BCS + PPS Flashcards

Question

Heart Failure ✓ 1- Define cor pulmonale + recall common causes 2- Def, RFs, Eti, Pathophys, SSX, Diagnostic Criteria, Ddx, Ix, 1st line Mx, Complica'ns

Answer 1

1. 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) 2. 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 *

Answer 2

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 1. ECG to r/o STEMI 2. TTE or CT if TTE isn't available → CT will show widened mediastinum 3. Consider TOE for definitive diagnosis Tx for type A = open repair w/ graft Tx for type B 1) Conservative Mx i.e IV morphine + IVF if hypotensive / β blocker or non-dihydropyridine CCB if hypertensive 2) EVAR repair if there is aortic rupture or end organ ischemia Complica'ns - cardiac tamponade - aortic incompetence * Know for OSCE *

Answer 3

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 *

Answer 4

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 *

Answer 5

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 !

Answer 6

" 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

Answer 7

→ 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 = 1. 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 2. Left common carotid artery → 2 branches = left internal carotid + left external carotid 3. 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 = 1. Celiac trunk → 3 branches = left gastric, splenic + common hepatic artery 2. Superior mesenteric artery 3. 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

Answer 8

" 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

Answer 9

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 * Know for OSCE *

Answer 10

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's 2. Ventila'n w/ 100% O2 3. Treat underlying cause

Answer 11

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 1. 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 2. Duplex U/S 3. 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 1. Smoking cessa'n + BP / glucose control 2. Exercise training i.e structured + supervised program of regularly walking to point of near-maximal claudica'n pain, resting + repeating again 3. Medical Tx i.e 75mg clopidogrel daily + high dose statin 4. Sx . . . - endovascular angioplasty + stenting - endarterectomy i.e cutting vessel open + removing atheromatous plaque - bypass Sx = using graft to bypass blockage * Know for OSCE *

Answer 12

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

Answer 13

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 * Know for OSCE *

Answer 14

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

Answer 15

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 * Know for OSCE *

Answer 16

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

Answer 17

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 1. 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" 2. 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" 3. 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" 4. Add LABA to low dose ICS + SABA - end in “EROL” ⚠️ LABAs MUST ALWAYS BE USED W/ ICS ! 5. 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 *

Answer 18

Trachea bifurcates into left + right main bronchi @ carina (T5)

Answer 19

B/c right main bronchus = wider, shorter + more vertical than left main bronchus

Answer 20

Inferior por'n of right lower lobe

Answer 21

Superior por'n of right lower lobe

Answer 22

Right = 3 → upper/superior lobe → middle lobe → lower/inferior lobes Left = 2 → upper/superior lobe → lower/inferior lobe

Answer 23

Right lung has 2 fissures → Horizontal fissure btw superior + middle lobe → Oblique fissure btw middle + inferior lobe Left lung has 1 fissure = Oblique fissure

Answer 24

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)

Answer 25

To sweep mucus secre'ns + debris out of lungs + towards mouth

Answer 26

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

Answer 27

- 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

Answer 28

To prevent it from collapsing

Answer 29

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

Answer 30

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

Answer 31

Hgb bound to CO ⚠️ Recall that Hgb binds to CO w/ 250x more affinity than it does O2 !

Answer 32

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 !

Answer 33

HYPOXEMIA = low O2 content in blood which can lead to HYPOXIA = when tissues are O2 starved

Answer 34

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 !

Answer 35

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

Answer 36

1. @ Rest = -70mV b/c of higher [Na ions] outside compared to inside (-ve means polarized); there's more [K ions] inside than outside 2. 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 * 3. Na channels close + K channels open causing K ions to move out ∴ inside becomes -ve again = REPOLARIZA'N 4. 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) 5. K channels finally close → hyperpolariza' n = corrected + inside goes back to initial resting Ψ

Answer 37

- 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 *

Answer 38

⚠️ 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

Answer 39

⚠️ 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

Answer 40

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

Answer 41

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

Answer 42

- SSX = HA, confus'n, nausea, chest pain, SOB, bright red cheeks - Ix for diagnosis = ABG → will show low O2 satura'n + high carboxyHgb

Answer 43

- 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

Answer 44

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

Answer 45

- 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 !

