o - Inflammatory / IBD associated arthritis
- Reactive arthritis = inflammatory arthritis subsequent to infec’n such as chlamydia but the arthritis = in diff spot from infec’n
→ SSX = conjunctivitis + urethritis (yellow penile discharge) + arthritis (“can’t see, pee or climb a tree”)
⚠️ THERE MUST BE FHx in 1st ° RELATIVES i.e parents / siblings / children
Ankylosing Spondylitis ✓
Def - inflammatory arthritis of axial skeleton (vertebral column jts in spine + sacroiliac jts) that causes progressive jt pain + stiffness
→ always occurs before 45 y/o
→ 90% of AS pts will have HLA-B27 gene
RFs
- FHx
- male in their 20s
SSX
- chronic pain + stiffness in lower back that is better w/ activity + worse w/ rest
- pain in buttock reg’n (sacroiliac pain)
SSX on lumbar exam = < 20 cm on Schober’s test
Ix’s
- HLA B27 genetic testing
- X ray of spine + sacrum
- spine MRI → in early stage of disease might show of bone marrow edema
X ray finding = bamboo spine due to fus’n of sacroiliac + spinal jts (in later stages of AS)
Tx
1. NSAIDs
2. Anti-TNF medica’ns such as adalimumab, etanercept or infliximab
3. Secukinumab or ixekizumab
Complica’n = spine + sacroiliac jt fus’n
- Know for OSCE *
Reactive Arthritis ✓
Def - synovitis in ≥ 1 jt in response to infective trigger
→ SSX onset = 1-4 wks after infec’n
RFs
- HIV
- male
- HLA B27
Eti / infective trigger
- gastroenteritis
- salmonella
- campylobacter
- shigella
- chlamydia
SSX = “can’t see, pee or climb a tree”
- b/l non infective conjunctivitis and/or anterior uveitis
- urethritis + circinate balanitis (dermatitis of head of penis)
- monoarticular or polyarticular arthritis of lower limb jts
Ddx
- RA
- gout
- septic arthritis
Ix’s
- ESR / CRP → will be elevated
- rheumatoid factor to r/o RA
- jt aspira’n to r/o septic arthritis + gout
Tx = NSAID → corticosteroid → sulfasalazine
- Know for OSCE *
Sepsis ✓
SIRS criteria for sepsis = infec’n + ≥ 2 of the following . . .
- temp < 36 °C or > 38 °C
- RR > 20
- HR > 90
- WCC > 11,000 or < 4,000
→ severe sepsis = sepsis + ≥ 1 of the following . . .
- HypoTN
- RR > 25
- HR > 130
- AMS i.e confus’n / drowsiness
- pt hasn’t passed urine in the past 18 hrs or has passed < 0.5ml/kg of urine/hr
RFs
> 60 y/o
- pregnancy
- IV drug use
- hemodialysis
- immunocompromised
- recent Sx / invasive procedure
Pathophys of severe sepsis - release of IL-1
→ vasodila’n → BP ↓ → HypoTN
Emergency Tx = start w/ broad spectrum IV Abx + then give specific Abx based on pathogen
⚠️ NEVER SEND SEPTIC PT HOME !
Ix / Tx = Sepsis 6
1- IV Abx
2- IV fluids
3- Measure lactate
4- Take blood cultures +/- urine / sputum cultures to identify causative pathogen
5- Measure urine output w/ hrly fluid balance
→ may be ↓ed i.e < 0.5 ml / kg / hr
⟹ means kidneys are starting to fail
6- Administer O2 to keep satura’ns > 94% or btw 88 + 92% if pt = @ risk of CO2 reten’n
Complica’ns
- septic shock
- renal dysfunc’n
- hepatic encephalopathy
- Know for OSCE *
Bites ✓
- Dog bites can lead to osteomyelitis
- Tx of human bite wound requires Abx
Indicators of severe illness ✓
lactate > 2 + base excess > -2 (i.e more -ve) +
What is shock and what are the 4 types of shock ? ✓
Def - state where tissue perfus’n = inadequate ∴ leading to reversible cell injury + then to irreversible cell injury if prolonged
Types
- Hypovolemic shock = caused by loss of blood volume (i.e blood loss, dehydra’n, fluid shift such as in peritonitis)
→ Tx = fluid replac’nt w/ balanced crystalloids - Cardiogenic shock = caused by heart pb i.e MI, arrhythmia, valve / septal defect
- Obstructive shock = something is obstructing circula’n
→ ex’s = P.E, tens’n pneumothorax, tamponade - Distributive shock = due to pathological redistribu’n of blood volume, Tx = fluid replac’nt + vasoconstrictors
→ Anaphylactic shock = caused by allergic rxn
→ Septic shock = caused by infec’n
→ Neurogenic shock = caused by damage to nervous system - Know for OSCE *
Crystalloids v.s Colloids ✓
- Crystalloids = solu’ns w/ small molecules, move rapidly throughout body
→ ex’s = NS, LR/Hartmann’s, dextrose - Colloids = large molecule solu’ns ∴ stay in bloodstream longer
Flow of bile ✓
- Liver produces + secretes bile → right + left hepatic ducts → common hepatic duct
→ common hepatic duct joins w/ cystic duct from gallbladder to form common bile duct
→ half of that bile from common bile duct goes directly into duodenum + other half is stored + [ ]ed in gallbladder
→ when we eat fatty food CCK = released from duodenum → CCK triggers gallbladder contrac’n ∴ releasing that stored bile into duodenum to help break down digested fats
→ pancreatic juice = secreted by acinus (exocrine part of the pancreas) + released from pancreatic duct that joined w/ common bile duct (they join @ ampulla of vater)
⟹ it’s alkaline b/c in addi’n to digestive enzymes for fats, sugars + proteins
→ has to be alkaline b/c digestive enzymes of small intestine = pH-sensitive
→ protein-digesting enzymes pancreas secretes = inactive initially + get activated in duodenum (this is on purpose b/c if they were already in their active from, they would digest the pancreas = what happens in pancreatitis)
⚠️ Cholesterol = excreted in BILE ONLY !
Small Bowel Obstruc’n (SBO) ✓
Def - when passage of food / gas through intestines becomes blocked = surgical emergency !
→ results in a build up of gas + fecal matter proximal to obstruc’n
Eti
- hernias
- malignancy (Tx in this case = urgent surgical resec’n)
- adhes’ns b/c of abdominal / pelvic Sx, peritonitis, abdominal or pelvic infec’n such as PID (= most common cause of SBO)
SSX
- bilious vomiting (highlighter green)
- abdominal distent’n
- diffuse colicky abdominal pain
- constipa’n / obstipa’n
- tinkling bowel sounds may be heard in early bowel obstruc’n
Ddx
- ileus
- appendicitis
- pancreatitis
Ix’s
- AXR → will show distended loops of bowel
- CTAP w/ oral + IV contrast to identify level + cause of obstruc’n
How to know if particular loop of bowel is distended
- small bowel should be max 3 cm
- colon should be max 6 cm
- cecum should be max 9 cm
Tx
1. ABCDE
2. Drip + suck i.e IV fluids + wide bore NG tube for decompress’n
3. Exploratory laparotomy if non-operative Tx ≠ successful after 72 hrs
⚠️ Keep these pts NPO to ↓ risk of aspira’n + in case they need to have Sx
Complica’ns
- sepsis
- multi organ failure
- bowel ischemia
- bowel necrosis
Ileus ✓
Def - lack of peristalsis in small bowel
= diagnosis of exclu’n after mechanical obstruc’n = r/o
→ most common cause = after Sx
RFs
- abdominal Sx
- systemic illness such as sepsis, MI, pneumonia, cholecystitis, pancreatitis
Eti = response to physiological stress such as . . .
- sepsis
- after Sx
- electrolyte imbalance such as HypoK or HypoNa
- infec’n / inflamma’n such as peritonitis, appendicitis, pancreatitis or pneumonia
SSX
- bilious vomiting
- abdominal pain / discomfort
- no bowel sounds
- obstipa’n i.e no stools + no flatus
Ddx = mechanical obstruc’n
Ix’s
- FBC → to check if it’s b/c of response to infec’n
- CTAP → will show fluid filled intestines + distended stomach
⟹ evidence of transi’n zone btw dilated + collapsed bowel = indicative of obstruc’n instead
Tx = treat underlying cause + supportive care i.e . . .
- NG tube + keep pt NPO
- IVF to prevent dehydra’n + correct any electrolyte imbalance
- encourage ambula’n to help stimulate peristalsis
- ttl parenteral nutri’n while waiting for bowel to regain its normal func’ning
- Know for OSCE *
Intestinal obstruc’n in children ✓
Def - physical obstruc’n that prevents flow of feces through intestines hence causing obstipa’n + vomiting (can be bilious vomiting)
Eti
- intussuscep’n
- meconium ileus
- strangulated hernia
- Hirschsprung’s disease
- esophageal or duodenal atresia
SSX
- not keeping down food
- abdominal pain + distens’n
- vomiting b/c obstruc’n causes backpressure through GI system
- high pitched bowel sounds in early obstruc’n + then completely absent bowel sounds
Ix = AXR → will show dilated loops of bowel proximal to obstruc’n, collapsed loops of bowel distal to obstruc’n + absence of air in rectum
Tx
1. Refer to pediatric Sx
2. Make them NPO
3. NG tube to help drain stomach + stop the vomiting
4. IVF to correct dehydra’n / electrolyte imbalance while awaiting definitive Tx
Appendicitis ✓
Def - acute inflamma’n of appendix
→ usually occurs in pts 10-20 y/o
Pathophys - appendix = small, thin tube arising from cecum (retrocecal) Iocated @ point where the 3 teniae coli meet → obstruc’n @ point where appendix meets bowel → pathogen gets trapped → infec’n + inflamma’n → if / when appendix ruptures, fecal contents + infective material = released into peritoneal cavity → peritonitis
SSX
- fever
- N + V
- anorexia
- central abdominal pain that moves down to RIF (w/in first 24 hrs)
- tenderness @ McBurney’s point = 1/3 of distance from ASIS to umbilicus
- Rovsing’s sign = when palpa’n of LIF causes pain in RIF
- peritonitis SSX if appendix ruptured
Ddx = other causes of RIF pain
- Crohn’s
- ovarian cysts
- ovarian tors’n
- ectopic pregnancy
Ix’s
- Alvarado score to determine likelihood of appendicitis
- FBC → leuocytosis
- CRP → will be elevated
- pregnancy test in female pts
- abdominal U/S if could not diagnose clinically
Tx = appendectomy
Complica’ns
- perfora’n
- peritonitis
- Know for OSCE *
Pancreatic enzymes ✓
- lipase for fat digest’n
- proteases for B12 + protein absorp’n
Pathophys of how pancreatic juices get released ✓
Entry of acidic chyme in duodenum stimulates release of secretin → secretin causes pancreatic duct cells to release pancreatic juice → CCK also stimulates release of pancreatic juice by enhancing activity of secretin
Acute Pancreatitis ✓
Def - self limiting inflamma’n of pancreas = most common complica’n of ERCP
Eti = “ I GET SMASHED”
- Idiopathic
- Gallstones (#2 cause)
- EtOH i.e alcohol (#1 cause)
- Trauma
- Steroids
- Mumps + malignancy i.e pancreatic cancer
- Auto immune such as polyarteritis nodosa + ascarsis infec’n
- Scorpion bite
- Hypertriglyceridemia / HyperCa / Hypothermia
- ERCP = endoscopic retrograde cholangio-pancreatography
- Drugs such as azathioprine or diuretics
Pathophys - pancreatic enzymes released as a result of inflamma’n autodigest pancreas → can lead to necrosis
SSX
- N + V
- anorexia
- sometimes signs of pleural effus’n
- epigastric pain (might radiate to back)
- signs of hypovolemic shock = emergency in this case
- rare SSX = Cullen’s sign (periumbilical bruising) + Grey-Turner’s sign (flank bruising)
Ddx = other causes of epigastric pain
- GERD
- peptic ulcer disease
Ix’s
- serum amylase → elevated > 3x upper limit of normal = enough to diagnose
- FBC → leukocytosis + elevated hematocrit (if hematocrit > 44% pt = @ risk of developing necrotizing pancreatitis)
- U+E → urea + creatinine might be elevated → means hypovolemic shock has caused renal failure
- CRP → if > 200 = indicative of necrotizing pancreatitis
- pulse oximetry → might show hypoxemia
⟹ pts w/ acute pancreatitis = at high risk of hypoxia b/c of of abdominal splinting / atelectasis / pulmonary edema / ARDS - LFTs → elevated AST > 3x times upper limit = gallstones is the cause
- CXR → to check for atelectasis / pleural effus’n
- transabdominal U/S → will show inflamed pancreas
- Ca b/c HyperCa can cause acute pancreatitis even if that’s a rare cause
- Ranson’s Criteria / Glasgow-Imrie score = done up to 48hrs after SSX develop in order to assess severity of acute pancreatitis (“PANCREAS”)
→ PaO2 < 60 mmHg or 7.9 kPa
→ Age > 55 y/o
→ Neutrophils i.e WBC > 15
→ Ca < 2 mmol/L
→ Renal i.e Urea > 16
→ Enzymes i.e LDH > 600 or AST > 200
→ Albumin < 32 g/L
→ Sugar i.e glucose > 10 mmol/L
⟹ give pt 1 point if they have it
≥ 3 points = severe so pt has to be admitted
< 3 points = not severe so pt doesn’t have to be admitted
Emergency Tx if in hypovolemic shock = fluid resucita’n i.e 500mL fluid challenge over 15 mins + morphine for analgesia
Mx in ICU
- ABCDE
- IV fluids
- Keep pt NPO
- analgesia
- Sx if pancreatitis = due to gallstones
- IV Abx IFF pt has infected necrotizing pancreatitis
Complica’ns
- sepsis
- pancreatic abscess
- chronic pancreatitis if it becomes recurrent
- acute renal failure due to hypovolemic shock
- abdominal compartment syndrome = organ dysfunc’n due to intra-abdominal HTN
- pancreatic ascites / pleural effus’n = accumula’n of pancreatic fluid in peritoneal cavity
- enteric fistulas due to inflamma’n surrounding pancreas + adjacent duodenum / transverse colon.
- acute lung injury / ARDS b/c produc’n + excre’n of inflammatory mediators during pancreatitis can damage alveolo-capillary membrane
- Know for OSCE *
Chronic Pancreatitis ✓
Def - chronic pancreatic inflamma’n
RFs
- FHx
- celiac disease
- smoking + alcohol
Eti
- alcohol (80% of cases)
- ductal obstruc’n i.e tumor / gallstones
- CF
- hemochromatosis
SSX
- N + V
- steatorrhea (usually occurs 5-25 yrs after onset of pain)
- malnutri’n due to steatorrhea
- weight loss due to malnurtri’n
- epigastric pain that is worse 15-30 mins after eating (pain might radiate to back)
- T2D if due to long-term alcohol consump’n - pancreas = damaged over time → destruc’n of islet of Langerhans cells which are responsible for producing insulin → deple’n of insulin → ↑ed levels of serum glucose (usually develops 20 yrs later after initial onset of pain)
Ddx
- GERD
- acute pancreatitis
- pancreatic cancer
- peptic ulcer disease
Ix’s
- CT / MRI = 1st line → will show pancreatic calcifica’ns, focal or diffuse enlarg’nt of pancreas + ductal dila’n
- endoscopic U/S (EUS) if diagnosis still uncertain
→ will show ductal / parenchymal abnormalities - secretin enhanced magnetic resonance cholangiopancreatography (s-MRCP) if diagnosis still uncertain → will show abnormal pancreatic exocrine func’n
Tx = treating SSX w/ analgesia + pancreatic enzyme supplements + sometimes ERCP w/ stent
Lifestyle Δs = abstinence from alcohol + smoking
Complica’ns
- ascites
- fistulae
- biliary obstruc’n
- pancreatic pseudocysts
- pancreatic exocrine + endocrine insufficiency
- pancreatic duct obstruc’n due to calcifica’n
- Know for OSCE *
Pancreatic Cancer ✓
→ 65% of tumors = w/in the head of pancreas
→ 15% = in body of pancreas
→ 10% = in tail of pancreas
→ has poor prognosis b/c = often diagnosed lte
Most common histological subtype = ductal adenocarcinoma → metastasizes to liver, lung, skin + brain
RFs
> 55 y/o
- FHx
- high BMI
- red meat intake
- alcohol + smoking
- familial cancer syndromes i.e BRCA1 / BRCA2, familial adenomatous polyposis / Lynch syndrome
SSX
- weight loss + anorexia
- non specific abdominal pain / discomfort (in epigastric reg’n)
- painless jaundice (in pancreatic head tumor due to obstruc’n of common bile duct) → dark urine, pale stools + pruritus
- back pain due to tumor cells invading retroperitoneal nerves of celiac plexus → later presenta’n hence the poor prognosis
- new onset of diabetes or worsening glycemic control in pt already diagnosed w/ diabetes
Referal
- jaundice + > 40 y/o = 2 wk wait referral
- weight loss + < 60 y/o + any of the following SSX = direct access CT abdomen
→ diarrhea
→ back pain
→ abdominal pain
→ N/V
→ constipa’n
→ new onset of diabetes
Ddx
- hepatitis
- gastric cancer
- bile duct stones
- cholangiocarcinoma
- chronic pancreatitis
- autoimmune pancreatitis
- perforated ulcer
⚠️ Always do erect CXR in pt presenting w/ severe epigastric pain to r/o perforated ulcer + then do CTAP if u still suspect perforated ulcer
Ix’s
- LFTs
- U/S to identify loca’n of ductal obstruc’n
- CT scan + histology from Bx for diagnosis
- CTAP for staging
- Ca 19-9 tumor marker (can also be ↑ed in cholangiocarcinoma)
Staging
- stage 1 → tumor = limited to pancreas
- stage 2 → tumor has infiltrated bile duct and/or other near structures but there’s NO lymph node involv’nt
- stage 3 = lymph node involv’nt
- stage 4A = metastasis into nearby organs (stomach / liver / diaphragm / adrenals)
- stage 4B = metastasis into distant organs
Tx for Stage 1 + 2 = surgically resectable so Sx + pancreatic enzyme supplement so pt can maintain weight + QoL
→ if tumor = in head of pancreas → Whipple procedure or pylorus-preserving pancreaticoduodenectomy
⟹ Whipple = removal of head of pancreas, stomach pylorus, duodenum, gallbladder, bile duct + relevant lymph nodes
→ if tumor = in body or tail of pancreas → distal pancreatectomy + splenectomy
→ neoadjuvant combina’n chemo or fluorouracil-based chemoradiotherapy for pts that u clinically suspect there’s metastasis but there isn’t any radiological evidence of metastatic disease
Tx for Stage 3 or 4 → palliative Tx i.e ERCP + biliary stent b/c it isn’t resectable
- Know for OSCE *
Gallstones / Cholelithiasis ✓
Def - presence of solid stones in gallbladder (usually cholesterol stones but can also be Ca bicarb stones)
RFs = “5 F’s”
> 40 y/o
- Female
- Fair i.e white
- Fertile i.e pregnant
- Fat i.e obesity / T2D / metabolic syndrome
SSX (can be asymptomatic)
- N/V sometimes
- biliary colic i.e constant pain in right hypochondrium, especially after fatty meal
⟹ pathophys of biliary colic - fat enters digestive system → triggers duodenum to secrete CCK
→ CCK triggers gallbladder contrac’n
Ddx = other causes of right hypochondrium pain
- hepatitis
- cholangitis
- cholecystitis
- pre eclampsia (HELLP syndrome specifically)
Ix’s
- abdominal U/S to diagnose b/c is the most sensitive test for gallstones
- LFTs → elevated ALP + elevated bilirubin
Tx for symptomatic or stone > 2.5 cm lap chole
→ post-cholecystectomy syndrome involves = nonspecific SSX that can occur after a cholecystectomy (improve over time)
⟹ nausea
⟹ diarrhea
⟹ epigastric or RUQ pain / discomfort
⟹ intolerance of fatty foods
⟹ flatulence
⚠️ Children w/ gallstones need to have cholecystectomy !
Complica’ns
- acute cholecystitis
- choledocholithiasis i.e gallstones w/in common bile duct and / or acute cholangitis
- acute biliary pancreatitis- stones pass distally through bile duct duct → cause obstruc’n @ ampulla → ↑ in pancreatic ductal pressure → reflux of pancreatobiliary secre’ns into pancreatic duct
- gallstone erodes through gallbladder wall
→ cholecystoduodenal fistula can develop in that hole → duodenal obstruc’n / Bouveret syndrome - gallstone erodes through gallbladder wall
→ cholecystoduodenal fistula can develop → obstruc’n in narrowest segment of healthy bowel → gallstone ileus - Know for OSCE *
Cholecystitis ✓
Def - gallbladder inflamma’n, may resolve itself spontaneously 5-7 days later
RFs
- T2D
- gallstones
Eti = gallstones usually
Pathophys - gallstone causes bile to become trapped in gallbladder → trauma caused by gallstone stimulates PG synthesis (PGI2, PGE2) which mediate inflammatory response
SSX
- fever
- palpable mass i.e palpable gallbladder
+ve Murphy sign = pain on inhala’n when u deep palpate RUQ
- pain + tenderness in right hypochondrium (might radiate to btw scapulae / shoulder blades)
Ddx = other causes of right hypochondrium pain
- hepatitis
- gallstones
- cholangitis
- pre eclampsia (HELLP syndrome)
Ix’s
- abdomen CT or MRI if sepsis = suspected
→ will show irregular thickening of gallbladder ,↑ed density of fatty tissue around gallbladder, gas in gallbladder lumen or wall + peri‐gallbladder abscess → will also show gallbladder perfora’n if present - FBC → leukocytosis
- ESR / CRP → elevated
- LFTs → may show elevated ALP + elevated gamma + elevated bilirubin
- serum amylase / lipase to r/o pancreatitis
Tx = analgesia → Abx if there’s sepsis
Complica’ns = gallstone ileus + cholecysto-enteric fistula
- Know for OSCE *
What is Calot’s triangle / Hepatocystic triangle, what are its borders + its contents ? ✓
- Calot Triangle = anatomical space in abdomen located @ porta hepatis of liver which is where hepatic ducts + neurovascular structures enter/exit liver
- Borders
→ superior border = inferior surface of liver
→ medial border = common hepatic duct
→ inferior border = cystic duct - Contents = Cystic artery + R. hepatic artery + Lymph node of Lund (sentinel lymph node of gallbladder)
Acute Cholangitis ✓
Def - infec’n + inflamma’n of bile ducts = surgical emergency b/c sepsis + septicemia can cause death !
RFs
> 50 y/o
- gallstones
- bile duct Sx
Eti = gallstones in common bile duct or infec’n introduced during ERCP
Most common causative pathogens
- E. coli
- Klebsiella
- Enterococcus species
SSX = Charcot’s triad = fever + jaundice + right hypochondrium pain
→ Reynold’s pentad = Charcot’s triad + shock / hypoTN + AMS = SSX of acute toxic cholangitis = surgical emergency !
⚠️ Only cholangitis + acute pyelonephritis will cause fever w/ chills !
Ddx = other causes of right hypochondrium pain
- hepatitis
- gallstones
- cholecystitis
- pre eclampsia (HELLP syndrome)
Ix’s
- ERCP = 1st line Ix = live imaging
- transabdominal U/S → will show dilated bile duct
- FBC → leukocytosis
- U + E → urea + creatine might be elevated if there’s severe sepsis
- LFTs → hyperbilirubinemia + elevated AST + ALP
- blood cultures to identify causative pathogen
Tx = Sepsis 6 + then ERCP → Percutaneous transhepatic cholangiogram (PTC) if ERCP fails = IR drain that relieves obstruc’n
Complica’ns
- inadequate biliary drainage
- hepatic abscess (usually in sclerosing cholangitis)
- acute pancreatitis b/c of ERCP or obstruc’n of pancreatic duct or common channel joining common bile duct + pancreatic duct
- Know for OSCE *
Ddx of abdo pain based on quadrant ✓
R. HYPOCHONDRIUM
- hepatitis
- gallstones (pain ≥ 30 min)
→ Ix’s = LFTs, FBC + abdominal U/S - cholangitis = RUQ pain + fever + jaundice
→ Ix’s = FBC, CRP, LFTs - cholecystitis (pain might radiate to R. scapula / base of R. shoulder)
→ Ix’s = FBC, CRP, bilirubin, LFTs - pre eclampsia = HA + R. hypochondrium pain
→ bedside exams = BP + urine dipstick
→ Ix’s = FBC, LFTs + fetal U/SHELPP due to pre-eclampsia
EPIGASTRIC REG’N
- peptic ulcer disease
- pancreatitis or pancreatic cancer
→ pancreatitis = epigastric pain + nausea + vomiting
→ bedside exam = Glasgow pancreatitis scoring chart (must be done w/in 48hrs)
→ Ix’s = FBC, CRP, Serum lipase or amylase - GERD = burning epigastric pain worse @ night + after spicy meals (RF = obesity + old age)
L. HYPOCHONDRIUM = ruptured spleen
R. FLANK
- kidney cancer
- kidney stones
- pyelonephritis = flank pain + fever + N + V
→ bedside exam = urine dipstick
→ Ix’s = FBC, U + E + blood culture
UMBILICAL REG’N
- ruptured AAA
- SBO
- early appendicitis
L. FLANK
- kidney cancer
- kidney stones
- pyelonephritis
RIF
- appendicitis = RIF pain + N + V
→ Ix’s = FBC + CRP + abdominal U/S
- ovarian cysts
- ovarian tors’n → Ix = transvaginal U/S
- ectopic pregnancy → Ix = transvaginal U/S
- Crohn’s
- inguinal / femoral hernia
SUPRAPUBIC REG’N
- STI
- regular pregnancy
LIF
- diverticulitis→ Ix’s = FBC, U + E, CRP
- ovarian cysts
- ovarian tors’n → Ix = transvaginal U/S
- ectopic pregnancy → Ix = transvaginal U/S
- volvulus
- inguinal / femoral hernia
- Know for OSCE *
Mesenteric ischemia / Ischemic bowel disease ✓
Def - ↓ed blood flow to GI tract
→ acute mesenteric ischemia = caused by rapid blockage in blood flow through SMA due to blood clot stuck in artery, RFs = Afib (b/c can cause clot to form in RA), vascular disease
→ chronic mesenteric ischemia = due to narrowing of mesenteric blood vessels 2° to atherosclerosis, RFs = same as CVD
3 main branches of abdominal aorta that supply abdominal organs
- celiac artery
- SMA
- IMA
Blood supply of abdominal organs
- foregut i.e stomach, part of duodenum, biliary system, liver, pancreas + spleen = supplied by celiac artery
- midgut i.e from distal part of duodenum to first half of transverse colon = supplied by SMA
- hindgut i.e from the second half of transverse colon to rectum = supplied by IMA
SSX of acute
- fever
- nausea
- diarrhea
- hematochezia / melena
- out of propr’n abdominal pain + tendernes
- SSX of chronic = central colicky abdominal pain after eating, weight loss (due to food avoidance as this causes pain) + abdominal bruit on ausculta’n
Ix for chronic = CT angiography
Ix’s for acute
- urgent contrast CT → will show bowel dilata’n + bowel wall thickening
- ABG + lactate → lactic acidosis
- FBC → leukocytosis due to lactic acidosis
- U + E → urea + creatinine will be elevated if pt = in shock
- coagula’n study / D dimer to see if due to hypercoagulable state / embolism / thrombosis
Tx for chronic
- fixing modifiable RFs such as quitting smoking (e.g.,
- statins + antiplatelet medica’ns
- revasculariza’n to improve blood flow to intestines
→ via endovascular procedure such as percutaneous mesenteric artery stenting
Tx for acute = Sx to remove necrotic bowel
or open Sx / endovascular procedure to bypass thrombus in blood vessel
- Know for OSCE *
Volvulus ✓
Def - when loop of bowel twists around itself / on its mesentery → causes bowel obstruc’n = medical emergency !
RFs
- male
- pregnancy
- high fiber diet
- enlarged bowel
- abdominal adhes’ns
- previous abdominal opera’s
- chronic constipa’n or laxative use
Types
- cecal volvulus → originates in RIF
- sigmoid volvulus → twist originates in LIF
Pathophys of sigmoid volvulus - Eti → sigmoid colon becomes dilated +loaded w/ stools ∴ making it susceptible to tors’n → direc’n of volvulus = counterclockwise → blood supply = compromised
SSX
- vomiting
- constipa’n
- bloody stools
- abdominal distens’n
- colicky abdominal pain
Ddx
- bowel obstruc’n
- diverticular disease
Ix’s
- abdomen pelvis CT w/ contrast = 1st line Ix
→ will show very dilated sigmoid colon w/ a whirl sign - AXR → coffee bean sign in sigmoid volvulus
Tx = decompress’n w/ sigmoidoscope→ inser’n of a flatus tube (stays in pt for up to 24 hrs to allow continued passage of bowel contents)
→ Sx if there’s colonic ishemia, if decompress’n fails or if there’s perfora’n / necrotic bowel on endoscopy
Complica’ns = bowel necrosis + perfora’n
- Know for OSCE *
Bowel Cancer ✓
Def - cancer of the colon or rectum = 4th most common cancer in the UK
→ majority = adenocarcinomas derived from epithelial cells
RFs
> 50 y/o
- FHx
- IBD
- obesity
- smoking + alcohol
- Lynch syndrome = hereditary nonpolyposis
- familial adenomatous polyposis (FAP) = benign polyps
⚠️ Pts w/ FAP should have prophylactic panproctocolectomy i.e removal of colon, rectum + anus to ↓ risk of them getting colorectal cancer
SSX
- rectal mass
- rectal bleeding
- Δ in BM
- unexplained weight loss
- unexplained abdominal pain
- Fe deficiency anemia
Pts who should get urgent 2 wk wait urgent cancer referral . . .
> 40 y/o + abdominal pain + unexplained weight loss
> 50 y/o + unexplained rectal bleeding
> 60 y/o + Fe deficiency anemia or Δ in BM
Ddx
- IBD
- IBS
- anal fissure
- hemorrhoids
- diverticular disease
Ix’s
- FBC → might show anemia
- colonoscopy = gold std
- CT colonography if colonoscopy ≠ indicated or pt doesn’t want
- CT scan of chest, abdomen pelvis to check for metastasis
- genetic testing for Lynch once diagnosis = confirmed
Screening = every 2 yrs for ppl btw 60 + 74 y/o via fecal blood kit
→ colonoscopy referral if occult blood = found
TNM Staging
T0 = no evidence of 1° tumor
T1 = tumor has invaded submucosa
T2 = tumor has invaded muscularis propria
T3 = tumor has invaded through the muscularis propria + into the pericolorectal tissues
T4a = tumor has penetrated surface of visceral peritoneum
T4b = other organs or structures have been invaded
NX = lymph nodes can’t be assessed
N0 = no regional lymph node involv’nt
N1a = 1 regional lymph node
N1b = 2-3 regional lymph nodes
N2a = 4-6 lymph nodes
N2b = ≥ 7 regional lymph nodes
M0 = No metastasis
M1 = metastasis
M1a = metastasis confined to 1 organ or site
M1b = metastasis in peritoneum in > 1 organ / site
Duke classifica’n
- A = confined to mucosa + part of muscle of bowel wall
- B = extends through muscle of bowel wall
- C = lymph node involvement
- D = metastatic disease
Emergency Tx i.e acute obstruc’n by tumor or significant diverticular disease = Hartmann’s procedure i.e resec’n of rectosigmoid colon + forma’n of end colostomy
→ colostomy = either permanent or will get reversed later
Tx for colon cancer
→ A-C = surgical resec’n + post-op chemo
→ D = surgical resec’n + pre + post-op chemo
Tx for rectal cancer
→ A = local excis’n or chemo if not suitable for Sx
→ B-D = radical resec’n + pre-op chemoradiotherapy + post op chemo OR ttl neoadjuvant chemo
Mx after curative Sx i.e 3 yrs later
- CEA
- CTAP
Complica’n = anastomosis leak (any time there’s a bowel anastomosis there’s a risk of anastomosis leak, rectal resec’ns have the highest rate of anastomotic leaks)
⟹ SSX = worsening abdominal pain + sepsis
⟹ usually occurs in post days 3-5
⟹ Tx = IV Abx if pt = septic + then send back to OR
- Know for OSCE *
Diverticulosis / Diverticular Disease ✓
Def - diverticulae / outpouchings in lining of large bowel (usually sigmoid colon)
→ when diverticulae become infected it’s called diverticulitis
RFs
> 50 y/o
- low fiber diet
- obesity
- NSAIDs (↑ risk of diverticular hemorrhage)
Pathophys - wall of large intestine contains muscle layer called circular muscle → points where circular muscle = penetrated by blood vessels = areas of weakness b/c don’t have protec’n of teniae coli → ↑ed pressure inside lumen over time causes gaps to form in circular muscle → gaps allow mucosa to herniate through muscle layer → diverticulae form
⟹ diverticula doesn’t form in rectum b/c rectum has outer longitudinal muscle layer which provides extra support
SSX of diverticulitis
- fever
- LIF pain
- N + V
- diarrhea
- rectal bleeding
- peritonitis in severe cases
- palpable abdominal mass if abscess has formed
- Raised inflammatory markers + WCC
Ddx = other causes of LIF pain
- ovarian cysts
- ovarian tors’n (pain = sudden)
- ectopic pregnancy (must do urine dip w/ β HCG in all young women w/ LIF pain to r/o ectopic pregnancy !)
Ix’s
- CRP → will be elevated
- FBC → polymorphonuclear leukoctyosis (in diverticulitis)
- CTAP to check for complica’ns of diverticulitis → will show thickening of bowel wall, abscess, streaky mesenteric fat + may show gas in bladder in cases of fistula
- CT w/o contrast if contrast = contraindicated
- abdominal U/S if CT = contraindicated → will show abscess, perfora’n + obstruc’n if they’re present
Tx for diverticulosis = bulk-forming laxatives + ↑ing fiber consump’n b/c fiber adds bulk to stool which alleviates constipa’n + ↓ pressure in colon which minimizes risk of diverticulitis + ↑ed diverticulae forma’n
Complica’ns of diverticulitis
- fistulas
- abscess
- stricture
- perfora’n
- obstruc’n
- colorectal neoplasm
Tx for uncomplicated diverticulitis
- oral co-amoxiclav for ≥ 5 days
- analgesia (not NSAIDs or opiates if possible)
- clear liquid diet until SSX improve (usually 2-3 days)
- f/u w/in 48 hrs to review SSX
Tx if pt has complica’ns = admit them + then . . .
- NPO or clear liquid diet
- IV Abx
- IV fluids
- analgesia
- Hartman’s procedure if pt has diverticular perfora’n
- Know for OSCE *
How to drain an abscess ✓
- Get all ur equipment
- Posi’n pt + bed as u want
- Palpate fluctuence of abscess i.e where u would “pop it”
- Put cover around it
- Inject lidocaine into fluctuence + wait for it to take effect (pull back w/ syringe to make sure u don’t get blood before u inject)
- Poke area w/ needle + ask pt if they can feel it
→ if they can feel it, wait a bit longer + if they can still feel it inject more - make a straight incision 1cm deep across fluctuence
- Cut an ellipse around that
- Use kelly to open + close inside that cavity in all direc’ns to drain it
- Flush that cavity with saline as many times as u need to
- Pack it w/ iodoform in all direc’ns + leave a tail so pt can pull it out
- Tape it w/ ABD dressing
Types of Laxatives ✓
Bulk-forming laxative
- ispaghula husk
→ takes 72 hrs to act + is mainly for pts who don’t consume enough fiber
Osmotic laxatives (don’t give if pt feels bloated)
- lactulose
- macrogol
Softening laxative (don’t give if pt’s stools are already soft)
- docusate
Stimulant laxatives
- senna
- bisacodyl
→ C/I = bowel obstruc’n
- Know for OSCE *
What to give for opioid induced constipa’n ✓
Stimulant + osmotic laxative
Testicular Tors’n ✓
Def - when testicle twists on spermatic cord
= urological emergency that must be treated surgically w/in 6 hrs of presenta’n !
RFs
- neonate
- male < 25 y/o
Most common Eti = bell clapper deformity
→ normally testicle = fixed posteriorly to tunica vaginalis but in bell-clapper deformity fixa’n btw testicle + tunica vaginalis = absent ∴ testicle hangs horizontally instead of vertically hence can rotate freely w/in tunica vaginalis
Pathophys - constric’n of vascular supply → ischemia → necrosis of testicle if left untreated
SSX = sudden u/l testicular pain that started after physical activity
SSX on exam
- firm swollen testicle
- elevated / retracted) testicle
- absent cremasteric reflex
- abnormal testicular lie (often horizontal)
- rota’n (epididymis ≠ in normal posterior posi’n)
Ddx
- hydrocele
- varicocele
- spermatocele
- inguinal hernia
- testicular cancer
- epididymitis
- epdidymo-orchitis
- Fournier’s gangrene = rate life threatening bacterial infec’n of scrotum / penis / perineum
Ix to confirm diagnosis = scrotal U/S → will show whirlpool sign ⟹ spermatic cord + blood vessels have spiral appearance
Tx = surgical scrotal explora’n + orchiopexy = putting testicles in proper posi’n → orchidectomy (removal of testicle) if there’s necrosis
Complica’ns
- recurrence
- reactive hydrocele
- ischemia of testes → necrosis → infertility or subfertility
- Know for OSCE *
What’s a hydrocele ? ✓
Cyst w/in scrotum, feels like a bag of worms
What’s a varicocele ? ✓
= Enlarg’nt of veins in scrotum
→ 99% of varicoceles = left sided + 30% = both sides, right side = very rare (can indicate a malignant process blocking drainage on right side of abdomen)
→ left testes varicocele = more common b/c right testicular vein = tributary of IVC while left testicular vein = tributary of renal vein which is more narrow ∴ it’s easier to get pulling of blood on that side
Prostate cancer ✓
Def - cancer of the prostate
→ almost all prostate cancers = adenocarcinomas arising from epithelial cells lining ducts of prostate
→ prostatic Intraepithelial Neoplasia (PIN) = asymptomatic pre-malignant les’n that can progress into cancer
RFs
> 50 y/o
- FHx
- Afro Caribbean origin
SSX = asymptomatic or . . .
- ED
- hematuria
- bladder outflow obstruc’n
- persistent back pain (if there’s vertebral metastasis)
Ddx
- BPH
- chronic prostatitis
Ix’s
- PSA → will be elevated i.e > 4 (1/3 of men w/ elevated PSA will have prostate cancer)
⟹ be wary of things that can falsely elevate PSA such as . . .
> BPH
> UTI
> prostatitis
> vigorous exercise
> acute urinary reten’n
> ejacula’n w/in 24 hrs of test - Multiparametric MRI of prostate = 1st line Ix
→ 1 = very low suspici’n
→ 2 = low suspici’n
→ 3 = equivocal
→ 4 = probably cancer
→ 5 = definitely cancer - Transrectal U/S guided Bx of prostate (TRUS) for diagnosis if linkert score > 3
Grading = Gleason scoring system → tumor = given 2 scores from 3-5 according to microscopic appearance + both scores = added together to give overall grade
⟹ score of 6 = good prognosis
⟹ score of 7 = intermediate prognosis
⟹ score ≥ 8 = worse prognosis
Tx if no metastasis + pt = healthy = radical prostatectomy
→ bladder = rejoined to urethra after entire prostate = removed
⟹ side effects of Sx . . .
- ED
- urinary incontinence
- bladder neck obstruc’n
Tx for metastatic disease = testosterone inhibitors + palliative radiotherapy in bone metastasis
- Know for OSCE *
Bladder cancer ✓
Def - cancer of the bladder
→ most = transi’nal cell carcinomas
→ SUC (superficial urothelial carcinoma) = confined to mucosa OR invades into lamina propria but not into muscularis propria (detrusor muscle) = papillary tumor
⟹ Tx = TURBT (transurethral resec’n of a bladder tumor)
⟹ has high chance of recurrence even after removal hence all pts w/ SUC require cytoscopy checks at regular intervals
→ (MIC) muscle invasive urotherlia carcinoma
⟹ invades into or beyond detrusor muscle
⟹ tends to be soild rather than papillary
⟹ Tx = cystectomy i.e removal of bladder (organs such as uterus can also be removed)
⟹ has a worse prognosis than SUC b/c = more likely to spread to reg’nal lymph nodes + metastasize to distant sites
→ (CIS) carcinoma in situ = pre-cancer b/c although cells display nuclear features associated w/ malignancy such as pleomorphism or high amt of mitoses, there’s NO invas’n through base’nt membrane, which is a requirement for something to be called “cancer”
⟹ 40% of CIS will turn into MIC if left untreated hence = more ominous diagnosis than SIC b/c has higher likelihood of progressing to MIC
RFs
> 65 y/o
- FHx
- male
- pelvic radia’n
- exposure to dyes / solvents
- smoking (most important RF !)
- chronic bladder irrita’n i.e recurrent UTIs
SSX
- dysuria
- painless hematuria (macroscopic or microscopic)
⚠️ always do cystoscopy in smoker w/ painless hematuria to not miss bladder cancer !
Pts who require 2 wk wait urgent referral . . .
→ pt > 45 y/o w/ unexplained visible hematuria w/o UTI or after UTI Tx
→ pt > 60 y/o w/ microscopic hematuria + either dysuria or high WCC on FBC
Ix’s
- urine cytology (might not be +ve even if pt has bladder cancer)
- cystoscopy = used for diagnosis → should be followed by CT + MRI urogram
Tx = chemo if there’s metastasis + then immunotherapy if needed
Complica’ns = urinary reten’n + hydronephrosis
- Know for OSCE *
Testicular cancer ✓
Def - cancer of 1 testes
→ most common malignancy in men from 20-34 y/o
→ highly curable when diagnosed early + can still be cured even if there’s a relapse
→ grows from germ cells
RFs
- HIV
- FHx
- white
- infertility
- testicular atrophy
- cryptorchidism (most important RF)
Types
- seminoma = slow growing → can spread to lymph nodes = less common
→ have differentiated cells i.e already became respective cells types - non seminoma = faster growing = more common → ex’s = embryonal carcinoma, teratoma, yolk sac tumor
→ have undifferentiated cells i.e still have Ψ to become any cell lineage
SSX
- hard, painless nodule on 1 testes
- gynecomastia sometimes due to ↑ed estrogen : androgen ratio (usually in rare testicular tumor called Leydig cell tumor)
Ix’s
- scrotal U/S for diagnosis
- Bx to determine histology of mass
- CXR to check for lung metastasis
- β hCG → sometimes elevated in testicular cancer
- serum 𝛼 fetoprotein (AFP) → sometimes elevated in testicular cancer
- LDH → sometimes elevated in testicular cancer
Royal Marsden Staging System
- stage 1 = isolated to testicle
- stage 2 = cancer has spread to retroperitoneal lymph nodes
- stage 3 = cancer has spread to lymph nodes above diaphragm
- stage 4 = metastasis
Tx
- Radical inguinal orchiectomy (for any suspicious testicular mass irregardless of stage + type)
- For seminoma = chemo or external beam radia’n post-orchiectomy
For non seminoma stage 1 = retroperitoneal lymph node disses’n (RPLND) post orchiectomy followed by chemo
- For metastasis (irregardless of it’s seminoma or non seminoma) = combina’n chemo post orchiectomy
- For relapse (irregardless of it’s seminoma or non seminoma) = salvage chemo
Complica’n = infertility
- Know for OSCE *
Renal cancer ✓
Def - kidney cancer
→ most common type = renal cell carcinoma (RCC), specifically renal clear cell carcinoma
→ no Bx done in this type of cancer !
RFs
> 55 y/o
- FHx
- HTN
- male
- obesity
- smoking
- familial syndromes such as von Hippel Lindau syndrome = rare autosomal dominant disease that predisposes to certain benign + malignant tumors such as RCC + pheochromocytoma
SSX
- flank/ loin mass
- flank / loin pain
- hematuria
- weight loss
Ddx
- renal cyst
- bladder cancer
Ix’s
- FBC → RBC count might be elevated due to ↑ed EPO
- LDH → if elevated = poor prognostic marker
- corrected Ca → if elevated = poor prognostic marker
- U + E → urea + creatinine might be elevated
- GFR → might be ↓ed
- abdominal / pelvic U/S for diagnosis of renal cancer in general
- CT abdomen + pelvis w/ contrast for diagnosis + staging of RCC i.e lymph node spread / metastasis
- MRI abdomen + pelvis if contrast = contraindicated
Tx if no metastasis = ttl nephrectomy
Tx if there’s metastasis = palliative
ED ✓
Def - inability to achieve or maintain sufficient erec’n for sexual performance
RFs
- PVD
> 40 y/o
Pathophys - parasympathetic system stimulates vasodila’n of helicine arteries of corpora cavernosa
→ erec’n → prostatic plexus cavernous + pudendal nerves carry sympathetic fibers → sympathetic fibers release NE → NE vasoconstricts helicine arteries of corpora cavernosa → erer’n stops
⚠️ If there’s a pb w/ or lack of input from sympathetic fibers of prostatic plexus we get priapism b/c there’s nothing to end erec’n
Tx = sildenafil
→ MOA - phosphodiesterse inhibitor ∴ ↑ [cGMP] which vasodilates through NO signaling ∴ overriding sympathetic vasoconstric’n + allowing erec’n to take place
→ side effects = flushing, HAs, dizziness
→ C/Is = taking nitrates b/c will cause too much vasodila’n
→ end in “NAFIL”
Hypertrophy v.s Hyperplasia ✓
- Hypertrophy = ↑ in SIZE of cells which causes ↑ size of tissue/organ
- Hyperplasia = ↑ in # of cells which also causes ↑ size of tissue/organ
BPH ✓
Def - benign prostatic hyperplasia
RF = > 50 y/o
Pathophys - subtle hormonal imbalance that occurs w/ aging → overgrowth of prostatic tissue in transi’n zone → forma’n of large nodules
SSX
- urgency
- weak flow
- frequency
- nocturia
- straining
- hesitancy i.e difficulty starting + maintaining stream
Ddx
- UTI
- prostatitis
- overactive bladder
- bladder / prostate cancer
Ix’s
- rectal exam to check prostate size
- urine dipstick to check for possible UTI or bladder cancer
- Interna’nal prostate SSX score to assess severity
→ 0-7 = mild BPH
→ 8-19 = moderate BPH
→ 20-35 = severe BPH - PSA to not miss prostate cancer
Tx if SSX don’t interfere w/ QoL = lifestyle Δs
Tx for bothersome SSX = 𝛼 blocker such as tamsulosin (relaxes smooth muscle in prostate ∴ allowing urine to flow more freely through urethra) → add 5 𝛼 reductase inhibitor → add phosphodiesterase 5 inhibitor → TURP (transurethral resec’n of prostate)
⟹ complica’ns of TURP Sx . . .
- HypoNa
- ED or retrograde ejacula’n
- bleeding
- infec’n
- urinary incontinence
- urethral stricture
→ MOA of 5 𝛼 reductase inhibitor - inhibits 5 𝛼 reductase ∴ it can’t convert DHT to testosterone which is responsible for prostatic growth so less testosterone → less prostatic growth, also help w/ baldness
→ side effects = gynecomastia + sexual dysfunc’n i.e ED / ↓ in libido + volume of ejacula’n
→ end in “STERIDE”
Complica’ns
- obstructive uropathy → infec’n + HTN
- b/l hydroureter + hydronephrosis if bladder outflow obstruc’n isn’t relieved
- untreated hydronephrosis → progressive atrophy of renal parenchyma → CKD + progressive loss of renal func’n bilaterally
- urinary tract obstruc’n due to compress’n of prostatic urethra b/c transi’n zone = adjacent to urethra
- Know for OSCE *
Epididymitis ✓
Def - u/l inflamma’n of epididymis (SSX should be < 6 wks in dura’n)
→ if testes = inflamed as well = epididymo-orchitis
RFs
- unprotected sex
- bladder outflow obstruc’n
Eti - STI like chlaymdia or gonorrhea in sexually active men or pathogens like mumps or E.coli in non-sexually active men
Pathophys - inflamma’n process starts in tail + subsequently spreads to body + head of epididymis
SSX
- u/l SSX of inflamma’n on scrotum i.e pain, swelling, hot + red
- urethral discharge if due to gonorrhea or chlamydia
Ddx = testicular tors’n
Ix’s
- gram stain of urethral secre’ns to identify causative pathogen
- urine dipstick → +ve for leukocytes
- urine microscopy, culture + sensitivity (MCS)
- chlamydia + gonorrhea NAAT testing
- PCR from saliva swab or mumps antibodies if mumps = suspected
Tx
- if you suspect it’s due to gonorrhea = IM CTX + doxycycline
- if due to chlamydia = oral doxycycline for 10-14 days or oral ofloxacin for 14 days
→ oral co-amoxiclav for 10 days if quinolone Abx = contra-indicated
→ MOA of quinolones - broad spectrum Abx that kills bacterial cells by inhibiting DNA synthesis
→ side effects = tendinopathy (especially in Achilles tendon) + ↓ in seizure threshold
→ C/Is = pregnant women + children
→ end in “QUINOLONE” or “FLOXACIN”
- if due to E. coil = levofloxacin for 10 days
Complica’ns
- abscess
- infertility
- testicular ischemia
- epididymal obstruc’n
- Know for OSCE *
Prostatitis ✓
Def - inflamma’n of prostate
Eti = usually due to E. coli infec’n
RFs
- UTI
- BPH
Types
- acute = due to bacteria
- chronic
→ due to active bacterial infec’n
→ not due to an active infec’n
SSX of chronic (≥ 3 months of SSX)
- pelvic pain
- pain w/ BM
- lower urinary tract SSX i.e dysuria, hesitancy, frequency + urinary reten’n
- sexual dysfunc’n such as ED, pain on ejacula’n or hematospermia (blood in semen)
- tender + enlarged prostate
SSX of acute = SSX of chronic + systemic SSX i.e . . .
- fever
- nausea
- myalgia
- sepsis
Ix’s
- urine dipstick → will be +ve for leukocytes
- urine culture / blood culture + MCS → will be +ve for bacteria (usually E.coli)
Emergency Tx i.e if pt = in septic shock = IV Abx + NSAIDs → then switch to oral Abx for regular Tx
Complica’ns
- sepsis
- urinary reten’n
- prostate abscess
- chronic prostatitis
- Know for OSCE *
Urinary Incontinence in women ✓
RFs
- older age
- pregnancy
- obesity
- pelvic organ prolapse
- post-menopausal
- diuretic use
Types
- stress incontinence = pt leaks when they cough or sneeze
- urge incontinence = feeling of urinary urgency followed by involuntary leakage
- overactive bladder / detrusor muscle overactivity
Ix’s = urodynamic testing
- cystometry to measure detrusor muscle contrac’n
- uroflowmetry to measure flow rate
- leak point pressure test to check for stress incontinence
→ pt = asked to cough / move when bladder = filled to various capacities - post-void residual measurement to check for urinary reten’n
- empty supine stress test = +ve if leakage = observed while pt does valsava maneuver
Tx for stress incontinence
- Behavioral modifica’ns . . .
- Kegel / pelvic muscle exercises (PT referral)
- vaginal devices such as pessary
- weight loss in women w/ BMI > 25
- ↓ing caffeine intake
- smoking cessa’n
- treating any constipa’n if present - Sx
- sling
- colposuspens’n
- TVT (tens’n-free vaginal tape) / TOT (transobturator tape) → narrow band of tape = placed under urethra to support urethra + bladder like a hammock
Tx for urge incontinence / overactive bladder (NO Sx b/c can make it worse !)
1. Above behavioral modifica’ns
2. Anti cholinergic drug such as oxybutynin
3. Mirabegron = β3 agonist that stimulates sympathetic nervous system = contraindicated in pts w/ uncontrolled HTN !
4. Invasive methods such as . . .
- botulinum toxin type A injec’n into bladder wall
- percutaneous sacral nerve stimula’n where device = implanted in pt’s back that stimulates sacral nerves
- augmenta’n cystoplasty = using bowel tissue to enlarge bladder
- urinary divers’n = redirec’n of urinary flow via urostomy on abdomen
Tx for overactive bladder = neuromodula’n / electric stimula’n via sacral nerve or injec’n of botulinum toxin type A into bladder wall
- Know for OSCE *
Breast Cancer ✓
90% of breast cancers = ductal + 10% = lobular
RFs
> 50 y/o
- HRT
- obesity
- alcohol
- nulliparity
- not breastfeeding
- long term use of COCP
- FHx (most important RF)
- atypical ductal hyperplasia
- female sex (99% of cases = women)
- early menarche or late menopause
SSX
- nipple invers’n
- nipple discharge
- ulcera’n / funga’n
- hard, painless lump
- palpable axillary nodes
- skin dimpling or puckering
- mass = fixed to chest wall or overlying skin
- nipple eczema (in Paget‘s disease of nipple)
- peau d‘orange (= cutaneous edema due to lymphatic obstruc’n)
Who gets 2 wk wait urgent referral for suspected breast cancer . . .
- unexplained breast lump in pt ≥ 30 y/o
- u/l nipple SSX in pt ≥ 50 y/o
When to suspect inflammatory breast cancer . . .
- young breastfeeding woman w/ recurrent mastitis that doesn’t improve even after 2 diff courses of Abx
→ must refer to breast surgeon !
→ has very poor prognosis
- Fibrocystic Δ / Fibroadenoma = most common benign breast tumor
→ SSX . . . - breast pain / tenderness just before period
- lump itself = smooth, well circumscribed + painless
- usually in 15-35 y/o women
Breast cancer v.s Fibrocystic Δ
- u/l v.s b/l
- single nodule v.s multiple nodules
- no menstrual varia’n v.s menstrual varia’n
- no regress’n during pregnancy v.s Ψ regress’n during pregnancy
- DCIS (Ductal carcinoma in situ) = pre-cancerous or cancerous, if left untreated can progress to invasive breast cancer which is why we do lumpectomy + radia’n
- Paget disease of the nipple = disease affecting skin of nipple + areola = manifesta’n of DCIS, but NOT ALL DCIS cases will have Paget !
→ commonly occurs around menopause
→ SSX = - erythematous erup’n / ulcera’n
- scaling + flaking of skin
- u/l eczema of nipple
- crusted les’n w/ irregular borders
- Eczema of the nipple
→ Paget v.s Eczema of the Nipple - u/l v.s b/l
- around menopause v.s around lacta’n
- mild v.s marked itching
- no vesicles v.s vesicles / blisters
- nipple = retracted / destroyed v.s nipple = preserved
- may have underlying lump v.s no underlying lump
- discharge +/- bleeding v.s may have atopic Hx i.e asthma / eczema / hay fever
Ix’s
- Triple assess’nt (“CRP”)
a) Clinical i.e Hx + phys. exam
b) Radiological
- U/S for pts < 40 y/o → will distinguish btw solid + cystic les’ns
- mammogram for pts > 40 y/o → will identify micro-calcifica’ns + densities
→ BI-RADS score = used to assess likelihood that breast les’n is malignant - 0 = incomplete exam
- 1= -ve for cancer
- 2 = very likely to be benign
- 3 = probably benign
- 4 = suspicious for cancer
- 5 = HIGHLY suspicious for cancer
c) Pathological i.e FNA or Core Bx
- Sentinel lymph node = 1st node that drains a cancer → if -ve, that means cancer has NOT spread to any other nodes ∴ NO further Sx in axilla = required but if +ve then MUST remove axillary lymph nodes !
Breast cancer prognostic factors from most to least important . . .
- Stage = most important prognostic factor in all cancers not just breast Ca
- Grade
- Histological subtype
- Vascular invas’n
- Whether or not all margins can be excised
- ER status
→ +ve ER status = better prognosis than -ve ER status b/c can respond to hormonal therapy such as tamoxifen or anastrozole
→ HER2 +ve = poorer prognosis than HER2 -ve but at least can respond to herceptin or trastuzumab
Complica’n = metastasis to bone, lungs, liver, brain (in that order)
Screening = every 3 yrs for all GP registered women btw 47 + 71 y/o via 2 mammograms on each breast
- Know for OSCE *
Duct Ectasia ✓
Usually in elderly women + is caused by shortening + widening of mammary ducts
SSX
- b/l nipple retrac’n
- b/l green or white nipple discharge
- Know for OSCE *
Back pain + what u should suspect based on SSX ✓
- Suspect malignancy if . . .
→ pt > 50 y/o
→ pain = worse @ night + doesn’t get better w/ rest - Suspect infec’n such as osteomyelitis / discitis if . . .
→ pt had recent infec’n or = IV drug user + there’s fever + spinal tenderness - Suspect inflammatory if . . .
→ pain improves w/ activity - Suspect mechanical pb such as muscle strain if . . .
→ neuro exam = normal but there’s paraspinal tenderness
→ pain = worse w/ activity + better w/ rest
→ pt = older - Suspect radiculopathy / nerve root damage (such as due to disk hernia’n) if . . .
→ pain radiates below knee
→ straight leg test = +ve + pt has neurological deficits - Suspect spinal stenosis if . . .
→ pt has pseudoclaudica’n i.e intermittent leg pain + pain = relieved by leaning forward - Suspect compress’n if . . .
→ pt has osteoporosis + onset of SSX = following recent trauma
Radiculopathies ✓
- causative disc = always 1 level above affected nerve
→ C3/C4 radiculopathy
- causative disc = C2-C4
- sensory deficits = in shoulder + neck
- motor SSX = scapular winging
→ C5 radiculopathy
- causative disc = C4-C5
- sensory deficits = in anterior shoulder
- motor deficits = weak biceps + deltoid muscles + ↓ed biceps reflex
→ C6 radiculopathy
- causative disc = C5-C6
- sensory deficits = from upper lateral elbow over radial forearm up to thumb + radial side of index finger
- motor deficits = weak biceps + wrist extensors + ↓ed biceps + brachioradialis reflex
→ C7 radiculopathy
- causative disc = C6-C7
- sensory deficits on palmar side = ulnar side of index finger + entire middle finger + radial side of ring finger
- sensory deficits on dorsal side = medial forearm up to index, middle + ring finger
- motor deficits = weak triceps, wrist flexors + finger extensors + ↓ed triceps reflex
→ C8 radiculopathy
- causative disc = C7-T1
- sensory deficits = ulnar side of ring finger, entire pinky, hypothenar eminence + ulnar side of distal forearm
- motor deficits = weak finger flexors
→ L3 radiculopathy
- causative disc = L2-L3
- sensory deficits = in anterior thigh
- motor deficits = weak hip flex’n, knee extens’n + hip addc’n + ↓ed patellar / knee jerk reflex as well as +ve femoral stretch test
→ L4 radiculopathy
- causative disc = L3-L4
- sensory deficits = anterior aspect of knee + medial malleolus
- motor deficits = weak knee extens’n + hip adduc’n + ↓ed patellar reflex as well as +ve femoral stretch test
→ L5 radiculopathy
- causative disc = L4-L5
- sensory deficits = dorsum of foot
- motor deficits = weak foot + big toe dorsiflex’n as well as +ve sciatic nerve stretch test
→ S1 radiculopathy
- causative disc = L5-S1
- sensory deficits = posterolateral aspect of leg + lateral aspect of foot
- motor deficits = weak plantar flex’n + ↓ed Achilles reflex as well as +ve straight leg test
→ S2-S4 radiculopathy
- causative disc = S1-S4
- sensory deficits = posterior aspect of thigh + leg (S2), perineum (S3-S4) + peri anal area (S4)
- motor deficits = ↓ed peroneal + bulbocavernous reflex
Why do we check for neck injury after MVA ? ✓
B/c MVA can cause incomplete C7 spinal cord injury
→ SSX = spasticity
⟹ generalized spasticity = treated w/ oral baclofen
⟹ focal or multifocal spasticity = treated w/ 1 of the following . . .
- botulinium toxin
- phenol nerve
- muscle block
⟹ regional spasticity = treated w/ intrathecal phenol or intrathecal baclofen
Bell’s Palsy ✓
Def - acute u/l LMN facial nerve palsy ∴ forehead is NOT spared
→ most patients fully recover after several wks but recovery can take up to 1 yr
→ 1/3 of pts will have residual weakness
Most common Eti = reactiva’n of HSV-1
SSX
- eyebrow asymetry
- mouth droop +/- drooling
- inability to close 1 eye
- facial pain / abnormal sens’an
Ix = clinical diagnosis + diagnosis of exclus’n
Tx if pt presents w/in 72 hrs of SSX onset = prednisone + lubricating eye drops
- Know for OSCE *
Causes of LMN Facial Nerve Palsy ✓
“SITT”
Systemic diseases
- MS
- diabetes
- sarcoidosis
- leukemia
- Guillain Barré
Infec’ns
- HIV
- Lyme disease
- otitis media
- otitis externa
Tumors
- parotid tumor
- acoustic neuroma
Trauma
- Sx
- direct nerve trauma
Guillain Barré ✓
Def - immune-mediated demyelina’n of PNS usually triggered by an infec’n
→ SSX usually start w/in 4 wks of preceding infec’n
Eti = preceding infec’n (Campylobacter jejuni, EBV or CMV usually)
Pathophys - B cells create antibodies against antigens on triggering pathogen → antibodies accidentally also attack target proteins on myelin sheath or axon due to structural similarity
SSX
- progressive, ascending weakness i.e legs are affected 1st
- ↓ed or absent reflexes
- peripheral neuropathy
Ddx = myasthenia gravis
Ix’s
- nerve conduc’n study → will show ↓ed signal
- LP → elevated CSF protein + normal or slightly high lymphocytes
- LFTs → liver enzymes may be elevated during first few days but will then normalize 1-2 wks later
- spirometry every 6hrs
Diagnosis = based on SSX + CSF
Tx if pt doesn’t have renal failure or IgA deficiency = IV Ig or plasma exchange
Tx if pt has renal failure or IgA deficiency = plasma exchange
Complica’ns
- DVT
- severe respiratory failure → ICU for intuba’n + ventila’n
- Know for OSCE *
Myasthenia Gravis ✓
Def - chronic autoimmune disorder of post-synaptic membrane @ NMJ in skeletal muscle
→ usually affects women < 40 y/o + men > 60 y/o
Pathophys - Ach receptor antibodies bind to postsynaptic Ach receptors ∴ Ach can’t bind to its receptors so not enough Ach → muscle weakness
SSX
- progressive muscle weakness that gets worse w/ activity + improves w/ rest
→ affected muscles = proximal muscles of limbs + small muscles of head + neck ∴ causing . . .
⟹ dysphagia
⟹ diplopia + ptosis due to extraocular muscle weakness
⟹ weakness in facial mov’nts
⟹ fatigue in jaw when chewing
⟹ slurred speech
⟹ difficulty climbing stairs, standing from a seat or raising hand above head
Phys. Exam
- Ask pt to count from 1 to 100, if voice becomes progressively weaker = +ve fatigue test
Ix’s
- FVC → might be low
- CT of chest to check for thymoma
- Ach receptor antibodies (AchR) → will be +ve in 85-90% of pts
- MuSKS antibodies → might be +ve
- repeated nerve stimula’n if antibodies = unremarkable → will show > 10% ↓
- single fiber electromyography if nerve stimula’n = unremarkable → will show complete failure of neuromuscular transmiss’n in muscle fiber or jitter = ↑ed variability in motor latencies
- edrophonium test when still unsure of diagnosis
→ give pt IV Tensilon / edrophonium injec’n → blocks Achesterase → +ve result = immediate SSX improv’nt = diagnostic for myasthenia gravis
Tx = pyridostigimine = long acting Achesterase inhibitor ∴ helps to ↑ Ach levels @ NMJ
Complica’n = mysasthenic crisis = emergency b/c it’s life-threatening !
= precipitated by recent illness, such as respiratory tract infec’n
→ SSX =
- limb weakness
- respiratory failure due to respiratory muscle weakness
- hypercapnia + its associated SSX i.e double vi’sn / slurred speech
→ FVC will be < 1L
→ Tx = IV Igs + plasmapheresis
- Know for OSCE *
Cauda equina syndrome / spinal cord compress’n ✓
Def - compress’n of lumbosacral nerve roots that extend below spinal cord = neurosurgical emergency !
→ can cause irreversible damage if ur too late
RFs
- anticoagulants
- spinal trauma / Sx
- lumbar disk hernia’n
Eti
- hematoma
- disc prolapse
- spinal stenosis
- epidural abscess
- metastatic compress’n
- trauma that caused vertebral fracture
SSX
- lower back pain
- saddle anesthesia i.e gradual ↓ in perianal sensa’n (early sign)
- urinary / fecal incontinence (VERY LATE sign)
- u/l or b/l sciatica i.e muscle weakness, numbness + tingling in entirety of lower limb(s)
Ix = urgent lumbar spine MRI w/o contrast
→ CT of lumbar spine w/o contrast if MRI ≠ available
Tx = lumbar decompress’n Sx
Complica’ns
- bladder dysfunc’n
- bowel dysfunc’n
- sexual dysfunc’n
- Know for OSCE *
Trigeminal neuralgia ✓
Def - facial pain in ≥ 1 divis’n of trigeminal nerve
RFs
- MS
- old age
Types = based on Eti
- idiopathic = no known Eti
- classical (most common) = due to intracranial vascular compress’n of trigeminal nerve root
- 2° = due to another pathological process such as malignancy or MS
SSX = severe stabbing pain triggered by sensory stimulus such as cold wind / brushing hair or teeth or touching face
Ix = clinical diagnosis
Tx
- Carbamazepine (anti-convulsant)
→ MOA = Na channel blocker (just like Na valproate) - Gabapentin or pregabalin = for neuropathic pain
- Ablative Sx for idiopathic + microvascular decompress’n for classical
- Know for OSCE *
Idiopathic intracranial HTN / pseudotumor cerebri ✓
Def - disorder of ↑ed ICP
RF = obese, fertile female
SSX
- HA
- transient visual obscura’ns
- pulse synchronous tinnitus
- photobia
- retrobulbar pain
- papilloedema / optic disc swelling on fundoscopy
- ↓ed visual acuity due to papilloedema
Ix’s
- perimetry (visual field testing) → visual field defects and/or enlarged blind spot
- dilated fundoscopy → use Frisén grading to grade severity of papilloedema = from 0-5
⟹ 0 = normal optic disc + 5 = severe papilloedema
Tx
- acetazolamide
→ MOA - ↓ CSF produc’n
→ side effect = tingling of fingers + toes - shunt to drain CSF
Complica’n = vis’n loss
What is the Tx for cerebral edema ? ✓
Dexamethasone
Nasopharyngeal tumor ✓
SSX
- lump in neck
- u/l hearing loss
- tinnitus
- blocked or stuffed nose
- recurrent nose bleeds
- blood in saliva
- sore throat
- HAs
RFs
- FHx
- male
- EBV
- being from Southeast Asia or North Africa
- salt-cured food
- smoking
- alcohol
Order of Ix’s
1. Nasoendoscopy for diagnosis
2. CT/MRI + Bx for staging
Tx = chemoradiotherapy after discuss’n w/ MDT
Complica’n = can metastasize to reg’nal lymph nodes + then to bone, lung or liver
Ddx for each type of hearing loss ✓
- Sensorineural = damage to inner ear structures, sensory cells or nerve fibers
→ causes = presbycusis, acoustic neuroma, ototoxic medica’ns, labyrinthitis, meniere’s
→ Tx for b/l sensorineual hearing loss = b/l hearing aids - Conductive = pb conducting sound waves from outer or middle ear to inner ear
→ causes = blockage i.e fluid / wax / infec’n / ossicle fracture / perfora’n of tympanic membrane
Rinne → tests CONDUCTIVE only
- if AC > BC = +ve which could be normal or sensorineural pb
- if BC > AC = conductive pb
Weber → test both
- if both ears = same = normal or b/l equivalent pb
- if healthy ear = louder = sensorineural pb in sick ear
- if sick ear = louder = conductive pb in sick ear
Vertigo Ddx ✓
a) Vestibular neuronitis
Def - inflamma’n of vestibular nerve
Eti = viral URTI usually
SSX
- NO tinnitus or hearing loss b/c cochlear nerve ≠ affected
- constant vertigo that is worsened by head mov’nt
- balance pb
- N + V → admit pt if they become severely dehydrated
Ix = head impulse test
Tx = prochlorperazine
b) Labyrinthitis
Def - infamma’n of optic capsule bony labyrinth of inner ear
Eti = viral URTI but can also be 2° to meningitis
SSX
- acute onset vertigo
- hearing loss
- tinnitus
- ear discharge sometimes
- N/V sometimes
Ix = clinical diagnosis
Tx if due to viral infec’n = same as vestibular neuronitis i.e prochlorperazine for 3 days
c) Benign Paroxysmal Posi’nal Vertigo (BPPV)
Def - sudden onset of dizziness + vertigo triggered by Δs in head posi’n = peripheral cause of vertigo
→ avg age of onset = 55 y/o
RFs
- female
- older age
- head trauma
- vestibular neuronitis
- labyrinthitis
- migraines
Eti
- idiopathic
- head trauma
- aging
- viral infec’n
Pathophys - Eti → CaCO3 crystals called otoconia displace into semicircular canals → normal flow of endolymph through canals = disrupted
SSX = recurrent episodes of vertigo triggered by Δs in head posi’n i.e rolling over in bed / gazing upwards
→ episode lasts 20-60 secs
→ no SSX in btw episodes
Diagnostic Ix = +ve Dix-Hallpike maneuver on exam
→ pt sits upright on flat examina’n couch w/ head turned 45° to side that ur testing → support pt’s head + rapidly lowering pt backwards until their head is hanging off @ end of couch → check for nystagmus
Tx - usually resolves spontaneously after a couple wks
→ half of pts w/ BPPV will have recurrence 3-5 yrs after initial diagnosis
SSX relief
- Epley maneuver (successful in around 80% of cases)
- Vestibular rehab = teaching pt exercises they can do themselves at home such as Brandt-Daroff exercises = pt sits on end of bed + lies sideways while slightly rotating head such that it faces ceiling → should be done several times / day until SSX improve
d) Meniere’s
Def - long term inner ear disorder that causes recurrent episodes of SSX + feeling of fullness in ear
→ causes sensorineural hearing loss
⟹ low frequencies = affected first
RF = 40-50 y/o
Eti - idiopathic
Pathophys - excessive buildup of endolymph in labyrinth of inner ear
→ endolymphatic hydrops i.e higher endolymph pressure than normal
→ sensory signals = disrupted
SSX = u/l tinnitus + hearing loss + vertigo
→ SSX last for 20 mins
Ix’s
- clinical diagnosis by ENT
- audiology assess’nt to evaluate hearing loss
Lifestyle Δs
- smoking cessa’n
- limiting dietary salt
- limiting caffeine intake
- should ↓ alcohol consump’n
Tx = prochlorperazine + β histine for Ppx
- Know for OSCE *
Presbycusis ✓
Def - age related gradual + symmetrical sensorineural hearing loss
RFs
- male
- old age
- FHx
- exposure to loud noise
- diabetes
- smoking
- HTN
Eti - loss of neurons + hair cells in cochlea
SSX = gradual + symmetrical hearing loss
→ high frequencies = affected first
Diagnostic Ix = audiogram → will show a sloping high frequency hearing loss
Tx
- avoiding loud noise
- hearing aids → cochlear implants
Acoustic neuroma / Vestibular schwannoma ✓
Def - benign les’n of Schwan cells of vestibular por’n of CN 8
→ as tumor grows, can press on other CNs as well such as CN 7
→ usually u/l but tumor = b/l it means that pt has neurofibromatosis type II
RFs = 40-60 y/o + neurofibromatosis
SSX
- u/l sensorineural hearing loss (usually = 1st SSX)
- ul tinnitus
- dizziness or lack of balance
- ataxia
- CN 5 SSX = absent corneal reflex
- CN 7 SSX = facial palsy
Ix’s
- brain MRI w/ contrast for diagnosis → enlarged internal acoustic meatus
- audiometry to assess hearing loss → sensorineural hearing loss
Tx for grade 1
1- observa’n
2- radia’n or Sx
Tx for grade 2-3 + < 3 cm = radia’n or Sx
Tx for grade 4 or > 3 cm = Sx
Complica’ns of Sx
- vestibulocochlear nerve injury → permanent hearing loss or dizziness
- facial nerve injury → facial weakness
- Know for OSCE *
Cholesteatoma ✓
Def - non cancerous accumula’n of squamous epithelial cells in middle ear
RFs
- ear Sx
- blast injury to ear
- middle ear disease
- congenital ear anomaly
- being born w/ cleft palate
- eustachian tube dysfunc’n
Eti = congenital or acquired
SSX
- foul smelling ear discharge
- u/l conductive hearing loss
- keratin crust in attic / upper part of middle ear on otoscopy
- dizziness if inner ear = also affected
Ix’s
- audiogram to asses hearing status
- CT head to confirm diagnosis → will show middle ear + mastoid opacifica’n
Tx = surgical removal of cholesteatoma
Complica’ns
- recurrence
- hearing loss
- bone eros’n
- Know for OSCE *
Otitis Media ✓
Def - middle ear bacterial infec’n, most commonly affects children + usually happens subsequent to a respiratory viral infec’n such as RSV, influenza + adenovirus
RFs
- FHx
- lower SES
- young age
- lack of breastfeeding
Eti - usually caused by strep pneumoniae but can also be caused Hemophilus influenzae, Moraxella catarrhalis or Staph. aureus
SSX
- fever
- otalgia
- ↓ed hearing in affected ear
- myringitis i.e erythema of tympanic membrane (looks bulged + cloudy)
- might have cough + sore throat
⚠️ if there’s discharge from ear it means tympanic membrane = perforated !
Ix = otoscopy → will show bulging opacified tympanic membrane instead of being pearly-grey translucent as it should
Tx = Tylenol / ibuprofen for pain + fever b/c most otitis media cases will resolve spontaneously w/in 3-7 days
→ 5-7 days of amoxicillin for those who are systemically unwell, have otorrhea, or < 2 y/o w/ b/l otitis media
Complica’ns
- mastoiditis (very rare)
- tympanic membrane perfora’n
- effus’n → must be treated b/c can cause speech / hearing impairment
⟹ Tx = grommet in anterior inferior tympanic membrane to drain fluid
- Know for OSCE *
Otitis Externa ✓
Def - inflamma’n of external ear canal, also known as “swimmer’s ear”
RFs
- swimming
- trauma to ear
- diabetes
- humid env’nt
- ear canal obstruc’n
- excessive ear wax removal (protects against infec’ns)
Eti
- bacterial infec’n (pseudomonas aeruginosa or staph. aureus)
- fungal infec’n (aspergillus or candida)
- eczema
- contact dermatitis
SSX
- ear pain
- otorhea
- itchiness
- conductive hearing loss if ear becomes blocked
Findings on exam
- erythema + swelling in ear canal
- tenderness of ear canal
- pus or discharge in ear canal
- neck lymphadenopathy
Ix = otoscopy for clinical diagnosis
Tx for mild = 2% acetic acid
Tx for severe = steroid + topical aminoglycoside Abx such as neomycin or gentamicin
⚠️ Aminoglycoside Abx = Ψly ototoxic ∴ must exclude perforated tympanic membrane before prescribing it for otitis externa !
Tx for fungal = clotrimazole otic drops
- Know for OSCE *
UK childhood vaccine schedule (those capitalized = live vaccines except HPV) ✓
- all vaccines prior to 3 y/o = 2 doses except 6 in 1 + MenB = 3 doses
2 months
- 6 in 1 (diphtheria, polio, tetanus, pertussis, Hib, HepB) dose 1/3
- ROTAVIRUS dose 1/2
- MenB dose 1/3
3 months
- 6 in 1 dose 2/3
- ROTAVIRUS dose 2/2
- Pneumococcal/PCV dose 1/2
4 months
- 6 in 1 dose 3/3
- MenB dose 2/3
1y/o
- Hib/MenC
- MMR dose 1/2
- Pneumococcal/PCV dose 2/2
- MenB dose 3/3
2-10y/o
FLU shot every yr
3 y/o
- MMR dose 2/2
- 4 in 1 preschool booster (diphtheria, pertussis, polio, tetanus)
12-13 y/o
- HPV (greatest RF for cervical cancer)
→ vaccine protects against strains 6, 11, 16 + 18
⟹ strains 6 + 11 cause genital warts, whereas 16 + 18 ↑ risk of oropharyngeal cancer, cervical cancer, anal cancer, penile cancer + vulval cancer
14 y/o
- 3 in 1 teenage booster (diphtheria, polio, tetanus)
- MenACWY
Vaccine C/Is ✓
- Live vaccines if pt = pregnant or immunocompromised
- anaphylactic rxn to previous dose or vaccine component
“MOPS” ✓
= the 4 diseases in children that pneumoccoccal vaccine protects against
- Meningitis
- Otitis media
- Pneumonia
- Sinusitis
Pediatric Normal HR + RR ✓
< 1 y/o
- HR → 100-180
- RR → 30-55
1-2 y/o
- HR → 90-140
- RR → 20-40
3-5 y/o
- HR → 80-120
- RR → 20-30
6-9 y/o
- HR → 75–120
- RR → 18-25
Infectious Mono ✓
Def - oropharynx infec’n caused by EBV
→ incuba’n period = 3-7 wks
→ route of transmiss’n = saliva i.e by kissing or sharing cups / toothbrushes
RFs
- sex
- kissing
Eti = EBV → infects B lymphocytes in oropharynx
SSX
- fever
- fatigue
- sore throat
- splenomegaly
- lymphadenopathy
- tonsillar enlargement
- causes intensely itchy maculopapular rash in response to amoxicillin or cefalosporins
Ix’s
- FBC → lymphocytosis
- heterophile antibodies (not specific for EBV)
via Monospot or Paul-Bunnell test → will be +ve - EBV specific antibodies → will be +ve if due to EBV → +ve IgM antibody suggests acute infec’n
→ +ve IgG antibody suggests immunity i.e already had disease - LFTs → will be elevated
Tx = self limiting
Mx
- avoid alcohol b/c EBV impacts liver’s ability to process alcohol
- avoid contact sports due to risk of splenic rupture
Complica’ns
- splenic rupture
- glomerulonephritis
- hemolytic anemia
- thrombocytopenia
- chronic fatigue
- Know for OSCE *
Rhinosinusitis ✓
Def - inflamma’n of mucosal lining of nasal cavity + paranasal sinuses
→ SSX < 10 days = viral
→ 10 days < SSX < 4 wks = bacterial
RFs
- viral URTI
- allergic rhinitis
Eti - usually viral but can also be due to bacterial infec’n
SSX
- nasal discharge
- nasal obstruc’n
- facial pain
Ix = clinical diagnosis + sinus culture
Tx = Abx for bacterial + self limiting for viral
Complica’ns
- chronic sinusitis
- cavernous sinus thrombosis
- Know it for OSCE *
Epistaxis ✓
Def - nosebleed (usually u/l)
→ most common loca’n of bleed = Kiesselbach’s plexus in Little’s area = nasal mucosa @ front of nasal cavity w/ lots of blood vessels
RFs
- dry weather
- nasal trauma
Triggers
- nose picking
- colds
- sinusitis
- vigorous nose blowing
- trauma
- Δ in weather
- anticoagulant
- snorting cocaine
Ix = clinical diagnosis
Tx
1. Tell pt to tilt their head forward
2. Pinch soft part of nose for 10-15 mins
3. Tell pt to spit out any blood in their mouth
4. If bleeding doesn’t stop after 10-15 mins . . .
→ electrocautery or cautery w/ AgNO3 sticks for minor bleeding from an accessible site
→ anterior or posterior nasal packing w/ nasal tampons for profuse bleeding from site that is difficult to localize
5. Consider reversing INR
6. After bleed consider prescribing Naseptin nasal cream to ↓ crusting, inflamma’n + infec’n
→ C/I = soy or peanut allergy
Laryngitis ✓
Def - inflamma’n of larynx
RFs
- recent URTI
- tobbacco use
- immunocompromised
- contact w/ infected person
- incomplete or absent Hib vaccine
Eti
- viral
- fungal
- bacterial
- autoimmune
- irritant / toxin
- trauma such as heavy vocal use
SSX
- cough
- sore throat
- hoarse voice
- dysphagia
- odynophagia
Ix = largynoscopy + culture
Tx = phenoxymethylpenicillin if due to bacteria
Complica’n = compromised airway
- Know for OSCE *
Croup / Viral Laryngitis (URTI in kids) ✓
→ mainly occurs in pts 6 months - 6 y/o
Eti = parainfluenza virus (types 1 or 3)
SSX
- barking seal cough
- hoarse voice
- stridor (in moderate ~ severe croup)
- labored breathing
- low grade fever
Ix = clinical exam but will see Steeple sign (subglottic narrowing) on PA CXR
Tx = single dose dexamethasone → add nebulized adrenaline if pt has stridor
Admit if pt < 3 months or if uncertain about diagnosis
- Know for OSCE *
Epiglottitis (URTI in kids) ✓
Def - inflamma’n of epiglottis due to infec’n = medical emergency !
→ rare nowadays thnx to Hemophilus influenzae B vaccine
RFs
- immunocompromised
- didn’t get Hib vaccine
Eti = Hib
SSX
- high fever
- drooling
- dysphonia
- dysphagia
- tripod posi’n
- stridor
- sore throat
Ddx
- croup
- tonsillitis
- foreign body aspira’n
Ix = lateral X-ray of neck to r/o foreign body → will show characteristic thumbprint sign
⚠️ Don’t waste time w/ Ix’s if pt = unwell, just treat !
Tx
1. Alert senior pediatrician + anesthesiologist
2. Ensure airway = secure
3. Steroid such as dexamethasone + IV Abx such as CTX once airway = secured
Prognosis - most pts will not require intuba’n
Complica’n = epiglottic abscess
- Know for OSCE *
Tonsilitis (URTI in kids) ✓
Def - inflamma’n of tonsils (of palatine tonsils usually) due to infec’n (usually viral)
→ palatine tonsils = on each side @ back of throat
→ usually occurs in children
RFs
- 5-15 y/o
- contact w/ infected ppl
Eti
- virus (self-limiting)
- Strep A when due to bacterial infec’n
SSX
- odynophagia
- swollen anterior cervical lymph nodes
- red, inflamed + enlarged tonsils w/ or w/o tonsillar exudate = white patches of pus on tonsils
Ix’s
- Centor criteria (alternative = FeverPAIN score) to see if due to bacteria
→ 1 point if pt has that SSX, ttl score ≥ 3 = 40- 60 % prob that bacteria = cause . . . (“FATT”)
⟹ Fever > 38ºC
⟹ Absence of cough
⟹ Tonsillar exudate
⟹ Tender anterior cervical lymph nodes - RADT or throat culture
Tx for viral = paracetamol + ibuprofen to control pain + fever
→ tell pt to return pain hasn’t stopped after 3 days or if fever ↑ above 38.3ºC
Tx for bacterial = penicillin V / phenoxymethylpenicillin for 10 days
→ clarithromycin instead if pt has penicillin allergy
Complica’ns
- quincy i.e peritonsillar abscess
→ Tx = needle aspira’n by ENT
- scarlet fever
- rheumatic fever
- post streptococcal glomerulonephritis
- post streptococcal reactive arthritis
- otitis media if infec’n spreads to inner ear
- Know for OSCE *
What is trismus ? ✓
When pt has difficulty opening jaw
Bronchiolitis (URTI in children) ✓
Def - infec’n + inflamma’n of bronchioles (small airways of lungs)
→ most common in pts < 6 months old
→ leading cause of hospital admiss’n for pts < 1y/o
RFs
- winter
- air pollu’n
- prematurity
- passive tobacco smoke exposure
- immunodeficiency
Eti - RSV usually
SSX
- cough
- coryzal symptoms i.e UTRI SSX = runny nose, sneezing, mucus in throat + watery eyes
- dyspnea
- tachypnea
- expiratory wheeze + crackles on ausculta’n
- SSX of pediatric respiratory distress i.e . . .
→ cyanosis
→ grunting
→ nasal flaring
→ tracheal tugging
→ use of accessory muscles of respira’n
→ intercostal / subcostal recess’ns
Indica’ns to admit pt . . .
- CF
< 3 months old
- RR > 70
- premature
- O2 sat < 92%
- Down syndrome
- moderate-severe respiratory distress
- clinical SSX of dehydra’n
≥ 50% ↓ in milk intake
- apneas i.e episodes where pt stops breathing
Ddx
- CF
- croup
- asthma
- pneumonia
Ix = clinical diagnosis + pulse oximetry to check for hypoxemia
Tx = self limiting → SSX usually last 7-10 days ttl + most pts fully recover w/in 2-3 wks
Mx
- starting w/small frequent feeds + then gradually ↑ing
- saline nasal drops + nasal suc’ning of nasal secre’ns (especially before they feed)
Ventilatory support if needed
- High-flow humidified O2 via tight nasal cannula
→ delivers air +O2 continuously w/ some added pressure → +ve end-expiratory pressure (PEEP) helps to maintain airway @ end of expira’n + prevent lung collapse - CPAP - also involves using sealed nasal cannula but delivers much higher + more controlled pressures
- Intuba’n + ventila’n → involves inserting endotracheal tube in trachea
⟹ monitor these pts w/ capillary blood gases
RSV ppx for high risk pts such as congenital heart disease or born premature
→ monthly injec’ns of palivizumab
Complica’ns
- recurrent wheezing
- cough may persist even after infec’n resolves
- Know for OSCE *
Pertussis / Whooping Cough (URTI in kids) ✓
Def - URTI caused by Bordetella pertussis = gram -ve bacteria = NOTIFIABLE DISEASE !
RFs
- unvaccinated
- close contact w/ infected person
SSX chronology
1. mild coryzal SSX + low grade fever +/- mild dry cough
2. severe paroxysmal coughing (i.e in waves) 1 wk later
Ddx
- TB
- pneumonia
- foreign body aspira’n
Ix’s
- nasal or nasopharyngeal or nasal swab w/ PCR or bacterial culture for diagnosis
→ should be done w/in 2-3 wks of SSX onset
- anti-pertussis toxin Ig G if cough has been present for > 2 wks
→ from oral fluid or from blood instead if pt > 17 y/o
Tx
- macrolide Abx such as azithromycin → SSX should resolve w/in 2 months
- Abx Ppx for close contacts of infected patient IF are part of vulnerable popula’n i.e . . .