Answer 46

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

Answer 47

1. Inotropic/channel-linked = directly coupled to an ion channel → fast (millisecs) 2. 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) 3. Tyrosine-kinase linked receptors, ex = insulin → slow response but not as slow as nuclear receptors 4. 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

Answer 48

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) 1. Microcytic = MCV < 80 (causes = "TAILS") - Thalassemia = normal ferritin + the microcytic anemia is NOT new - Anemia of chronic disease (can also be normocytic) = 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 - Sideroblastic anemia 2. Normocytic = MCV w/in normal range aka 80-100 ➔ Hemolytic = high reticulocyte count, ex: sickle cell, hem. anemia (can be inherited or acquired) → 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 = due to aplastic anemia or anemia of chronic disease 3. 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 !

Answer 49

+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

Answer 50

- 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 *

Answer 51

- 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

Answer 52

- 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

Answer 53

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 = 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’s: TB, MS, scabies, Guillain-Barre, Mantoux test

Answer 54

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 1. Mark areas w/ pen or marker + include +ve + -ve control → +ve control = histamines + -ve control = water 3. Apply 1 drop of each allergen / control on their marked spot 4. Prick each of those spots (use diff needle for each spot) 5. Press entire forearm w/ paper towel 6. 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 *

Answer 55

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 on minimal 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 ⟹ ↑ risk of DVTs ⟹ can cause myelofibrosis = when bone marrow becomes fibrotic ∴ spleen has to take over RBC prodcuc'n ∴ causing splenomegaly - 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 1. Smoking cessa'n therapy + both pneumococcal / influenza vaccina'ns + pulmonary rehab if they had an exacerba'n 2. inhaled SABA or SAMA 3. What to add if pt is still symptomatic . . . → if FEV1 >50% = inhaled LAMA or LABA → if FEV1 <50% = Inhaled LAMA or LABA+ICS 4. If still symptomatic add LABA+ICS or if already on LABA+ICS add LAMA 4. 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 *

Answer 56

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 *

Answer 57

- septic pts w/ ↓ed consciousness - intoxicated pts i.e alcohol overuse - acute stroke pts w/ impaired swallowing - pts w/ dysphagia Tx for aspira'n pneumonia = co-amoxiclav

Answer 58

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)

Answer 59

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 *

Answer 60

1. 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 - 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 2. 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 3. 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 4. 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 5. 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 *

Answer 61

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

Answer 62

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

Answer 63

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 *

Answer 64

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

Answer 65

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 *

Answer 66

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 *

Answer 67

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

Answer 68

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

Answer 69

“CP4MT2A” - Costochondritis - P.E - Pleural Effus'n - Pneumothorax - Pericarditis - MI - Cardiac Tamponade - Aortic dissec'n - Abdominal pb like GERD

Answer 70

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) 1. 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 2. High flow O2 3. 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 *

Answer 71

- 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

Answer 72

("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 / pericarditis uremia * Know for OSCE *

Answer 73

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 the past 48 hrs → ↑ in serum Cr to ≥ 1.5x BL 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 > 10,000) → 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 rhabdo, 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 *

Answer 74

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 + proteinuria/hematuria - G2 = GFR from 60-89 + proteinuria/hematuria - 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 1. Statin 20mg to ↓ risk of CVD 2. 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 3. 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 ! Main cause of death in CKD pts = CVD * Know for OSCE *

Answer 75

C/Is - HIV - active infec'n - life expectancy < 2 y/rs - active malignancy → there should be ≥ 2 yrs btw remiss'n + transplant for pts w/ prior malignancy Addi'nal Mx = the following 3 immonusppressants for life . . . - tacrolimus → side effects = HTN, HLD + nephrotoxic - prednisolone - mycophenolate mofetil or azothiprine → side effects = leukopenia, anemia + GI toxicity Early complica'ns of transplant - arterial or venous thrombosis → Ix = renal U/S - delayed graft func'n (DGF): → 20-60% of grafts from wont' start working immediately ⟹ most common eti for this = ATN - stenosis → can occur in anastomoses → Tx = balloon dilata'n Late complica'ns - cancer due to long-term immunosuppress'n especially . . . → HPV → lymphoma → Karposi Sarcoma (HHV8) * Know for OSCE *

Answer 76

= 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 such as PR diclofenac 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 *

Answer 77

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"

Answer 78

NEPHROTIC SSX - severe PROteinuria (≥ 3.5 g/L/day, urine might have frothy appearance) - hypoalbuminemia (≤ 30 g/L) - edema + HLD + hypercoaguability 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 Ix = Renal Bx Tx = furosemide Complica'ns - HTN - HLD - thrombosis NEPHRITIC SSX - 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 *

Answer 79

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 LP - end stage renal failure (usually occurs around 50 y/o for dominant + before adulthood for recessive) * Know for OSCE *