→ pregnant
→ unvaccinated infant
→ healthcare workers that have contact w/ children or pregnant women
Complica’ns
- vomiting, fainting, pneumothorax due to severe coughing
- bronchiectasis
Ddx of red eye ✓
Painful red eye = all the “itis” except conjunctivitis + episcleritis
- acute angle closure glaucoma
- scleritis
- anterior uveitis
- corneal abras’n or ulcera’n
- keratitis
- foreign body in eye
- traumatic or chemical injury
Painless red eye
- conjunctivitis (red all around eye)
- episcleritis (small sec’n of red)
- subconjunctival hemorrhage (bright red in corner of eye + no irrita’n)
Conjunctivitis ✓
Def - inflamma’n of conjuntiva
⚠️ DOES NOT cause eye pain, photophobia or ↓ed visual acuity
RFs
- contact lens use
- allergen exposure
- exposure to irritant
- exposure to infected person
- 1 eye that’s already infected
- mechanical / UV light / chemical trauma
Eti
- bacterial or viral (adenovirus usually if viral)
- allergic conjunctivitis = seasonal or related to exposure to allergen
SSX (u/l or b/l)
- red, itchy eye
- eyelids stuck together in the morning
- pre auricular lymphadenopathy in viral
- b/l swelling of conjunctival sac + eyelid + watery discharge in allergic
Ix’s
- clinical diagnosis
- rapid adenovirus immunoassay → 2 lines means +ve → will be +ve in viral
Tx for allergic olopatadine / opatanol eye drops + mast cell stabilizer
→ MOA of olopatadine / opatanol = antihistamine / selective H1 receptor antagonist
Tx for viral or mild bacterial = usually self-limiting w/in 1-2 wks so just hygiene measures i.e . . .
- regular hand washing
- avoiding towel sharing + close contact w/ others
Addi’nal Tx for severe bacterial = chloramphenicol or fusidic acid eye drops
⚠️ Neonatal conjunctivitis i.e conjunctivitis in pt < 1 month old requires urgent ophtho assess’nt b/c can cause permanent vis’n loss !
- Know it for OSCE *
Periobrbital + orbital cellulitis ✓
- periorbital cellulitis = infec’n of eyelid tissues superficial to orbital septum
→ in children can rapidly progress to orbital cellulitis - orbital cellulitis = involv’nt of tissues BEHIND orbital septum = medical emergency !
RFs
- sinusitis
- male + young
- lack of Hib vaccine
Eti = sinusitis (b/c can spread from ethmoid sinuses)
SSX for periorbital = swollen, red, hot skin around eyelid + eye
SSX for orbital
- pain w/ eye mov’nt
- ↓ed eye mov’ts
- vis’n Δs
- abnormal pupil rxn
- proptosis
Ix’s
- clinical diagnosis
- CT to distinguis btw orbital + periorbital
- FBC → elevated neutrophils
Emergency Tx for orbital cellulitis = IV CTX
→ surgical drainage if abscess forms
- Know for OSCE *
Glaucoma ✓
Acute angle closure glaucoma
Def - acute ↑ in IOP = ophthalmological emergency b/c can lead to permanent vis’n los !
RFs
- FHx
- old age
- shallow anterior chamber
- Chinese / East Asian ethnicity
- female (4x more likely than men)
Eti
- 1°
- 2° to underlying eye disease
- drug induced i.e . . .
→ adrenergic drugs such as noradrenaline
→ anticholinergic medica’ns such as oxybutynin
→ TCAs
Pathophys - iris bulges forward + seals off trabecular meshwork from anterior chamber ∴ preventing drainage of aqueous humour → ↑in IOP
SSX
- severely painful red eye
- blurry vis’n
- seeing halos around lights
- HA
- N+V
SSX on exam
- hazy cornea
- ↓ed visual acuity
- mid-dilated pupil
- fixed-size pupil
- hard eyeball on gentle palpa’n
Ix for both =
- slit lamp exam to check cup disc ratio + optic nerve health → in open angle will show cupping i.e cup disc ratio > 0.5
- goldmann applana’n tonometry to measure IOP → will be > 21
- visual field assess’nt to check for peripheral vis’n loss
- gonioscopy to assess angle btw iris + cornea to distinguish btw acute + open → trabecular meshwork will NOT be visible in acute due to obstruc’n v.s no obstruc’n in open
- central corneal thickness assess’nt
Emergency Tx
1. Lie pt on their back w/o a pillow
→ pilocarpine eye drops (2% for blue eyes + 4% for brown eyes) → oral
acetazolamide
2. Laser iridotomy - small hole = created in iris ∴ allowing aqueous humour to flow through
⟹ MOA of pilocarpine - causes ciliary muscle contrac’n + acts on muscarinic receptors in iris sphincter muscles to cause pupil constric’n ∴ moving iris away from trabecular meshwork
⟹ MOA of acetazolamide = carbonic anhydrase inhibitor ∴ ↓ aqueous humour produc’n
Complica’ns
- retinal vein occlus’n
- permanent vis’n loss
- permanent ↓ in visual acuity
Open angle glaucoma
Def - ↑ in IOP due to progressive degenera’n of optic nerve fibers = most common type of glaucoma
RFs
- FHx
- black
- old age
- myopia
Pathophys - gradual ↑ in resistance to flow through the trabecular meshwork → pressure slowly builds w/in eye
SSX - asymptomatic for a long time ∴ is usually diagnosed incidentally during eye check up
Tx if IOP ≥ 24
- 360° selective laser trabeculoplasty
→ 2nd procedure may be needed later on but this will at least delay or prevent need for eye drops - Latanoprost eye drops (PG analog) if trabeculopasty failed or = contraindicated
→ MOA - ↑ uveoscleral outflow
→ side effects - eyelash growth, eyelid + iris pigmenta’n (iris will become more brown) - Other eye drops to ↓ aqueous humor produc’n such as CA inhibitor or timolol = β blocker
- Trabulectomy
Complica’n = vis’n loss
- Know both for OSCE *
Keratitis ✓
Def - inflamma’n of cornea = ocular emergency !
→ most common cause = HSV
RFs
- corneal trauma
- corneal abras’n / eros’n
- immunocompromised
- contact lens wear (these pts can get acanthamoeba keratitis)
Eti
- viral infec’n (HSV usually)
- bacterial infec’n (Pseudomonas or Staph.)
- fungal infec’n (Candida or Aspergillus)
- CLARE (contact lens induced acute red eye)
- exposure keratitis = caused by inadequate eyelid coverage
SSX in 1st time
- red eye
- blurry vis’n
- light sensitivity
- tearing of the eye
- foreign body sensa’n
SSX in recurrence
- painful red eye
- photophobia
- vesicles
- foreign body sensa’n
- watery discharge
- ↓ed visual acuity
Ix’s
- diagnostic Ix = slit lit exam
→ fluorescein dye → will appear green → means there are dendritic corneal ulcers - MCS of corneal scrapings
- urgent ophthalmology referral
Tx for viral = aciclovir 3% eye ointment 5x/day for 10-14 days + for ≥ 3 more days once there’s apparent healing
Tx for bacterial = tobramycin or gentamicin fortified eye drops
Complica’ns
- perfora’n
- endophthalmitis
- corneal scarring (can cause vis’n impairement)
⟹ Tx = prednisolone eye drop → corneal transplant
- Know for OSCE *
Uveitis ✓
Def - inflamma’n of uvea i.e iris, ciliary body + choroid
→ anterior uveitis = most common type = inflamma’n in anterior chamber
RFs
- HLA-B27 arthropathies ( i.e “PAIR”)
- MS
- TB
- HSV
- VZV
- syphilis
- sarcoidosis
Eti
- infectious = due to TB, HSV, VZV, syphilis, Lyme disease
- autoimmune = due to sarcoidosis / MS
Types
- anterior uveitis = inflamma’n of iris and/or ciliary body
- intermediate uveitis = inflamma’n of area behind ciliary body
- posterior uveitis = inflamma’n of choroid + retina
SSX
- painful red eye (dull, aching pain)
- photophobia due to ciliary muscle spasm
- ↓ed visual acuity
- epiphora i.e excessive lacrima’n
SSX on exam
- miosis (due to sphincter muscle contrac’n)
- ciliary flush i.e ring of red spreading from cornea outwards
- abnormally shaped pupil due to posterior synechiae (adhes’ns) pulling iris
- hypopyon = white fluid in anterior chamber that contains inflammatory cells
Ix = clinical diagnosis
Tx
- ophtho referral
- corticosteroid eye drops to ↓ inflamma’n
- cycloplegic eye drops such as cyclopentolate or atropine → paralyze ciliary body which relieves pain + also helps to prevent adhes’ns btw iris + lens
⟹ cyclopentolate or atropine = antimuscarinic ∴ inhibit iris sphincter muscles + ciliary muscles - antimicrobial drugs for infectious causes
Complica’ns (aim of Tx = to ↓ inflamma’n + avoid these complica’ns . . .)
- adhes’ns
- ↑ed risk of glaucoma
- cataracts
- vis’n loss
- Know for OSCE *
Scleritis ✓
Def - inflamma’n of sclera (visible white part of eye)
→ requires immediate referral to ophthalmologist via emergency eye clinic
→ most severe type = necrotizing scleritis b/c can cause scleral perfora’n
RF = female
Eti
- idiopathic
- 2° to underlying systemic inflammatory condin such as RA or granulomatosis w/ polyangiitis
- 2° to pseudomonas or staph. aureus infce’n (less common)
SSX = gradual onset (can be u/l or b/l)
- red, inflamed, tender sclera
- congested vessels
- severe pain
- pain w/ eye mov’nt
- photophobia
- epiphora
- ↓ed visual acuity
Tx
- ophtho referral
- treat underlying cause
Ddx of painless ↓ in visual acuity w/ no red eye ✓
- CRVO
- CRAO → sudden vis’n loss + afferent pupillary defect
- retinal detach’nt → shadow in vis’n
- AMD → gradual central vis’n loss, scotoma, metamorphopsia
Retinal detach’nt ✓
Def - painless condi’n where neurosensory layer of retina (contains nerves + photoreceptors) separates from retinal pigment epithelium (base layer attached to choroid) = medical emergency b/c since neurosensory retina relies on blood vessels of choroid for its blood supply, pt can lose their vis’n
RFs
- FHx
- trauma
- lattice degenera’n = thinning of retina
- posterior vitreous detachment
- diabetic retinopathy
- retinal malignancy
Classifica’n based on Eti
- rhegmatogenous = most common type = due to retinal tear
- trac’nal = due to scar tissue on retina puling retina away from back of eye
- exudative = due to fluid buildup b/c of . . .
→ AMD
→ tumor in eye
→ injury or trauma to eye
→ inflammatory eye condi’n
Pathophys - Eti → above layers separate vitreous fluid fills space btw layers → blood supply = disrupted → permanent damage to photoreceptors
SSX
- painless peripheral vis’n loss → pt might describe it as a shadow in their vis’n
- blurry or distorted vis’n
- flashes + floaters in vis’n
Ddx of painless vis’n loss w/o red eye
- retinal detach’nt
- CRVO / CRAO
- vitreous hemorrhage due to diabetic retinopathy
Ix’s
- visual acuity testing → ↓ed visual acuity
- slit lamp exam → will show retinal break
- indirect ophthalmoscopy → will show retinal break
- ophthalmology referral
- Tx for rhegmatogenous = pneumatic retinopexy / scleral buckle and/or vitrectomy
- Tx for trac’nal = vitrectomy
- Tx for exudative = treat underlying cause
- Know for OSCE *
Retinal vein occlus’n (CRVO) ✓
RFs
- HTN
- diabetes
- smoking
- high cholesterol
- high plasma viscosity such as in MM
- myeloproliferative disorders
- inflammatory condi’ns such as SLE
Pathophys - thrombus forms in retinal veins ∴ blocking drainage of blood from retina
Types
→ branch = thrombus forms in branch retinal veins
⟹ only specific area drained by that branch = affected
→ central = thrombus forms in central retinal vein
⟹ whole retina = affected
SSX
- painless blurry vis’n or vis’n loss for branch
- central vis’n loss if macula was an affected area
Ddx of painless vis’n loss w/o red eye
- retinal detach’nt
- CRVO
- central retinal artery occlus’n, central retinal vein occlusion
- vitreous haemorrhage due to diabetic retinopathy
Ix’s
- fundoscopy → 5 specific features (features will be present in all 4 quadrants in central !) . . .
- retinal edema / optic disc swelling
- cotton wool spots
- hard exudates
- dilated tortuous retinal veins
- widespread flame + dot hemorrhages i.e “stormy sunset” appearance
- fluorescein angiogram for confirma’n of diagnosis
→ will show areas of blocked fluorescence + delayed venous filling during transit phase - ophtho referral
Tx for CRVO w/o maculoedema = observing + managing RFs → intravitreal ranibizumab = VGEF inhibitor
Tx for CRVO w/ maculoedema = intravitreal dexamethasone
Tx if there’s neovasculariza’n = laser photocoagula’n
Complica’ns
- vis’n loss
- vitreous hemorrhage
- Know for OSCE *
Central retinal artery occlus’n (CRAO) ✓
Def - occlus’n of central retinal artery = branch of ophthalmic artery, which is a branch of internal carotid = vis’n threatening emergency !
RFs
- CVD RFs
- GCA RFs
Eti = GCA or atherosclerosis
→ atherosclerosis = most common cause
SSX
- sudden painless vis’n loss of vision → can be described as like a curtain coming down over vis’n
+ve RAPD i.e > constric’n of affected eye when light is shined on other eye compared to when light is shined on itself
Ddx of painless vis’n loss w/o red eye
- retinal detach’nt
- CRVO
- central retinal artery occlus’n, central retinal vein occlusion
- vitreous hemorrhage due to diabetic retinopathy
Ix = fundoscopy → will show pale retina w/ a cherry red spot @ macula
⟹ retina = pale due to lack of perfu’n + cherry red spot = fovea
Emergency Tx = resolving blockage via . . .
- ocular massage
- anterior chamber paracentesis
- sublingual isosorbide dinitrate to dilate artery
- oral pentoxifylline to dilate artery
- IV acetazolamide or IV mannitol to ↓ IOP
Long term Mx = treating modifiable RFs
Complica’n = vis’n loss
- Know for OSCE *
Subconjunctival hemorrhage ✓
Def - when small blood vessel w/in conjunctiva ruptures ∴ releasing blood into space btw sclera + conjunctiva
→ often appear after trauma to the eye or after episodes of strenuous activity, such as heavy coughing, weight lifting or straining when constipated
RFs
- HTN
- non accidental injury
- whooping cough
- bleeding disorders such as thrombocytopenia
- medica’ns that can cause bleeding i.e antiplatelets, DOACs, warfarin
Eti - idiopathic
SSX = painless bright red blood underneath conjunctiva w/ no visual impairment
Ix = clinical diagnosis
Tx - nothing b/c = harmless + will resolve spontaneously in around 2 wks
→ lubricating eye drops can be used if there’s mild irrita’n
Age-related Macular Degenera’n (AMD) ✓
Def - progressive condi’n affecting the macula
→ most common cause of blindness in the UK
→ usually u/l but can be b/l
RFs
- FHX
- smoking
- older
- obesity
- CVD such as HTN
Types
- wet (neovascular)
- dry (non-neovascular) = more common
Pathophys of wet - abnormal angiogenesis in macula → those abnormal new blood vessels leak ∴ causing fluid accumula’n, hemorrhage + fibrosis which can lead to rapid central vis’n loss
SSX (wet presents more acutely)
- ↓ed visual acuity (hence affecting everyday tasks like reading or driving)
- gradual central vis’n loss
- scotoma i.e enlarged central area of vis’n loss
- metamorphopsia = straight lines look wavy or crooked
Ix’s
- optical coherence tomography → gives cross-sec’nal view of retinal layers = for diagnosis + monitoring
- Fluorescein angiography → in wet AMD will show edema + neovasculariza’n
- Snellen chart → ↓ed visual acuity
- Amsler grid (also used to monitor SSX)
→ metamorphopsia - fundoscopy → Drusen = yellowish deposits of proteins + lipids btw retinal pigment epithelium + Bruch’s membrane
⟹ small amt in old person = normal but large amt = suggestive of AMD - slit lamp exam
Tx for wet = ophtho referral → anti-VEGF intravitreal injec’ns once / month
- Know for OSCE *
Blepharitis ✓
Def - inflamma’n of eyelid margins
Types
→ anterior
→ posterior
Eti for anterior = Staph. epidermid eyelid infec’n
Eti for posterior = Meibomian gland dysfunc’n
→ Meibomian glands = responsible for secreting meibum (oil) on eye
SSX
- b/l burning sensa’n in eyes
- b/l itching sensa’n in eyes
- b/l eyelid crusting
- b/l dry eyes
Ddx = malignancy
Ix’s
- lid Bx to r/o malignancy
- lid margin culture to identify causative pathogen
- microscopic evalua’n of epilated eyelashes to check if there are demodex mites
Tx = warm compresses + gentle cleaning of eyelid margins to remove debris
- Know for OSCE *
Cataracts ✓
Def - gradual opacifica’n / clouding of lens due to denatura’n + accumula’n of lens protein
→ mainly affects old ppl
→ each eye = affected differently ∴ SSX are usually asymmetrical
RFs = “PADS”
- Prolonged corticosteroid use
- AGE
- Diabetes mellitus and/or HTN
- Smoking + Alcohol
Causes = “C DATED”
- Congenital (screened for @ birth w/ red reflex test)
- Drugs especially steroids
- Age
- Trauma
- Eye disease / eye Sx
- Diabetes
SSX
- slow ↓ in visual acuity
- progressive blurry vis’n
- colors becoming more faded or more yellow or brown
- starbursts / glares around lights especially @ night
Ddx = glaucoma
Ix
- glare test → will show ↓ed visual acuity under glare
- slit lamp exam for diagnosis → will, show cataract
- ophthalmoscopy → loss of red reflex w/ normal fundus + optic nerve
- IOP → will be normal
Tx = treat modifiable RFs → surgically remove cloudy lens + replace by artificial / acrylic lens
Complica’n of cataract Sx = endophthalmitis = inflamma’n of inner contents of eye (usually due to an infec’n) → can lead to vis’n loss
⟹ Tx = intravitreal Abx
- Know for OSCE *
Tx for various drug overdoses ✓
- Tx for opioid overdose of such as heroin overdose = naloxone (initial dose = 0.4 mg IV + repeat every 2-3 mins until pt improves)
→ MOA - competitive opioid antagonist
→ side effects - anxiety, aggress’n, N + V, diarrhea, abdo. pain + rhinorrhea - Tx for amphetamine or cocaine overdose = benzodiazepines to prevent seizures
- Know for OSCE *
Cocaine induced ACS ✓
SSX
- chest pain
- sweating
- tachycardia
Pathophys = cocaine causes coronary artery spasm
Ix = ECG → will show sinus tachycardia w/ ST eleva’n in lateral leads +/- ventricular ectopics
Depress’n ✓
Def - mood disorder characterized by persistent low mood + loss of interest
RFs
- low SES
- female sex
- major life event(s) / trauma
SSX
- Sleep ↓
- Interest ↓
- Guilt ↑
- E ↑/ ↓
- [ ] ↓
- Appetite ↑/↓
- Psychomotor agita’n
- Suicidal idea’n
Diagnostic criteria . . .
- Pt must experience ≥ 5 depressive SSX including ≥ 1 core SSX (i.e low mood/sad, loss of interest or fatigue/low E)
- SSX must be present at least most days for ≥ 2 wks
Tx
- SSRI such as Sertraline (Selective Serotonin Reuptake Inhibitor) → MOA- inhibits SERT @ pre-synaptic terminal which is a serotonin transporter ∴ inhibits re-uptake of serotonin which ↑ amt of serotonin remaining in synaptic cleft
→ C/I’s = MAO-B’s, linezolid (b/c also ↑ serotonin levels which can cause serotonin syndrome = life threatening), triptains + pregnancy b/c = teratogenic
→ side effects = nausea, HA, sexual dysfunc’n, anxiety initially
→ monitoring - initial f/u after 2 wks U+E before prescribing + then yrly
→ pt will be on it for ~ 9 months then will be tapered off
→ end in “TINE” (except duloxetine) or “PRAM” - Venlafaxine = SNRI (Serotonin / Norepinephrine Reuptake Inhibitor)
→ MOA- blocks serotonin + NE transporters ∴ inhibits their reuptake
→ C/I’s = SSRIs, MAOI’s, TCAs + psychotics
→ side effects = HTN, HA, bone reabsorp’n, diaphoresis (excessive sweating) + widening of QRS complex
→ ends in “PRAN” or “XINE”
3.
- TCA (Tricylic Antidepressants) → block muscarinic receptors for Ach
→ C/I’s = SNRIs, FHx of sudden cardiac death or prolonged QT interval + closed angle glaucoma
→ side effects = para inhibited so dry mouth, blurred vis’n, urinary reten’n + constipa’n as well as QRS prolonga’n, seizures + orthostatic hypoTN
→ end in “TYLINE”
⚠️ TCA overdose can cause QRS prologa’n
⟹ Tx = IV Na Bicarb - MAO B inhibitors → block monoamine oxidase which breaks down dopamine, serotonin + NE so by inhibiting it, their levels can ↑
→ C/I’s = SSRI / SNRI
→ side effects = HA, dyskinesia, postural hypoTN, psychological disorders + QRS prolonga’n
→ end in “GILINE”
Complica’n = psychotic depress’n
→ usually presents as a distorted percep’n of reality
Important info to give to pts starting an anti-depressant ✓
- More likely to commit suicide in 1st 4 wks of usage which is why 1 wk f/u = required for suicidal pt that just got started on antidepressant
- Can take up to 6 wks before they start seeing beneficial effects
The 4 indica’ns for ECT ✓
- Tx resistant depress’n
- catatonia i.e pt can’t eat, talk or move
- prolonged manic episode such as in manic phase of bipolar disorder or in pts who have mix of mania + depress’n
- pregnant pt @ high risk to commit suicide
Suicide ✓
RFs
- male
< 19 or > 45 y/o
- depress’n
- previous attempt
- alcohol / drug abuse
- loss of rational thinking
- lack of social support
- organized suicide plan
- chronic / debilitating illness
Risk assess’nt after attempt - pt attempted to take their life → ask about their feelings about having survived b/c if sad = @ high risk of attempting again but if happy about it = @ low risk of attempting again
GAD (Generalized Anxiety Disorder) ✓
Def - chronic, excessive worry which isn’t related to particular circumstances along w/ SSX of physiological arousal such as restlessness / insomnia / muscle TN
RFs
- FHx
- female
- substance abuse
- childhood trauma
- chronic pain and/or illness
Eti
- trauma
- genetic
- drugs / medica’n
- parenting style
Diagnostic criteria = anxiety for ≥ 6 months unrelated to another mental disorder + ≥ 3 of the following SSX . . .
- restlessness
- easily tired
- poor [ ]
- irritability
- muscle tens’n
- sleep pbs
Tx
1. Pharmacological interven’ns i.e SSRI / SNRI
2. Psychological interven’ns i.e CBT or interpersonal therapy
- Know it for OSCE *
Bipolar disorder ✓
Def - chronic + episodic mood disorder characterized by manic or hypomanic episodes
→ manic episode = persistently elevated or irritable mood + ↑ed E / way more talkative for ≥ 1 wk + func’nal impairment +/- psychosis
→ hypomanic episode = ≥ 4 days + no func’nal impairment + no pyschosis
RFs
- FHx
- substance abuse
- other mood disorders
- GAD
- childhood trauma
- stressful life events
- previous Hx of depress’n
Diagnostic criteria = too much E + ≥ 3 of the following or irritable mood + ≥ 4 of the following . . .
- fight of ideas i.e saying so much @ once + pt feels like their thoughts are too fast or them to keep up w/
- ↓ed need for sleep
- pressured / accelerated speech
- inflated self esteem / grandiosity
- more distracted than usual
- risk-seeking behavior i.e excessive shopping / having sex w/ everyone around them
Types
- Type 1 = ≥ 1 manic episode
- Type 2 = no manic episode but ≥ 1 hypomanic episode + ≥ 1 major depressive episode
Ix’s
- mood disorder questionnaire
- bipolarity index → will be +ve
Tx = mood stabilizers such as quetiapine, Li or lurasidone
→ Li side effects = nausea, abdo pain, metallic taste, tremor, polydipsia, polyuria
→ C/Is = pregnancy, breastfeeding, low Na diet
→ SSX of Li toxicity = ataxia, twitching
⚠️ Do not stop Li abruptly !
Complica’n = suicide
- Know it for OSCE *
Panic Disorder ✓
Def - recurrent unexpected panic attacks for ≥ 1 month (pt might be tachycardic during panic attack)
RFs
- female
- asthma
- smoking
- caffeine
- 18-39 y/o
- major life events
- FHx (1st ° relatives)
SSX of panic attack
- sudden excessive sweating
- dry mouth
- sensa’n of “butterflies” in stomach
- difficulty breathing
- feeling of impending doom
Ix = clinical diagnosis
Tx = psychotherapy
- Know it for OSCE *
OCD ✓
Def - persistent obsess’n / compuls’n that takes > 1 hr / day
RF = FHx
Ix = clinical diagnosis
Tx = psychotherapy
Complica’n = suicidal idea’n
Phobias ✓
Def - fear of a specific object or situa’n
= triggered by actual or anticipated exposure to stimulus
Ex’s
- agoraphobia = fear of being trapped / unable to escape
- social phobia = fear of social situa’ns or public speaking
RFs
- somatiza’n
- mood disorder
- axniety disorder
- FHx (in 1st ° relative, especially in twin)
Ix = self report
Tx = exposure + response preven’n CBT
PTSD / Acute stress rxn ✓
RFs
- low social support
- Hx of mental disorder
- drug / alcohol misuse
Eti
- war
- natural disaster
- serious accident
- victim of torture
- victim of sexual violence
- sudden loss of a loved one
SSX (SSX have to be for ≥ 1 yr for it to be PTSD or else it’s acute stress rxn)
Re-experiencing
- pain
- trembling
- flashbacks
- nightmares
- suddenly startled
Avoidance
- distracting themselves
- drug / alcohol / risky behavior
- emo’nally numbing themselves
- avoiding ppl or certain places / things
Hyperarousal
- insomnia
- difficulty [ ]ing
- anger outbursts
Tx = trauma focused CBT
Diagnostic criteria for Delus’nal disorder ✓
Persistent delus’n for ≥ 1 month that DOESN’T impact their daily func’ning
Diagnostic criteria for Brief psychotic disorder ✓
≥ 1 of the following SSX for 1 wk - 1 month max . . .
- delus’ns
- hallucina’ns
- disorganized speech
Diagnostic criteria for Schizoaffective disorder ✓
Uninterrupted period where pt has an episode of a mood disorder i.e manic episode or MDD + ≥ 1 of the brief psychotic disorder SSX + ≥ 2 of the following SSX . . .
- delus’ns
- hallucina’ns
- social w/drawal
- disorganized speech
- appearing flat / emo’nless
- lack of interest in social intera’n
Schizophrenia ✓
Def - significant altera’n in person’s thoughts, percep’n, mood + behavior
RF = FHx
Diagnostic criteria = ≥ 6 months of func’nal decline + ≥ 2 of the following SSX for ≥ 1 month (pt must have ≥ 1 +ve SSX) . . .
- hallucina’ns, delusn’s, disorganized thoughts / speech (+ve SSX)
- social w/drawal, lack of interest in social intera’n, appearing flat / emo’nless (-ve SSX)
Ix = clinical diagnosis
Tx
- Typical / 1st genera’n anti-pyschotics (not clozapine) or Atypical / 2nd genera’n
- Switch to diff typical / 1st genera’n anti-pyschotics (not clozapine) or atypical / 2nd genera’n
- Clozapine = associated w/ agranulocytosis ∴ pts need to get constant FBCs (usually occurs 6-18 wks after being started on it)
→ MOA of typical antipsychotics - dopamine receptor antagonists ∴ will ↓ synaptic activity of dopamine in substantia nigra
→ side effects - NMS due to extrapyramidal effects + side effects of not enough para
→ end in “ZINE”, includes haloperidol
⟹ SSX of NMS = “LEVER” . . .
- Lead pipe muscle rigidity i.e dystonia / hypertonia
- Encephalopathy i.e confus’n
- Vital signs high i.e fever, HTN, tachycardia + tachypnea
- Elevated CK b/c of rhabdomyolysis
- Rhabdomyolysis = when damaged muscle tissue release their proteins + electrolytes into blood = Ψly fatal !
→ MOA of atypical antipsychotics = serotonin-dopamine antagonists
→ side effects - weight gain (olanzapine especially)
→ PIP/ZIP in the middle OR end in “DONE”, “PINE” . . .
- risperidone (associated w/ hyperprolactinemia)
- quetiapine (associated w/ somnolence)
- olanzapine
- clozapine
- Know for OSCE *
Avoidant v.s Schizoid personality disorder ✓
Avoidant
- feelings of inadequacy
- hypersensitivity to criticism
- strong desire for affec’n + acceptance
- pts tend to avoid social situa’ns + have few close rela’nships
- often rely heavily on a single
attach’nt figure
- can experience physical SSX such as
headaches / stomach aches in stressful situa’ns
Schizoid
- limited emo’nal express’n
- prefer solitary activities
- have little to no interest in
forming close interpersonal connec’ns
- prefer activities that involve little to no social interac’n
Stroke ✓
RFs
> 65 y/o
- FHx
- HTN
- HLD
- diabetes
- smoking
- frequent falls + connective tissue disorders for hemorrhagic
Types
- Ischemic = ↓ in blood supply causing focal neurological deficits for > 24 hrs due to occlus’n by embolus / thrombus or low systemic pressure i.e hypo-perfus’n = 80% of strokes
→ Pathophys of ischemic - rupture of atherosclerotic plaque in an internal carotid artery → thrombus forma’n at this site → detach’nt of thrombus + emboliza’n of a cerebral artery → sudden occlus’n of that cerebral artery → abrupt ↓ blood flow to particular locus of brain that artery supplies → infarc’n of that area
- Hemorrhagic = neural damage due to intracranial bleeding = 20% of strokes
→ extradural hemorrhage (bleeding btw skull + dura mater) = head injury → transient LOC → lucid for a bit → several hrs’ worth of deteriora’n in conscious level + focal neuro deficit(s)
→ subdural hemorrhage = bleeding btw dura mater + arachnoid mater (grey crescent shape on CT)
→ epidural / extradural hematoma (boggy swelling + grey lemon on CT b/c of raised ICP)
→ intracerebral hemorrhage (bleeding into brain tissue) = most likely diagnosis in pt w/ acute focal neurology, ↓ed level of consciousness + known Hx of HTN
→ subarachnoid hemorrhage = bleeding into arachnoid space (often described by pts as worst HA of their life, entire periphery will be bright on CT)
SSX = “FAS”
- Face droopiness
- Arm weakness
- Slurred speech
→ for subarachnoid hemorrhage = thunderclap/rapid onset HA + stiff neck + photophobia
⚠️ If SSX last < 24hrs it’s a TIA NOT a STROKE (won’t show up on CT scan) !
→ after diagnosing it as a TIA do carotid duplex scan to r/o carotid stenosis → carotid endarterectomy if scan shows > 50% stenosis w/ ischemic event OR > 70% stenosis + asymptomatic
Ix’s
- Non-contrast head CT = quick so order it if ur almost certain it’s a stroke
→ hyperdense = hemorrhagic stroke
→ hypodense = ischemic stroke (might not show up on CT though) - Brain MRI (Gold std but can start Tx w/ just CT findings)
→ con w/ this = takes too long + pt has to stay still which they might not be able to do - Lumbar puncture 12hrs after doing CT → in subarachnoid haemorrhage will show xanthochromia
⚠️ Always do brain CT before doing LP to make sure pt doesn’t have high ICP or else can cause hernia’n which can kill pt ! - CT Angiography to identify blocked vessel + locate source of bleed
- ECG to r/o arrhythmias
- Carotid U/S
Tx for TIA = MRI + referral w/in 24 hrs + 300mg aspirin + statin
Tx for ischemic
1. Immediate CT to r/o hemorrhagic stroke
2. Aspirin 300mg daily for 2 wks
3. Admit pt to stroke center
4. Allow permissive HTN to not make ischemia worse
5. Thrombolysis i.e IV alteplase if SSX started w/in 4.5 hrs + pt = SYMPTOMATIC
→ MOA of alteplase = tissue plasminogen activator (tPA) i.e converts plasminogen to plasmin so it can lyse fibrin ∴ getting rid of clot
→ side effects = bleeding, angioedema, anaphylaxis + fever
→ C/Is = hemorrhage, stroke or neuroSx in past 3 months i.e any condi’n that ↑ risk of bleeding
6. Clopidogrel 75mg once daily
7. Atorvastatin 20-80mg 48hrs later
8. Neurorehab
9. Treating modifiable RFs i.e smoking, obesity, exercise, BP / diabetes control
Tx for hemorrhagic = β blockers, CCBs + Sx
Addi’nal Tx for stroke pt w/ Afib = anticoagulant
→ either Warfarin or factor Xa inhibitor such as Apixaban
- Know for OSCE *
Subarachnoid hemorrhage ✓
RFs
45-70 y/o
- HTN
- smoking + alcohol
- black women
- FHx
- cocaine use
- connective tissue disorders
- neurofibromatosis
Eti = ruptured cerebral aneurysm or trauma
SSX
- thunderclap HA i.e like someone hit the back of ur head
- N/V
- neck stiffness
- photophobia
Ix’s
- Non-contrast head CT
→ will show hyperattenua’n i.e be hyperdense
→ less reliable if taken > 6 hrs after onset of SSX
⚠️ A normal head CT doesn’t t exclude a subarachnoid hemorrhage ! - Lumbar puncture 12hrs after doing CT → will show xanthochromia + raised RBC count
⚠️ Always do brain CT before doing LP to make sure pt doesn’t have high ICP or else can cause hernia’n which can kill pt ! - CT angiography after confirming diagnosis to locate where bleed is coming from
Tx = neuroSx referral + nimodipine to prevent vasospasms
- Know it for OSCE *
Cavernous sinus thrombosis ✓
Def - when thrombus forms w/in cavernous sinus
RFs
- recent Hx of acute sinutis
- Hx of peri-orbital infec’ns
Eti = bacterial infec’n usually
SSX
- fever
- HA
- ophthalmoplegia
- lateral gaze palsy
- peri orbital edema
- proptosis = eye bulging
- chemosis = swelling of inner eyelids
Ix’s
- FBC → polymorphonuclear leukocytosis if due to infec’n
- head CT w/ contrast
- head MRI w/ contrast if CT doesn’t diagnose
- blood culture to identify causative pathogen if due to infec’n
Tx = high dose IV vancomycin + heparin
→ MOA of vancomycin - glycopeptide Abx ∴ inhibits peptidoglycan synthesis in cell wall of gram +ve bateria
→ side effects - nephrotoxic, hypoTN
→ end in “PLANIN” or “VANCIN” (vancomycin = the excep’n)
Complica’ns
- hemorrhage
- death
- Know it for OSCE *
Causes of coma ✓
- Ischemic stroke
- Hemorrhagic stroke
- Cerebral venous thrombosis
- Hypertensive encephalopathy
- Cardiac arrest
- Sepsis-associated encephalopathy
- Meningitis
- Viral encephalitis
- Brain abscess
- Traumatic brain injury
- Brain tumor
- Seizure disorder
- Syncope
- Wernicke’s encephalopathy
- Hypo or hyperthermia
- Burns
- Alcohol / MetOH/ ethylene glycol / CO poisoning
- Know for OSCE *
What is Prolonged Disorder Of Consciousness (PDOC) ?
Unconsciousness or ↓ed GCS that persists for > 4 wks after injury
MS ✓
Def - chronic + progressive autoimmune condi’n involving demyelina’n of CNS
RFs
< 50 y/o
- FHx
- female
Eti - immune system attacks myelin sheath of myelinated neurons
SSX
- loss of sensa’n
- optic neuritis i.e u/l ↓ in visual acuity due to demyelina’n of optic nerve + can also present as . . .
→ central scotoma enlarged central blind spot)
→ pain w/ eye mov’nt
→ impaired color vis’n
→ RAPD in affected eye i.e consesual rxn > direct rxn - UMN SSX such as hyper-reflexia or muscle spams
- sensory ataxia (propriocep’n specifically) → pt will have +ve Romberg’s test
- cerebellar ataxia if there’s a cerebellar les’n
Types / disease patterns
- relapsing-remitting (most common pattern when first diagnosed) = episodes of SSX followed by recovery + SSX tend to occur in diff areas w/ each episode
→ active = new SSX or MRI shows new les’ns
→ not active = no new les’ns on MRI or new SSX
→ worsening = overall worsening of disability
→ not worsening = no worsening of disability over time - 2° progressive MS = relapsing-remitting disease but w/ progressive worsening of SSX + remiss’ns = incomplete
- 1° progressive = worsening disease w/o any relapse or remiss’n
Ix’s
- brain MRI / spinal MRI → will show demyelinating les’ns that are “disseminated in time + space” i.e vary in loca’n
- LP → will show oligoclonal bands in CSF
Tx for relapses = methylprednisolone
SSX Tx
- exercise to maintain strength
- amitriptyline or gabapentin for neuropathic pain
- baclofen or gabapentin for muscle spasmps
→ baclofen = GABA receptor agonist that acts on CNS
Complica’ns
- ED
- UTIs
- impaired mobility
- visual impairment
- osteopenia / osteoporosis
- Know for OSCE *
Encephalitis ✓
Def - inflamma’n of brain parenchyma
→ most common cause = viral infec’n
⟹ HSV-1 specifically in children
⟹ HSV-2 in neonates
RFs
< 1 y/o or > 65 y/o
- immunodeficiency
- post infec’n
- animal / insect bite
Eti
- HSV
- EBV
- VSV
- polio
- MMR
SSX
- fever
- altered cogni’n
- altered level of consciousness
- acute onset of focal neuro SSX
- acute onset of focal seizures
Ddx = malaria (if in endemic reg’n)
Ix’s
- ask about vaccina’n
- FBC → elevated WCC
- peripheral smear (in malaria endemic reg’n)
- HIV testing
- U + E → might show HypoNa
- LFTs b/c Coxiella burnetii, Rickettsia, tick-borne disease, EBV + CMV cause elevated LFTs
- LP → send CSF for viral PCR testing → followed by MRI to visualize brain in detail
⟹ CT scan instead of LP if LP = contraindicated
Tx
1. Aciclovir while waiting for results
2. Repeat LP prior to stopping antiviral therapy to ensure successful Tx
Complica’ns
- death
- seizures
- HAs
- chronic pain
- mov’nt disorder
- learning disability
- hormonal imbalance
- Δs to memory + cogni’n
- Δ in mood or personality
- Know for OSCE *
Brain abscess ✓
Def - life threatening condi’n in brain parenchyma caused by infec’n
RFs
- sinusitis
- otitis media
- dental procedure or tooth infec’n
- meningitis
- recent neuroSx or head + neck Sx
- congenital heart disease
- endocarditis
- diabetes
- immunocompromised
- IV drug use
- hemodialysis
- prematurity
Eti
- bacterial
- fungal
- parasitic
Diagnostic Ix = head CT w/ + w/o contrast
→ will show ≥ 1 ring enhancing les’n
Tx = AB
Complica’ns
- death
- seizures
- hydrocephalus
CNS + PNS cells ✓
Neurons / nerve cells + Glial cells / supporting / non-neuronal
- Neurons = non ÷ing
= cell body + receiving dendrites + projecting axon - Glial cell types = 4 CNS + 1 PNS
→ 4 CNS = astrocytes, oligodendrocytes, microglia + ependymal cells
a) ASTROCYTES = largest + most abundant
→ respond to CNS injury i.e gliosis
→ buffer extracellular [ K ] by mopping up leaked K ions
→ metabolize + recycle certain neurotransmitters (glutamate, serotonin, + γ-aminobutyric acid/GABA)
→ make up blood–brain barrier + contain glial fibrillary acidic protein (GFAP) = marker used in brain cancers such as astrocytoma + glioblastoma
b) OLIGODENDROCYTES = myelinate CNS neurons (1 can myelinate many neurons)
→ get damaged in MS + leukodystrophies
c) MICROGLIA = resident macrophages of CNS
→ when brain = damaged or infected, they become activated + quickly multiply to perform func’ns such as phagocytosis + antigen presenta’n
d) EPENDYMAL CELLS = ciliated cells that line CNS cavities
→ produce CSF + form part of blood-CSF barrier
→ beating of their cilia helps to circulate CSF that fills CNS cavities
- 1 PNS = SCHWANN CELLS = myelinate neurons w/in PNS (1 schwann cell can only myelinate 1 neuron)
Brain tumors ✓
Types
- Frontal lobe tumor
→ SSX = Δs in personality and/or behavior - Gliomas = tumor in glial cells (graded from grade 1-4)
→ astrocytoma (most common + also most aggressive form = glioblastoma)
→ oligodendroglioma
→ ependymoma - Meningiomas = tumors from meninges
→ usually benign but can take up space + hence cause ↑ in ICP - 2° metastases (“BLRM”)
→ breast
→ lung
→ RCC
→ melanoma - pituitary tumors
→ if they grow large enough can press on optic chiasm + hence cause bitemporal hemianopia
Ix = Brain MRI + Bx
Seizures ✓
If seizure > 5 mins or pt has multiple seizures w/o regaining consciousness = status epilepticus = medical emergency !
Types in adults
- generalized tonic-clonic = tonic (muscle tensing) + clonic (muscle jerking) mov’s associated w/ complete LOC
→ pts might expereince aura or abnormal sens’an prior to seizure
→ there might be tongue biting, incontinence, groaning + irregular breathing
→ after seizure there is a prolonged post-ictal period, where pt = confused, tired + irritanle - focal / partial seizure = occur in an isolated brain area (temporal lobes usually ∴ affecting hearing, memory + emo’ns
→ associated SSX depend on loca’n but can include . . . - déjà vu
- unusual emo’ns
- Δ in ≥ 1 of 5 senses
- abnormal behaviors
→ pt remain awake in this type of seizure during partial seizures
⟹ remain aware during simple partial seizures but lose awareness during complex partial seizures
Myoclonic = brief + sudden muscle contrac’ns i.e like a jolt
Tonic = sudden onset of hypertonia i.e entire body stiffens, resulting in pt falling backwards if they’re standing
→ last a few secs (a couple minutes max)
Types in children
- absence seizures = pt becomes blank, stares into space + then abruptly returns to normal
→ last 10-20 sec
→ during episode, pt = unresponsive + unaware of their surroundings and do not respond - infantile spasms / West syndrome = custers of full-body spasms
→ poor prognosis + = associated w/ developmental regress’n
→ Tx = prednisolone + vigabatrin - febrile convuls’ns = tonic-clonic seizures that occur in children during a high fever
→ are ≠ caused by any pathology
→ no lasting damage usually
Ddx
- TIA
- hypoglycemia (always do capillary blood glucose in syncopal pt to r/o this out)
- pseudoseizures (non-epileptic attacks)
- vasovagal syncope (can happen during flights + pt can also have jerking mov’nts)
- cardiac syncope due to arrhythmia or structural heart disease
Ix’s
- EEG → used for classifica’n, prognostica’n + risk of recurrence
- brain MRI to diagnose structural problems in adults + children if they have ≥ 1 of the following SSX . . .
- 1st seizure + pt < 2 y/o
- focal seizure
- no response to first line Tx for that type of seizure
- ECG to exclude cardiac causes
- U+ E
- blood glucose to check or hypoglycemia + diabetes
- blood / urine / LP cultures if either sepsis, encephalitis or meningitis = suspected
Emergency Tx i.e in status epilepticus
Before ambulance arrives . . .
1. Put pt in a safe posi’n (on carpeted floor for ex)
2. Place pt in recovery posi’n if possible
3. Put something soft under pt’s head to protect against head injury
4. Remove obstacles that could lead to injury
5. Make a note of time @ which seizure started + stopped
6. Call an ambulance if lasting > 5 mins it’s their first seizure
Once ambulance arrives . . .
1. ABCDE
2. Benzodiazepine
3. Another dose of above after 5-10 mins if seizure continues
4. IV phenobarbital or phenytoin
→ side effects of phenytoin = folate + Vit D deficiency + Dupuytren’s contracture
→ SSX of phenytoin overdose = nystagmus, diplopia, slurred speech, confus’n + hyperglycemia
→ MOA of benzos - facilitate + enhance binding of GABA to its receptor to create seda’n + muscle relax’an effect
→ side effects - confus’n, aggress’n (worse in elderly pts + when administered @ night)
→ C/Is - angle closure glaucoma b/c will relax sphincter pupillae muscle of iris
→ end in “PAM”
Regular Tx based on seizure type . . .
- absence = Na valproate or ethosuximide (this only in adults)
→ side effects of ethosuximide = rash + night terrors - GTCS = Na valproate or lamotrigine / levertiracetam in women able to have children
→ side effects of Na valproate . . . - hair loss
- teratogenic
- tremor
- live damage
- ↓ed fertility
- tonic or atonic
→ Na valproate or lamotrigine in women able to have children
⟹ that other for atonic in children - myoclonic = Na valproate or levetiracetam in women able to have children
⟹ Na valproate only for children - partial / focal seizures
→ levetiracetam or lamotrigine in adults
→ carbamazepine or lamotrigine in children + then ⟹ side effects of carbamazepine = agranulocytosis
+ aplastic anemia
Seizure advice for parents
- take showers rather than baths
- be very cautious w/ swimming unless seizures = well controlled + pt = closely supervised
- be cautious w/ heights
- be cautious w/ traffic
- be cautious w/ anything heavy or hot or any electrical equipment
- Know for OSCE *
Febrile Convuls’ns (kids) ✓
Def - seizure + high fever (i.e > 38°C) in child btw 6 months + 5 y/o
Eti = viral infec’n usually
Type
→ simple = generalized tonic clonic seizure that lasts < 15 min (only occurs once during a single febrile illness)
→ complex = ≥1 of the following . . .
- 15 min long
- focal seizure
- recurs w/in 24 hrs / single febrile illness
When u should get pediatric assess’nt for a kids who seizes . . .
< 18 months
- 1st time
- complex seizure
- focal neurological deficit
- fever w/ no apparent focus
Ddx
- epilepsy
- neuro infec’n i.e meningitis / encephalitis/ cerebral malaria
- brain tumor
- intracranial hemorrhage
- syncopal episode
- electrolyte abnormality
- accidental / NAI
Ix = clinical diagnosis but can do urine dipstick to quickly check for infec’n
Emergency Tx i.e if it lasts > 5 mins
1. Buccal midazolam
2. Another dose after 10 mins if seizure is still going
3. IV phenytoin
Regular Tx
1. Give ibuprofen / paracetamol for pyrexia + diazepam if it’s pt’s 1st complex febrile convuls’n
2. Long term anti convulsant Tx if pt has had ≥ 2 complex febrile seizures + diazepam Tx was ineffective
Advice to give parents if a further episode occurs
- stay w/ child
- put child in a safe place (on a carpeted floor)
- place them in recovery posi’n + away from Ψ sources of injury
→ place arm that is nearest to you @ a 90° angle to their body w/ their palm facing upwards
→ place back of hand of pt’s other arm on cheek nearest to you
→ while keeping that hand pressed against their cheek, pull leg such that it’s at a 90° angle
- place a pillow under their head
- don’t put anything in their mouth
- call an ambulance if seizure lasts > 5 mins or it’s the pt’s 1st ever seizure
Complica’ns
- 2-7.5% risk of developing epilepsy after simple febrile convuls’n
- 10-20% risk of developing epilepsy after complex febrile convuls’n
Prognosis - 1/3 of pts will have another seizure
- Know for OSCE *
Seizure v.s Syncope ✓
Seizure = confus’n / amnesia AFTER regaining consciousness i.e post-ictal state
Syncope = amnesia only lasts as long as person is blacked out
Syncope ✓
Def - sudden LOC
Eti
- Neurally mediated syncopes . . .
→ vasovagal = triggered by noxious stimuli i.e heat, bad news, prolonged standing
⟹ usually accompanied by prodromal SSX i.e pallor, diaphoresis
→ situa’nal = triggered by coughing, swallowing, peeing or defecating
→ carotid sinus hypersensitivity = triggered by head rota’n, shaving or wearing neck collar
- Orthostatic hypotens’n
→ Def - drop in SBP by ≥ 20 mmHg + drop in diastolic by ≥ 10 mmHg when going from sitting to standing
→ Eti . . .
- inadequate fluid intake
- excessive fluid loss
- diuretic use (especially in older pt)
- β blockers
- opiates
- alcohol consump’n
- Cardiac
→ Eti . . .
- AV block
- Brugada
- LBBB or RBBB
- Sinus Brady
What imaging should all pts at least 16 y/o presenting w/ LOC or amnesia after injury get ✓
Head CT
DVLA driving rules for specific diseases ✓
Diseases where pt must notify DVLA
- insulin treated diabetes
- 1st seizure = 6 months no driving + 5 yrs for commercial vehicle unless risk/yr < 2%
- epilepsy or multiple unprovoked seizures = 1 yr no driving but can drive once are 1yr seizure-free (w/ or w/o meds) + 10 yrs for commercial vehicle
- MI requiring stenting = 1 wk no driving + 6 wks for commercial vehicle
- MI treated by CABG = 1 month no driving + 4 months for commercial vehicle
- unexplained syncope = 6 months no driving + 1 yr for commercial vehicle
⚠️ Tell pt prosecu’n = possible if they don’t notify + are in involved in a traffic incident + confidentiality must be broken if patient refuses i.e Dr will inform DVLA
Pt doesn’t have to notify
Stroke / TIA = 1 month no driving or 1yr for commercial vehicle but can return if there are no deficits that might prevent them from driving safely
Types of child abuse from most to least common ✓
- Neglect
- Emo’nal abuse
- Multiple i.e > 1 type
- Physical abuse
- Sexual abuse
FTT / Growth Faltering ✓
Def - < expected weight + height in first 3 yrs of life
RFs
- cerebral palsy
- premature birth
Eti
- Pre natal
→ IUG restric’n
→ chromosomal abnormalities such as Down’s
→ toxin exposure in utero (drugs / alcohol / smoking) - Post natal
→ inadequate intake
- neglect
- food insecurity
- feeding pb (GERD / cleft lip)
→ Malabsopr’n
- CKD
- celiac
- chronic vomiting / diarrhea
→ ↑ed demand
- infec’n
- malignancy
Ix’s
- growth charts
- FBC + serum ferritin to identify check for IDA
- U + E
- LFTs
- TFTs
- Inflammatory markers
- Sweat test + CXR to r/o CF
- Know for OSCE *
Duodenal atresia ✓
Def - narrowing or complete obstruc’n of duodenal lumen = most common cause of upper GI obstruc’n in children w/ Down syndrome
Pathophys - obstruc’n of duodenal lumen → accumula’n of gastric contents + bile → body has to forcefully expel those contents by vomiting
SSX
- recurrent vomiting + abdominal disten’n
→ green vomit i.e bilious vomiting means that there’s obstruc’n beyond Ampulla of vater
Down syndrome ✓
Def - most common VIABLE chromosomal disorder + most common genetic cause of intellectual disability
RFs
- previous child w/ Down’s
- advanced maternal age (i.e > 35 y/o)
Pathophys - meiotic nondisjunc’n during meiosis I (most of the time) OR unbalanced Robertsonian transloca’n btw chromosomes 14 + 21 → extra chromosome 21
SSX
- small stature
- duodenal atresia
- develop’ntal delay
- floppy / hypotonic
- Brushfield spots (= whitish spots @ periphery of iris)
- dysmorphic features i.e . . .
→ low set ears
→ largish tongue
→ epicanthic fold
→ flat nose bridge
→ single palmar crease
→ upslanting palpebral fissures
Ix’s
- Nuchal translucency > 3mm
→ -ve predictive value for Down’s = high since Down’s = pretty rare - 1st trimester screening
→ ↑ed β-hCG + ↓ed PAPP-A - 2nd trimester screening
→ ↑ed β-hCG + inhibin A + ↓ed estriol + AFP - karyotype for diagnosis
- hearing + vis’n tests
Complica’ns
- hearing / vis’n pbs
- ↑ed risk of AML + ALL
- earlier than expected onset of Alzheimer’s
- atrio ventricular septal defect
Physiological Δs in pregnancy ✓
CARDIO
- heart physiologically dilates
- RBC volume will ↑ by 20-30%
- plasma volume will ↑ by up to 50% ∴ SV + HR will ↑ + so will CO → CO will ↑ by 20% by 8th wk + by 40-45% by 20-28 wks
- ↓ in systemic + pulmonary vascular resistance by 25–30%
- ↓ in BP in 1st + 2nd trimesters + ↑ back to non-pregnant levels in 3rd trimester
- ↑ in coagula’n factors + platelet activity + ↓ in fibrinolysis + coagula’n inhibitors such as antithrombin, protein C + S which is why risk of VTE in pregnancy + postpartum ↑, even though actual prevalence of VTE in pregnancy = low
⚠️ Discrepancy btw ↑ in plasma + RBC volume, hematocrit + Hgb ↓ is what causes dilu’n effect + hence anemia in pregnancy
VAGINA + CERVIX
- vagina becomes more elastic
- ↑ in blood supply to uterus + vagina
- mucus glands of cervix enlarge + mucus plug called operculum forms to protect against infec’ns
KIDNEY
- ↓ in serum Ca
- ↓ in serum Urea + Cr
- ↑ in GFR but ↓ in oncotic pressure
- ↑ in renal blood flow + ↑ kidney size
- ↑ in uric acid excre’n due to ↑ed GFR
- ↑ in protein excre’n but not beyond normal levels
- glucose = freely filtered in glomerulus b/c of ↓ed tubular reabsorp’n
- glomerular hydrostatic pressure remains stable which ↓ risk of glomerular HTN
RESP
- ↑ in metabolic rate by 15%
- ↑ in O2 consump’n by 20%
- ↑ in minute ventila’n by 40-50%
- ↑ in tidal volume but not RR (= MATERNAL HYPERVENTILA’N)
- ↑ in arterial pO2
- ↓ in arterial pCO2 along w/ serum bicarb
- PEFR + FEV1 = unaffected
- ABG will show compensated respiratory alkalosis (arterial pH = 7.44)
GI
- N/V
- ↓ in motility + sphincter tone hence causing reflux + constipa’n
- ↑ in intra gastric pressure ∴ stomach = ↑gly displaced upwards
HORMONES
- Relaxin peaks @ end of 1st trimester + falls to an intermediate value throughout 2nd + 3rd trimester → stimulates forma’n of endothelin, which in turn mediates vasodila’n of renal arteries via NO synthesis
- ↑ in hCG (should 2x every day otherwise could be ectopic pregnancy)
- ↑ in insulin but then tissues become resistant to insulin = good b/c we want glucose to ↑ (resistance begins in 2nd trimester + peaks in 3rd trimester)
- ↑ in prolactin to prepare breast for lacta’n
- ↑ in progesterone which ↑ LDL / fat absorp’n which is why pregnant women gain weight
- ↑ in estrogen which will ↑ oxytocin receptors in prepara’n for delivery
What is given to pregnant women w/ hyperemesis ? ✓
- IV fluids
- anti emetics
- thiamine b/c hyperemesis can cause encephalopathy
Antenatal visit schedule ✓
- every 4 wks up to wk 28
- every 2 wks from wk 28-wk 36
- every wk from wk 36 onwards
- Booking visit (4-8 wks) = urinanalysis for proteinuria, CBC for anemia, HIV, syphilis, Hep B, blood group + Rh antibody status via indirect Coomb’s, screening for thalassaemia (all women) , sickle cell disease (women @ higher risk), retinopathy screening for pt w/ T2D + pt educa’n i.e . . .
- what to expect @ different stages of pregnancy
- lifestyle advice in pregnancy
- supplements (i.e folic acid + Vit D)
- plans for birth
- screening tests
- antenatal classes
- breastfeeding classes
- discussin mental health
Every subsequent visit will have
- discuss plans for remainder of pregnancy + delivery
- urine dipstick for proteinuria for pre-eclampsia
- BP for pre-eclampsia
- urine microcopy + culture to check for asymptomatic bacteriuria
- 10 wks - 13 and 6 = dating scan i.e gesta’nal age = calculated via CRL + multiple pregnancies = identified, cell free DNA / nuchal translucency (Down’s, Edward’s, Patau’s), blood type, CBC for anemia, Cr, fasting glucose, HIV, syphilis, Hep B+C, Varicella + Rubella immunity
- 16 wks = AFP for spina bifida, pertussis vaccine
- 20 wks = anatomy U/S
- 24-28 wks = 2hr OGTT for women w/ RFs or if there is LGA / polyhydramnios / glucose on urine dipstick to screen for gesta’nal diabetes + retinopathy screening @ 28 wks for pt w/ T2D
→ RFs for gesta’nal diabetes . . .
- previous gesta’nal diabetes
- previous macrosomic i.e ≥ 4.5 kg
- BMI > 30
- Black Caribbean, Middle Eastern or South Asian
- FHx of diabetes in first ° relatives
→ symphysis–fundal height = checked from here onwards
- 28 wks = HIV + syphilis again, blood group + Rh antibody status again
- 30 wks
- 32 wks
- 34 wks
- 36 wks = Group B strep, fetal presenta’n = assessed @ very visit from here onwards
- 37 wks
- 38 wks
- 39 wks
- 40 wks if it gets to that
General advice for pregnancy ✓
- folic acid 400mcg from before pregnancy to 12 wks to ↓ risk of neural tube defects
- Vit D supplementa’n (10 mcg or 400 IU daily)
- avoid Vit A supplements + eating liver or pate b/c Vit A in high amts = teratogenic
- don’t drink or smoke during pregnancy
- avoid unpasteurized dairy or blue cheese due to risk of listeriosis
- avoid undercooked or raw poultry due to risk of salmonella
- can continue moderate exercise but avoid contact sports
- sex is safe
- flying ↑ risk of VTE
- place car seatbelts above + below the bump not across it
Meds to stop
- ACE/ARBs
- Thiazide + thiazide-like diuretics
- β blockers that aren’t labetolol
- NSAIDs (avoid)
Pregnant women should avoid alcohol + smoking b/c causes or ↑ risk of the following . . .
Alcohol
- miscarriage
- small for dates
- preterm delivery
- fetal alcohol syndrome
→ microcephaly (small head)
→ learning disability
→ behavioural difficulties
→ hearing + vis’n issues
→ cerebral palsy
Smoking
- fetal growth restric’n (FGR)
- miscarriage
- stillbirth
- preterm labor + delivery
- placental abrup’n
- pre eclampsia
- cleft lip or palate
- sudden infant death syndrome (SIDS)
Flying in Pregnancy
- Per RCOG = safe in uncomplicated healthy pregnancies up to . . .
→ 37 wks if it’s a single pregnancy
→ 32 wks if it’s a twin pregnancy - After 28 wks, most airlines need a note from a midwife, GP or OB stating that pregnancy is going well + that there are no addi’nal risks
Describe gamete transport, fertiliza’n, blastocyst forma’n, blastocyst implanta’n + the develop’nt of the trophoblast, extra-embryonic mesoderm + amnion ✓
Sperm goes from vagina to cervix to fallopian tube (some go to empty fallopian tube + some get trapped in cilia) → once in fallopian tube, sperm become hyperactive i.e start swimming harder + faster (@ this point only a dozen = left) → sperm penetrate corona radiata + ZP
→ sperm attaches to ZP via sperm receptors on surface → attach’nt triggers acrosome of sperm to release digestive enzymes that eat through ZP
→ 1st sperm to make contact w/ ovum = the one that will fertilize it → fus’n
→ other sperm can no longer attach b/c of rehardening of ZP + repellant chemicals released by egg → fus’n triggers egg to continue meiosis II
→ microtubules pull pronuclei of each together to form diploid zygote → cilia of fallopian tube sweep zygote towards uterus
→ as zygote is moving through fallopian tube towards uterus it undergoes cleavage i.e mitotic ÷n’s → at 16 cells has reached uterus + is called morula (= day 4 post fertiliza’n)
→ at 32 cells = blastocyst (day 5) → blastocyst = filed w/ fluid called blastocele + has 2 groups of cells called trophoblast + inner cell mass → trophoblast will form chorionic sac + fetal por’n of placenta while inner cell mass will form fetus itself
→ trophoblast excretes enzymes that degrade ZP so blastocyst can “hatch” i.e break free from ZP (day 6)
→ implanta’n in endometrium of uterus (day 7)
→ placenta begins forming around wk 4 + is completely formed by wk 10
Anatomy + Physiology of Lacta’n ✓
- 9 lobes / breast
- w/in lobes = many lobules that have lactiferous ducts + alveoli
Lactogenesis
1) Breast becomes milk-producing gland at wk 16-22 w/ produc’n of colostrum → milk secre’n = prevented due to the high levels of estrogen + progesterone in pregnancy b/c they inhibit prolactin
2) Progesterone + estrogen levels ↓ ∴ prolactin is no longer inhibited
→ baby sucking stimulates release of prolactin (for milk produc’n) + oxytocin (contracts myoepithelial cells which forces milk from alveoli into ducts + sinuses i.e milk ejec’n / galactokinesis)
3) Maintenance of milk produc’n via autocrine control i.e galactopoiesis
4) Breast involu’n i.e apoptosis of milk-making epithelial to ↓ + eventually completely arrest milk produc’n
Outline the steps of lacta’n ✓
- Mammogenesis - estrogen + progesterone↑ to ↑ # ducts/lobules/alveoli
- Lactogenesis - prolactin↑
⚠️ Mom doesn’t make milk during pregnancy due to inhibi’n from estrogen + progesterone but after delivery, placenta ≠ there to produce estrogen + progesterone ∴ that inhibi’n = lost
→ breastfeeding delays period b/c prolactin causes -ve feedback on estrogen + progesterone - Galactokinesis - suckling triggers oxytocin which triggers milk expuls’n
- Galactopoiesis - maintenance of milk = due to prolactin, which surges every time baby suckles
What is puerperium ? ✓
Period from delivery till 42 days after delivery
Important notes about C-sec’n ✓
- prophylactic Abx = always given
- bladder = always catheterized
- reg’nal anesthesia = preferred over general anesthesia
- post op TED stockings
- not all women will be NPO
Success of trial of vaginal delivery after 1 previous C-sec’n ✓
Most will have successful vaginal delivery !
Gyn Ddx for common SSX ✓
Amenorrhea i.e lack of periods
→ 1° = due to hyper or hypogonadotropic hypogonadism such as Turner’s
⟹ in addi’n to amenorrhea pt w/ Turner’s will be shorter in stature, FSH / LH will be raised
→ 2°
- PCOS
- pregnancy (most common cause)
- menopause
- hormonal contraceptives
- premature ovarian insufficiency
- hyper or hypoTSH
- excessive prolactin secre’n due to prolactinoma
- Cushing’s syndrome
Intermenstrual Bleeding i.e bleeding btw menstrual periods
- STI
- pregnancy
- hormonal contracep’n
- cervical / endometrial polyps or cancer
- medica’ns such as SSRIs + anticoagulants
Dysmenorrhea i.e painful periods
- 1° i.e no underlying cause
- PID
- fibroids
- Cu coil
- adenomyosis
- endometriosis
- ovarian or cervical cancer
Menorrhagia i.e heavy menstrual bleeding
- 1° i.e no underlying cause
- PID
- fibroids
- Cu coil
- adenomyosis
- endometriosis
- anticoagulants
- bleeding disorders such as Von Willebrand disease
- endocrine disorders such as diabetes or hypo-thyroidism
Postcoital Bleeding
- polyps
- trauma
- atrophic vaginitis
- cervical / endometrial / vaginal cancer
Pelvic Pain
- UTI
- IBD
- IBS
- PID
- appendicitis
ovarian cysts
- ovarian tors’n
- endometriosis
- pelvic adhes’ns
- ectopic pregnancy
- Mittelschmerz = cyclical pain during ovul’an
Vaginal Discharge (abnormal if excessive, discolored or foul-smelling)
- BV
- thrush
- chlamydia / gonorrhea
- trichomonas vaginalis
Pruritus Vulvae i.e itching of vulva + vagina
- thrush
- eczema
- atrophic vaginitis
- irritants i.e soaps, detergents, barrier contracep’n
- Know for OSCE *
PMS ✓
Def - psychological, emo’nal + physical SSX in the days preceding onset of menstrua’n (i.e during luteal phase)
→ SSX resolve once menstrua’n begins
→ obviously cannot occur prior to menarche, during pregnancy or once woman reaches menopause
SSX
- low mood
- anxiety
- mood swings
- irritability
- bloating
- fatigue
- HAs
- breast pain
- clumsiness
- cognitive impairment
- ↓ed confidence
- ↓ed libido
Diagnostic Ix = SSX diary that spans 2 menstrual cycles → will show cyclical SSX that occur just before + resolve immediately after onset of menstrua’n
Mx
- general healthy lifestyle Δs such as improving diet, exercise, alcohol, smoking, stress + sleep
- COCP that has drospirenone such as Yasmin
- SSRI / CBT
- referral if SSX = severe
- Know for OSCE *
Gesta’nal Diabetes ✓
Def - when woman w/o previous diagnosis of diabetes develops high blood glucose level during pregnancy b/c of the ↓ed insulin sensitivity that occurs during pregnancy
RFs
> 40 y/o
- PCOS
- elevated BMI
- FHx of diabetes
- non white ancestry
- previous macrosomic baby
- previous gesta’nal diabetes
Complica’ns
- LGA (↑ risk of shoulder dystocia)
- macrosomia i.e ≥ 4.5 kg (↑ risk of shoulder dystocia)
- T2D after pregnancy
- neonatal hypoglycemia
Ix = 2hr OGTT (“ 5 6 7 8 “ for normal values) @ 24-28 wks if mom has glycosuria, RFs or polyhydramnios
→ fasting should be < 5.6
→ 2hr should be < 7.8
⚠️ Woman w/ pre-existing diabetes should get retinopathy screening during pregnancy !
Mx during pregnancy
- fasting < 7 = diet + exercise for 1-2 wks → metformin → insulin
- fasting > 6 + macrosomia or fasting > 7 = insulin +/- metformin
- women should monitor blood glucose at home + aim for . . .
→ fasting of 5.3 (≤ 4 = TOO LOW !)
→ 1 hr post-meal of 7.8
→ 2 hrs post-meal of 6.4
Mx after delivery
- can stop diabetes medica’ns immediately after birth
- f/u in ≥ 6 wks to test post delivery fasting glucose
- women w/ existing diabetes should ↓ their insulin doses b/c of physiological postnatal hypoglycemia
- Know it for OSCE *
Pre natal care for women w/ pre-existing diabetes who want to get pregnant ✓
- should take 5mg of folic acid from preconcep’n until 12 wks gesta’n
- should delay concep’n for 6 months until they achieve better glycemic control to ↓ risk of congenital abnormalities
- Know it for OSCE *
Labor ✓
Def - process of uterine contrac’ns + cervical dila’n that enables uterus to deliver viable fetus (i.e > 24 wks)
- Labor = diagnosed when contrac’ns = regular + ↑ing both in frequency + severity
- 1st stage = period btw the onset of regular painful uterine contrac’ns to full cervical dilata’n
→ when contrac’ns = weak, irregular + DONT ↑ in intensity or dura’n they’re known as Braxton Hick contrac’ns (usually occur in 2nd or 3rd trimester)
a) Latent phase = dura’n for cervix to be be dilated to 3 cm
b) Active phase = dura’n for cervix to be be fully dilated to 10 cm - 2nd stage = from full cervical dilata’n to delivery of fetus
- 3rd stage = from delivery of fetus to delivery of placenta + membranes (usually < 15min)
⚠️ if @ 41 wks pt hasn’t delivered yet, labor = induced w/ PGE2 + then tocolysis w/ terbutaline
→ complica’n of this = uterine hyperstimula’n which can be treated by removing agent of induc’n
Induc’n of Labor ✓
Bishop score = used to predict if induc’n of labor will be successful (ttl score ≥ 8 = successful IOL)
- fetal sta’n = scored from 0-3
- cervical posi’n = scored from 0-2
- cervial dilata’n = scored from 0-3
- cervical effacement = scored from 0-3
- cervical consistency = scored from 0-2
Main Induc’n op’n = vaginal prostaglandin E2 (dinoprostone) → gel, tablet (Prostin) or pessary (Propess) = inserted into vagina
Other induc’n op’ns
- CRB (cervical ripening balloon) → silicone balloon = inserted into cervix + gently inflated to dilate cervix
→ = alternative when vaginal prostaglandins ≠ preferred such as in women w/ previous C sec’n, multiparous women (≥ 3) or if vaginal prostaglandins failed - artificial rupture of membranes w/ oxytocin infus’n → can be used to monitor progress of induc’n after vaginal prostaglandins have been used
- oral mifepristone (anti-progesterone) + misoprostol = used when intrauterine fetal death has occurred
Complica’n = uterine hyperstimula’n i.e prolonged + frequent uterine contrac’n
→ can lead to fetal distress + compromise
→ diagnostic criteria = individual uterine contrac’ns that are > 2 mins in dura’n + > 5 uterine contrac’ns every 10 mins
Mx of Breech Presenta’n ✓
< 37 wks = do nothing
≥ 37 wks + no C/I = external cephalic vers’n
≥ 37 wks + ≥ 1 of the following C/Is = planned C sec’n @ 39 wks . . .
- multiple pregnancy
- ruptured membranes
- vaginal bleeding (currently or up to 1 wk ago)
- Rh isoimmuniza’n
- placental abrup’n
- pre e / HELPP
- fetal distress
CTG / Fetal Heart Tracing ✓
” VEAL CHOP “
- Variable decel = Cord compress’n
- Early decel = Head compress’n
- Accels = OK i.e Normal !
- Late decel i.e after contrac’ns = Placental insufficiency / fetal compromise
Pre-eclampsia ✓
Def - new onset of HTN in pregnant woman at > 20 wks gesta’n (BP ≥140/90 mmHg on 2 occas’ns ≥ 4 hrs apart) + significant proteinuria (2+ on dipstick) = medical emergency so must admit pt to hospital immediately !
→ = significant cause of both maternal + fetal morbidity + mortality
→ if just high BP but no proteinuria = pregnancy induced HTN NOT pre eclampsia !
→ if there are seizures = eclampsia
⟹ seizures in eclampsia = generalized tonic clonic usually
High-risk RFs
- pre existing HTN
- previous pre eclampsia / HTN in pregnancy
- diabetes
- CKD
- autoimmune condi’n such as SLE
Moderate RFs
> 40 y/o
> 10 yrs since since previous pregnancy
- FHx
- BMI > 35
- first pregnancy
- multiple pregnancy i.e twins
⚠️ Offer aspirin from 12 wks onward if pt has 1 HIGH RF or ≥ 2 MODERATE RFs !
SSX = HTN + proteinuria + edema +/- . . .
- HA
- vis’n Δs
- N / V
- right hypochondrium abdominal pain (due to liver swelling)
Mild
- systolic = 140-149
- diastolic = 90-99
Moderate
- systolic = 150-159
- diastolic = 100-109
Severe
- systolic > 160
- diastolic > 110
Pathophys - spiral arteries of placenta form abnormally → high vascular resistance in those vessels
Ix’s
- BP → will show HTN
- urinanalysis → will show proteinuria
- Urine protein : Cr ratio > 30 or albumin : Cr ratio > 8
- PlGF btw 20-35 wks to r/o pre-e (will be low in pre-e)
Diagnostic criteria = BP > 140/90 + ≥ 1 of . . .
- proteinuria (should be ≥ 1+ on dipstick)
- organ dysfunc’n i.e ↑ed Cr / elevated liver enzymes / thrombocytopenia / hemolytic anemia / seizures
- placental dysfuc’n such as fetal growth restric’n or abnormal fetal doppler
Complica’ns
- placental abrup’n
- pulmonary edema
- fetal growth restric’n
- HELLP syndrome
→ Hemolysis
→ Elevated Liver enzymes
→ Low Platelets
Tx
1. Labetolol b/c provides maternal cerebral protec’n
2. Nifedipine (modified-release)
3. Methyldopa (stop w/in 2 days of delivery)
4. IV hydralazine for severe pre-e
5. IV MgSO4 for eclampsia
Tx during labor
- IV Mg SO4 during labor + 24 hrs later to prevent seizures
- fluid restric’n during labor in severe pre-e or eclampsia to avoid fluid overload
Mx
- BP measur’nt ≥ 4x/day
- quantify proteinuria if not done previously
- Monitor FBC, U + E, LFTs + bilirubin 2-3x/wk to check for SSX of HELLP syndrome
- severe pre-e + pt > 34 weeks = complete corticosteroids + deliver when BP = controlled
After delivery
- maternal BP monitoring +/-antihypertensives (Safe to use some ACE-Is / β blockers / CCBs = safe while breastfeeding
- OB f/u
- Know for OSCE *
TORCH infec’ns ✓
Def - congenital infec’ns that fetus can get if mom has it during pregnancy
- Toxoplasmosis = protozoan parasite infec’n caused by eating raw/undercooked meat or being exposed to feces of recently infected cats
→ risk of congenital toxoplasmosis = higher later in pregnancy
→ SSX = intracranial calcifica’n + hydrocephalus
+ chorioretinitis (inflamma’n of choroid + retina)
Others i.e Hep B, syphilis, Zika
→ Zika = endemic to Africa, caused by Aedes mosquito
⟹ spreads through intercourse w/ infected person
⟹ SSX of congenital Zika syndrome . . .
- fetal growth restric’n
- microcephaly
- other intracranial abnormalities, such as ventriculomegaly + cerebellar atrophy
⟹ Ix’s in pregnancy = viral PCR + Zika virus antibodies to the Zika virus → fetal medicine referral if test +ve
⟹ No Tx
- Rubella → caused by maternal infec’n during first 20 wks of pregnancy
→ risk = highest before 10 wks gesta’n
→ women planning to become pregnant should make sure they received MMR vaccine + if unsure of vaccina’n status can be tested for rubella immunity
⟹ if they do not have antibodies to rubella, they can be vaccinated with 2 doses of MMR, 3 months apart
→ SSX . . . - congenital deafness
- congenital cataracts
- congenital heart disease (PDA + pulmonary stenosis)
- learning disability
- CMV
→ most cases of CMV in pregnancy DO NOT lead to congenital CMV
→ spread via saliva or urine of infected symptomatic children
→ SSX . . . - hearing loss
- vis’n loss
- fetal growth restric’n
- microcephaly
- learning disability
- seizures
- Herpes Simplex
- Know it for OSCE *
Cord Prolapse ✓
Def - when umbilical cord descends below presenting part of fetus after rupture of fetal membranes
→ complica’n = fetal hypoxia
RFs
- abnormal fetal lie after 37 wks gesta’n → strongest RF b/c provides space for the cord to prolapse below the presenting par
- multiple pregnancy
- polyhydramnios
- premature
- high head,
- unusually long cord
Ix’s
- CTG → will show variable decels
- vaginal exam to confirm diagnosis
Tx = emergency C sec’n
- Know it for OSCE *
Shoulder dystocia ✓
Def - when anterior shoulder of baby becomes stuck behind pubic symphysis of pelvis after head has been delivered = obstetric emergency !
Emergency Tx = “ HELPERR”
1. Call for HELP i.e ob + peds + anesthesiologist
2. Evaluate for Epistiotomy to enlarge vaginal opening + ↓ risk of perineal tear
3. Legs i.e McRobert’s maneuver - hyperflex’n of mother @ hip i.e mom’s knees to her abdomen
→ provides a posterior pelvic tilt ∴ lifting pubic symphysis up + out of the way
4. Pressing on suprapubic reg’n of abdomen → puts pressure on posterior aspect of baby’s anterior shoulder ∴ encouraging it down + under pubic symphysis
5. Enter / internal maneuvers i.e Rubin’s + Woodscrew or reverse Woodscrew
→ Rubin’s = reach into vagina to put pressure on posterior aspect of baby’s anterior shoulder to help it move under pubic symphysis
→ Woodscrew = during Rubin’s use other hand to reach in vagina → top shoulder = pushed forwards + bottom shoulder = pushed backwards
→ Reverse Woodscrew if regular woodscrew doesn’t work → top shoulder = pushed forward
6. Remove baby’s posterior arm from birth canal
7. Roll pt i.e make them get on all 4’s
Complica’ns
- postpartum hemorrhage
- fetal hypoxia + subsequent cerebral palsy
- brachial plexus injury + Erb’s palsy
- perineal tears
- Know it for OSCE *
Severity of antepartum hemorrhage ✓
Minor = < 50 ml of blood loss
Major = 50-1000 ml of blood loss
Massive = > 1000 ml or blood loss or SSX of shock
Mx for major or massive hemorrhage
1. Call senior ob midwife + anesthesiologist
2. 2 grey cannula
3. Bloods i.e FBC, U+E, LFTs, coag panel + crossmatch 4 units of blood
5. Fluid + blood resuscita’n as required
6. CTG for fetal monitoring + close monitoring of mom
- Know it for OSCE *
Placenta previa ✓
Def - when placenta = over cervical os i.e directly covers it (normally should be ≥ 2 cm from cervical os)
→ if placenta edge is < 2 cm from cervical os = low lying placenta NOT placenta previa !
RFs
> 40 y/o
- previous C sec’n due to uterine scarring
- previous termina’n of pregnancy
- multiparity
- multiple pregnancy
- maternal smoking
- assisted concep’n
SSX = painless vaginal bleeding
Findings on exam
- vaginal bleeding
- non tender uterus
- low lying placenta on 20 wk anomaly scan
- fetal lie + presenta’n may be abnormal
Ddx of antepartum hemorrhage
- placenta previa
- vasa previa
- placental abrup’n
Ix’s
- U/S w/ fetal doppler
- FBC
- type + cross match
Tx
1. If identified @ 16-20 wk scan check again @ 32 wks
2. If still there @ 32 wks, check again @ 36 wks
3. Give corticosteroids btw 34 wks and 35 + 6
4. C sec’n if still there @ 36 wks
Complica’ns
- antepartum hemorrhage
- maternal anemia
- preterm birth + low birth weight
- stillbirth
- Know for OSCE *
Vasa previa ✓
Def - when the 3 fetal vessels (2 arteries + 1 vein) are exposed i.e travel through chorioamniotic membranes + across / over internal cervical os instead of directly into placenta
RFs
- IVF
- multiple pregnancy
- low lying placenta
SSX
- rupture of membranes + then painless vaginal bleeding right after
- fetal bradycardia
Types
- Type I → fetal vessels = exposed as a velamentous umbilical cord
- Type II → fetal vessels = exposed as they travel to an accessory placental lobe
Ddx of antepartum hemorrhage
- placenta previa
- vasa previa
- placental abrup’n
Ix = U/S + fetal doppler
Tx = corticosteroids from 32 wks onwards to promote fetal lung develop’nt + elective C-sec’n @ 34-36 wks
→ emergency c sec’n if there is antepartum hemorrhage to prevent fetal death
Complica’ns
- fetal blood loss
- fetal death
- Know for OSCE *
Placental abrup’n ✓
Def - complete or partial detach’nt of placenta from uterine wall before delivery
→ concealed = when cervical os remains closed so bleeding that occurs remains w/in uterine cavit
→ overt / revealed = blood loss = observed via vagina
RFs
- HTN
- smoking
- trauma
- multiparity
- thrombophilia
- previous abrup’ns
- advanced maternal age
- smoking during pregnancy
- anti-phospholipid syndrome
- cocaine use during pregnancy
- current pre-e or HELLP syndrome
SSX
- vaginal bleeding
- sudden + continuous lower abdominal pain
- “woody” tender uterus on palpa’n
Ddx of antepartum hemorrhage
- placenta previa
- vasa previa
- placental abrup’n
Ix’s
- clinical diagnosis
- U/S to r/o placenta previa
- Kleihauer test for Rh -ve women b/c will require anti D Ppx → quantifies how much fetal blood = mixed w/ maternal blood in order to determine required dose of anti-D
Tx
- fetus dead → induce vaginal delivery → C sec’n instead if pt = hemodynamically unstable or hemorrhaging
- fetus alive + no SSX of distress
→ < 36 wks = close observa’n + antenatal steroids btw 24 and 34 + 6 wks
→ > 36 wks = induce + deliver vaginally - fetus alive + SSX of distress = C-sec’n
Complica’ns
- shock
- stillbirth
- hemorrhage
- premature birth
- placental insufficiency
- post partum hemorrhage
- Know for OSCE *
Post-partum hemorrhage ✓
Def - ≥ 500 ml of blood loss (in vaginal delivery) or ≥ 1000 ml (in C sec’n) once both baby + placenta are delivered
= obstetric emergency !
RFs
- pre e
- obesity
- large baby
- previous PPH
- placenta accreta
- multiple pregnancy
- prolonged 3rd stage
- failure to progress into 2nd stage of labor
Eti = “4 T’s”
- Tone i.e uterine atony (most common cause) = failure of uterus to contract after delivery
- Trauma i.e perineal tear or uterine rupture
- Tissue i.e retained placenta
- Thrombin i.e bleeding disorder
Tx
1. ABCDE
2. Lie mom flat, keep her warm
3. Insert 2 large-bore cannulas
4. Bloods i.e FBC, U&E + clotting screen
5. Group + cross match 4 units of blood
6. Warmed IV fluid + blood resucita’n as required
7. Oxygen (regardless of O2 sat)
8. Fresh frozen plasma if there are clotting abnormalities or after 4 units of blood transfus’n
Preven’n measures
- treating anemia in antenatal period
- giving birth w/ empty bladder b/c full bladder ↓ uterine contrac’n
- IV tranexamic acid in C sec’n (for higher-risk pts only)
Complica’ns
- infec’n
- anemia
- maternal death
- Know for OSCE *
Placenta accreta ✓
Def - when placenta implants deeper, through + past endometrium ∴ making it difficult to separate placenta after baby = delivered
RFs
- previous placenta accreta
- previous C sec’n
- advanced maternal age
- low lying placenta or placenta previa
- previous endometrial curettage procedure (such as for abor’n or miscarriage)
SSX = asymptomatic usally but can present w/ antepartum hemorrhage in 3rd trimester
Ix = U/S + fetal doppler
Tx = scheduled C sec’n btw 35 and 36 + 6 wks + antenatal steroids btw 24 and 34 + 6 wks
- Know for OSCE *
Post natal care ✓
- Immediate things
- analgesia as required
- help mom establish breast or bottle-feeding
- VTE risk assess’nt
- monitor for PPH
- monitor for sepsis
- monitoring BP if mom had pre-e
- monitoring surgical recovery after C - sec’n or perineal tear - 6 wk post natal visit (10 B’s)
- Baby blues i.e screen for post natal depress’n
- Breastfeeding
- Baby’s overall wellbeing
- BM
- Bladder
- Boinking i.e intercourse
- Birth control (don’t need it for first 21 days + for after can use progesterone only pill, implant or COCP 6 wks after delivery if breastfeeding)
- Belly i.e C sec’n scar if applicable
- Bleeding i.e normal initial lochia (mix of blood, endometrial tissue) ? has period returned ?
→ period will return 6 months later if breastfeeding + 3 wks later if bottle feeding
- BP + urine dipstick in mom who had pre-e + blood glucose in mom who had gesta’nal diabetes
- Know for OSCE *
Miscarriage ✓
Def - spontaneous pregnancy termina’n @ ≤ 24 wks
→ occurs in up to 1/3 of pregnancies)
→ 80% of miscarriages = in 1st trimester
⟹ early miscarriage = < 12 wks
⟹ late miscarriage = 12-24 wks
Types
- missed miscarriage = fetus is no longer alive but no SSX occurred + cervical os = closed
- threatened miscarriage = fetus is alive + painless vaginal bleeding + closed cervical os
- inevitable miscarriage = heavy, painful vaginal bleeding w/ clots + cervical os = open
- incomplete miscarriage = painful vaginal bleeding + retained products of concep’n are still in uterus
- full / complete miscarriage = no products of concep’n = left in uterus
- recurrent miscarriage = spontaneous loss of ≥ 3 consecutive pregnancies
- anembryonic pregnancy = present gesta’nal sac but it’s empty
RFs
- advanced maternal age
- uterine malforma’n
- BV
- thrombophilia
- parental chromosomal anomaly
Ddx = ectopic pregnancy
Ix’s
- transvaginal U/S for diagnosis
- β hcG to r/o ectopic pregnancy
Tx for confirmed diagnosis of miscarriage
1. Expectant Mx for 7-14 days i.e do nothing
2. Medical or surgical Mx
- Know for OSCE *
Stillbirth ✓
Def - spontaneous pregnancy termina’n after 24 wks
RFs
- smoking
- alcohol
- fetal growth restric’n
- advanced maternal age
- maternal obesity
- multiple pregnancy
- sleeping on back as opposed to on sides
Eti
- unexplained (around 50%)
- pre e
- placental abrup’n
- vasa previa
- cord prolapse
- cord wrapped around the fetal neck
- obstetric cholestasis
- diabetes
- thyroid disease
- TORCH infec’ns
- genetic abnormalities or congenital malforma’ns
Diagnostic Ix = U/S + fetal mov’nts + repeat U/S +
anti-D Ppx w/ Kleihauer test for Rh -ve moms
→ w/ parental consent, testing = carried out after stillbirth to determine cause i.e genetic testing of fetus + placenta, postmortem examina’n of fetus (including x-rays), testing for maternal + fetal infec’n, testing the mom for condi’ns associated w/ stillbirth such as diabetes, thyroid disease + thrombophilia
Tx op’ns
- vaginal birth = preferred method (must do this method there is sepsis, hemorrhage or mom has pre-eclampsia)
- expectant Mx → moms must be closely monitored
- induc’n of labor w/ mifepristone + vaginal or oral misoprostol
- Know for OSCE *
Termina’n of pregnancy ✓
Can be performed legally @ up to 24 wks of gesta’n @ approved site + by approved Dr IFF 2 Dr’s agree that ending pregnancy would cause less damage to pt’s physical or mental health than continuing w/ pregnancy or @ any point in pregnancy in any of these scenarios . . .
- risk to life of pregnant woman > risk of terminating pregnancy
- termina’n = necessary to prevent grave permanent injury to physical or mental health of pregnant woman
- there’s a substantial risk that if child were born it would suffer from such physical or mental abnormalities that would leave them seriously handicapped
Abor’n Op’ns
- medical abor’n (most approprate in early pregnacy) = mifepristone + then misoprostol 1-2 days later + anti D Ppx for Rh -ve women ≥ 10 wks
- surgical abor’n → involves cervical priming before Sx i.e softening + dilating cervix w/ misoprostol / mifepristone or osmotic dilator devices
⟹ cervical dilata’n + suc’n of uterine contents if ≤ 14 wks
⟹ cervical dilata’n + evacua’n w/ forceps if btw 14 + 24 wks
Complica’ns
- pain
- infec’n
- bleeding
- failure of abor’n i.e pregnancy continues
- damage to uterus or cervix
Puerperal psychosis ✓
Def - rare but serious psychosis in woman who just gave birth (days or wks ago)
RFs
- personal or FHx of mental illness
- difficult or traumatic childbirth
- lack of social support
SSX
- delus’ns
- confus’n
- hallucina’ns
- agita’n
- lack of insight into illness
Tx = hospitaliza’n + medica’n
- Know for OSCE *
Toxic shock syndrome ✓
RFs
- diabetes
- alcohol
- prolonged tampon use i.e > 6 hrs
- using highly absorbent tampons
Eti
- group A strep (Strep pyogenes)
- MSSA
- MRSA
Types
- menstrual TSS → occurs in women during menstrua’n w/ extended use of a single tampon
- non menstrual TSS → due to staphylococcal post-partum vaginal or cesarean wound infec’n
Diagnostic criteria
- temp > 38.9ºC
- SBP < 90 mmHg
- diffuse erythematous rash following prolonged tampon use
- involv’nt of ≥ 3 organ systems such as . . .
→ GI i.e diarrhea or vomiting
→ renal failure
→ hepatitis
→ thrombocytopenia
→ CNS i.e confus’n
Ix’s
- blood / wound culture
- FBC
- U + E to check for renal failure
- LFTs to check for liver involv’nt
Tx = remove tampon + admit for IVF + IV Abx
→ for streptococcal = clindamycin + benzylpenicillin (vancomycin instead if pt has penicillin allergy)
→ for MSSA = clindamycin + oxacillin (vancomycin instead if pt has penicillin allergy)
→ for MRSA = clindamycin + vancomycin
Complica’ns
- bacteremia
- DIC
- renal failure
- Know for OSCE *
AUB ✓
Def - varia’n from normal menstrua’n in terms of volume / dura’n / frequency or regularity
RFs
- PCOS
- obesity
- anovulatory disorders
- endocrine disorders
- just after puberty or right before menopause
Eti / Ddx = “PALM COEIN”
- Polyps / PCOS / perimenopause
- Adenomyosis
- Leiomyoma
- Malignancy / Metabolic i.e high prolactin or thyroid abnormalities
- Coagulopathy / Cushing’s syndrome
- Ovulatory dysfunc’n
- Endometrial disorder
- Iatrogenic i.e med induced (POCP, antidepressants antipsychotics)
- Not known
Tx
- Estrogen / COCP
- Tranexamic acid
→ MOA = anti-fibrinolytic - binds to lysine receptor on plasminogen → plasminogen becomes plasmin → can no longer bind to fibrin mesh → fibrinolysis + clot destruc’n = inhibited ∴ clotting = promoted → by promoting clotting, helps w/ heavy bleeding - Hysterectomy
- Know for OSCE *
Uterine fibroids ✓
Def - benign uterine tumors
RFs
- black
- in her 40s
Types
- intramural = w/in myometrium
- pedunculated = on a stalk
- subserosal = just below outer layer of uterus
→ grow outwards + can become so large that they fill abdominal cavity
- submucosal = just below endometrium
SSX = usually asymptomatic or . . .
- heavy mensal bleeding
- irregular firm + central pelvic mass
Ix = hysteroscopy ifor submucosal fibroids presenting w/ heavy menstrual bleeding + pelvic U/S for larger fibroids
Tx
- If fibroid < 3 cm . . .
1. Mirena coil
2. SSX Mx w/NSAIDs + tranexamic acid
3. COCP
4. cyclical oral progestogens GnRH agonists such as leuprorelin - If fibroid > 3 cm = gyn referral
→ Tx = above medical Mx / Sx i.e . . . myomectomy (only Tx known to improve fertility in pts w/ fibroids) / endometrial abla’n / hysterectomy
Complica’ns
- UTIs
- ↓ed fertility
- constipa’n
- urinary outflow obstruc’n
- tors’ of fibroid (usually in pedunculated fibroids)
- Fe deficiency anemia due to heavy menstrual bleeding
- pregnancy complica’ns such as miscarriage or premature labor
- red degenera’n = ischemia, infarc’n + necrosis of fibroid due to disrupted blood supply
→ more likely to occur during 2nd + 3rd trimester of pregnancy + in fibroids > 5 cm
→ SSX = severe abdominal pain + tachycardia + low-grade fever +/- vomiting
→ Tx = supportive i.e rest, fluids + analgesia
- Know for OSCE *
Ovarian cysts ✓
RF = premenopausal
Types
- func’nal
→ follicular cysts (most common ovarian cyst)
= harmless + tend to disappear after a few menstrual cycles
⟹ on U/S will have thin walls + no internal structures
→ dorpus luteum cysts = whe ncorpus luteum fails to break down + instead fills w/ fluid (often occur in early pregnancy)
- other i.e . . .
→ serous cystadenomas = benign epithelial cell tumors
→ mucinous cystadenoma = benign epithelial cell tumors
→ endometrioma = endometriosis in ovaries ∴ cause pain + disrupt ovula’nn
→ dermoid cysts / germ cell tumor = benign ovarian teratoma associated w/ ovarian tors’n → can contain skin / teeth / hair / bone
SSX = usually asymptomatic but can present w/ acute pelvic pain if there is ovarian tors’n, hemorrhage or rupture of cyst
Ix’s
- U/S for premenopausal women w/ simple ovarian cyst < than 5cm
- Ca 125 tumor marker for ovarian cancer but can also be ↑ed in fibroids, endometriosis, adenomyosis, pelvic infec’n or liver disease → 2 wk wait gyn onc referral if pt has raised Ca 125 or complex cysts
- women < 40 y/o w/ complex ovarian mass will also require LDF, AFP + HCG to screen for germ cell tumor
Mx for simple ovarian cysts in premenopausal women
< 5 cm cysts will self resolve w/in 3 menstrual cycles + no f/u U/S needed
5-7cm = yrly U/S monitoring w/ obgyn
> 7 cm = consider MRI scan or surgical evaulua’n
Tx for postmenopausal women
- simple cysts < 5 cm + normal Ca 125 = U/S monitoring every 4-6 months
- Sx for persistent or enlarging cysts i.e cystectomy or oophorectomy
Complica’ns
- ovarian tors’n
- hemorrhage into cyst
- rupture of cyst w/ bleeding into peritoneum
- Know for OSCE *
Ddx of Hirsutism ✓
- PCOS
- Cushing’s syndrome
- hyperprolactinemia
- androgenic drugs
- Know for OSCE *
How might anovula’n present ? ✓
Prolonged menstrual cycle i.e > 21-32 days
PCOS ✓
RFs
- obesity
- FHx in 1st ° relative
- premature adenarche
SSX
- infertility
- weight gain
- acne due to androgens
- hirsutism due to androgens
- oligomenorrhea (almost all PCOS pts will have this)
Diagnostic criteria (Rotterdam criteria) = ≥ 2 of the following . . .
- anovula’n or oligoovula’n
- hyperandrogenism i.e hirsutism / acne
- polycystic ovaries on U/S
Ix’s
- serum prolactin → might be elevated
- LH → will be elevated
- high LH : FSH ratio
- testosterone
- sex hormone-binding globulin
- TSH to r/o thyroid disease
- pelvic U/S
- transvaginal U/S = gold std for visualizing ovaries
→ diagnostic criteria = ≥ 12 developing follicles in one ovary (“string of pearls” appearance) OR ovarian volume > 10 cm^3
- 2hr 75g OGTT = performed in morning (pre-prandial)
→ Procedure
1. take pt’s BL fasting plasma glucose
2. pt drinks a 75g glucose drink
3. measure plasma glucose 2 hrs later
Results (refer pts w/ impaired glucose or severe SSX to specialist)
- impaired fasting glucose = BL of 6.1-6.9 mmol/l
- impaired glucose tolerance = 2 hr plasma glucose btw 7.8 + 11.1 mmol/l
- diabetes = 2 hr plasma glucose > 11.1 mmol/l
Complica’ns
- CVD
- subfertility due to anovula’n
- metabolic syndrome
- impaired glucose tolerance / T2D (in the long term)
- obstructive sleep apnea
- pregnancy complica’ns including gesta’nal diabetes, pregnancy-induced HTN + pre-eclampsia
SSX Tx
- amenorrhea / oligomenorrhea → COCP or cyclical progestogen such as medroxyprogesterone 10mg OD for 2 wks (every 3-4 months) to induce w/drawal bleed + then do TVUS to assess thickness = necessary to ↓ risk of endometrial hyperplasia + endometrial cancer
⟹ > 10mm thick or unusual appearance = refer for sampling / Bx to exclude Hyperplasia or Cancer - hirsutism / acne → COCP +/- topical therapies as required for acne (retinoids for ex)
- subfertility
→ full asses’nt to consider other causes of subfertility → weight loss, smoking
→ fertility Tx referral (might give Clomiphene to induce ovula’n or recommend IVF)
Mx
- lifestyle Δs i.e . . .
→ weight loss
⟹ weight loss alone can result in ovula’n + hence restora’n of fertility, better insulin resistance, ↓ed hirsutism + ↓ed risk of complica’ns
⟹ orlistat can be used for pts w/ BMI > 30
→ exercise
→ smoking cessa’n
→ antihypertensive medica’ns when required
- screen for CVS RFs via QRISK2 Score
→ statins if QRISK score > 10% - screen for OSA
- ask about emo’nal wellbeing + screen for depress’n / anxiety / eating disorder / -ve body image
- Know for OSCE *
Endometriosis ✓
Def - chronic inflammatory condi’n where endometrium grows in parts of body other than endometrium
→ most common sites of endometriosis = pelvic peritoneum + ovaries
→ when it grows in myometrium = adenomyosis
RFs
- FHx
- nulliparity
- Mullerian anomalies
- being of reproductive age
Pathophys of SSX - cells of endometrial tissue outside uterus respond to hormones in same way as endometrial tissue in actual uterus ∴ shed their lining + bleed during menstrua’n just like regular endometrial tissue → causes irrita’n + inflamma’n of tissues around the sites of endometriosis → cyclical, dull, heavy or burning pain that occurs during menstru’n → bleeding + iflamma’n causes develop’nt of scar tissue that binds organs together
→ inflamma’n can lead to adhes’ns
SSX
- dyspareunia (in adenomyosis)
- dysmenorrhea (in adenomyosis)
- menorrhagia (in adenomyosis)
- chronic or cyclic pelvic pain during mentrua’n = main SSX
- deposits of endometriosis in bladder or bowel can lead to blood in urine or stools
Ix’s
- pelvic U/S may reveal large endometriomas + chocolate cysts
- laparoscopic Sx + Bx = gold std to diagnose pelvic + abdominal endometriosis
- transvaginal U/S of pelvis for adenomyosis
Tx for endometriosis = ibuprofen / naproxen + OCP → GnRH agonist such as oserelin or leuprorelin → hysterectomy
Tx for adenomyosis when woman DOES NOT want contracep’n
- tranexamic acid if pt doesn’t have associated pain - mefenamic acid (NSAID) if pt does have associated pain
Tx for adenomyosis when pt wants contracep’n
1. Mirena coil
2. COCP
3. cyclical oral progestogens
Complica’n = infertility b/c scarring + overproduc’n of PGs interferes w/ fertiliza’n + implanta’n
→ can be treated w/ Sx
Adenomyosis pregnancy complica’ns
- SGA
- PROM
- miscarriage
- preterm birth
- need for C sec’n
- postpartum hemorrhage
- Know it for OSCE *
Cervical Cancer ✓
Epi
- 2nd most common cancer in women worldwide
- peak incidence in 30-39 y/o + > 70 y/o
RFs
- FHx
- HIV
- smoking
- ↑ed # of full term pregnancies
- COCP use for > 5 yrs
- early sexual activity
- ↑ed # of sexual partners
- not using condoms
- not engaging in cervical screening b/c most cases of cervical cancer = preventable w/ early detec’n
Most common Eti = HPV 16 + 18
Types
- squamous cell carcinoma (most common)
- adenocarcinoma
SSX = asymptomatic or . . .
- intermenstrual, postcoital or post-menopausal bleeding
- pelvic pain
- dyspareunia
- abnormal vaginal discharge
Ix = speculum → urgent colposcopy referral if cervix looks abnormal i.e has . . .
- ulcera’n
- bleeding
- inflamma’n
- visible tumor
Pap smear cervical screening (for women + transgender men who still have a cervix)
- every 3 yrs for pts btw 25 + 49 y/o
- every 5 yrs for pts btw 50 + 64 y/o
Pam smear
1. speculum exam
2. cells from cervix = collected w/ a small brush
3. cells from brush = deposited into preserva’n fluid
4. sample = transported to lab
5. sample = tested for HPV
6. if pt = HPV +ve, cells = examined under microscope for dyskaryosis (precancerous Δs)
⟹ possible pap smear cytology results . . .
- inadequate
- normal
- borderline Δs
- low-grade dyskaryosis
- high-grade dyskaryosis moderate or high-grade dyskaryosis severe
- possible invasive SCC
- possible glandular neoplasia
⚠️ Dyskaryosis = found from cervical smear + dysplasia = found on colposcopy !
Cervical screening special rules
- women w/ HIV = screened annually
- women > 65 y/o can request a smear if they haven’t had one since age 50s
- pregnant women due for routine smear should wait until 12 wks post-partum
Colposcopy Steps
- Speculum + equipment called colposcope = used to magnify cervix
- Acetic acid causes abnormal cells to appear white = called acetowhite (probably CIN or cancer)
- Schiller’s iodine test - cervical cells = stained w/ iodine solu’n
→ normal cells = brown stain
→ abnormal areas will NOT stain - Large loop excis’n of transforma’nal zone (LLETZ) can be performed during colposcopy to get a tissue sample → local anesthetic = applied → loop of wire w/ electrical current = used to remove abnormal epithelial tissue on cervix + electrical current cauterizes tissue + stops the bleeding
Grading of cervical intraepithelial neoplasia (CIN) from colposcopy = premalignant
- CIN I = mild dysplasia, affects 1/3 of thickness epithelial layer, likely to return to normal so no need for any Tx
- CIN II = moderate dysplasia, affects 2/3 of thickness of epithelial layer, likely to progress to cancer if left untreated
CIN III / cervical carcinoma in situ = severe dysplasia, VERY likely to progress to cancer if left untreated
→ via LLETZ or cone Bx = where cone-shaped piece of cervix - removed w/ scalpel + sample = sent for histology to assess for malignancy
Staging for cervical cancer (FIGO)
- stage 1a = confined to cervix + < 5mm
- stage 1a = confined to cervix + ≥ 5 mm
- stage 2a = has invaded uterus or upper 2/3 of vagina but no parametrial inva’sn
- stage 2b = has invaded uterus or upper 2/3 of vagina + there is parametrial inva’sn
- stage 3a = has invaded lower 1/3 of vagina but doesn’t extend to pelvic wall
- stage 3a = has invaded lower 1/3 of vagina + extends to pelvic wall
- stage 4a = has spread to adjacent organs i.e bladder
- stage 4b = has spread to distant (15% 5 yr survival rate whereas for stage 1a = 98%)
Tx for cervical cancer
- CIN or early stage 1a = LLETZ or cone Bx
- stage 1b-2a = radical hysterectomy + removal of local lymph nodes + chemo + radi’an
- stage 2b-4a = chemo + radia’n
- stage 4b = Sx + chemo + radia’n + palliative care
- Know for OSCE *
Ovarian Cancer ✓
Epi
→ most common histologic subtype = serous adenocarcinoma
→ leading cause of death from gynecological malignancy b/c presents late + w/ non specific SSX
RFs
- around age 60
- BRCA1/ BRCA2 gene
- ↑ed # of ovula’ns
- obesity
- smoking
- recurrent use of clomifene
- early menarche
- late menopause
- lack of pregnancies
Protective factors
- COCP
- breastfeeding
- pregancy
SSX
- bloating
- early satiety
- loss of appetite
- weight loss
- pelvic pain
- urinary SSX such as frequency or urgency
- ascites (warrants 2 wk wait urgent refereal)
- abdominal or pelvic mass (warrants 2 wk wait urgent referral unless clearly due to fibroids)
- hip or groin pain if mass presses on obturator nerve
Initial Ix’s
- Ca125 + pelvic U/S
- risk of malignancy index (RMI) to estimate risk that an ovarian mass is malignant , takes into account . . .
→ menopausal status
→ Ca 125 level
→ U/S findings
Later Ix’s
- CT scan to establish diagnosis + stage cancer
- histology of sample via CT guided Bx, laparoscopy or laparotomy
- paracentesis / ascitic tap can be used to test ascitic fluid for cancer cells
- women < 40 y/o w/ complex ovarian mass will required AFP + HCG b/c could be germ cell tumor
Staging (FIGO)
- stage 1 = confined to ovary
- stage 2 = has spread past ovary but still inside pelvis
- stage 3 = has spread past pelvis but is still in abdomen
- stage 4 = distant mets i.e outside abdomen
Tx = chemo + Sx
- Know for OSCE *
Endometrial Cancer ✓
Def - usually seen in post-menopausal women
→ most common type = adenocarcinoma
→ good prognosis due to early detec’n
⚠️ women w/ postmenopausal bleeding have endometrial cancer until proven otherwise !
RFs = unopposed estrogen aka too much estrogen
- diabetes
- obesity
- ↑ed age
- early menarche
- late menopause
- estrogen only HRT
- little or no pregnancies
- tamoxigen
- PCOS → lack of ovula’n ↑ estrogen
- Lynch syndrome (nothing to do w/ estrogen)
Proactive factors
- COCP
- Mirena coil
- ↑ed pregnancies
- cigarette smoking
Main SSX = post menopausal bleeding → must do urgent 2 wk wait referral
Ddx
- endometriosis
- cervical cancer
- endometrial hyperplasia = precancerous endometrial thickening
→ hyperplasia w/o atypia
→ atypical hyperplasia
Ix’s
- TRUS to asses endomtrical thickness → normally shoudl be < 4 mm in post menopausal women
- Hysteroscopy + endometrial Bx if > 4 mm
- Always do TRUS in women > 55 y/o w/ unexplained vaginal discharge + visible hematuria w/ anemia / hyperglycemia or ↑ed platelets *
Staging of endometrical cancer (FIGO)
- stage 1 = confined to uterus
- stage 2 = has invaded cervix
- stage 3 = has invaded vagina, ovaries, fallopian tubes or lymph nodes
- stage 4 = has invaded bladder, rectum or beyond pelvis
Tx for endometrial hyperplasia = progestogen via . . .
- mirena coil or via
- continuous oral progestogens such as medroxyprogesterone or levonorgestrel
Tx for endometrial cancer
- for stage 1 + 2 = TAH + b/l salpingo-oophorectomy
- pts w/ high-risk disease may have post-op radiotherapy
- progestogen therapy = sometimes used in frail elderly women who aren’t suitable for Sx
- Know for OSCE *
Contracep’n ✓
- REVERSIBLE = LARCs (long acting reversible contracep’n) / everyday use / only used during sex
1a) LARCs = depo provera injec’ns + implants + IUD
→ DEPO INJEC’N = inhibits ovulat’n, last about 3 months + should not be used after 50 y/o
⟹ side effect = weight gain + ↓ed bone mineral density
⟹ C/I = women > 45 y/o due to ↓ed bone mineral density b/c can cause osteoporosis
→ IMPLANT= in upper inner aspect of arm, inhibits ovula’n + lasts 3 yrs
⟹ side effects = bleeding, HA, acne, bloating, mood, weight gain + hair loss
→ IUD (most effective) = prevent implanta’n + sperm entry + have to be fitted by medical professional
⟹ C/Is = PID in past 3 months, suspected / known pregnancy, unexplained vaginal bleeding + uterine abnormalities
⟹ Mirena (last 5yrs) - releases hormones which change the womb to make it unfavorable for pregnancy, causes stop menstrual cycle to stop completely in 1/3 women
→ if inserted w/in first wk of LMP or previously on reliable contracep’n no addi’nal contracep’n needed, if not then pt should use barrier contracep’n for 7 days
⟹ Ci IUD (lasts 5-10yrs) - releases Cu which kills eggs + sperm + changes womb to make it unfavorable for pregnancy
→ can have unprotected intercourse immediately
→ side effects = more heavy + painful period, intermittent vaginal bleeding
1b) Must use everyday = COCP, POP, vaginal rings + patches
→ POP side effects = disturbed menstrual bleeding + weight gain
⟹ C/I = breast cancer
→ COCP MOA = act on anterior pituitary + hypothalamus to ↓ FSH + LH
→ How to take it → 21 pills in one pack + 7-day pill-free interval
1. start on 1st day of next period or can start on any day but must use alternative contracep’n for 7 days
2. ideally should be taken @ the same time every day
3. What to do if missed pill
→ if 1 pill missed + < 24-48 hr take missed pill immediately + resume normal pill-taking w/o any extra precau’n
→ if ≥ 2 missed pills take 1 as soon as remembered + use addi’nal contracep’n for the next 7 days
→ COCP side effects . . .
- HTN ⟹ should get regular check-ups
- migraines
- thrombosis ⟹ calf pain, leg swelling, CP, SOB
→ COCP C/Is where disadvantages > advantages . . .
- BMI > 35
- controlled HTN
- BRCA1/BRCA2 carrier
- current gallbladder disease
- immobility i.e. wheel chair use
> 35 y/o + smokes < 15 cigarettes/day
- FHx of thromboembolic disease in 1st degree relatives who are < 45 y/o
→ COCP Absolute C/Is . . .
- migraine w/ aura
- uncontrolled HTN
- current breast cancer
- Hx of thromboembolic disease
> 35 y/o + smoking > 15 cigarettes/day
- Hx of stroke or ischemic heart disease
- breast feeding + < 6 wks post-partum
- major surgery w/ prolonged immobiliza’n
+ve antiphospholipid antibodies (such as in SLE)
1c) Only during sex = male condoms, female condoms + diaphragms
→ condoms = easily available + protect against STIs but can cause allergies
- IRREVERSIBLE = male + female steriliza’n
→ male = vasectomy + female = tubal liga’n or tubal occlusive device
- EMERGENCY CONTRACEP’N
- Cu IUD = best op’n = for up to 120hrs after intercourse = effective for up to 5 yrs
→ C/Is = PID in past 3 months, pregnancy, unexplained genital bleeding, ancer - Hormonal methods
→ Ulipristal Acetate EllaOne = w/in 120 hrs but the earlier the better = selective progesterone receptor modulator that inhibits ovula’n
→ Levonelle / Levonorgestrel = w/in 72 hrs but the earlier the better - Know for OSCE *
What are the 2 gynecological emergencies ? ✓
Ectopic pregnancy + ovarian tors’n
- ectopic pregnancy = life threatening
- ovarian tors’n = pt can lose ovary
Ectopic Pregnancy ✓
Def - implanta’n of fertilized ovum outside of uterine endometrial cavity
→ most commonly occurs in fallopian tube (ampulla specifically)
RFs
- IVF
- PID
- smoking
- Hx of STIs
- endometriosis
- pelvic or tubal Sx
- IUD use while pregnant
- precious ectopic pregnancy (recurrence = 10-20%)
SSX = painful vaginal bleeding + amenorrhea + abdominal or adnexal tenderness
Ddx
- ruptured ovarian cyst
- miscarriage
Ix’s
- serum β hCG (= more accurate than urine pregnancy test b/c can detecte even small levels of hCG)
= secreted by synctio-trophoblast in early pregnancy but then placenta takes over (placenta also produces hPL, GnRH, GHRH, calcitonin + relaxin)
→ should 2x every 24-28 hrs if not SUSPECT ECTOPIC !
- Transvaginal U/S → in normal pregnancy we expect to see gesta’nal sac IN uterus so if that’s not the case you should suspect an ectopic pregnancy
⟹ takes 5 wks for sac to be visible
⟹ @ 6 wks yolk sac = visible + fetal heartbeat = audible - Fetal doppler → in ectopic pregnancy, fetal heartbeat might be OUTSIDE of uterine cavity
Tx for ruptured ectopic pregnancy = surgical extrac’n + fluid resucita’n
Tx if moderate risk of rupture = methotrexate + surgical extrac’n
Tx if low risk of rupture i.e minimally symptomatic + hemodynamically stable = expectant Mx
Complica’ns
- recurrence
- maternal death due to rupture of implanta’n site + intraperitoneal hemorrhage
Ovarian tors’n ✓
Def - when ovary twists in rela’n to surrounding structures
→ more likely to occur w/ benign tumors + during pregnancy
Eti - ovarian mass > 5cm whether that be a cyst or a tumor
SSX chronology
1. sudden onset severe u/l pelvic pain
2. pain gets progressively worse + might be accompanied by N + V
SSX on exam
- localized tenderness
- palpable
→ absence of mass does not exclude diagnosis
Ix’s
- 1st line Ix = pelvic U/S → might show “whirlpool sign” free fluid in pelvis + edema of ovary
- definitive diagnosis = via laparoscopic Sx
Tx
1. urgent gyn admiss’n
2. laparoscopic Sx for detors’n i.e untwisting + fixing ovary in place OR oophorectomy
Complica’ns
- loss of that ovary
→ fertility ≠ usually affected when this happens b/c other ovary can compensate
- if necrotic ovary ≠ removed
→ may become infected → abscess forms → sepsis OR abscess ruptures → peritonitis + adhes’ns
Molar pregnancy SSX ✓
- larger than normal fundal height for gesta’nal age
- severe early onset pre-eclampsia
- exaggerated SSX of pregnancy such as excessive vomiting + rapidly ↑ing uterine size = due to prolifera’n of abnormal trophoblastic tissue
Subfertility ✓
Def - failure to conceive after 1 yr of regular unprotected sexual intercourse (UPSI)
→ warrants referral to fertility doctor
→ the more yrs of subfertility a couple has, the lower their chances of successfully conceiving in the future
Epi
- very common
- 1 in 6 couples seek specialist help
- 84% will achieve pregnancy in 1yr w/ regular UPSI
- 92% will achieve that w/in 2yrs
Eti
- ovula’n disorders
- tubal factors
- male factors (25%)
- no cause
Ix’s
- BL FSH (day 2-5), LH, TSH, prolactin + testosterone
- mid luteal progesterone to confirm ovula’n (7 days before bleeding)
- semen analysis to see if due to male subfertility
- U/S to assess tubal patency
Tx = IVF
→ criteria for fertility Tx for 40-42 y/o pts . . .
- 2 yr Hx of infertility
- never had IVF
- no evidence of low ovarian reserve
- had tests done that show that their ovaries would respond normally to fertility drugs
- have discussed risks of IVF + becoming pregnant @ this age w/ their Dr
What’s the most important sperm parameter for successful concep’n ✓
Sperm motility b/c sperm has to be able to reach egg !
Absolute C/Is to breastfeeding ✓
- anti mitotic drugs
- breast reduc’n w/ nipple transplant
- any radioactive substance (diagnostically or therapeutically)
Immediate Mx of neonate born w/o adequate pulse or respira’n ✓
- Dry, stimulate + wrap in warm towel
- AIRWAY - check for obstruc’n, meconium + intubate if very premature or HR = low
- BREATHING - if not breathing by 90 secs, do 5 infla’n breaths w/ bag + then O2 mask ventila’n
- CIRCULA’N - if chest is moving + airway is ≠ obstructed but pt is still bradycardic start chest compress’ns
- DRUGS - if none of the above worked give adrenaline / Na bicarb / dextrose
Fetal circula’n + how fetal ducts close ✓
Fetal circula’n
- Umbilical veins carry O2ated blood that they got from placenta
- DUCTUS VENOSUS allows umbilical veins to bypass liver b/c they split @ liver + O2ated blood from umbilical veins goes to IVC → RA
→ normally would go to RV next but due to low O2 in baby, there’s high vasoconstric’n so pulm. artery + pressure on right side = high + blood can’t move from low to high ∴ most of blood goes to LA via FORAMEN OVALE instead, but a tiny bit makes it to RV
→ normally RV would send blood to lungs, but baby’s lungs = fluid-filled so we need to bypass lungs + instead go straight to aorta (via DUCTUS ARTERIOSUS) - DeO2ated blood = returned to placenta via umbilical arteries
- Once umbilical cord = cut, alveolar fluid = cleared from lungs via expuls’n + absorp’n
→ baby’s lungs fill w/ O2 so vessels dilate i.e vasoconstric’n → ↓ pulm.artery + right side pressure
⚠️ Umbilical cord has 3 vessels (2 arteries + 1 vein)
- Now that lungs = cleared of fluid, surfactant = produced (↓ surface tens’n of air-liquid interface w/in alveolar walls which ↓ tendency of alveoli to recoil on expans’n + ↑ lung compliance which prevents lung + alveolar collapse) → alveoli capillaries fill w/ blood + start gas exchange
Fetal duct closure
- Foramen ovale closes mechanically initially + then permanently by fibrosis + becomes Fossa ovalis but if remains open = Patent Foramen Ovale (PFO) ≠ true Atrial Septal Defect (ASD) b/c no atrial septal tissue = missing but it does ↑ risk of stroke
- Ductus venosus closes + becomes Ligamentum venosum
- Ductus arteriosus closes due to ↑ in bradykinin + becomes Ligamentum arteriosum but if remains open = Patent Ductus Ateriosus (PDA) = maintained open by PGE2, so medica’ns like indomethacin or ibuprofen which inhibit PG synthesis = effective for closing duct
→ sometimes Sx may be required to close particularly large PDAs
→ in case of some congenital heart defects like pulm. atresia / critical pulmonary stenosis / transposi’n of great arteries, PDA = kept open - Umbilical veins become ligamentum teres
Prematurity ✓
Def - baby born before 37 wks
→ < 28wks premies have the worse prognosis
RFs
- poly or oligohydramnios
- substance use during pregnancy
- maternal infec’n during pregnancy
- vaginal bleeding during pregnancy
Complica’ns
- chronic bronchopulmonary disease
- retinopathy of prematurity = incomplete retinal vasculariza’n
→ can lead to severe visual impairment in childhood - periventricular leukomalacia = injury of white matter that’s responsible for lower limb motor control
- PVH (Periventricular-Intraventricular Hemorrhage) = bleeding of blood vessels of germinal matrix in periventricular area → bleed can extend into ventricles + cause death
- necrotizing enterocolitis = ischemic necrosis of intestinal mucosa → creates hole in intestine through which bacteria can leak through → severe abdominal infec’ns
Necrotizing enterocolitis ✓
Def - disorder affecting premature neonates where part of their bowel becomes necrotic = life-threatening emergency
Eti = prematurity
Pathophys - ischemic necrosis of intestinal mucosa
→ bowel perfora’n i.e hole in intestine → bacteria can leak through that hole → severe abdominal infec’ns
→ peritonitis + shock
SSX
- intolerance to feeding
- vomiting (particularly w/ green bile)
- generally unwell
- distended, tender abdomen
- absent bowel sounds
- blood in stools
Ix’s
- FBC
- CRP
- Capillary blood gas → will show metabolic acidosis
- Blood culture
- AXR for diagnosis → will show . . .
⟹ dilated loops of bowel
⟹ thickened bowel walls b/c of bowel wall edema
⟹ pneumatosis intestinalis i.e gas in bowel wall
⟹ pneumoperitoneum i.e free gas in peritoneal cavity (means there’s pefora’n)
⟹ gas in portal veins
Tx
1. NPO + IV fluids, ttl parenteral nutrit’n (TPN) + IV Abx
2. NG tube can be inserted to drain fluid + gas from stomach + intestines
3. Might need Sx to remove dead bowel
→ babies may be left w/ a temporary stoma if significant amt of bowel = removed
Complica’ns
- perfora’n
- peritonitis
- sepsis
- death
- strictures
- abscess forma’n
- long term stoma after Sx
- short bowel syndrome after Sx
3 common neonatal emergencies i.e TTN, RDS + meconium aspira’n ✓
- Transient tachypnea of the newborn (TTN)
Def - impaired gas exchange due to alveolar fluid from lungs not being cleared (most common neonatal emergency)
→ occurs in term or late preterm infants
→ w/ supportive therapy can spontaneously resolve after 24-78 hrs w/o leaving any long-term complica’n
RFs
- lack of labor i.e C-sec’n b/c no vaginal delivery to clear liquid
- maternal diabetes b/c insulin delays matura’n of type 2 pneumocytes ∴ ↓ing surfactant produc’n
Ix = CXR → may show over-inflated lungs w/ interstitial edema
- Meconium Aspira’n Syndrome (MAS)
Def - respiratory distress in newborn due to meconium in baby’s trachea
RFs
- gesta’nal age > 42 wks
- pregnancy-induced HTN
- maternal diabetes
- maternal smoking or substance misuse
- fetal distress
- oligohydramnios
- thick meconium
- Apgar > 7
- chorioamnionitis
- C sec’n
SSX
- hypoxia
- recess’n
- cyanosis
- tachypnea
- poor feeding
- barrel shaped chest
- meconium stained skin, nails + umbilicus
Diagnostic Ix = CXR → will show patchy perihilar infiltrates + lung hyperinfla’n due to air trapping
Tx
1. suc’n baby’s mouth as soon as head = visible
2. O2 therapy if mild + CPAP if moderate or severe
Complica’ns
- pneumothorax
- persistent pulmonary HTN
- Respiratory Distress Syndrome (RDS)
RFs
- prematurity b/c lungs = immature
- C-sec’n b/c there was no labor to stimulate surfactant produc’n + secre’n
- gesta’nal diabetes b/c of delayed surfactant produc’n
Eti
- sepsis
- pneumonia
- acute pancreatitis
- fat embolism
- being pre-term
Pathophys - not enough surfactant → high surface ten’sn w/in alveoli → atelectasis (lung collapse)
→ inadequate gaseous exchange → hypoxia, hypercapnia + respiratory distress
SSX
- cyanosis
- hypoxia
- grunting
- tachypnea
- tachycardia
- nasal flaring
- subcostal + intercostal retrac’ns
- ground glass appearance on CXR
Tx
- Dry
- A, B, C
- Drugs
a) antenatal steroids to mom such as dexamethasone → speeds up surfactant produc’n in lungs
b) exogenous surfactant
- CPAP → assists in keeping airways + alveoli open by delivering +ve expiratory pressure right when alveoli = most likely to collapse
Short term complica’ns
- apnea
- infec’n
- pneumothorax
- pulmonary hemorrhage
- necrotizing enterocolitis
- intraventricular hemorrhage
Long term complica’ns
- retinopathy of prematurity
- chronic lung disease of prematurity
Hypoxic Ischemic Encephalopathy (kids + adults) ✓
Def / pathophys - prolonged hypoxia → restric’n in blood flow to brain i.e ischemia → brain malfunctioning i.e encephalopathy
Eti = anything that leads to brain asphyxia i.e . . .
- maternal shock
- intrapartum hemorrhage
- prolapsed cord
- nuchal cord (when cord = wrapped around baby’s neck)
Grading based on SSX + prognosis
→ mild
- poor feeding
- irritability
- resolves w/in 24 hrs
→ moderate
- poor feeding
- lethargi
- hypotonic
- seizures
- can take wks to resolve + up to 40% of pts will develop cerebral palsy
→ severe
- ↓ed consciousness
- apneas
- flaccid tone
- ↓ed or absent reflexes
- up to 90% of pts develop cerebral palsy
- up to 50% mortality
Ix = ABG
Tx
1) Supportive care i.e neonatal resuscita’n, optimal ventila’n, circulatory support, nutri’n, Tx of seizures
2) Therapeutic hypothermia in neonatal ICU → baby’s temp = lowered for 4 days w/ cooling blankets + cooling hat (target temp = 33-34°C) → after the 4 days baby = gradually warmed to normal body temp over 6 hrs
⟹ goal = to ↓ inflamma’n + neuron loss after hypoxic injury + hence ↓ risk of complica’ns
Complica’ns
- cerebral palsy
- death
- blindness
- develop’ntal delay
- learning disability
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Cerebral palsy (in kids) ✓
Def - non progressive permanent neurological problems resulting from damage to brain around time of birth
RFs
- prematurity
- low birth weight
- birth asphyxia
- multiple births
- maternal illness
- fetal brain malforma’n
- major birth defects
- familial metabolic or genetic disorder
- neonatal complica’ns
Eti
- Antenatal
→ maternal infec’n
→ tauma during pregnancy - Perinatal
→ birth asphyxia
→ pre term birth - Postnatal
→ meningitis
→ severe neonatal jaundice
→ head injury
Types
- spastic / pyramidal hypertonia = due to UMN damage
→ monoplegia = only 1 limb affected
→ hemiplegia = limbs one 1 side affected (left or right)
→ diplegia = all 4 limbs affected but legs = worse
→ quadriplegia = all 4 limbs affected + seizures, speech disturbance + other neuro impairments
- dyskinetic / athetoid / extrapyramidal = pbs w/ controlling muscle tone due to basal ganglia damage
- ataxic = pbs w/ coordinated mov’nt due to cerebellar damage
Ddx
- brain tumor
- muscular dystrophy
- myelodysplasia
Ix = brain MRI → will show periventricular leukomalacia, congenital malforma’n, stroke or haemorrhage
Tx = MDT w/ PT, OT, dietician
Complica’ns
- feeding difficulties
- intellectual disability
- hearing / visual impairment
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Muscular dystrophies ✓
Def - progressive motor muscle diseases caused by defective or absent glycoproteins in the muscle membrane
Common types
- Duchenne muscular dystrophy (X linked recessive) = most common one (presents in children usually)
- Myotonic dystrophy → presents in adulthood w/ . . .
⟹ progressive muscle weakness
⟹ prolonged muscle contrac’ns
⟹ cataracts
⟹ cardiac arrhythmias
⟹ difficulty releasing grip
RFs
- FHx
- male + 3-5 y/o for Duchenne
Eti of Duchenne = defective dystrophin gene on X chromosome = protein that helps hold muscles together at the cellular level
SSX
- intact sensa’n
- hypotonia
- hyporeflexia
- difficulty ambulating, running + jumping
- calf hypertrophy
- Gower’s sign in children due to proximal muscle weakness = putting their hands on their legs to help themself stand up (SSX of Duchenne)
Ix’s
- creatine kinase → elevated in Duchenne
- genetic testing b/c = often due to genetic muta’n
Tx = oral corticosteroids + PT/OT + exercise
Tx for bedwetting in children ✓
- Lifestyle Δs i.e not drinking too much before bed + setting alarm to pee @ certain time
- Desmopressin b/c ↓ nighttime urine produc’n
Biliary atresia (kids) ✓
Def - progressive necroinflammatory congenital condi’n where part of bile duct = narrowed or completely absent
Pathophys - liver = able to conjugate bilirubin but conjugated bilirubin can’t be excreted b/c of absent bile duct
SSX
- persistent neonatal jaundice i.e ≥ 2 wks
- dark urine
- pale stool
Ix’s
- ttl bilirubin
- conjugated bilirubin → will be elevated
- LFTs
- PT + INR to check if liver is damaged + hence unable to make clotting factors
- abdominal U/S
- sweat Cl test to r/o CF
- 𝛼 antitrypsin b/c when deficient can cause neonatal cholestasis
Tx
- Sx called Kasai portoenterostomy → a sec’n of small intestine = attached to liver opening i.e where bile duct would normally attach but even after Sx inflammatory process can continue to ascend through intrahepatic biliary tree
- Liver transplant in end stage liver disease
Complica’ns
- fibrosis
- cirrhosis
- portal HTN
- GI bleed
- deficiency in fat soluble vitamins
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Constipa’n in children ✓
RFs
- low fiber diet
- poor fluid intake / dehydra’n
- psychosocial problems such as issues at home or at school
SSX
- < 3 stools / wk
- hard stools that are difficult to pass
- rabbit dropping stools
- straining
- painful passages of stools
- abdominal pain
- avoiding going to bathroom b/c of anticipated pain
- hard stools may be palpable in abdomen
- encopresis (fecal incontinence)
Ix = clinical diagnosis
Tx
- high fiber diet
- hydra’n
- laxatives (movicol) → should be continued long term + slowly weaned off as child develops normal, regular bowel habit
Complica’ns
- anal fissure
- abdominal pain
- anal fissure
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Hirschsprung’s disease ✓
Def - congenital condi’n where parasympathetic ganglion cells of Myenteric plexus = absent in distal bowel + rectum
→ usually diagnosed in 1st yr of life
RFs
- FHx
- Down syndrome
- neurofibromatosis
- endocrine neoplasia type 2A
Eti - congenital absence of ganglion cells of Myenteric / Auerbach plexus
Pathophys - myenteric plexus = part of enteric nervous system + is responsible for stimulating peristalsis in large bowel → during fetal develop’nt parasympathetic ganglion cells of myenteric plexus start higher up in GI tract + gradually migrate down towards distal colon + rectum → in Hirschsprung’s the ganglion cells don’t travel all the way down ∴ leaving a sec’n of colon or whole colon in ttl w/o innerva’n
→ aganglionic sec’n becomes constricted → feces can’t move → bowel obstruc’n → proximal to obstruc’n bowel becomes distended + full
SSX
- delay in passing meconium i.e > 24 hrs
- chronic constipa’n since birth
- abdominal pain + disten’n
- vomiting
- poor weight gain / FTT
Ddx
- CF
- chronic constipa’n
Ix’s
- AXR → will show dilated loops of bowel + air-fluid levels
- Rectal Bx + histology to confirm diagnosis → will show absence of ganglion cells
Tx
1. Bowel irriga’n (doesn’t work for pts w/ ttl colonic Hirschsprung’s disease)
2. Surgical removal of aganglionic sec’n of bowel
→ most pts patients will have a normal life after Sx but they might have long term disturbances in bowel func’n + some ° of incontinence
3. Ileostomy + Sx for ttl colonic Hirschsprung’s
Complica’ns
- Hirschsprung associated enterocolitis (HAEC) = inflamma’n + obstruc’n of intestine occurring in ~ 20% of neonates w/ Hirschsprung’s = life threatening b/c can lead to toxic megacolon + bowel perfora’n
→ presents w/in 2-4 wks of birth w/ . . .
- fever
- abdominal disten’n
- diarrhea +/- blood + features of sepsis
→ Tx = IV Abx, fluid ressuscita’n + decompress’n of obstructed bowel
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Gastroenteritis in children ✓
Def - inflamma’n of stomach all the way to intestines
RFs
< 5 y/o
- other sick ppl in household
- contaminated food / water
- poor hand hygiene
- lack of immuniza’n against rotavirus
- lack of breastfeeding
- immunodeficiency
Eti = viral usually in children (rotavirus + norovirus)
SSX
- high fever i.e > 39° C
- N + V
- abdominal pain
- pooping 6-7x w/in 24hr period
Ddx
- IBS
- IBD
- intussuscep’n
- lactose intolerance
- CF
- celiac
- medica’ns such as Abx
Ix’s
- clinical diagnosis
- U + E to check for dehyrdra’n
- FBC
- MCS of stool (rarely required)
Tx
1. Isolate pt so they don’t spread it to others (in ward)
2. IV fluids if pt = dehydrated
3. Fluid challenge to see if they can be managed at home i.e give pt small volume of fluid orally every 5-10 mins + see if they tolerate it
4. After SSX have resolved pt needs to be off from school for an addi’nal 48 hrs
Complica’ns
- IBS
- Guillain Barré
- hypoglycemia
- reactive arthritis
- metabolic acidosis
- lactose intolerance
- electrolyte imbalance
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Most common cause of diarrhea in children w/o any weight loss or FTT ✓
Toddler’s diarrhea → usually resolves by age 5
Intussucep’n (in kids) ✓
Def - condi’n where bowel invaginates / telescopes into the lumen of a more distal adjoining part of bowel
→ most common site of intussuscep’n = ileocecal
→ usually affects infants btw 6 + 18 months old but peak age = 5-9 months
RFs
- male
- CF
- concurrent viral URTI
- Henoch-Schonlein purpura
- intestinal polyps
- Meckel’s diverticulum
- Peyer patch in terminal ileum
SSX
- severe, progressive colicky abdominal pain
- inconsolable crying
- pale / lethargic / unwell child
- vomiting
- diarrhea
- red currant jelly stool b/c of blood + mucus (late sign)
- palpable sausage-shaped mass in RUQ
- constipa’n
Ddx
- gastroenteritis
- pyloric stenosis
Ix’s
- AXR as usual whenever obstruc’n = suspected
- U/S for diagnosis → will show a target-like mass or doughnut sign
- Barium enema (= contraindicated if there’s peritonitis, shock, perfora’n or pt = clinically unstable)
Tx
1. Fluid resucita’n + therapeutic enema
→ contrast, water or air = pumped into colon to force folded bowel out of bowel + into its normal posi’n
2. Fluid resucita’n + surgical reduc’n if enema fails
3. Fluid resucita’n + surgical resec’n if pt has bowel necrosis or perfora’n
Complica’ns
- bowel obstruc’n → peristalsis = disrupted → mesentery becomes compressed → blood vessels = trapped in layers of bowel → intestinal ischemia → gangrenous / necrotic bowel → bowel perfora’n → death (very rare)
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Pyloric stenosis (in kids) ✓
Def - thickening / hypertrophy of pyloric sphincter
RFs
- FHx
- male
- btw 2-12 wks old
Pathophys - thickening / hypertrophy of pyloric sphincter → narrowing of pyloric canal
SSX
- recurrent projectile non-bilious vomiting after feeding b/c of peristalsis (even after changing formula)
- weight loss / FTT
- palpable olive shaped mass in RUQ
Ix’s
- U + E + ABG → HypoCl, HypoK, HypoNa + metabolic alkalosis
- U/S for diagnosis → pyloric channel length > 15 mm + pyloric muscle thickness > 3 mm
Tx = IV fluid + electrolyte replacement + Ramstedt pyloromyotomy (open or laparoscopic)
→ incis’n = made in smooth muscle of pylorus to widen canal so that food can pass from stomach to duodenum as normal
→ prognosis after opera’n = excellent
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Meningitis (in kids + adults) ✓
Def - inflamma’n of meninges due to infec’n
→ bacteria meningitis + meningococcal infec’n = NOTIFIABLE DISEASES !
RFs
< 2 y/o b/c of incomplete immuniza’n
- immunocompromised
- crowded living
Eti
- TB meningitis (usually doesn’t present acutely)
→ usually in pts < 5 y/o in TB endemic reg’n - viral meningitis (most common eti)
→ enteroviruses (coxsackie B virus = most common viral pathogen)
→ HSV
→ VZV - bacterial meningitis pathogens based on age . . .
≤ 3 months = Group B Strep, E. coli, Listeria (also common in elderly + immunocompromised pts)
1 month - 6 y/o = N meningitidis, S pneumoniae, Hib
> 6 y/o = N meningitidis + in adults S pneumoniae
- fungal meningitis
SSX
- fever
- HA
- neck stiffness
- photophobia
- poor feeding / vomiting
- lethargy
- irritability
- seizures
- AMS / Δ in level of consciousness
- non-blanching rash in children if there is meningococcal septicemia
Ddx
- encephalitis
- cerebral malaria
- TB meningitis
Ix’s
- LP + culture / viral PCR to determine pathogen
⚠️ Anywhere below L3 = safe for LP b/c spinal cord stops @ L1/L2
⚠️ LP C/Is = GCS < 9, active seizures / post ictal or pt = hemodynamically unstable
→ bacterial meningitis LP = elevated neutrophils, elevated protein, very low glucose, high pressure inflammatory
exudate + cloudy / turbid appearance
→ viral meningitis LP = elevated lymphocytes, normal protein, normal glucose, + clear appearance
- Kernig’s test → lie pt on their back, flex one hip + knee to 90° + then slowly straighten knee while keeping hip flexed @ 90°
⟹ if there is spinal pain or resistance to mov’nt = suspicious for meningitis - Brudzinski’s test → lie pt flat on their back → gently use your hands to lift their head + neck off the bed
→ flexing their chin to their chest
⟹ +ve test = pt involuntarily flexes their hips+ knees = diagnostic for meningitis - FBC / blood culture
Tx for bacterial meningitis (clinical suspic’n = enough to treat)
→ < 3 months old = IV cefotaxime + IV amoxicillin
→ > 3 months old = IV CTX
⚠️ Administer benzylpenicillin parenterally in the meantime if pt hasn’t arrived to hospital yet
⚠️ Any febrile child w/ purpura should be given IM Benzylpenicillin + admitted immediately
⚠️ Always do LP in pt w/ suspected sepsis if pt = febrile + < 1 month old OR 1-3 months old + unwell / has low or high WCC
Post exposure Ppx if exposed to pt w/ meningococcal infec’n = single dose of ciprofloxacin (ideally w/in 24 hrs of diagnosis)
→ risk of transmiss’n = highest if person had prolonged contact w/ pt w/in 7 days prior to onset of illness
⟹ risk ↓ after that ∴ if 7 days following exposure to pt the haven’t developed any SSX = unlikely that they have it
Tx for HSV or VZV viral meningitis = aciclovir
Complica’ns of bacterial meningitis
- hearing loss due to inflammatory damage to cochlear hair cells (always do auditory assess’nt after meningitis)
- hydrocephalus
- cerebral abscess → will have to be drained
- seizures / epilepsy
- cognitive impairment
- learning disability
- memory loss
- focal neuro deficits i.e limb weakness / spasticity
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Obstructive sleep apnea (OSA) ✓
Def - when pt stops breathing for up to a few minutes while they’re sleeping
→ obstructive = due to collapse of pharyngeal airway
→ central = pb is in brain
RFs
- male
- middle age
- obesity
- alcohol
- smoking
- severe cases can cause HTN, HF + ↑ risk stroke or MI
⚠️ Pts that need to be fully alert for work such as vehicle operators require an urgent referral to ENT or sleep specialist + may have to amend their work duties while waiting for assess’nt !
SSX
- partner notices episodes of apnea @ night
- snoring
- always tired
- daytime somnolence
- waking up w/ HAs
Ddx
- narcolepsy
- insufficient sleep
- inadequate sleep hygiene
- periodic limb mov’nt disorder
- hypersomnia due to drug or substance use
- hypoTSH
Diagnostic Ix = sleep study or polysomnography
Tx
1. Managing modifiable RFs i.e weight loss, smoking cessa’n + ↓ing alcohol consump’n
2. CPAP machine
3. Upper airway Sx if it reaches that point
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Develop’ntal / congenital hip dysplasia ✓
Def - structural abnormality in children’s hips due to abnormal develp’nt of fetal bones during pregnancy
RFs
- female
- FHx in 1st ° relative
- breech presenta’n at / after 36 wks
- multiple pregnancy
- birth weight > 5 kg
Screening = done via neonatal exam @ birth + @ 6-8 wks to check for any suspicious findings such as . . .
- different leg lengths
- restricted hip abduc’n on one side
- significant b/l restric’ in abduc’n
- difference in knee level when hips = flexed
- clunking of the hips on Ortolani + Barlow
→ have high specificity in detec’n of hip instability
⟹ ortolani test (goal = to relocate) = +ve if distinctive clunk is heard as hip relocates
⟹ barlow test (goal = to dislocate) = +ve if hip can be popped out of socket w/ maneuver
Diagnostic Ix = hip U/S if clunking = heard or child has multiple RFs → will show subluxa’n on provocative testing + abnormal rela’nship btw femoral head + acetabulum
⟹ subluxa’n = not fully dislocated or dislocatable
⟹ disloca’n = femoral head sits fully outside of acetabulum (whether at rest or w/ provocative testing)
Tx
- if pt presents @ < 6 months old, Tx = Pavlik harness
→ keeps the pt’s hips flexed + abducted
→ purpose = to hold femoral head in its correct posi’n so that acetabulum (hip socket) can develop into a normal shape
→ requires regular review + harness = removed after 6-7 wks if hip = stable - if pt presents @ > 6 months old or harness fails Tx = Sx
→ after Sx hip spica cast = used to immobilize hip for a prolonged period of time
Complica’ns if persists into adulthood
- muscle weakness
- abnormal gait
- early degenerative Δs
- recurrent subluxa’n or disloca’n
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Osgood-Schlatter disease (in kids) ✓
Def - inflamma’n of tibial tuberosity in teenagers = where patella ligament inserts
→ usually u/l but can also be b/l
→ pt can have 1 episode or multiple episodes
→ lasts for a couple wks or months but eventually SSX will fully resolve
⟹ pt = left w/ hard boney lump on knee
RFs
10-15 y/o
- male
- athlete
SSX (gradual onset)
- visible or palpable hard + tender lump on tibial tuberosity
- pain in anterior aspect of knee that is worse w/ knee extens’n, kneeling + physical activity
Tx
- less physical activity
- ice
- NSAIDS (ibuprofen) for symptomatic relief
- PT
Complica’n (very rare) = avuls’n fracture
= separa’n of tibial tuberosity from rest of tibia
→ Tx for this = Sx
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Slipped upper femoral epiphysis (in kids) ✓
Def - when head of femur slips / = displaced along growth plate ∴ femoral head will be displaced postero-inferiorly + metaphysis + epiphysis will be misaligned
→ most common hip disorder in teenagers
→ only left hip = usually affected but can also be b/l
RFs
- 8-16 y/o + obese
- more common in boys but presents earlier in girls (11 y/o v.s 12 y/o)
SSX
- antalgic gait
- sudden hip / groin / thigh or knee pain
- limb can appear shortened
- restricted range of hip mov’nt (internal rota’n = most affected ∴ pt will prefer to keep hip externally rotated)
Ddx
- hip fracture
- Perthes
- avascular necrosis
- hip dysplasia
- osteomyelitis
- septic arthritis
- ankylosing spondylitis
Ix’s
- b/l anterior posterior + frog leg lateral x rays
for diagnosis
→ on b/l anterior posterior x ray Klein’s line will not intersect w/ femoral head as it normally should
→ on frog leg lateral x ray Klein’s line will not intersect w/ femoral head + physis will be blurry or widened (+ve Bloomberg sign) - FBC + inflammatory markers to r/o Ddx
Tx = Sx i.e internal fixa’n of femoral head + fixing it in place so that it’s in its correct posi’n + doesn’t slip further
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Legg-Calvé-Perthes / Perthes (in kids) ✓
Def - spontaneous avascular necrosis of head of hip due to disrup’n in blood flow to femoral head
→ affects epiphysis of femur = bone that’s distal to physis (aka growth plate)
→ over time there is revasculariza’n / neovasculariza’n, healing of femoral head + bone remodeling as bone heals
RFs = male, thin + 4-8 y/o
Eti - idiopathic
SSX
- pain @ hip jt especially w/ mov’nt
- antalgic gait
- ROM of hip = restricted
- limited abduc’n + internal rota’n
- gluteal wasting
+ve Trendelenburg sign
Ddx
- septic arthritis
- slipper upper femoral epiphysis
Ix’s
- b/l hip x-ray for diagnosis → will show femoral head collapse + fragmenta’n + subchondral fracture
⟹ in early disease will show widening of jt space
⟹ in later disease will show flattening / ↓ed size of femoral head - FBC + inflammatory markers to r/o Ddx
Tx
< 5 y/o = mobiliza’n + monitoring + non surgical containment
7-12 y/o = surgical containment → salvage procedure
> 12 y/o = salvage procedure → replac’nt arthroplasty if there’s arthritis (after pt reaches skeletal maturity)
Mx
- bed rest
- trac’n
- crutches
- analgesia
- PT
Complica’ns
- early hip osteoarthritis (long term)
- limb length inequality (long term)
- stiffness
- loss of rota’n
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Transient synovitis of the hip (in kids) ✓
Def - self-limiting inflammatory disorder of synovial membrane of hip jt in children
→ most common cause of hip pain in 2-12 y/o pts
→ often occurs a couple wks after viral URTI
→ SSX should start to improve after 24-48 hrs + should completely resolve after 1-2 wks
RFs = male + 2-12 y/o
SSX
- limp
- hip or groin pain
- refusal to bear weight
Ix’s
- log roll for diagnosis → ask pt to lie supine + gently roll their leg from side to side = +ve if that mov’nt causes involuntary muscle guarding in affected limb
- FBC + inflammatory markers to r/o septic arthritis
- X ray to r/o Perthes
Tx = supportive i.e analgesia (NSAID or paracetamol)
Talipes / Clubfoot (in kids) ✓
Def - fixed abnormal ankle posi’n that presents @ birth
RFs
- male
- FHx
- associated congenital abnormalities such as spina bifida, Down syndrome, cerebral palsy
SSX
- ankle = in equinus
- forefoot = adducted
- hindfoot = in varus
Ix = clinical diagnosis
Tx
- Ponseti method (ideally should be done immediately after birth) - foot = manipulated towards a normal posi’n + a cast = applied to hold it in posi’n → this is repeated over + over until foot = in right posit’n
⟹ at some point achilles tenotomy = performed to release tens’n in achilles tendon
⟹ has initial correc’n rate of 98%
⟹ compliance = strong predictor of recurrence - Surgical interven’n if Ponsetti fails, if there’s recurrence or if there are residual deformities
Kawasaki disease (in kids) ✓
Def - self-limiting systemic medium vessel vasculitis that typically affects children < 5 y/o
→ 2nd most common childhood vasculitis after IgA vasculitis
RF = asian
Eti - no known cause
SSX
- persistent high fever for > 5 days (i.e > 39ºC)
- red palms w/ desquama’n i.e peeling of skin on finger + toes
- widespread erythematous maculopapular rash
- strawberry tongue
- dry, cracked lips
- b/l conjunctivitis
- cervical lymphadenopathy
Ddx = scarlet fever b/c both can have strawberry tongue
Disease course
1- Acute phase (last 1-2 wks) → child = unwell w/ fever, rash + lymphadenopathy
2- Subacute phase (lasts 2-4 wks) → acute SSX settle but desquama’n + arthralgia occur + there is now risk of coronary artery aneurysm forming
3- Convalescent stage (lasts 2-4 wks) → remaining SSX settle, blood tests slowly return to normal + any coronary aneurysm may regress
Ix’s
- FBC → might show anemia, leukocytosis + thrombocytosis
- LFTs → might show hypoalbuminemia + elevated liver enzymes
- CRP / ESR → will be elevate (ESR especially)
- Urinalysis → leukocytes
- Echocardiogram to check for any coronary artery pathology
Tx = high dose aspirin to ↓ risk of thrombosis + IV Igs to ↓ risk of coronary artery aneurysms
⚠️ Kawasaki disease = one of few scenarios where aspirin = used in children !
⚠️ Aspirin = usually avoided in children due to risk of Reye’s syndrome !
Complica’ns
- coronary artery aneurysms
- myocarditis
- pericarditis
- Know for OSCE *
Mesenteric Adenitis (in kids) ✓
Def - swelling of abdominal lymph nodes due to viral gastroenteritis = self-limiting
→ common cause of stomach pain in pts < 16 y/o
SSX
- sore throat or cold SSX before stomach pain even started
- abdominal pain (in umbilicus or RIF)
- fever
- nausea
- diarrhea
Ix = clinical diagnosis
Mumps ✓
Def - self-limiting viral infec’n characterized by parotid gland swelling (resolves after 1 wk) = NOTIFIABLE DISEASE !
→ spreads via respiratory droplets
→ incuba’n period = 14-25 days
RFs
- unvaccinated status
- interna’nal travel
Eti - Mumps virus = RNA paramyxovirus
SSX chronology
1. Prodrome i.e flu-like SSX . . .
- fever
- HA
- muscle aches
- lethargy
- dry mouth
- ↓ed appetite
2. Parotid gland swelling a couple days later
→ can be u/l or b/l
SSX of complica’ns
- abdominal pain b/c of pancreatitis
- testicular pain + swelling b/c of orchitis
- confus’n, neck stiffness + HA b/c of meningitis or encephalitis
Ix
- reverse transcriptase PCR of saliva swab for diagnosis
- mump antibodies
→ +ve IgM = ACTIVE infe’n
→ +ve IgG = vaccinated or past infec’n
Tx = supportive i.e rest, fluids + analgesia
Complica’ns
- orchitis
- meningitis
- pancreatitis
- encephalitis
- sensorineural hearing loss
Hand foot + mouth disease (in kids) ✓
Def - highly contagious self-limiting childhood viral infec’n (itchy vesicular rash + illness resolve after 7-10 days)
→ incuba’n period = 3-5 days
RFs
< 10 y/o
- immunosuppress’n
- family or school contacts w/ infec’n
Eti = coxsackie A virus
SSX chronology
1. URTI SSX such as fever, sore throat, dry cough + fatigue
2. small painful ulcers on mouth + tongue 1-2 days later
3. painful blistering red spots across body (hands + feet)
Ix = clinical diagnosis
Mx
- supportive i.e paracetamol + hydra’n
- avoiding sharing towels + bedding
- washing hands regularly
- careful handling of dirty diapers
- Know for OSCE *
Scarlet fever (in kids) ✓
Def - exotoxin-mediated infectious disease associated w/ group A strep infec’n (tonsillitis usually)
= NOTIFIABLE DISEASE !
RFs
3-6 y/o
- GAS pharyngitis
- close contact w/ person w/ scarlet fever
SSX
- fever > 38°C
- lethargy
- sore throat
- red-pink, blotchy, blanching macular rash w/ rough “sandpaper” texture that starts on trunk + spreads outwards but spares palms + soles
- pts can have red, flushed cheeks
- desquama’n after 7 days i.e rash peels
- strawberry tongue
- cervical lymphadenopathy
Ddx = kawasaki b/c both can have strawberry tongue
Ix = clinical diagnosis
Tx = 10 days of Phenoxymethylpenicillin (Penicillin V) or Azithromycin instead if pt has if penicillin allergy
→ school exclus’n until 24 hrs after starting Abx
- Know for OSCE *
Viral exanthema in kids i.e widespread eruptive rash due to viral infec’n ✓
a) Measles
b) Rubella / german measles
c) Parvovirus B19
d) Roseola
A) MEASLES = NOTIFIABLE DISEASE !
Def - highly contagious self-resolving viral infec’n (resolves 7-10 days after SSX onset)
→ spreads via respiratory droplets
→ incuba’n period = 10-12 days
RF = unvaccinated status
Eti - measles virus = RNA virus
SSX
- fever
- cough
- coryzal SSX
- conjunctivitis
- Koplik spots i.e greyish white spots on buccal mucosa that appear 2 days after fever = diagnostic of measles
- erythematous, macular rash w/ flat les’ns that starts 3-5 days after fever on face (behind ears usually) + then spreads to rest of body
Diagnostic Ix = measles antibodies
→ +ve IgM = ACTIVE infe’n
→ +ve IgG = vaccinated or past infec’n
Mx = supportive + after SSX resolve children need to be isolated for 4 addi’nal days
Complica’ns (30% of pts will develop a complica’n)
- diarrhea
- pneumonia
- dehydra’n
- encephalitis
- meningitis
- hearing / vis’n loss
- death
B) RUBELLA / GERMAN MEASLES
Def - highly contagious self-limiting viral infec’n
= NOTIFIABLE DISEASE !
→ spreads via respiratory droplets
→ incuba’n period = 2 wks
→ = rare due to MMR vaccine
RFs
- incomplete immuniza’n
- exposure to infectious contact
- interna’nal travel
Eti - Rubella virus = a togavirus
SSX
- fever
- jt pain
- sore throat
- petechial rash that starts on face, then spreads to rest of body + lasts 3 days
- hepatosplenomegaly
- post auricular / cervical lymphadenopathy
Ix’s
- salivary rubella IgM → +ve means acute
- Diagnostic Ix = rubella antibodies
→ +ve IgM = ACTIVE infe’n
→ low avidity IgG = past infec’n but not too long ago
→ high avidity IgG = past infec’n way back or vaccina’n
Mx
- supportive
- offer MMR vaccine w/in 72 hrs if pt ≠ vaccinated
- once rash appears, pt should stay home for ≥ 5 days + avoid pregnant women
Most common complica’n = otitis media but pneumonia = most common cause of death in these pts
C) PARVOVIRUS B19 / slapped cheek / 5th disease
Def - childhood self-limiting viral infec’n (rash + SSX disappear 1-2 wks later)
→ transmitted by respiratory secre’ns or through placenta
→ pt = infectious 7-10 days before rash appears + no longer infectious once rash appears
RFs = spring + close contact w/ infected individual
SSX chronology
1. non-specific viral SSX i.e mild fever, muscle aches + lethargy
2. after 2-5 days, diffuse bright red rash appears on both cheeks
3. a few days later = reticular (net like) mildly erythematous rash affecting trunk + limbs appears
→ can be raised + itchy
Ddx = rubella
Ix in non pregnant pt = clinical diagnosis
Ix’s in pregnant women w/ possible parvovirus
- IgM → tests for acute infec’n wi/in past 4 wks
- IgG → tests for immunity to virus after past infec’n
- Rubella antibodies b/c rubella = Ddx
Tx = paracetamol → NSAIDs for arthritis SSX
Pts @ risk of complica’ns
- immunocompromised pts
- pregnant women
- pts w/ hematological disorders such as sickle cell anaemia, thalassaemia, hereditary spherocytosis or hemolytic anemia
Regular complica’ns
- aplastic anemia
- encephalitis
- meningitis
Complica’ns in pregnancy
- miscarriage
- fetal death
- severe fetal anemia
- hydrops fetalis i.e fetal heart failure
- mirror syndrome / pre-eclampsia-like syndrome in mom = hydrops fetalis + placental edema + edema in mom + HTN + proteinuria
D) ROSEOLA
Def - childhood febrile illness
RFs = < 2 y/o or immunocompromised
Eti
- human herpes virus 6 (more common)
- human herpes virus 7
SSX chronology
1. high grade fever (> 39.5°C) for 3-7 days + then fever resolves
2. non-itchy rose colored maculopapular rash that starts on torso + spreads to limbs, spares face
→ pt = no longer infectious once rash appears
Ix = clinical diagnosis
Tx = supportive i.e antipyretic such as paracetamol or ibuprofen
Complica’n = febrile convuls’n
- Know for OSCE *
Molluscum contagiosum (in kids) ✓
Def - self limiting contagious infec’n in kids mainly but can also occur in adults
→ caused by molluscum contagiosum virus (type of poxvirus)
→ can take up to 18 months for papules to disappear
RFs
- close contact w/ infected individual
- sexual contact w/ infected individual
- atopic dermatitis
- immunocompromised such as HIV pts
- tropical climate
SSX
- smooth pearl-like papules w/ central dimple
→ in HIV pts = larger + more numerous + predominantly over genital reg’n + face
Diagnostic Ix = clinical diagnosis w/ dermatoscope
Mx
- avoid scratching or picking les’ns b/c can lead to spreading, scarring + infec’n
- avoid sharing towels to minimize spread of infec’n
Cryptorchidism (undescended testes) ✓
Def - when ≥ 1 testes hasn’t descended yet
→ testes have to descend for optimal sperm produc’n + to avoid cancer !
RFs
- FHx
- SGA
- low birth weight i.e < 2.5 kg
- prematurity
- maternal smoking during pregnancy
Pathophys of testicular descent
1) Transabdominal stage - begins @ 8wks gesta’n
→ gubernaculum enlarges + anchors testes to what will become the inguinal reg’n (via trac’n)
→ gubernaculum shortens as it progressively incorporates into gubernacular bulb
2) Inguinoscrotal stage - begins @ 26wks
→ testes = initially in posterior abdominal wall
→ processus vaginalis forms
→ gubernacular bulb dilates inguinal canal
→ abdo. pressure + gubernaculum contrac’n pushes testes through inguinal canal + into scrotum
→ as testes descend through inguinal canal they take layers of abdominal wall w/ them, which will become layers of scrotum + also take vessels, nerves + vas deferens
→ abdominal contents exit abdominal cavity through internal / deep inguinal ring + external / superficial inguinal ring + extend into scrotum
→ by 33 wks, testicular descent = complete
→ gubernaculum regresses
→ remnant of testo-scrotal attach’nt = left behind
⚠️ indirect inguinal hernias = due to processus vaginalis failing to close after migra’n of testes into scrotal sac
Ix = clinical diagnosis
Tx - give it 6 months initially + then do
orchidopexy Sx if testes still hasn’t descended by then
Complica’ns = ↑ed risk of . . .
- testicular tors’n
- infertility
- testicular cancer
ADHD (in kids) ✓
Def - neuro-developmental disorder that starts in childhood + is characterized by inatten’n, hyperactivity + that affects child’s ability to carry out everyday tasks, develop normal skills + perform well academically
RFs
- FHx
- male
- low birth weight
- epilepsy
- tic disorder
Inatten’n SSX
- poor listening skills
- misplaces items needed to complete activity or task
- distracted by external or unimportant stimuli
- forgets daily activities
- small atten’n span
- lack of ability to complete work or follow instruc’ns
- disinclined to start HW any activity requiring [ ]
- inability to focus on details
- thoughtless mistakes in schoolwork or assignments
Hyperactive SSX
- squirms when seated
- constantly fidgets w/ feet or hands
- marked restlessness that is difficult to control
- seems to always be on the go
- lack of ability to play in a quiet manner
- can’t staying seated in class
- overly talkative
Impulsive SSX
- difficulty waiting for their turn
- interrupts or intrudes conversa’ns / others’ activities
- impulsively blurts out answers w/o hearing quest’n
Diagnostic criteria = ≥ 6 SSX in pts < 17 y/o or ≥ 5 SSX in pts ≥ 17 y/o for ≥ 6 months in ≥ 2 settings
Classfiica’n
- combined type = pt has both inattentive + hyperactive/impulsive SSX
- predominantly inattentive type
- predominantly hyperactive / impulsive type:
Ix = clinical diagnosis
Tx for < 6 y/o
1. classroom behavior interven’n
2. methylphenidate
3. guanfacine
Tx for > 6 y/o
1. psychoeduca’n + behavioral therapy +/- stimulant
2. start stimulant or try diff stimulant
- Know for OSCE *
Autism spectrum disorder (in kids) ✓
Def - lifelong genetic neurodevelopmental condi’n characterized by receptive behavior + deficit in communica’n + social interac’n
RFs = male + FHx
Impaired social interac’n SSX
- difficulty w/ normal back + forth conversa’n
- failure to initiate or respond to social interac’ns
- difficulty in understanding + forming rela’nships
- gaze avoidance
- socially / emo’nally inappropriate behavior
- can’t do imagine play
Repetitive behavior SSX
- lining up toys or flipping objects / echolalia / idiosyncratic phrases
- ritualized behavior
- strong attachment or preoccupa’n w/ unusual object
- hyper or hyporesponsive to visual or sensory input
Diagnostic criteria = impaired social interac’n SSX + ≥ 2 repetitive behavior SSX + SSX must start in childhood
Ix = autism questionnaire
Tx
1. behavioral interven’n
2. early interven’n
3. family support + educa’n
- Know for OSCE *
Where are Fe, B12 + B9 absorbed ? ✓
“FedBiL”
Fe = duodenum
→ side effect of Fe supplement = constipa’n
B12 = ileum
B9 = jejunum
The 6 Anterior pituitary v.s the 2 Posterior pituitary hormones ✓
- Anterior
→ ACTH- stimulates adrenal glands to produce hormones
→ LH
→ FSH
→ GH
→ TSH
→ Prolactin - Posterior
→ ADH
→ Oxytocin
1° + 2° retroperitoneal organs ✓
“ADIPUC KER”
1° = “ADIPUC”
A = Adrenal glands + aorta
D = Duodenum (except duodenal cap)
I = IVC
P = Pancreas (except tail which is intraperitoneal)
U = Ureters
C = Colon (ascending + descending)
2° = “KER”
K = Kidneys
E = Esophagus
R = Rectum
What are the meninges ? What are its 3 layers from most superficial to deep ? ✓
= membranous covering of brain + spinal cord w/ 3 layers . . . (from superficial to deep)
- dura mater
- arachnoid mater
- pia mater
Where is CSF located, where is it produced, how does it flow + how does it get reabsorbed ? ✓
CSF = located in subarachnoid space btw pia mater + arachnoid membrane
CSF = produced in choroid plexus of each ventricle by ependymal cells
Flow of CSF (“L 34S”) - Lateral ventricles to 3rd ventricle via foramen of Monro → 3rd to 4th ventricle via cerebral aqueduct → 4th ventricle to subarachnoid space of CNS (medially via foramen of Magendie + laterally via foramen of Luschka) → gets reabsorbed into dural venous sinuses via arachnoid granula’ns
Vertebrae structure ✓
Vertebrae = separated by intervertebral discs that have fibrous outer ring called annulus + gel-filled center called nucleus
All vertebrae have vertebral body anteriorly + foramen + 2 transverse processes + 1 spinous process
- 7 cervical (C1 = atlas, C2 = axis)
→ y shaped spinous process
→ triangular foramen
→ has extra spinal nerve but for others matches # of vertebrae - 12 thoracic
→ circular foramen - 5 lumbar
→ round spinous process
→ triangular foramen - 5 sacral (fused vertebrae)
The 3 types of spine curvature ✓
- Lordosis = swayback
- Kyphosis = hunchback (think “knotre dame”)
- Scoliosis = curved left or right
⚠️ We naturally have cervical lordosis, thoracic kyphosis + lumbar lordosis
The 5 antibody classes ✓
- all have 2 heavy chains (must be the same) + 2 light chains (2 𝛼 or 2 kappa)
- all have 2 binding sites → Fab + Fc
→ Fab role = bind antigen
→ Fc role = bind other things
“GAMED”
G = most abundant in bloodstream, only one that can cross placenta, has 4 subclasses
A = most commonly produced Ig in the body, monomer or dimer, mainly present in secre’ns of digestive, respiratory + urogenital tracts systems i.e breast milk / tears / mucus
M = 1st to be produced + is a pentamer
E = monomer
D = monomer, mainly a receptor since is initially there w/ M
What are the 2 types of adaptive immunity ? ✓
1) Humoral = for extracellular pathogens = B cell + antibody mediated
- B cells = produced in bone marrow → go to spleen for final matura’n → are now mature but still inactive → T independent activa’n for nonprotein antigens + T dependent activa’n for protein antigens
- helper T cell (Th) has CD4 component + antigen component → CD4 component interacts w/ MHC-II of antigen presenting cell + antigen component interacts w/ antigen → produces cytokine that activates B cells + triggers clonal expans’n → daughter cells from clonal expans’n are either short lived fully differentiated plasma cells or long lived memory cells → those that become plasma cells secrete IgM 1st
2) Cell-mediated = via T cells
= for intracellular phagocytosed microbes that survived + escape to cytoplasm or viruses that replicate inside infected cells
- Naive T cells express antigen receptors + reside in lymphoid organs → microbes have antigens on their surfaces + get transported to lymphoid organs → in these organs antigens = processed + displayed by MHC molecules on APCs → after antigen recogni’n, antigen-specific T cells secrete cytokines that stimulate prolifera’n of antigen specific T cells
(= CLONAL EXPANS’N)
→ a por’n of them will undergo differentia’n into effector T cells or memory T cells → effector T cells can be cytotoxic CD8 T cells or CD4 T-helper cells or NK’s
→ CD4 helper T cells secrete cytokines to ↑ antibody produc’n → plasma cells induce differentia’n of cytotoxic CD8 T cells into CTL‘s so they can perform cytolysis of infected cell or produce cytokines that inhibit viral replica’n
Familial v.s Sporadic Cancer ✓
- Familial = due to inherited muta’n
- Sporadic = due to acquired muta’n whether that be as a result of exposure to radia’n or just random chance
Unique features of Latent TB ✓
- asymptopmatic
- normal CXR
- non-contagious
2 main meningitis Ix’s ✓
CSF microscopy + culture
Bacteria most likely to cause meningitis in 6 y/o pt ✓
Neisseria mengitidis
What Ix should u do for a symptomatic suspected TB pt ? ✓
Sputum culture → +ve means active TB
When there’s an acute inflamma’n such as in appendicitis, what cells are most likely to be seen microscopically / histologically ? ✓
Neutrophils
What’s the biggest RF for diabetic foot disease ? ✓
Peripheral arterial disease
What do the left gastric artery, right gastric artery, left gastroepiploic artery + short gastric artery supply ? ✓
- left gastric artery supplies distal esophagus + upper right por’ns of fundus + body of stomach
- right gastric artery supplies lesser curvature of stomach
- left gastroepiploic artery supplies fundus + upper por’n of gastric body
- short gastric artery supplies fundus of stomach on the side of greater curvature of stomach
What is horseshoe kidney ? ✓
Abnormal kidney where inferior kidney poles of kidneys = fused hence result = U shaped kidney located lower than it normally would be
→ pts = asymptomatic
Diff parts of nephron + their roles ✓
- PO4 = co-transported w/ Na across semi-permeable membrane along w/ up to 2/3 of filtered water in PCT + up to 2/3 of filtered water = reabsorbed by PCT
- Thin ascending limb of Loop of Henle = impermeable to water but highly permeable to Na + Cl → reabsor’n of Na + Cl ions then occurs in thick ascending limb
- Thick descending limb of Loop of Henle = permeable to water but impermeable to solutes
- The PCT has the highest metabolic demand so is the most sensitive to anoxia *
Why should MMR vaccine not be given before 1 y/o ? ✓
B/c pt will have suboptimal immune response due to maternal antibodies still present
How many ribs do we have ? ✓
12 pairs
- 7 pairs of true ribs
- 3 pairs of false ribs
- 2 floating ribs
What are the 7 shoulder ligaments ? ✓
- anterior glenohumeral ligaments (x3)
- coraco clavicular ligament
- coraco humeral ligament
- coraco acromial ligament
- transverse humeral ligament
What are the 4 shoulder jts ? ✓
- glenohmeral (does external rotata’n)
- sterno clavicular
- acromioclavicular
- scapulothoracic
What are the 9 possible shoulder mov’nts + what muscle(s) = responsible for each ? ✓
- Initia’n of abduc’n i.e up to 15° = supraspinatus
- Abduc’n of 15-90° = deltoid
- Abduc’ beyond 90° = trapezius + serratus anterior
- Adduc’n = pec minor/major + lat dorsi + teres major
- Extens’n = lat dorsi + teres major + long head of triceps + posterior fibers of deltoid
- Flex’n = pec major + biceps brachii + coracobrachialis + anterior fibers of deltoid
- Medial/Internal rota’n = pec major + lat dorsi + teres major + anterior fibers of deltoid + subscapularis (injury to this muscle = hard to detect b/c pec major compensates for it)
- Lateral/External rota’n = teres minor + posterior fibers of deltoid + infraspinatus
- Circumduc’n = pec major + lat dorsi + teres major/minor + deltoid + subscapularis + biceps brachii + coracobrachialis + long head of triceps + supraspinatus + infraspinatus
What nerve is damaged when the neck of the humerus is fractured ? ✓
Axillary nerve
How many muscles compartments does the arm have ? ✓
2 compartments
- Anterior (flex’n + slight abduc’n)
→ innerva’n = musculocutaneous nerve
→ muscles = biceps brachii + coracobrachialis + brachialis - if it ends in brachialis it means blood supply = brachial artery *
- Posterior (does extens’n + slight adduc’n)
→ innerva’n = radial nerve
→ muscles = triceps brachii + anconeus
Consequences of musculocutaneous nerve damage ✓
Weakness in arm flex’n + sensory loss in lateral forearm
What are the 3 superficial muscles of the pectoral reg’n ? ✓
Deltoid (shoulder) + pec major + serratus anterior
What causes lateral + medial winged scapula ? ✓
Lateral = due to spinal accessory nerve palsy which causes absent pull of trapezius + rhomboid muscles (very rare)
Medial = absent pull of serratus anterior muscle due to long thoracic nerve palsy (most common) → pt will have pb w/ arm abduc’n since that muscle = involved w/ that
Our 4 superficial back muscles ✓
- Trapezius → trapezoid looking muscle from back of neck to shoulders
- Lat dorsi → equivalent of serratus anterior but at the back
- Levator scapulae → equivalent of SCM but at the back
- Rhomboid minor + major (to the left of scapula if you’re looking at the back)
→ thin strip on top = minor + large square at the bottom = major
Shoulder v.s Elbow jt ✓
- Shoulder = ball + socket
- Elbow = hinge jt
The 3 articula’ns of the elbow jt ✓
- Humero radial
- Humero ulnar
- Proximal radioulnar
What are the 3 elbow jt ligaments ? ✓
- Annular
- Medial - ulnar collateral
- Lateral - radial + lateral collateral
What 3 important things does the cubital fossa contain ? ✓
brachial artery + median + radial nerve
How many compartments does the forearm have ? ✓
2 compartements
- Anterior = flex’n (8 muscles ttl)
→ 5 superficial =
- FDS (Flexor Digitorum Superficialis)
- Flexor Carpi Ulnaris
- Flexor Carpi Radialis
- Palmaris Longus
- Pronator Teres
⟹ all insert in medial epicondyle of humerus so can be injured in medial epidcondyltis / golfer’s elbow
→ 3 deep =
- Flexor Digitorum Profundus
- Flexor Pollicis Longus
- Pronator Quadratus
⟹ innerva’n = median nerve except FCU + FDP = ulnar
- Posterior = extens’n (12 muscles ttl)
⟹ innerva’n = radial nerve
→ 3 “Carpi”
- Extensor carpi radialis longus
- Extensor carpi radialis brevis
- Extensor Carpi Ulnaris
→ 3 “Digit …”
- Extensor Digitorum
- Extensor Indicis
- Extensor Digiti Minimi
→ 3 “Pollicis”
- Extensor Pollicis longus
- Extensor Pollicis brevis
- Abductor Pollicis Longus
→ 3 randoms
- Brachiradialis
- Supinator
- Anconeus
⚠️ All the “carpi” + “digit…” that begin w/ extensor = injured in lateral epicondylitis / tennis elbow
Muscles of the hands ✓
3 thenar muscles (“FOA”)
- Flexor Pollicis Brevis
- Opponens Pollicis
- Abductor Pollicis Brevis
→ innerva’n = median nerve
4 hypothenar muscles (“POAF”)
- Palmaris Brevis
- Opponens Digiti Minimi
- Abductor + Flexor Minimi Brevis
→ innerva’n = ulnar nerve
4 others (“PADL”)
- Palmar Interossei (does ADduc’n)
- Abductor Pollicis
- Dorsal Interossei (does ABduc’n)
→ innerva’n = deep ulnar
- x4 Lumbricals (innerva’n = mix of median + ulnar)
Fibromyalgia ✓
Def - syndrome characterized by widespread pain for ≥ 3 months
RFs
20-60 y/o
- FHx
- female
- rheumatological condi’n
- life stressors
SSX
- widespread pain
- 2° fatigue / irritability / sleep disturbances
Ix = clinical diagnosis
Tx
1. exercise / PT / relaxa’n
2. SNRI
- Know for OSCE *
What are bursa ? ✓
Sacs created by synovial membrane filled w/ synovial fluid = found @ bony prominences i.e knee, greater trochanter, shoulder, elbow
→ their func’n = to ↓ fric’n btw the bones + soft tissues during mov’nt
- Know for OSCE *
Chronic fatigue syndrome X
X
Greater Trochanter Bursitis / Trochanteric Bursitis ✓
Def - inflamma’n of a bursa over greater trochanter of hip
SSX
- greater trochanteric pain syndrome i.e gradual onset aching or burning pain in outer hip that may radiate down to outer thigh
→ pain = worse after activity or sitting / standing for a prolonged amt of time - tenderness over greater trochanter but no swelling like in other types of bursitis
- pain on resisted hip mov’nts
+ve tredelenburg test
Tx
- rest
- ice
- analgesia w/ NSAID
- physio
- steroid injec’ns
Complica’n = difficulty sleeping b/c pain makes it hard to find comfortable posi’n
- Know for OSCE *
Olecranon Bursitis / student’s elbow ✓
Def - inflamma’n + swelling of an elbow bursa
Eti
- trauma
- fric’n from repetitive mov’nts or leaning on elbow
- inflammatory condi’n such as gout or RA
- infec’n (in this case = septic bursitis)
SSX = warm, tender + swollen elbow
Addin’al SSX in septic bursitis
- fevere
- hot to touch
- very tender
- erythema on surrounding skin
- sepsis SSX
Ddx
- septic arthritis
- gout
- pseudogout
Ix = jt aspir’an + microscopy, culture + gram staining
→ pus = infec’n
→ straw colored fluid = less likely to be infec’n
→ blood stained fluid = trauma, infec’n or inflamma’n
→ milky fluid = gout or pseudogout
Tx for septic bursitis = AB such as flucloxacillin
Regular Tx
- rest
- ice
- compres’n
- analgesia w/ paracetamol or NSAID
- protec elbow from pressure or trauma
- steroid injec’ns may be used in problematic cases + only if + after infec’n has been excluded
- Know for OSCE *
Epicondylitis (medial + lateral) ✓
Def - inflamma’n @ point where tendons of forearm insert into epicondyles @ elbow = type of repetitive strain injury
→ medial epicondyle = wrist flex’n
→ lateral epicondyle = wrist extens’n
RFs = repetitive activity + > 40 y/o
Types (“LT MG”)
- lateral epicondylitis / tennis elbow
- medial epicondylitis / golfer elbow
SSX
- pain + tenderness @ that epicondyle that radiates down forearm
- weakness in grip strength
Ix’s for tennis elbow = Mill’s test + Cozen’s test
Tx
- rest
- analgesia
- PT
- orthotics such as elbow braces or straps
- steroid injec’ns
- platelet-rich plasma (PRP) injec’ns
- extracorporeal shockwave therapy
- Know for OSCE *
Compartment Syndrome ✓
Def - orthopedic emergency where pressure w/in a fascial compartment = abnormally elevated ∴ blood flow to that compartment = cut off
Eti
- tight cast / dressing
- trauma (fractures most commonly) but can also be crush injury or contus’n
SSX = 6 P’s
- pain that is disproportionate to clinical situa’n (analgesia doesn’t help)
- pallor
- paresthesia (in chronic compartment syndrome)
- perishingly cold (body loses ability to auto regulate temp = late sign)
- paralysis (late + worrying sign)
- pulseless (late sign)
Ix = clinical diagnosis but needle manometry can be used to measure compartment pressure
Emergency Tx
1. remove any tight cast / dressing
2. urgent fasciotomy to release pressure
→ compartment = explored to identify + debride any necrotic muscle tissue → wound = left open + is then covered w/ dressing
3. elevating leg to heart level
4. avoiding hypoTN
Complica’ns
- tissue necrosis if left untreated
- limb loss
- Know for OSCE *
Hip fracture ✓
RFs
- old age
- female
- osteoporosis
- frequent falls
- low BMI
Eti = trauma or 2° to osteoporosis
Types
- intra capsular fracture = break in femoral neck w/in capsule of hip jt
→ affects area proximal to intertrochanteric line
Garden classifica’n for intra-capsular fractures
Grade I = non-displaced + incomplete fracture
Grade II = non-displaced but complete fracture
Grade III = partial displacement i.e trabeculae are @ an angle
Grade IV = full displacement i.e trabeculae = l l
Tx for Grade 1 or 2 = internal fixa’n w/ screws to hold femoral head in place while fracture heals
Tx for Grade 3 or 4 who can walk independently = ttl hip replac’nt i.e femoral heads + acetabulum = removed + replaced
Tx for Grade 3 or 4 w/ limited mobility or significant comborbidities = hemiarthroplasty i.e replacing femoral head but leaving acetabulum in place
- extra capsular fracture = hip fracture where blood supply to femoral head = intact ∴ no need to replace femoral head
→ intertrochanteric fractures = ones that occur btw greater + lesser trochanter
⟹ Tx = dynamic hip screw i.e sliding hip screw
→ subtrochanteric fractures = ones that occur proximal to femoral shaft but distal to + w/in 5cm of lesser trochanter
⟹ Tx = intramedullary nail - metal pole = inserted through greater trochanter into central cavity of femoral shaft
SSX
- shortened, abducted + externally rotated leg
- unable to bear weight
- pain in hip or groin that might radiate to knee
Ix’s
- anterior to posterior (AP) + lateral hip X-ray for diagnosis
→ disrup’n of Shenton’s line = NOF (neck of femur) fracture
- MRI or CT if X-ray = -ve but you still suspect hip fracture
Fall Ix’s if pt fractured due to fall i.e . . .
- FBC to check for anemia
- U + E to check for electrolyte imbalances
- ECG to check for arrhythmias / MI
- BNP to check fo heart failure
- CT to check for stroke
Complica’ns
- avascular necrosis
- half of pts become less independent after a hip fracture
- Know for OSCE *
Ankle fracture ✓
Eti = low E fall
SSX
- ankle pain + swelling
- inability to bear weight
Ddx
- lateral ankle ligament tear
- achilles tendon rupture
Ix for diagnosis = X-ray
Tx for open fracture = emergency Sx
Tx for closed fracture w/ disloca’n - closed reduc’n + splint → open reduc’n + fixa’n
- Know for OSCE *
What are the 4 knee ligaments ? ✓
- anterior cruciate ligament → attaches @ anterior intercondylar area on tibia + stops tibia from sliding forward in rela’n to femur
- anterior drawer test + Lachlan test *
- posterior cruciate ligament → attaches @ posterior intercondylar area one tibia + stops tibia frim sliding backwards in rela’n to femur
- lateral collateral ligament
- medial collateral ligament
According to Ottawa knee rules which pts presenting w/ knee injury require an X-ray ? ✓
Pts w/ ≥ 1 of the following . . .
≥ 55 y/o
- patellar tenderness + no tenderness elsewhere
- fibular head tenderness
- unable to flex knee to 90°
- can’t bear weight i.e can only take a max pf 3 steps
⚠️ Rapid swelling in knee injury = suggestive of hemarthrosis !
Meniscal tear ✓
Def - knee injury where meniscus (cartilage in knee jt) = damaged
RFs
- american football
- rugby
- basketball
- trauma
- prior knee injury
Eti = twisting mov’nts in knee i.e playing sports
SSX
- “pop” sound when injury initially happens
- pain that may refer to hip or lower back
- swelling
- stiffness
- restricted ROM
- locking of knee
- instability or the knee
Ddx = tear or sprain one of the 4 knee ligaments
Ix’s
- MRI scan = 1st line
- Arthroscopy = gold std for diagnosis → allows us to visualize meniscus w/in jt
Tx
1. conservative Mx i.e analgesia w/ NSAIDs + RICE
2. Sx sometimes
- Know for OSCE *
ACL injury ✓
RFs
- athlete
- trauma
Eti = twisting injury to knee
SSX
- pain
- knee swelling
- sudden “pop” sound accompanied by pain
Ddx = other knee ligament injury
Ix’s
- anterior drawer test
- Lachmann test
- MRI scan = 1st line
- Arthroscopy = gold std for diagnosis → allows us to visualize ACL
Tx
1. conservative Mx i.e analgesia w/ NSAIDs + RICE
2. crutches + knee braces may be required to help protect knee while mobilizing
3. arthroscopic Sx to reconstruct ACL (often but not always required)
- Know for OSCE *
Shoulder Disloca’n ✓
Def - when ball of shoulder i.e head of humerus comes entirely out of socket (socket = glenoid cavity of scapula)
→ most common = anterior shoulder disloca’n
→ subluxa’n = partial shoulder disloca’n i.e ball isn’t entirely out of socket + naturally pops back into place soon after
Eti
- 90% of time = anterior
- only seizure or electric shock will cause posterior disloca’n
SSX
- deltoid will appear flattened
- humeral head will cause a palpable bulge
Ix’s
- apprehens’n test to assess for shoulder instability
- X ray for diagnosis + also after reduc’n to confirm shoulder = reduced
- MRI prior to Sx + to check for any Bankart or Hill Sachs les’ns
Tx
- analgesia
- arm sling to support arm
- closed shoulder reduc’n (must r/o fracture first !)
- PT
- Shoulder stabiliza’n Sx sometimes
Complica’ns
- axillary nerve damage (C5/C6) → loss of sensa’n in regimental badge area over lateral deltoid + motor weakness in deltoid + teres minor muscles
- tear of glenoid labrum that surrounds glenoid cavity
- Hill Sachs les’ns = compress’n fractures of posterolateral part of humeral head
- Bankart les’ns = tears to anterior por’n of labrum b/c of repeated shoulder disloca’ns / subluxa’ns
- rotator cuff tear (especially in older pts)
- Know for OSCE *
What are the 4 rotator cuff muscles ? ✓
” SITS AEI “
- Supraspinatus → abducts arm
- Infraspinatus → externally rotates arm
- Teres minor → externally rotates arm
- Subscapularis → internally rotates arm
- Know for OSCE *
Rotator cuff tear ✓
Def - partial or complete tear of tendons of rotator cuff muscles
→ usually supraspinatus tendon
RFs
- active ppl
- older ppl i.e > 60 y/o
Eti
- acute injury such as falling on outstretched hand
- degenerative Δs due to older age
- overhead activities such as tennis or construc’n work
Cofield classifica’n of rotator cuff tears
- small = < 1 cm
- medium = 1-3 cm
- large = 3-5 cm
- massive = >5 cm
SSX
- shoulder pain
- weakness + pain w/ specific mov’nt based on what that muscle does
- difficulty finding comfortable sleeping posi’n due to pain
Diagnostic Ix = U/S or MRI b/c tendon = soft tissue
Tx
- rest
- analgesia
- PT
- arthroscopic rotator cuff repair sometimes
- Know for OSCE *
Adhesive capsulitis i.e frozen shoulder ✓
Def - chronic fibrosing condi’n where shoulder capsule, which is normally elastic + allows for large ROM becomes inflamed ∴ causing ↓ in ROM
→ very common cause of shoulder pain
RFs
40-70 y/o
- diabetes
- prior Hx of frozen shoulder
- prior shoulder Sx
Eti
- 1° = occurred spontaneously w/o any trigger
- 2° = b/c of trauma / Sx or immobiliza’n
SSX chronology (each phase lasts ~ 6 months)
- painful phase i.e shoulder pain (worse @ night)
- stiff phase i.e no more pain but shoulder is now stiff
→ both passive + active mov’nt = affected
→ external rota’n = more affected than internal rota’n - thawing phase i.e gradual improv’nt in stiffness
Ddx for shoulder pain preceded by trauma / injury
- fractre
- shoulder disloca’n
- rotator cuff tear
Ddx for shoulder pain NOT preceded by trauma
- glenohumeral jt arthritis
- acromioclavicular jt arthritis
- supraspinatus tendinopathy (empty can test)
Diagnostic Ix = clinical diagnosis but U/S, CT or MRI might show a thickened jt capsule
Tx
- NSAIDs
- PT
- intra-articular steroid injec’ns
- hydrodila’n i.e injecting fluid into jt to stretch capsule
- Sx in extreme cases
- Know for OSCE *
What’s a contracture ? ✓
Shortening of soft tissues that leads to restricted mov’nt of related jt
Dupuytren’s Contracture ✓
Def - inherited AD condi’n where palmar fascia becomes thickened
→ ring finger = finger that is most often affected
→ index finger = least likely to be affected
RFs
- male
- FHx
- manual labor especially w/ vibrating tools
- diabetes (type 1 > type 2)
- epilepsy
- smoking
- alcohol
Pathophys - palmar fascia becomes thickened + tight → finger contracture → finger = tightened into a flexed posi’n + becomes unable to fully extend
SSX
- painless hard nodules on palm +/- skin thickening / pitting → fascia becomes progressively thicker
→ becomes impossible to fully extend affected finger - thick, nodular cord can be palpated all the way from palm to affected finger
Grading
- grade 1 = thickened nodule + band in palmar aponeurosis
- grade 2 = peritendinous band + limited affected finger extens’n
- grade 3 = presence of flex’n contracture
Ix’s
- clinical diagnosis
- table top test → ask pt to put their hands flat on a table = +ve if they can’t do that = suggestive of Dupuytren’s
Tx if pt has no MCP or PIP contracture = do nothing just f/u every 6 months
Tx if pt has MCP or PIP contracture
- Intrales’nal collagenase injec’ns
- Sx such as . . .
- needle fasciotomy → involves inserting a needle through skin to divided + loosen cord that is causing the contracture
- limited fasciectomy → involves removing abnormal fascia + cord to release contracture
- dermofasciectomy → involves removing abnormal fascia + cord + associated skin
⟹ skin graft = used to replace removed skin - Know for OSCE *
Trigger Finger / Stenosing tenosynovitis ✓
Def - painful condi’n where pt has difficulty moving a specific finger
→ part of sheath that is usually affected = 1st annular pulley / A1pulley @ MCP jt
→ some resolve spontaneously
RFs
- female
- 40-55 y/o
- diabetes (especially T1D)
Pathophys - flexor tendons of our fingers pass through several tunnels (sheaths) along the length of the fingers
→ in trigger finger, there is thickening of the tendon or tightening of the sheath which prevents tendon from smoothly moving through sheath when finger = flexed + extended
SSX = worse in the morning + improve during the day . . .
- painful + tender finger (usually around MCP jt on palm side of hand)
- finger that doesn’t move
smoothly
- finger that makes popping / clicking sound
- finger stuck in flexed posi’n
Ix = clinical diagnosis
Tx
- rest + analgesia
- splinting
- steroid injec’ns
- Sx to release A1 pulley
- Know for OSCE *
Ganglion Cysts ✓
Def - painless smooth, soft, benign cysts filled w/ synovial fluid = most common benign hand / wrist les’n
→ mainly occur in wrist or fingers but can occur anywhere where there’s a jt or tendon since that’s where they originate from
→ will transilluminate if you shine light through it b/c = fluid filled
→ 40-50% of cysts will resolve spontaneously, but this can take several yrs
Diagnostic Ix = clinical diagnosis
Tx
1. observa’n
2. needle aspira’n i.e draining cyst by aspirating fluid w/ needle → has high rate of recurrence i.e ≥ 50%
3. surgical excis’n (do this 1st if there’s vascular compromise) → has low rate of recurrence
- Know for OSCE *
What is the flexor retinaculum ? ✓
Strong, fibrous band near wrist that covers carpal bones on palmar side of hand
→ on ulnar side attaches to pisiform bone + hook of hamate bone
→ on radial side attaches to tubercle of scaphoid bone + ridge of trapezium bone
Nerves that control sensa’n in arms / hands / fingers ✓
- Thumb, index, middle finger + half of ring finger = median nerve
- Other half of ring finger + pinky = ulnar nerve
- musculocutaneous nerve (C5-C7) = lateral part of forearm
- radial nerve (C5-C8) = dorsal aspect of 1st + 2nd metacarpals
Contents of carpal tunnel ✓
Median nerve + 9 flexor tendons
Carpal Tunnel Syndrome ✓
Def - compress’n of median nerve in carpal tunnel
RFs
- RA
- female
- obesity
- diabetes
- hypoTSH
- acromegaly
- perimenopausal
- computer job / constant hand strain
Diagnostic Ix = nerve conduc’n study on median nerve → we except to see slow velocity
SSX
- atrophy of thenar muscles (next to thumb)
- weakness of all policis muscles b/c = supplied by median nerve
- pain / numbness / paresthesia in 1st 3.5 digits
+ve Tinel’s sign i.e tapping causes paresthesia
+ve Phalen’s sign i.e flex’n of wrist causes SSX
→ SSX might be worse at night
Tx
- wrist splint every night for 3 wks ~ 1 month
→ add corticosteroid injec’n if doesn’t help
→ carpal tunnel release Sx if SSX persist after 6 wk trial of above (flexor retinaculum = divided)
- Know for OSCE *
What does tenderness on palpa’n of anatomical snuffbox indicate ? ✓
Fracture of scaphoid bone
SSX of radial nerve injury ✓
- wrist drop i.e wrist + fingers are flexed + can’t be extended due weakened extens’n
Ulnar nerve injury ✓
- Eti = medial epicondyle injury
- SSX = claw hand deformity
De Quervain’s Tenosynovitis ✓
Def - condi’n where abductor pollicis longus (APL) + extensor pollicis brevis (EPB) tendon sheaths in wrist = swollen + inflamed
→ = a type of repetitive strain injury
SSX
- pain on radial aspect of wrist that might radiate to forearm
- weakness
- numbness
- burning sensa’n
- aching / tenderness
Ix’s
- Finkelstein’s test → ask pt to make a fist w/ their thumb inside their fingers + then adduct their wrist
⟹ +ve if that mov’nt causes pain radial aspect of wrist = diagnostic of De Quervain
Tx
- rest + adapting activities
- using splints to restrict mov’nt
- analgesia
- PT
- steroid injec’ns
- Know for OSCE *
What does Achilles tendon do ? ✓
Connects calf muscles (gastrocnemius + soleus) to heel (calcaneus bone)
Achilles Tendinopathy ✓
Def - damage, swelling, inflamma’n + ↓ed func’n of Achilles tendon
RFs
- sports that stress Achilles such as tennis, track, basketball
- inflammatory condi’ns such as RA or ankylosing spondylitis
- HLD
- diabetes
- fluoroquinolone Abx
Types
- inser’n tendinopathy = w/in 2 cm of inser’n point on calcaneus
- mid por’n tendinopathy = 2-6 cm above inser’n point
SSX = gradual onset of . . .
- pain w/ activity in Achilles tendon or heel
- stiffness
- tenderness
- swelling
- nodularity on palpa’n of Achilles tendon
Tx
- rest + altered activities
- ice
- analgesia
- PT
- Sx if above failed
Achilles tendon tear ✓
Def - rupture of Achilles tendon due to sudden onset injury
RFs
- FHx
- older age
- sports that stress Achilles
- Achilles tendinopathy
- systemic steroids
- fluoroquinolone Abx → rupture can occur spontaneously w/in 48 hrs of starting it
SSX
- sudden onset of pain in Achilles or calf
- snapping sound + sensa’n
- feeling as though something hit the back of their leg
- tenderness
- palpable gap in Achilles tendon (might be masked)
- Weakness of PLANTAR flex’n (dorsiflex’n ≠ affected)
- pt can’t on tiptoes on affected leg
+ve Simmond calf squeeze test i.e squeezing calf doesn’t cause plantar flex’n as it normally should
Diagnostic Ix = U/S
Tx
- rest + immobiliza’n
- VTE Ppx since there’s immobiliza’n
- ice
- eleva’n
- analgesia
Plantar Fasciitis ✓
Def - chronic self-limiting inflamma’n of plantar fascia (usually self-resolves w/in 6-18 months)
RF = elevated BMI
SSX
- plantar tenderness
- gradual pain on plantar aspect of heel that is worse w/ pressure i.e walking or standing for a long amt of time + better w/ rest
Ix = clinical diagnosis but should do x-ray to r/o fracture
Tx = supportive i.e . . .
- rest
- ice
- analgesia
- PT
- steroid injec’ns (can be very painful + very rarely can cause fat pad atrophy as well as rupture of plantar fascia)
Morton’s Neuroma ✓
Def - dysfunc’n of nerve in intermetatarsal space
→ abnormal nerve = usually located btw 3rd + 4th metatarsal
SSX
- pain @ front of foot + where nerve = located
- sensa’n that there’s lump in their shoe
- burning / numbness / paresthesia in distal toes
Ix’s
- applying deep pressure to affected intermetatarsal space causes pain
+ve metatarsal squeeze test i.e squeezing forefoot w/ one hand + using other hand to press affected area on plantar side of foot causes pain
+ve Mulder’s sign i.e painful click = felt when both hands = used on either side of foot to manipulate metatarsal heads
- U/S or MRI to confirm diagnosis
Tx
- adapting activities for ex avoiding high heels
- analgesia
- using insoles
- weight loss if appropriate
- steroid injec’ns
- radiofrequency abla’n
- surgical excis’n of neuroma
The 5 layers of the skin from superficial to deep ✓
- Corneum
- Lucidum (present in thick skin only)
- Granulosum
- Spinosum
- Basale / germinativum → gives rise to keratinocytes
+ contains melanocytes
What 4 types of cells are in the epidermis ? ✓
“KLMM”
- Keratinocytes
- Langerhan cells (immune cells)
- Merkel cells (mechanoreceptors)
- Melanocytes
Contents of dermis ✓
- sweat glands
- sebaceous glands
- collagen bundles
- fibroblasts
- monocytes
- phagocytes
- mast cells
- dermal dendrocytes
- glomus cell
Thalamus nuclei + corresponding sense ✓
- LGN = vis’n
- MGN = hearing
- Ventral posteromedial nucleus = facial sensa’n
- Ventral posterolateral nucleus (VPLN) = pain, pressure + vibra’n
- Ventral anterior nucleus = MOTOR
- postero = sensa’n but posteromedial = face sensa’n + posterolateral = pain, pressure + vibra’n *
Sensory/Ascending Tracts + Motor/Descending Tracts (“spino…” = sensory, ends in “spinal / bulbar” = motor) ✓
Sensory
- Anterior spinothalamic = crude touch + pressure, contralateral, decussates at same level nerve root enters spinal cord
- lateral spinothalmaic = pain + temp, contralateral, decussates at same level nerve root enters spinal cord
→ 1st order neurons (limbs) (1st order neutrons from upper limbs travel in lateral part of dorsal root + lower limbs medial part) → 2nd order neurons (medulla)
→ 2nd order neurons decussate w/in medulla
→ 3rd order neurons (VPLN of thalamus)
→ cerebral cortex - Dorsal columns / medial lemniscal = vibra’n, conscious propriocep’n + fine touch, ipsilateral, decussates at medulla
- Anterior spinocerebellar → decussates at medulla, unconscious propriocep’n
- lateral spinocerebellar → decussates at medulla, conscious propriocep’n
Motor
- Pyramidal (originate in cortex)
→ anterior corticospinal- ipsilateral, decussates at caudal end of medulla (10% of fibers don’t cross midline in medulla) = for innerva’n of more proximal muscles
→ lateral corticospinal- ipsilateral, decussates at caudal end of medulla (90% of fibers do so), UMNs synapse w/ LMNs at ventral horn
→ corticobulbar- neurons travel to brainstem, conscious control of skeletal muscles that move face, jaw, + certain muscles of neck + pharynx - Exrapyramidal (originate in brainstem)
→ rubropsinal
→ reticulospinal
→ tectospinal
→ vestibulospinal
What is Brown-Sequard syndrome ? ✓
1 entire side of spinal cord = affected (either left or right i.e hemisec’n), affects dorsal column, corticospinal + lateral spinothalamic = @ level of T8-T10
Which types of sensa’n are contralateral + which are ipsilateral ? ✓
Contralateral
- pain
- temp
- crude touch
- pressure
Ipsilateral
- vibra’n
- propriocep’n
Locked in syndrome ✓
= stroke in basilar artery ∴ causing ttl body paralysis including difficulty breathing + swallowing
→ all they can move is their eyes
Pupillary light reflex ✓
Para causes CIRCULAR muscles to contract + sympa causes RADIAL muscles to contract
UMN v.s LMN SSX ✓
UMN → originate in cerebral cortex / brain stem
- hypertonia
- spasticity = ↑ed resistance to passive movement of a jt due to abnormally high muscle tone i.e exaggera’n of stretch reflex
- clonus i.e involuntary muscle contrac’ns
- hyper-reflexia (can even be babinsky +ve)
→ UMN condi’ns = stroke, MS + myelopathy
LMN → originate in ventral horn or CN nuclei of brain stem
- hypotonia
- areflexia / hyporeflexia
- muscle atrophy b/c muscles are not being used
- fascicula’ns i.e muscle twitching b/c muscles are not being used
→ LMN condi’ns = poliomyelitis + spinal muscular atrophy
Both UMN + LMN can have weakness + paralysis
ACA, MCA, PCA + what they each supply ✓
MCA (largest of the 3)
→ lateral frontal lobe
- 1° motor cortex → contralateral hemiparesis in face + upper extremities
- Broca’s area (superior divis’n of MCA of dominant cerebral hemisphere which is left hemisphere in most ppl) → expressive aphasia
- frontal eye fields → ipsilateral gaze devia’n
→ lateral parietal lobe
- 1° somatosensory cortex → contralateral sensory loss in face + upper extremities
- optic radia’ns → contralateral homonymous hemianopia
→ lateral temporal lobes
- Wernicke’s area (superior temporal gyrus i.e inferior divis’n of dominant cerebral hemisphere which is left hemisphere in most ppl)→ receptive aphasia
- optic radia’ns → contralateral homonymous hemianopia
ACA → supplies . . .
→ medial frontal lobe
- 1° motor cortex → contralateral hemiparesis in lower extremities
→ medial parietal lobe
- 1° somatosensory cortex → contralateral sensory loss in lower extremities
⚠️ b/l SSX only occur in BRAIN STEM stroke !
- PCA → supplies occipital lobe
→ nystagmus
→ visual agnosia i.e inability to recognize visually represented objects
→ contralateral homonymous hemianopia w/ macular sparing
⚠️ 80% of carotid blood flow enters MCA + 20% enters ACA !
⚠️ Worst strokes = MCA b/c it supplies much more than the others !
5 main reflexes ✓
- Biceps = C5-C6
- Triceps = C7-C8
- Cremasteric = L1-L2
- Knee Reflex = L3-L4
- Ankle Reflex = S1-S2
GCS (Glasgow Coma Scale) ✓
(“eyes4 + mouth5 + legs6”)
- Ttl = /15
< 8 = severe
9-12 = moderate
> 13 = mild
Eyes - score of 4-1 (from best to worst)
→ 4 = spontaneous
→ 3 = eyes open to verbal stimulus
→ 2 = eyes open to pain stimulus
→ 1 = eyes don’t open at all
Verbal - score of 5-1 (from best to worst)
→ 5 = oriented
→ 4 = confused i.e you ask about date of today + they answer wrong
→ 3 = inappropriate words i.e say random words unrelated to question asked
→ 2 = incomprehensible sounds i.e grunting or moaning
→ 1 = no words / sounds at all
Motor - score of 6-1 (from best to worst)
→ 6 = follows commands
→ 5 = localizes / shows u where pain is
→ 4 = w/draws from pain
→ 3 = abnormal flex’n
→ 2 = abnormal extens’n
→ 1 = none
Parkinson’s ✓
Def - chronic progressive neurodegenerative disorder caused by degenera’n of dopaminergic neurons in substantia nigra
→ juvenile parkinsonism = < 21 y/o
→ young onset parkinsonism = 21-40 y/o
→ resting tremor cycles 4-6x / second
RFs
- men > 65 y/o
- FHx for young onset
Pathophys - neuronal death → indirect pathway of basal ganglia = affected → pt ≠ able to stop unwanted mov’nt
SSX = “TRRAPSS”
- Tremor (resting tremor that is worse on one side + performing a task w/ normal hand exaggerates it)
- Rigidity (cogwheel rigidity)
- Reduced facial mov’nts / express’ns (hypomimia)
- Akinesia or bradykinesia (slow mov’nt)
- Postural instability
- Shuffling gait
- Small handwriting (micrographia)
Ddx
- benign essential tremor
- drug induced parkinsonism
→ Li
→ dopamine depleting drugs such as tetrabenazine
→ dopamine receptor blocking drugs such as metoclopramide, risperidone, typical + atypical antipsychotics - progressive supranuclear palsy → will cause early postural instability, vertical gaze palsy i.e pt can’t look upwards, axial rigidity + speech / swallowing pbs
- multiple system atrophy = rare condi’n where neurons of multiple of systems in brain degenerate including basal ganglia → autonomic dysfunc’n ∴ causing . . .
⟹ orthostatic / postural hypoTN
⟹ constipa’n
⟹ sexual dysfunc’n
⟹ bladder dysfunc’n
⟹ abnormal sweating
⟹ ataxia b/c of cerebellar dysfunc’n - Lewy body dementia → SSX = . . .
⟹ parkinsonism
⟹ progressive cognitive decline
⟹ visual hallucina’ns
⟹ delus’ns
⟹ fluctuating levels of alertness
⟹ REM sleep disorders
Diagnostic Ix = clinical diagnosis but can do brain MRI to r/o Ddx
Diagnostic criteria (all must be met)
1) bradykinesia + ≥ 1 of the following SSX . . .
- rigidity
- 4-6 Hz tremor
- postural instability not caused by another condi’n
2) ≥ 3 of the following . . .
- u/l onset
- resting tremor
- progressive
- asymmetrical tremor i.e one side = worse
- has been going one for ≥10 yrs
- ≥ 70% response to levodopa
- levodopa response for ≥ 5 yrs
- severe levodopa-induced chorea
Tx
- Levodopa / Carbidopa (generic name = Sinemet)
- Levodopa MOA : gets converted to dopamine by DOPA decarboxylase @ presynaptic neuron + hence acts like endogenous dopamine
→ side effects = orthostatic hypoTN, hallucina’n + most importantly dyskinesia which can present as . . . ⟹ dystonia - excessive muscle contrac’n causes abnormal postures or exaggerated mov’nts
⟹ chorea - abnormal involuntary mov’nts such as jerking
⟹ athetosis - involuntary twisting or writhing mov’nts in fingers, hands or feet
⚠️ Dyskinesia due to levodopa can be treated w/ amantadine = glutamate antagonist
- Carbidopa MOA: inhibits DOPA decarboxylase activity in periphery ∴ prevents convers’n of L DOPA into dopamine ∴ ↑ing bioavailability of L DOPA in CNS + ↓ing systemic side effects that L-DOPA would normally have such as N/V
- Dopamine receptor agonist
→ MOA - binds on striatal dopamine receptors like endogenous dopamine
→ side effects = pulm. fibrosis w/ prolonged use, hallucina’ns, psychosis, impulse control disorders
→ ex’s = bromocriptine, pergolide or cabergoline - MAO-B inhibitors
→ MOA - inhibit breakdown of epinephrine
→ side effects = HA, dyskinesia + psychological disorders
→ end in “GILINE” - COMT inhibitors
→ MOA - inhibit catechol-O-methyl transferase ∴ ↓ peripheral metaboliza’n of L-DOPA → 3-OMD which helps to ↑ its bioavailability
→ side effects = GI, dyskinesia + psychiatric SSX
Complica’ns
- dementia
- dysphagia
- constipa’n
- bladder dysfunc’n
- orthostatic hypoTN
- Parkinson psychosis
- Know for OSCE *
Benign essential tremor ✓
RFs
- FHx
- older age
SSX (usually in heads but other tremors such as head tremor, jaw tremor or vocal tremor = possible)
- b/l postural tremor that cycles 6-12x / second
- improves @ rest + gets worse w/ inten’nal mov’nt (literal opposite of Parkinson’s)
- tremor improves w/ alcohol while in Parkinson’s alcohol neither worsens nor improves tremor
Ddx = same as Parkinson’s
Diagnostic Ix = clinical diagnosis
Tx if doesn’t interfere w/ daily life = nothing
Tx if interferes w/ daily life . . .
1. Propranolol or primidone = anti-epileptic barbiturate
2. Deep brain stimula’n
3. Focused U/S thalamotomy under MRI guidance
4. γ knife thalamotomy
- Know for OSCE *
Drugs that can cause tremor ✓
Drugs that cause tremor @ rest . . .
- dopamine depleting drugs such as tetrabenazine
- dopamine receptor blocking drugs i.e metoclopramide, risperidone, both typical + atypical antipsychotics
Drugs that cause postural tremor i.e tremor when limb isn’t supported by gravity . . .
- TCAs
- alcohol
- nicotine
- caffeine
- thyroxine
- β agonists
- theophylline
- anticonvulsants
- marijuana / cocaine / amphetamines
⚠️ Li can cause either type of tremor !
Tx for drug-induced Parkinsonism / extrapyramidal SSX ? ✓
Procyclidine HCl
HA red flag SSX i.e require urgent Ix ✓
“SNOOP”
- Systemic SSX i.e fever, myalgia, weight loss, Hx of cancer
- Neuro SSX such as blurry vis’n
- Onset = new or changed + pt > 50 y/o
- Onset = thunderclap presenta’n
- Papilledema / Pulsatile tinnitus / Positi’nal Provoca’n / Precipitated by exercise
Cluster v.s Migraine v.s Tens’n HA (kids + adults) ✓
- Cluster HA = severe, u/l, 15min-3hr + repetitive, more common in males
→ Acute Tx = Sumatriptan or 100% high flow O2
- MOA of triptans = serotonin 5-HT1 receptor agonist ∴ vasoconstrict cranial arteries, which are dilated during HA / migraine
- side effects = paresthesia, flushing, tingling, neck pain + chest tightness
- C/Is = Hx of MI / CAD / CVA / PVD, severe liver or renal failure, ≥ 65 y/o, breastfeeding + pregnancy
⟹ sumatriptan = only safe triptan if pt = pregnant or breast feeding
→ Ppx = Verapamil
- Migraine = u/l, 4-72 hr, pulsating pain +/- aura i.e N or V /seeing zigzags/flashing lights +/- central abdominal pain in kids that lasts > 1 hr
→ triggers . . .
⟹ stress
⟹ bright lights
⟹ strong smells
⟹ chocolate / cheese / caffeine
⟹ dehydra’n
⟹ poor sleep
⟹ trauma
⟹ menstrua’n
→ Acute Tx = NSAID such as ibuprofen or triptan
→ Ppx . . .
- lifestyle Δs
- β blockers
- amitriptyline
- topiramate (↓ frequency of migraine attacks)
⟹ C/I = pregnancy b/c = teratogenic
- Tens’n HA = b/l, > 30 min, feels like tight band
→ Acute Tx = NSAIDs / paracetamol
→ Chronic Tx = amitriptyline - Know for OSCE *
Thunderclap HA ✓
Def - sudden onset of 1st ever HA or worst HA ever w/in a minute w/ severity ≥ 7
Ix = CT 1st then wait 12hrs + do LP b/c takes 4-12 hrs for xanthochromia to develop which is diagnostic of SAH
Roles of cerebellum ✓
- Voluntary eye mov’nt
- Balance (vestibulocerebllum)
- Posture + gait (spinocerebellum)
- Coordina’n of voluntary mov’nt such as walking
- Motor learning i.e riding a bike or playing an instrument (cerebrocerebellum)
Is cerebellum contralateral or ipsilateral ? ✓
Ipsilateral
SSX of cerebellar stroke ✓
“DANISH”
D - Dysdiadochokinesia, Dysmetria (past-pointing), dysarthria
A - Ataxia
N - Nystagmus + N/V
I - Inten’n tremor
S - Slurred staccato speech
H - Hypotonia + Headache
Purpose of doll’s eye mov’nt examina’n in comatose pt ✓
To test oculocephalic reflex which involves CNIII + VI
→ hold pt’s eyelids open + move their head left to right + eyes should move in opposite direc’n
⟹ if eyes move in same direc’n or don’t move at all = absent reflex
What are the 3 parts of the basal ganglia ✓
- Corpus striatum = caudate nucleus + lentiform nucleus (putamen + globus palidus internis + externis, separated from caudate nucleus + thalamus by internal capsule) = in base of each hemisphere
- Subthalamic nucleus = in diencephalon
- Substantia nigra = in midbrain
Role of pineal gland ✓
Melatonin produc’n from serotonin
→ = stimulated by darkness + inhibited by light
Direct + Indirect Pathways of Basal Ganglia ✓
- Direct = initiates motor activity
- Indirect = inhibits unwanted motor activity
12 CN’s + their func’ns ✓
CN I = olfactory nerve → smell
CN II = optic nerve → visual acuity, visual fields, eye mov’nts, pupil rxns
CN III = oculomotor nerve → same as CNII
CN IV = trochlear nerve → same as CNII
CN V = trigeminal nerve
→ sensory = face + afferent part of corneal reflex
→ motor = mastica’n muscles + jaw jerk reflex
CN VI = abducens nerve → same as CNII
CN VII = facial nerve
→ sensory = taste for anterior 2/3 of tongue
→ motor = muscles of facial express’n + efferent part of cornea reflex
CN VIII = vestibulocochlear nerve → hearing + balance
CN IX + X = glossopharyngeal + vagus nerve
→ sensory = taste for posterior 1/3 tongue + posterior pharyngeal wall
→ gag reflex (afferent = glossopharyngeal, efferent = vagus)
→ motor = palate, swallowing + coughing
CN XI = accessory nerve = mov’nt of trapezius + sternocleidomastoid muscles
CN XII = hypoglossal nerve = tongue (motor)
⚠️ tongue devia’n = ipsilateral v.s uvula devia’n = contralateral !
Structures involved in storage + encoding of memory + emo’n i.e limbic system ✓
Storage
→ cortex for explicit + episodic memories
→ cerebellum for procedural memory
Encoding
→ hippocampus (= w/in temporal lobe) - facilitates transfer of short term to long term but ≠ involved in forma’n of new memories
→ amygdala (next to hippocampus so also in temporal lobe) = activated via release of adrenaline + triggers hippocampus to encode memories associated w/ emo’ns
What is aphasia + what are the 4 types of aphasia ? ✓
Aphasia = pb w/ speech or language
→ Broca’s aphasia or expressive aphasia = pb w/ language produc’n ∴ sentence forma’n = impaired but comprehens’n = normal
→ Wernicke’s aphasia or receptive aphasia = pb w/ language comprehens’n ∴ speech sounds fluent but what they’re saying has noting to do w/ what u just asked them
→ Conduc’n aphasia = pb w/ articulate fasciculus (connects Broca + Werncke) ∴ speech + comprehens’n = normal but repeti’n = impaired
→ Global aphasia = Wernicke’s area + Broca’s area + articulate fasciculus = affected ∴ pt has receptive + expressive aphasia + hence might communicate in gestures
⟹ could happen in ischemic infarct of MCA (especially if it’s in left hemisphere b/c is the dominant hemisphere in most ppl) b/c MCA supplies large por’ns of the lateral frontal, parietal + temporal lobes + Broca = in inferior frontal lobe, Wernicke in superoposterior temporal lobe + arcuate fasciculus connects the 2
Func’n of each lobe ✓
Frontal (= anterior to central sulcus)
- social behvavior
- emo’nal control
- insight
- planning + execu’n
- pb solving,
- language forma’n (Broca)
- voluntary mov’nt
Temporal
- memory
- auditory info
- language comprehens’n (Wernicke)
Parietal
- calcula’n
- visuo-spatial recogni’n i.e not needing map to get back home
- spelling
- writing
- sense of touch
Occipital = visual info
What are the 3 types of cartilage ? ✓
- Hyaline = most widespread but weakest of the 3
→ in ribs, sternum, nasal cartilage + trachea rings - Fibrocartilage = toughest of the 3 b/c contains both type II + type I collagen while the others only have type II
→ in intravertebral discs, pubic symphysis, menisci + ligaments - Elastic cartilage = springy, yellow, has the most ECM, only has type II collagen like hyaline
→ in ear + epiglottis
How many compartments does the leg have ? ✓
2 compatments
Anterior = dorsiflex’n i.e foot upwards
→ has 4 muscles
- Tibialis anterior
- Extensor digitorum longus
- Extensor hallucis longus
- Fibularis (peroneus) tertius
→ blood supply = anterior tibial artery
→ innerva’n = deep fibular/peroneal nerve
Posterior = plantar flex’n = i.e towards floor
→ has 6 muscles (3 superficial + 3 deep)
⟹ 3 superficial = Gastrocnemius + Plantaris + Soleus
→ blood supply = short + long saphenous veins
→ innerva’n = sural nerve
⟹ 3 deep = Tibialis posterior + Flexor digitorum longus + Flexor hallucis longus
→ blood supply = fibular + posterior tibial arteries
→ innerva’n = tibial nerve
Lateral = evers’n + plantar flex’n
→ has 2 muscles
- Fibularis / Peroneus longus + brevis
⟹ blood supply = anterior tibial artery for proximal + fibular artery for distal
⟹ innerva’n = superficial fibular/peroneal nerve
DAMAGE OF LEG NERVES + THEIR EFFECTS
- Common peroneal / fibular nerve = foot drop + numbness on dorsum + lateral aspect of foot
- Deep fibular nerve = supplies sensa’n to 1st web space i.e space btw 1st + 2nd toes + muscles involved in dorsiflex’n of foot + toes
- Superficial fibular nerve = altered sensa’n over dorsum of foot + can’t evert foot
- Sural nerve = SENSORY ONLY
- Tibial nerve = motor supply to intrinsic muscles of the foot + sensory for medial + plantar aspects
Common peroneal nerve injury ✓
Eti = knee trauma
SSX
- foot drop i.e pt = unable to dorsiflex + evert foot
- ↓ed sensa’n over lateral + dorsal aspects of foot
Muscle contrac’n ✓
Neuron ac’n Ψ arrives @ end of motor neuron → at NMJ, ac’n Ψ from neuron signals Ach release from pre-synaptic cleft
→ causes endplate Ψs on mycocyte membrane
→ endplate Ψs stimulate dihydropyridine receptors + subsequently ryanodine receptors
→ SR releases Ca
→ Ca binds to troponin (which is located in actin) + troponin binds to tropomyosin which was blocking myosin binding sites on actin but not anymore
→ myosin forms cross-bridge w/ actin
→ ATP binds to myosin head which has ATPase enzyme ∴ hydrolyzes ATP to ADP + Pi (b/c muscle contrac’n requires ATP)
→ ATP hydrolysis causes myosin heads to change posi’n + move to next actin binding site
→ myosin = released from actin + Ca moves out of sarcoplasm back into SR
- for muscle contrac’n to happen, both I band + length of sarcomere have to shorten *
What is the tarsal tunnel + what are its contents ? ✓
= passageway for tendons, nerves + vessels to travel btw posterior leg + foot
Contents = “ Tom Dick And Very Nervous Harry “
- Tibialis posterior tendon
- Digitorum i.e flexor digitorum longus tendon
- Artery (posterior tibial artery)
- Very (posterior tibial vein)
- Nerve (posterior tibial nerve)
- Hallucis i.e flexor hallucis longus tendon
Edward’s v.s Patau’s ✓
- Edward’s = Trisomy 18 = 2nd most common autosomal trisomy resulting in live birth (after Down’s)
- Patau’s = Trisomy 13
⚠️ Death usually occurs by age 1 for both !
What do the medulla + cortex of the adrenal glands secrete ? ✓
- Medulla = secrete catecholamines i.e adrenaline + noradrenaline
- 3 zones of the adreal cortex =
→ Zona gloMerulosa = secrete Mineralocorticoids like aldosterone
→ Zona fasciculata = secrete glucocorticoids like cortisol
→ Zona reticularis = secrete androgens
How does IVF work ? ✓
FSH = injected to stimulate ovaries to produce eggs ∴ instead of just letting follicles die we force them to become ovulatory follicle
Are trisomy 19 babies viable ? ✓
NO b/c will die after 1st wk
What’s the sign that placenta has separated i.e it’s time to deliver it ? ✓
Cord lengthening b/c once placenta separates it falls into cavity
Communicating v.s Non-Communicating Hydrocephalus ✓
- Communicating = full communica’n of CSF btw ventricles + subarachnoid space i.e no blockage which means pb = reabsorp’n
- Non-Communicating = CSF can’t flow out of ventricles due to blockage/ malforma’n / stenosis of aqueduct
→ ex = normal pressure hydrocephalus
→ SSX = normal ICP + urinary incontinence + cognitive dysfunc’n + gait apraxia i.e can’t lift feet off floor
The 4 errors of refrac’n that ↓ visual acuity ✓
Errors due to pb w/ eye length
MYOPIA = near-sightedness i.e can see near but not far b/c cornea = curved excessively + eyeball = too long ∴ instead of light being focused ON retina as it should be, it focuses IN FRONT of retina which makes far away objects blurry
→ correc’n = concave / diverging lens
HYPEROPIA = far-sightedness i.e can see far but not near b/c cornea ≠ curved enough + eyeball = too short ∴ instead of light being focused ON retina as it should be, it focuses BEHIND retina which makes close away objects blurry
→ correc’n = convex / converging lens
Errors due to pb w/ cornea + lens curvature
PRESBYOPIA = age related far-sightedness, loss of lens elasticity ∴ lens can’t change shape to focus on objects close by
→ correc’n = magnifiers / reading glasses
ASTIGMATISM = asymmetric curvature of cornea, normally as light enters cornea it should focus equally on all planes but b/c of asymmetric curvature image becomes blurry and / or distorted
→ correc’n = cylindrical lens
The 5 female ligaments ✓
- round ligament = uterine fundus to labia majora
- suspensory ligament of ovaries = ovaries to lateral pelvic wall
- cardinal ligament = cervix to lateral pelvic wall
- ovarian ligament = ovaries to uterus
- broad ligament = uterus, fallopian tubes + ovaries to pelvic wall
→ rupture of this ligament during labor, instrumental delivery or post-partum results in a spontaneous hematoma = obstetric emergency !
The 6 extra-ocular muscles ✓
Innervated by CN 3 (“3 SMI”)
- Superior rectus → elevates eye
- Medial rectus → adducts eye
- Inferior rectus (depresses eye) + Inferior oblique (lateral eye rota’n)
→ CN 3 palsy = down + out + droopy eyelid + dilated, fixed pupil
⟹ can be due to PCA aneurysm
Innervated by CN 4
- Superior oblique → medial eye rota’n
→ CN 4 palsy = defective downward gaze + vertical diplopia
Innervated by CN 6
- Lateral rectus → abducts eye
→ hence CN 6 palsy will cause defective abduc’n + horizontal diplopia
⚠️ Nerve palsies = ipsilateral !
3 C’s of Accommoda’n Reflex ✓
1) Convergence- CN III i.e oculomotor nerve innervates the medial recti muscles of each eye ∴ causing adduc’n which helps to maintain focused image on each fovea
2) Constric’n of pupils- para fibers from EDW nucleus travel w/ CN III via short ciliary nerves + ciliary ganglion to innervate sphincter pupillae ciliary muscles ∴ causing pupil constric’n (in the case of far away object) which helps to ↑ depth of focus
3) Change in lens curvature-
→ lens become flat + thin for objects faraway i.e ↑ curvature + become round + thick for objects nearby i.e ↓ curvature
General visual pathway + then specifically for superior + inferior visual field (remember “inferieur c’est meilleur”) ✓
Retina → optic nerve → optic chiasm → optic tract → LGN (nucleus on thalamus) → optic radia’ns i.e Barum or Meyer → visual cortex i.e occipital lobe
SIT ML
superior visual field → inferior retinal fibers
→ temporal lobe → meyer’s loop → lingual gyrus of occipital lobe
IS PBC
inferior visual field → superior retinal fibers
→ parietal lobe → barum’s loop
→ cuneus gyrus of occipital lobe
Eye les’ns ✓
Optic nerve les’n = ipsilateral b/c hasn’t crossed optic chiasm yet
- Left optic nerve les’n = blindness in all of left eye
- Right optic nerve les’n = blindness in all of right eye
Optic chiasm les’n = ipsilateral b/c only reached chiasm but hasn’t crossed it
= loss of vis’n in entire left visual field of left eye + entire right visual field of right eye = Bi-temporal Hemianopia
→ bi temporal = when it’s not the same visual field affected in each eye, when it’s the same visual field affected in each eye we use homonymous
Optic tract les’n = contralateral
- Left optic tract les’n = contralateral visual field affected i.e right visual field + on each eye ∴ we will have loss of vis’n in right visual field of left eye + in right visual field of right eye
→ = right homonymous hemianopia since only right visual field = affected + since it’s the same field in each eye that’s affected we use homonymous - Right optic tract les’n → visual field that is contralateral to les’n = affected + on each eye ∴ in this case we have loss of vis’n in left visual field of left eye + in left visual field of right eye
→ since only left visual field = affected = left homonymous hemianopia
Occipital lobe damage = contralateral
- Left occipital lobe damage but PCA infarct only i.e collateral blood supply sends blood to macula to save it = same as left optic tract les’n i.e loss of vis’n in right visual field of each eye EXCEPT in center which is where macula is ∴ we call this right homonymous hemianopia w/ macular sparing
- Right occipital lobe damage but PCA infarct only i.e collateral blood supply sends blood to macula to save it = same as right optic tract les’n i.e loss of vis’n in left visual field of each eye EXCEPT in center which is where macula is ∴ we call this left homonymous hemianopia w/ macular sparing
Meyer loop les’n (contralateral + opposite direc’n)
- Left meyer loop les’n = contaleteral + opposite ∴ since meyer = inferior retinal fibers, the damage will be on the right superior quadrant of each eye ∴ we call this Right homonymous superior quadrantanopia
- Right meyer loop les’n = contralateral + opposite ∴ since meyer = inferior retinal fibers, the damage will be on the left superior quadrant of each eye ∴ we call this Left homonymous superior quadrantanopia
Barum loop les’n (contralateral + opposite direc’n)
- Left barum’s loop les’n = contralateral + opposite ∴ since barum = superior retinal fibers, the damage will be on the right inferior quadrant of each eye ∴ we call this Right homonymous inferior quadrantanopia
- Right barum’s loop / dorsal optic radia’n les’n = contaleteral + opposite ∴ since barum = superior retinal fibers, the damage will be on the left inferior quadrant of each eye ∴ we call this Left homonymous inferior quadrantanopia
Macular les’n = ipsilateral
- Left macular les’n / central scotoma = black spot in center of left eye
- Right macular les’n / central scotoma = black spot in center of right eye
What is consonance ? ✓
Smooth transi’n from 1 stage of puberty to the next + in the normal order irregardless of if stage occurs earlier or later and/or lasts longe or shorter
Ddx of puberty disorders ✓
- PRECOCIOUS SEXUAL DEVELOP’NT = develop’nt of any 2° sexual characteristic before the age of 8 in girls + before the age of 9 in boys
→ Central = GnRH dependent = True, consonance still maintained, due to early activa’n of GnRH by hypothalamus, since GnRH is the pb there will be a +ve LH response to GnRH stimula’n
⟹ causes . . .
- idiopathic (ex: genetic)
- 2° (brain les’n, hypothalamic tumor, neuro-fibromatosis i.e café au lait spots)
- excess gonadotrophin secre’n (could be due to pituitary tumor)
→ Peripheral = GnRH independent = Pseudo, loss of consonance, due to excessive produc’n of sex hormones, since GnRH is not the pb there will be no LH response to GnRH stimula’n
⟹ ex’s . . .
- Sex steroid secreting tumor or exogenous steroids
- Testotoxicosis = activating muta’n of LH receptor leading to early androgen produc’n by Leydig cells, No FSH ↑
- McCune Albright = due to Gs-protein activating muta’n = survivable in pts w/ mosaicism but lethal if muta’n occurs before fertiliza’n b/c all cells will be affected !
→ presents w/ u/l café-au-lait spots w/ ragged edges - Congenital Adrenal hyperplasia = androgen produc’n by adrenal glands, pt will have low LH + FSH
- DELAYED PUBERTY = absence of menarche by 18 y/o or absence of pubertal signs in girls at 13 y/o (such as lack of breast develop’nt) + in boys at 14 y/o
→ Constitu’nal delay
- more common in boys
- can be genetic or 2° to chronic illness such as diabetes, CF, celiac, weight loss
→ Hypogonadotrophic hypogonadism (pt will have low LH + FSH)
⟹ causes . . .
- Hypopituitarism/impaired gonadotrophins
- High doses or long-term use of opioid or steroid / glucocorticoid medica’n
- Kallman’s syndrome = X-linked KAL gene impair’nt of GnRH neuron migra’n from olfactory placode ∴ causing impaired smell, small penis in males fully or partially undescended testicles
→ Hypergonadotrophic hypogonadism (pts will have low LH + FSH)
⟹ causes . . .
- chemo
- premature ovarian failure
- Klinefelter’s syndrome = XXY (affects 1 in 500 males)
- Turner’s syndrome = when girl only has 1 X chromosome (affects 1 in 3000 girls)
→ SSX = delayed puberty, short stature, webbed neck,
widely spaced nipples, lack of breast develop’nt
Explain male + female internal + external sex differentia’n ✓
MALE INTERNAL GENITALIA - Men have XY
→ Y chromosome contains SRY gene
→ SRY gene converts the initially biΨ gonadal/genital ridge into testes
→ testes contain Sertoli + Leydig cells
→ sertoli cells express AMH which inhibits growth of Mullerian ducts b/c we don’t want female genitalia + Leydig cells secrete testosterone which stimulates growth of Wolffian ducts
→ Wolffian ducts become male internal genitalia i.e epididymis, vas deferens, seminal vesicles + common ejaculatory duct
MALE EXTERNAL GENITALIA - 5 𝛼 reductase converts testosterone into DHT which will stimulate develop’nt of male external genitalia i.e penis, scrotum + prostate
FEMALE INTERNAL GENITALIA - No Y chromosome so no SRY gene ∴ by default biΨ gonadal ridge becomes ovaries → no testes so no Sertoli cells to express AMH ∴ Mullerian ducts are able to grow
→ Mullerian ducts become female internal genitalia i.e fallopian/uterine tubes, uterus, upper 1/3 of vagina + cervix
→ no testes also means no Leydig cells ∴ no testosterone produc’n which is needed for Wolffian duct develop’nt which we don’t want in females
FEMALE EXTERNAL GENITALIA - follicular / granulosa cells of ovaries express estrogen
→ estrogen stimulates develop’nt of vulva / external genitalia i.e clitoris, labia majora + minora + lower 2/3 of vagina
3 disorders of sexual differentia’n (DSD) i.e ambiguous genitalia ✓
- 46 XY DSD = deficiency in 5 𝛼 reductase ∴ no DHT
→ male internal genitalia will still form since they’re dependent on testes cells + NOT DHT BUT male external genitalia won’t develop b/c they’re dependent on DHT → female genitalia won’t form b/c AMH from testes cells = inhibiting Mullerian duct forma’n - 46 XY Androgen Insensitivity Syndrome (AIS) = testes present but no testosterone ∴ nothing to stimulate growth of Wolffian ducts which means no male internal genitalia
→ it’s like there’s estrogen instead, which means they could have female external genitalia - Turner’s (XO) = only 1 X ∴ ovaries = present but don’t develop properly
→ uterus + fallopian tubes = present but are small ∴ pt could have issues conceiving, pt went through adenarche but NOT gonadarche (possible b/c the 2 are independent events)
→ females w/ Turner’s = more likely to have X-linked recessive disorders b/c during develop’nt 1 of the X chromosomes in each XX cell = randomly deactivated + condensed into a Barr body but these pts have skewed inactiva’n ∴ may express X-linked recessive diseases like G6PD deficiency
Puberty in girls v.s boys ✓
Girls = from 8-12 y/o v.s boys = from 9-14 y/o ∴ puberty starts earlier in girls but lasts longer in boys
Girls
- Thelarche i.e breast develop’nt, due to estrogen = 1st visible sign of puberty in girls
- Adrenarche - ↑ in androgens from adrenal glands, zona reticularis of adrenal gland starts to develop as an independent zone, causes acne + sebum produc’n
- Gonadarche - lisspeptin hormone in hypothalamus → hypothalamus secretes GnRH → GnRH stimulates pituitary gland to release FSH + LH which act on gonads i.e ovaries so they can produce estrogen (HPG axis driven)
- Pubarche i.e pubic hair develop’nt, due to androgens
- Growth spurt, due to interac’n btw GH + estrogen (low levels of estrogen leads to initial rapid growth spurt + high levels of estrogen promotes epiphyseal fus’n @ the ends of bone ∴ causing growth to stop), starts 2 yrs earlier in girls
- Menarche i.e 1st period (due to estrogen)
- Androgenic hair growth i.e hair growth in other places expect pubic i.e axillary (due to androgens)
- Body shape change- widening of pelvis + ↑ adipose tissue (due to estrogen)
Boys (boys become fertile @ beginning of puberty)
- ↑ in testicular volume due to ↑ in # of seminiferous tubules (due to FSH) + penile growth (due to testosterone)
- Adrenarche - ↑ in androgens from adrenal glands, zona reticularis of adrenal gland starts to develop as an independent zone, causes acne + sebum produc’n
- Gonadarche - Klsspeptin hormone in hypothalamus → hypo secretes GnRH → GnRH stimulates pituitary gland to release FSH + LH which act on gonads i.e testes so they can produce testosterone (specifically via Leydig cells)
- Voice change (due to testosterone)
- Pubarche (due to androgens)
- Growth spurt (due to interac’n btw GH + estrogen)
- Androgenic hair growth i.e facial + axillary hair (due to testosterone)
Tanner staging for pubic hair (applies to both M + F) + female breast + male genitalia devlop’nt ✓
Pubic Hair | Breast | Male Genitalia
Stage 1 | None | None (pre-pubertal) | Pre-pubertal
Stage 2 | Few darker hairs along labia/base of penis | Areola enlarg’nt w/ firm, tender lump that is breast bud |Testes enlarge to 4 mL, scrotum = larger, reddened + skin = coarser
Stage 3 | Curly pigmented hair across pubis | Enlarg’nt of breast + areola as single mound| Penis enlarges (initially in length) + continued growth of testes + scrotum
Stage 4 | Small adult configura’n | Fill “pubic triangle” | Projec’n of areola above breast as double mound| Penis grows in length + breadth, continued growth of testes + scrotum + they become pigmented
Stage 5 | Adult configura’n |Spread to inner thighs / linea alba (i.e towards umbilicus) | Papilla projects out of areola (adult) | Adult size testes, scrotum + penis
At what level does the esophagus pass through the diaphragm ? ✓
T10
What are the borders + contents of the femoral triangle / adductor canal ? ✓
Borders = “SAIL”
Sartorius = lateral border
Adductor longus = medial border
Inguinal Ligament = superior border
Contents = “NAVY C”
- femoral Nerve
- femoral Artery
- femoral Vein
- Y fronts
- femoral Canal
What are the borders of Hesselbach’s triangle ? ✓
“RII”
- Rectus abdominis (medial border)
- Inferior epigastric vessels (lateral border)
- Inguinal ligament (inferior border)
Hernia ✓
Def - reducible or incarcerated / stuck protrus’n of any part of a cavity beyond its normal confines due to weak point in cavity wall
→ the more narrow the neck of the hernia, the more likely it is to strangulate
Types
A. Inguinal hernia = more common in men b/c in men inguinal canal carries spermatic cord w/ all those 11 structures + in females it only carries ilioinguinal nerve ∴ since there’s only 1 structure that goes through it, the tube = more narrow ∴ making it harder for females to get inguinal hernia
→ inguinal hernia = above + medial to pubic tubercle (where inguinal ligament attaches) OR lateral to mid-inguinal point
→ SSX = groin pain + swelling in groin that might get better when pt lies down
→ Indirect v.s direct (occur due to weakness in abdominal wall, specifically @ Hesselbach’s triangle)
- indirect = through both deep + superficial rings + = lateral to inferior epigastric
- direct = directly through posterior wall of inguinal canal / abdominal wall (usually b/l) + medial to inferior epigastric
- indirect = more common + tends to occur in younger men
- direct = less common + tends to occur in older men
B. Femoral hernia = hernia’on of abdominal contents through femoral canal = inferior + lateral to pubic tubercle OR inferior + medial to mid-inguinal point
→ more common in women due to ↑ed pelvic width (especially older women) but women still get more inguinal hernias
→ more likely to strangulate compared to inguinal hernias
⟹ strangula’n SSX = severe groin pain, tender, irreducible mass + SSX of inflamma’n such as erythema + warmth
C. Incis’nal hernia = hernia in abdomen that is only visible when pt tenses abdomen → occurs when scar tissue that has formed after a laparotomy weakens hence allowing a sac to form
D. Umbilical hernia - occur around umbilicus due to defect in muscle around umbilicus = more common in neonates + can resolve spontaneously
E. Spigelian hernia / lateral ventral hernia = rare hernia caused by defect in posterior sheath + lateral edge of rectus abdominis
F. Hiatus hernia = hernia’n of stomach up through diaphragm
→ SSX = GERD SSX so conservative Mx = PPI
→ Types . . .
- type 1 = sliding i.e stomach slides up through diaphragm
- type 2 = rolling i.e separate por’n of stomach such as fundus folds around + enters through diaphragm opening alongside esophagus
- type 3 = sliding + rolling
- type 4 = large opening w/ addi’nal abdominal organs in thorax such as omentum / bowel / pancreas
Tx = do nothing if it’s a wide neck hernia but otherwise = surgical repair
Complica’ns
- obstruc’n of feces → constipa’n
- strangula’n → base of th hernia becomes so tight that it cuts off blood supply ∴ causing bowel ischemia
Perianal abscess ✓
SSX
- pain when pt sits down
- visible tender anal mass (@ 2 o’ clock often)
Ix = clinical diagnosis
RFs for recurrent perianal abscess
- diabetes
- immunocompromised pts
- hidradenitis
Tx = incis’n + drainage
Complica’n = sepsis
- Know for OSCE *
Hemorrhoids ✓
Def - enlarg’nt of venous cushions in anal canal
→ anal cushions = submucosal tissue supplied by rectal arteries that help to control anal continence + internal + external sphincter
RFs
45-65 y/o
- pregnancy
- constipa’n
- obesity
- weightlifting
- chronic coughing
Eti = excessive straining such as in constipa’n
Where they usually occur
- 3 o’ clock
- 7 o’ clock
- 11 o’ clock
Grading of internal hemorrhoid
- grade 1 = w/in anal canal i.e does not protrude
- grade 2 = protrudes beyond anal canal but spontaneously reduces when pt stops straining
- grade 3 = protrudes outside anal canal + only reduces w/ manual reduc’n
- grade 4 = irreducible
SSX = asymptomatic or can present w/ . . .
- painless, bright PR bleeding on toilet tissue NOT ON STOOL
- feeling lump around anus
- external / prolapsed hemorrhoids = visible on anal inspec’n while internal hemorrhoids may be felt on rectal exam
Ddx
- anal fissure
- IBD
- colorectal cancer
- anal fistula
- rectal prolapse
Ix = proctoscopy i.e insert proctoscope into anal cavity to visualize mucosa
Tx for grade 1 + everyone else = high fiber diet + oral laxatives
Tx for grade 2 or 3 after step 1
1. rubber band liga’n
2. sclerotherapy / infrared coagula’n / hemorrhoid arterial liga’n / stapled hemorrhoidopexy
Tx for grade 4 after step 1 = hemorrhoidectomy
- Know for OSCE *
Anal Fissure ✓
Def - split in skin of distal anal canal
RFs
- pregnancy
- hard stools
SSX
- severe pain around anus during defaca’n → pt might describe it as trying to pass broken glass
- fresh blood PR during defeca’n (on toilet paper or on stool)
- marked spasm of sphincter muscle on examina’n
Ix = clinical diagnosis
Initial Tx
1. conservative Mx i.e high fiber diet, adequate fluid intake, sitz baths, topical analgesia, stool softeners
2. GTN or diltiazem gel
Tx for resistant or chronic anal fissures
1. botulinum toxin A injec’n or sphincterotomy
2. anal advancement flap → has higher failure rate than sphincterotomy but lower risk of incontinence
- Know for OSCE *
Contents of spermatic cord ✓
= “2 triple 3”
- 2 nerves
→ sympathetic nerve fibers
→ genital branch of the genitofemoral nerve - 3 arteries
→ testicular artery
→ deferential artery
→ cremasteric artery - 3 fascia
→ cremasteric fascia
→ internal + external spermatic fascia - 3 other things
→ vas deferens
→ pampiniform plexus
→ lymphatic vessels
What are the 3 accessory sex glands in men ? ✓
- Seminal vesicles
- During ejacula’n, its smooth muscle contracts to secrete fluid that contains fructose to provide E source for sperm, nutrients, PGs to stimulate urethra to contract, substances that suppress immune system against sperm in females + enzymes that enhance sperm mobility
= 60% of semen / seminal fluid
= alkaline + fructose rich
- Prostate gland
- During ejacula’n, its smooth muscle contracts to release milky white fluid that contains substances that enhances sperm mobility, thicken ejaculate + help w/ coagula’n + eventual breakdown of semen
= 30% of seminal fluid
- Bulbourethral glands / Cowper’s glands
Secrete mucus substance that lubricates urethra + tip of penis during intercourse + neutralizes acid from vagina + from urine in male urethra since both urine + semen come out of urethra
* occas’nally these secre’ns (also known as pre-ejaculate) may carry spermatozoa that remain in urethra from a previous ejacula’n b/c that leftover sperm can survive for > 48 hrs ! *
⚠️ Sperm = produced in seminiferous tubules of testes → = stored in epididymis for matura’n → vas deferens propels sperm forward w/ smooth muscle contrac’ns → sperm arrives at ampulla just above prostate where contents of seminal vesicles = added → as seminal fluid = propelled forward through ejaculatory ducts towards urethra, it passes prostate gland → prostate empties its contents → bulbourethral glands empty contents directly into urethra → semen = ejaculated from penis through urethra
What are the 2 zones of the prostate gland ? ✓
- Central zone = 25% of prostate = where BPH mainly occurs
- Peripheral zone = 75% of prostate = where prostate cancer mainly occurs
When are oocytes arrested ? ✓
@ Meiosis I + then again @ Meiosis II until fertiliza’n occurs
Steps of Folliculogenesis ✓
Granulosa cells multiply → oocyte secretes another protective acellular layer called zona pellucida → 2nd layer of cells called theca cells then differentiate around basal lamina → as follicle grows it ↑ rapidly in diameter + so do granulosa cells ÷’ns → gaps begin to form in granulosa cell layers → gaps consist of fluid-filled spaces which form an antrum + are filled w/ follicular fluid → follicles w/ an antrum = 3°/antral follicles
⚠️ Only antral follicles = visible on U/S, pre-antral follicles ≠ visible on U/S but are ALWAYS present (until menopause)
→ FSH drives most of late folliculogenesis but early follicle growth/initial follicle recruit’nt = independent of FSH
→ after initia’n + recruit’nt = selec’n i.e only 1 follicle = selected for ovula’n = follicle w/ highest mitotic index + largest diameter
⟹ once selected, chosen follicle will continue its growth while other follicles become atretic
⟹ selected antral follicle = rescued from atresia by responding to cyclic Δs in FSH secre’n
⟹ now becomes a pre-ovulatory follicle that is capable corpus luteum forma’n + oocyte release
- If exogenous FSH = supplied, unselected follicles can avoid atresia + proceed like the selected follicle which would obviously result in multiple ovula’ns *
Menstrual cycle steps ✓
- Follicular phase = days 1-13
- Ovula’n = day 14
- Luteal phase = days 15-28
- Hypothalamus secretes GnRH
- GnRH stimulates anterior pituitary to release FSH + LH
- FSH causes follicles to grow + 1 follicle gets selected (Graafian follicle) → that follicle starts releasing estrogen → estrogen = signal that follicle is growing so we don’t need GnRH/FSH/LH anymore so we get -ve feedback + their [ ]s start to ↓
- Estrogen keeps ↑ing + when it peaks it creates a +ve feedback instead so we get LH SURGE (pt might have RIF or LIF pain when this happens)
- LH converts Graafian follicle into corpus luteum + causes egg to unpause from being stuck in meiosis I so it can be released
- Egg = released into peritoneal cavity 24-36hrs after LH surge (released egg is now called ovum)
* ovula’n from both ovaries will make twins * - Ovum gets swept into fallopian tube via ciliated fimbriae + only has 24 hrs to be fertilized by sperm, which can remain in vagina for up to 5 days (fertiliza’n = most likely to occur @ ampulla)
- Corpus luteum releases progesterone to thicken endometrium in prepara’n for pregnancy + estrogen causes cervical mucus to thin so sperm can penetrate (also in prepara’n for pregnancy)
- If pregnancy doesn’t occur, corpus luteum disintegrates + becomes corpus albicans ∴ can no longer release progesterone + [progesterone] ↓ → causes stratum functionalis layer of endometrium to shed i.e menstrua’n
- If pregnancy does occur, hCG secreted by embryo is what is keeping CL alive + in that case CL will eventually become placenta
Menopause ✓
Def - > 12 months w/o menstrua’n due to loss of ovarian follicular func’n, avg age = 51 y/o
→ occurs b/c women have a fixed # of follicles so eventually follicles will run out
→ if occurs before 40 y/o = 1° ovarian insufficiency / premature ovarian failure which is PATHOLOGICAL !
→ perimenopause = transi’n period i.e 8 yrs prior to final period till 1 yr after final period
SSX = amenorrhea + “HAVOCS”
- Hot flashes / night sweats due to low estrogen
- Abnormal mood Δs due to low estrogen
- Vaginal atrophy i.e itching, painful intercourse (dyspareunia) + vaginal dryness → due to low estrogen
- Osteoporosis → due to low estrogen
- Coronary artery disease
- Sleep pbs
Ix’s
- estrogen + progesterone = both low
- LH + FSH = high due to absent -ve feedback from estrogen
Tx
- for pt w/ local SSX only = estrogen cream or tablet
- systemic SSX + no uterus = estrogen only HRT (either via pill or patch but patch = better)
- systemic SSX + pt has uterus = combined HRT i.e estrogen + progesterone (estradiol w/ norethisterone) in order to ↓ risk of endometrial hyperplasia + endometrial cancer
→ cyclical progesterone for perimenopausal pt i.e ≤ 12 months = given for 10-14 days / month which allows pts to have a monthly breakthrough bleed (just like a period) during estrogen-only part of cycle
→ continuous progesterone for postmenopausal pt
⟹ for 24 months if pt < 50 y/o
⟹ for 12 months if pt > 50 y/o - Ca + Vit D for osteoporosis
⚠️ Post-menopausal women w/ vaginal bleeding Ix = Transvaginal U/S → Pipelle endometrial to r/o endometrial pathology, including endometrial carcinoma
Discussing HRT w/ pts
- C/Is . . .
- VTE
- pregnancy
- liver disease
- breast cancer
- uncontrolled HTN
- active angina or MI
- endometrial hyperplasia or cancer
- undiagnosed abnormal bleeding - Risks (in women < 60 y/o benefits of HRT generally outweigh risks) . . .
→ risks of HRT = more significant in older women + w/ longer dura’n of Tx . . .
- ↑ed risk of breast cancer (especially w/ combined HRT)
- ↑ed risk of endometrial cancer (no risk @ all in women w/ no uterus)
- ↑ed risk of VTE (2-3x >)
- ↑ed risk of stroke + CAD w/ long term use + in older women (not in women on estrogen-only HRT) - Ways we ↓ those risks . . .
- adding progesterone to HRT for women w/ a uterus
- using patches rather than pills to ↓ risk of VTE - Assess’nt that has to be done before starting HRT . . .
- FULL HX to ensure there are no C/Is w/ FHx to assess risk of VTE + estrogen dependent cancers such as breast cancer
- must check BP + BMI
- ensure cervical + breast screening = up to date
- encourage lifestyle Δs that are likely to improve SSX + ↓ risks - Inform pt that it can be ↓ed gradually or stopped abruptly
Premature ovarian insufficiency ✓
Def - menopause before 40 y/o
Eti
- genetic
- idiopathic
- infec’s i.e TB / mumps / CMV
- Iatrogenic i.e due to chemo, radiotherapy or gyn Sx
- autoimmune (associated w/ celiac disease, adrenal insufficiency, T1D + thyroid disease)
SSX = amenorrhea + H + V of “HAVOCS”
- Hot flashes / night sweats → due to low estrogen
- Vaginal atrophy i.e itching, painful intercourse (dyspareunia) + vaginal dryness → due to low
Diagnostic criteria = pt < 40 y/o + menopausal SSX + elevated FSH
→ FSH needs to be persistently raised on 2 consecutive samples taken ≥ 4 wks apart
Tx = tradi’nal HRT (↓ BP + ↑ risk of DVTs) or COCP
Atrophic Vaginitis ✓
Def - atrophy + dryness of vaginal mucosa in menopausal women due to lack of estrogen
SSX
- V of “HAVOCS”
- recurrent UTIs, stress incontinence + pelvic organ prolapse in older women
Findings on examina’n of labia + vagina
- pale mucosa
- thin skin
- ↓ed skin folds
- inflamma’n + erythema
- vaginal dryness
- sparse pubic hair
Tx
- vaginal lubricants to help dryness SSX
- topical estrogen except if pt has C/I
→ estriol cream applied @ bedtime w/ syringe
→ estriol pessaries = inserted @ bedtime
→ estradiol tablets (Vagifem) once daily
→ estradiol ring (Estring) = replaced every 3months
Topical estrogen C/Is
- VTE
- angina
- breast cancer
- Know for OSCE *
Pelvic organ prolapse ✓
Def - descent of pelvic organs into vagina due to weakness + lengthening of surrounding muscles + ligaments
Types
- uterine prolapse = when uterus descends into vagina
→ occurs most commonly after menopause
→ mild cases can be treated w/ pessary but more severe cases may require Sx - vault prolapse = when vaginal vault (top of vagina) descends into vagina
→ occurs in women who had hysterectomy ∴ no longer have uterus - rectocele = when rectum prolapses forwards into vagina due to defect in posterior vaginal wall
→ associated w/ constipa’n, urinary reten’n (due to compress’n on urethra) + palpable lump in vagina
⟹ pt can use her fingers to press lump backwards ∴ correcting anatomical posi’n of rectum + stopping constipa’n - cystocele = when bladder prolapses backwards into vagina due to defect in anterior vaginal wall
→ prolapse of urethra = urethrocele
⟹ when both bladder + urethra prolapse = called cystourethrocele
RFs
- multiple vaginal deliveries
- advanced age
- post menopausal
- obesity
- chronic coughing
- chronic constipa’n → causes straining
SSX
- feeling of “something coming down” in vagina
- heavy sensa’n in pelvis
- urinary SSX such as incontinence, reten’n urgency, frequency
- bowel SSX such as constipa’n, incontinence, urgency
- sexual dysfunc’n, such as pain, altered sensa’n or ↓ed pleasure
Ix = physical exam
- pt should empty bladder beforehand → Sim’s speculum = U-shaped, single-bladed speculum that supports anterior or posterior vaginal wall while vaginal walls are examined
⟹ held on anterior wall to check for rectocele + on posterior wall to check for cystocele
- pt can be asked to cough or “bear down” to assess full descent the prolapse
Grading prolapse
- grade 0 = normal
- grade 1 = lowest part is > 1cm above introitus
- grade 2 = lowest part is w/in 1cm of introitus
- grade 3 = lowest part > 1cm below introitus
Tx
- Conservative Mx for pts w/ mild SSX, who don’t tolerate pessaries or aren’t suitable for Sx . . .
- weight loss
- pelvic floor exercise
- estrogen vaginal cream
- lifestyle Δs for associated stress incontinence such as using incontinence pads, ↓ing caffeine intake - Vaginal pessaries = inserted into vagina to provide extra support to pelvic organs
→ Types . . .
- cube pessaries
- donut pessaries (consist of a thick ring)
- hodge pessaries (are almost rectangular)
- ring pessaries → sit around cervix + hold uterus up
- shelf + gellhorn pessaries → consist of a flat disc w/ a stem, they sit below uterus w/ stem pointing downwards
→ Cleaning of pessary - should be removed + cleaned or changed periodically (every 4 months for ex) b/c can cause vaginal irrita’n + erosion over time
⟹ estrogen vaginal creams can be used to help protect vaginal walls from irrita’n
Sx (NOT MESH) = definitive Tx + has the following complica’ns . . .
- pain
- bleeding
- infec’n
- DVT
- damage to bladder or bowel
- recurrence
- Know for OSCE *
2 accidental consequences of thyroidectomy ✓
1) Hoarse voice due to accidental damage of recurrent laryngeal nerve b/c = inferior to thyroid artery
2) 1° HypoPTH due to accidental resec’n of parathyroid glands
→ pts will ∴ develop SSX of HypoCa i.e . . .
- perioral paresthesia = tingling or ‘pins + needles’ sensa’n in + around mouth, lips + extremities of hands + feet
- carpopedal spasm = painful, frequent + involuntary muscle contrac’ns in hands + feet
- laryngospasm i.e muscle spasm in vocal cords
- prolonged QT interval
- Chvostek sign i.e tapping of facial nerve on phys. exam leads to spasm of facial muscles
- Trousseau sign i.e inflated BP cuff causes carpopedal spasm
Drugs that are dangerous either b/c of narrow therapeutic index, deadly side effects or mutiple drug interac’ns ✓
- Narrow therapeutic index means dose to treat + dose to harm aren’t too far apart
“MIND THE GAP”
- Morphine
- Insulin
- Neoplasia drugs i.e chemo
- Digoxin (HF med) → inhibits Na/K ATPase pump hence can cause HypoK = +ve ionotrope b/c ↑ cardiac contractility + -ve chronotrope b/c ↓ cardiac rate which leads to ↑ in CO
→ SSX of digoxin toxicity = yellow-green vis’n discolora’n, N+ V, bradycardia, diarrhea, confus’n
⟹ which is why plasma digoxin should be measured 8-10 days after starting Tx (therapeutic range = 1-2 nmol/L)
⟹ pts will also have to do periodic renal func’n monitoring b/c poor renal func’n predisposes to digoxin toxicity
⟹ digoxin toxicity = worsened by hypoK - Theophylline / aminophylline
- Hyperglycemic agents (oral ones)
- Epilepsy drugs
- Gentamicin = aminoglycoside (end in “MICIN” w/ an I, main side effect = ototoxicity)
- Anticoagulants
- Psychiatric drugs like Li
→ SSX of Li toxicity = diarrhea, vomiting, lack of coordina’n, agita’n + coarse tremors
Drugs w/ narrow therapeutic index ✓
“L GDP”
- Li
- Gentamicin, vancomycin + amikacin
- Digoxin
- Phenytoin
What’s a hinge jt ? ✓
Jt that only allows mov’nt in 1 direc’n
→ ex = knee jt b/c only does flex’n + extens’n
Why is a posterior shoulder disloc’an a medical emergency ? ✓
B/c can cause avascular necrosis
Anterior v.s Posterior shoulder disloca’n on x-ray ✓
Anterior = loss of sharp angle
Posterior = shoulder has light bulb appearance
Contents of carotid sheath ✓
“ VIIC + CC ”
- Vagus nerve
- Internal jugular vein
- Internal carotid artery
- Common carotid artery
Ddx of malignant abdominal mass in pediatric pt ✓
< 2 y/o = neuroblastoma, Wilm’s tumor + hepato-blastoma
2-6 y/o = neuroblastoma + Wilm’s tumor
7-10 y/o = NHL (Non Hodgkin’s Lymphoma) + germ cell tumors
10-16 y/o = lymphoma, hepatocellular carcinoma + ovarian tumor
Pallative / End of life SSX Tx ✓
- For secre’ns = Hyoscine = anti muscarinic drug
- For restlessness = Midazolam
- For N + V = Domperidone
Bone structure ✓
- red + yellow marrow (fat)
→ until 7 y/o all of bone marrow = red but then becomes yellow - bone covering = periosteum
- shaft = diaphysis = tightly packed tissue i.e compact bone
- ends of bone = epiphyses = loosely packed tissue i.e spongy bone
⚠️ In children, epiphyseal plates HAVE NOT FUSED YET !
1° v.s 2° lymphoid organs ✓
1° lymphoid organs = where lymphocytes are FORMED + MATURE
→ include thymus + bone marrow
→ provide env’nt for stem cells to divide + mature into B or T cells
2° = where lymphocytes are ACTIVATED
→ include . . .
- spleen → for blood borne antigens
- lymph nodes → for antigens from skin or internal surfaces
⟹ drainage = periphery → thoracic duct → venous system - MALT (in tonsils) → for antigens directly through mucosal epithelium
- GALT (gut associated lymphatic tissue) i.e . . .
→ lymphatic patches in esophagus
→ lymphoid tissue in appendix + large intestine
→ Peyer’s patches in ileum (most numerous during puberty)
⚠️ Although T cells also originate in bone marrow like B cells, they have to migrate to thymus for matura’n mature whereas B cells = produced + also mature in bone marrow
⚠️ Thymus = largest during puberty + atrophies after puberty
What is a Robertsonian transloca’n ? ✓
Chromosomal transloca’n = one of the most common types of transloca’n, commonly involves chromosome pairs 13, 14, 15, 21 + 22 = when long arms of 2 acrocentric chromosomes (i.e chromosomes w/ centromeres near their ends) fuse at centromere + the 2 short arms = lost
→ balanced transloca’ns = no gain or loss of sig genetic material ∴ DO NOT cause phenotypic abnormalities
→ unbalanced transloca’ns i.e less or more genes can result in miscarriage, stillbirth + chromosomal disorders such as Down’s or Patau’s
What is Cri-du-chat syndrome ? ✓
Def - congenital dele’n on short arm of chromosome 5
SSX = “MECH”
- Microcephaly + moderate ~ severe intellectual disability
- Epicanthal folds
- Cardiac abnormalities (VSD usually)
- High pitched crying
Which vitamins are fat soluble ? ✓
“D E K A”
⚠️ Malabsorp’n diseases that cause steatorrhea such as CF + celiac disease can cause deficiencies in these vitamins !
→ steatorrhea = pale, greasy stools that are hard to flush
How is N2 metabolized so that ammonia doesn’t accumulate ? ✓
N2 = converted to urea by liver + excreted by kidneys via urine
What are the 3 ketone bodies + does urine disptick detect ALL ketone bodies ? ✓
- acetone, acetoacetate + β-hydroxybutyrate
→ urine dipstick CAN’T DETECT β-hydroxybutyrate !
HLA subtypes + their disease associa’ns ✓
- B27 = (“PAIR”) i.e Psoriatic arthritis, Ankylosing spondylitis, IBD-associated arthritis + Reactive arthritis
- DQ2 / DQ8 = Celiac disease
- DR3 = T1D, SLE, Graves disease, Hashimoto thyroiditis + Addison’s disease
- DR4 = RA, T1D + Addison’s disease
What does a preserved EF tell us ? ✓
Tells us that pb = diastolic heart failure ≠ systolic heart failure b/c preserved EF means heart is able to contract i.e EJECT blood but isn’t able to fill blood, which happens during diastole / relaxa’n
Neutrophil half-life ✓
7 hrs ∴ if u do FBC @ 7am + then again @ 3pm u might get diff neutrophil results
Why is TIBC high in anemia ? ✓
= compensa’n mechanism b/c ↑ in TIBC leads to ↑ in Fe binding spots ∴ more Fe can bind
U/S Analysis ✓
- Anechoic = completely black → means it’s fluid filled i.e blood vessel / cyst
- Hypoechoic = LESS bright i.e more grey → lymph nodes, tumors, muscle
- Hyperechoic = MORE bright than background i.e more white → bone
Palliative Care v.s Hospice ✓
- Palliative care = SSX Mx for pt w/ chronic condi’n
- Hospice = for pts who have < 6 months to live
DNR ✓
- DNR order = medical order issued by a physician or some other practitioner authorized to issue medical orders that directs clinicians NOT to provide cardiopulmonary ressuscita’n in the event pt goes into cardiac or respiratory arrest
- Medical futility = interven’n offers no chance of meaningful benefit to pt
→ interven’ns can usually be considered futile if prob of success (i.e being discharged alive from hospital) = close to 0 OR intervene’n could be successful but QoL = below what’s acceptable to pt
Advance Decis’n ✓
= Statement of refusal of specific Tx at a time when pt may no longer be competent
Crtieria for valid AD
→ only applies to refusals of Tx i.e can’t have an AD requesting a specific Tx to be given
→ pt must have been ≥ 18 y/o
→ pt had capacity at time of making AD
→ AD must clearly specify Tx to be refused + circumstances in which a refusal of Tx will apply
→ can be w/drawn or altered at any time if individual has capacity
→ must have been made voluntarily by a person who had capacity, was sufficiently informed + in the case of life-saving and/or life-preserving Tx, was written + witnessed
3 circumstances under which confidentiality can be breached ✓
- court order
- pt gives their consent
- pt or someone else’s life is directly threatened
3 criteria to diagnose someone w/ ID ✓
- IQ < 70
- Onset happened since birth
- Pt has impaired social adapta’ns
The 4 death awareness contexts ✓
- Closed awareness = when staff know about pt’s impeding death but pt doesn’t
- Suspic’n awareness = when Drs + nurses act in a way where they don’t talk about death, pt recognizes their terminality but doesn’t press the issue
- Mutual pretence = Dr + pt pretend that death isn’t imminent when the possibility is actually high
- Open awareness = when pt openly acknowledges that they’re dying + staff knows that pt knows
Non directed v.s directed organ dona’n ✓
- Non-directed = person offers to donate organ to anyone who might benefit
- Directed = person offers to donate organ to a specific person or group
Mental Capacity Act 2005 ✓
- Every adult has the right to make their own decis’ns + must be assumed to have capacity to do so unless proven otherwise
- Everyone should be encouraged + enabled to make their own decis’ns or to participate as fully as possible in decis’n-making process by being given the help and/or support they need to make + express their choice
- Individuals must retain the right to make what might be seen as eccentric or unwise decis’ns
- Decis’ns made on behalf of people w/o capacity should be made in their best interests, giving priority to achieving what they themselves would have wanted
- Decis’ns made on behalf of someone else should be those which are least restrictive of their basic rights + freedoms
Criteria for capacity according to MHA 2005 ✓
Pt = deemed to have capacity if they are unable to . . .
- understand the info relevant to the decis’n
- retain that info
- use or weigh that info as part of the decis’n-making process
- communicate their decis’n whether that be by talking / sign language or any other means of communica’n
Sec’ns 2, 3, 4 + 5.4 of MHA ✓
- Sec’n 2 = ADMISS’N FOR ASSESS’NT - pt must be suffering from a mental disorder of a nature or ° warranting admis’n for assesss’nt + must be in the interests of their own health or safety or for the protec’n of others
→ deten’n lasts 28 days
→ applica’n must be made by nearest relative or AMHP + be supported by 2 Drs (1 of which must be a specialist)
→ pt can appeal via mental health review tribunal
- Sec’n 3 = ADMISS’N FOR TX - pt must be suffering from mental disorder for which they need prescrip’n in hospital + it is necessary for their health or safety or that of others that prescrip’n be given + appropriate medical Tx is available
→ deten’n lasts for up to 6 months but is renewable @ 6 months + then every 12 months
→ applica’n must be made by nearest relative or AMHP + be supported by 2 Drs (1 of which must be a specialist)
→ pt can appeal via mental health review tribunal
- Sec’n 4 = EMERGENCY ADMISS’N - pt must be suffering from a mental disorder + there must be urgent need
→ deten’n lasts 72 hrs
→ recommenda’n must be made by 1 Dr (Dr doesn’t have to be a specialist but ideally should know pt)
- Sec’n 5.4 = DETAINING PT FROM LEAVING → if pt is already in hospital, Dr or nurse can stop pt from leaving until Dr has further evaluated them / decided what next step in Tx is
KM curve ✓
- compares the probability of achieving an outcome btw 2 groups
- if it’s a favorable outcome = plotted going up + if it’s an adverse outcome = plotted going downwards
- Y axis = probability of outcome
- has exact survival time + censored survival time
Which deaths must be reported to coroner ? ✓
- death of < 18 y/o (even if due to natural causes)
- deaths w/in 24 hrs of admiss’n to hospital
- deaths that might be linked to medical Tx, Sx or anesthesia
- deaths that might be linked to an accident, regardless of how long ago it happened
- deaths that might be linked to drugs or medica’ns (regardless of if they are prescribed or recrea’nal)
- If there’s a possibility of suicide
- deaths that might be related to the person’s occupa’n, for ex death due to asbestos exposure
What informa’n must be on death certificate ? ✓
- first + last name of deceased
- age
- sex
- birth details
- occupa’n
- cause of death if known
- when + where they died
- when death was registered
- signature of registrar
Can any Dr sign death certificate ? ✓
Yes as long as they saw pt ≥ 14 days before they died
ACLS Protocol ✓
Pt unconscious
1- yell + shake them
2 - check for breathing + pulse
3 - no pulse = start CPR immediately, bag (half a squeeze every 6 secs) + call for AED i.e defibrillator
4 - stil no pulse = call code blue, get IV/IO access
5 - more CPR (for 2 min, depth of 2 inches, rate of 100-120)
6 - pulse + rhythm check
a) Shockable rhythm i.e vfib or pulseless vtach
i. shock
ii. immediately resume compress’ns (for 2 mins)
iii. pulse + rhythm check
iv. shock again
v. immediately resume compress’ns (for 2 mins) + 1mg epi every 3-5 mins
vi. pulse + rhythm check
vii. shock again
viii. immediately resume compress’ns (for 2mins) + 300mg amiodarone IV push + can give 2nd dose of 150mg after
→ if no amiodarone available can give 1-1.5mg/kg lidocaine + 2nd dose of 0.5-0.75mg/kg after
b) Nonshockable rhythm (PEA or asystole) = compress’ns (for 2 mins) + 1mg epi every 3-5 mins
→ think of 6 H’s + 5 T’s for causes of PEA
- hypovolemia, hypoxia, hypoK, hyperK, H+ (acidosis), hypothermia
- toxins, tens’n pneumothorax, tamponade, coronary + pulmonary thrombosis,
b) Nonshockable rhythm (bradycardia i.e HR < 50)
i. Is pt stable or unstable (i.e has ≥ 1 of the following SSX . . .)
- SBP < 90
- diaphoresis
- chest pain
- dizziness
- ↓ed level of consciousness
→ stable = CTM
→ unstable . . .
1) 1mg atropine every 3-5 min, max dose = 3mg
2) transcutaneous pacing if pt is in complete heart block (warn pt will be painful + can give pain med / seda’n) or epi infus’n of 2-10 mg/min or dopamine infus’n of 5-20 mg/kg/min
b) Nonshockable rhythm (tachycardia i.e HR > 150)
i. Is pt stable or unstable (i.e has ≥ 1 of the following SSX . . .)
- SBP < 90
- diaphoresis
- chest pain
- dizziness
- ↓ed level of consciousness
→ unstable = synchronized cardiovers’n (warn pt will be painful + can give pain med / seda’n)
→ stable . . .
i. EKG
- wide i.e > 0.12 + monomorphic vtach = adenosine 6mg IV push (warn pt of feeling of impending doom; can give 2nd dose of 12mg) but if something else = amiodarone drip + consult cardiology
- narrow
1) vagal maneuvers i.e ask pt to bear down or blow through straw
2) adenosine 6mg IV push
3) β blocker / CCB + consult cardiology
7- ROSC is finally achieved
a) ABC
- intubate if airway = compromised i.e can’t breathe ≥ 10/min
- vitals → we want O2 sat to be btw 92 + 98% + SBP ≥ 90
∴ give 1-2 L NS if SBP < 90 + then check vitals again + then give vasopressors if SBP still < 90
b) 12 lead EKG + ABG + labs (call cath lab if EKG = suspicious for STEMI)
c) check if pt can follow commands
→ send pt to ICU for TTM if they can’t follow commands
⟹ TTM = 32-36°C for ≥ 24hrs
OPA (oropharyngeal airway) v.s NPA (nasopharyngeal airway) ✓
- OPA = when pt = unconscious or doesn’t have gag reflex
- NPA = conscious or unconscious
How to check proper size of each ?
- OPA = from corner of mouth to corner of mandible
- NPA = from tip of nose to lower earlobe
What type of airway protects against lung aspira’n ? ✓
Tracheal tube
What to give to babies if they have a fever ? ✓
Paracetamol
⚠️ Don’t give Ibuprofen to babies < 3 months old !
WHO Ladder of Pain (for post-op pain as well) ✓
- Paracetamol
- Weak opiate i.e codeine / tramadol / hydrocodone
- Strong opiate i.e morphine / oxycodone / methadone / hydromorphone / fentanyl
→ morphine = renally cleared so don’t give this to pts w/ kidney dysfunc’n
→ oxycodone = hepatically metabolized so = fine to give to pts w/ renal dysfunc’n
What type of pain is ibuprofen best for ✓
MSK pain
⚠️ Ibuprofen = NSAID, so always co-prescribe a PPI w/ it !