Answer 80

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 *

Answer 81

= 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 1. U + E → Na will be < 135 mmol/L 2. Serum glucose (random or fasting) to r/o hyperglycemia-associated HypoNa 3. 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 4. Physical Exam 5. If there are fluid overload SSX = Hypervolemic a) Urinary Na < 20 = due to CHF / cirrhosis / hypoalbuminemia b) Urinary Na > 20 = due to renal failure 6. 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 7. 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% NS - 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 *

Answer 82

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 - rhabdo (less common complica'n) * Know for OSCE *

Answer 83

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 → HypoMg → 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 for mild 2) 0.9% NaCl /KCl 0.3% 1L over 4 hrs for severe HypoK 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 *

Answer 84

Def - K > 6 = 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 ⟹ Tx = 500 mL NaCl over 15 mins → admin of mannitol b/c will cause ↑ in osmolality SSX - diarrhea - vomiting Ix = ECG → will show ≥ 1 of the following signs . . . - long PR interval - flat or completely absent P waves - broad/wide QRS - tall tented T waves in almost all leads aka tall + pty instead of broad - PVCs (premature ventricular contrac'ns) Emergency Tx i.e HyperK w/ ECG Δs = 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 ⚠️ If there's digoxin toxitiy, give insulin-glucose infus'n instead to treat HyperK ! * Know for OSCE *

Answer 85

Never unless pt = pregnant !

Answer 86

Def - infec'n of kidneys, bladder or urethra that are more common in women → usually caused by E. coli + 2nd by Klebsiella pneumoniae 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 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 UTI ppx 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 - 5-10 days for immunosuppressed women or pts w/ abnormal anatomy or impaired kidney func'n - 7 days for men, pregnant women + CAUTIs 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 *

Answer 87

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 *

Answer 88

1. Urgent referral for peds assess'nt in hospital + paracetamol to lower fever ⚠️ Never give Ibuprofen to pt < 3 months old ! 2. Ix's - FBC - CRP - blood culture - urinanalysis - stool culture if baby has diarreha - CXR if baby has resp SSX * Know for OSCE *

Answer 89

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 *

Answer 90

1. Activated charcoal 2. IV Na Bicarb to enhance elimina'n of aspirin in urine

Answer 91

- coma - seizures - acute renal failure - pulmonary edema - serum [salicylate] > 700mg/L

Answer 92

- 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

Answer 93

- gabapentin - pregabalin - duloxetine - amitriptyline → side effect in elderly pts = urinary reten'n, might appear as suprapubic mass on exam

Answer 94

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 1. Lifestyle Δs + check in 3-6 months if pt reached target HbA1c, if not . . . 2. Metformin OR DPP-4 inhibitor / pioglitazone / sulfonylurea if metformin = contraindicated OR SGLT-2 inhibitor if the other 3 aren’t appropriate for pt 3. 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 4. ↑ dose of metformin 5. 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 *

Answer 95

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 1. 0.9% NaCl 10ml/kg for 10 mins 2. 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

Answer 96

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 i.e . . . 1. Fluid replac'nt w/ NS 2. Insulin infus'n 3. Subq Heparin for VTE Ppx

Answer 97

Ix = A1c → btw 39-47 mmol/L = pre-diabetes → > 48 = diabetes Mx for pre-diabetes = refer to diabetes preven'n program for diet + lifestyle Δs to prevent them from actually getting diabetes

Answer 98

"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

Answer 99

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 i.e ↓ed consciousness / AMS 1. ABC 2. Recovery posi'n 3. if pt is on insulin infus'n STOP IT ! 4. If pt already has an IV give 100 ml of 10% Glucose or 1mg of IM Glucagon * Know for OSCE *

Answer 100

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 should avoid 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)

Answer 101

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 1. Dietary Δs + ↑ in physical activity 2. BMI ≥ 30 OR BMI ≥ 28 + comorbidity = treat w/ medica'n i.e orlistat → orlistat = lipase inhibitor ∴ ↓ absorp’n of dietary fat 3. 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 *

Answer 102

≥ 3/4 of the following . . . - HTN - BMI > 30 - Impaired glucose tolerance - Dyslipidemia i.e ↓ed LDL or triglycerides >150 mg/dL * Know for OSCE *

Answer 103

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 HyperTSH - 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 ↓ 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 *

Answer 104

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 *

Answer 105

Def - clinical syndrome of hyper-metabolism due to ↑ed free thyroxine (T4) and / or free triiodothyronine (T3) serum levels regardless of etiology → HyperTSH = 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 HyperTSH = most common cause of thyrotoxicosis → pathophys of Grave's - immune system produces TSH receptor antibodies that stimulate TSH receptors on thyroid → Grave specific SSX in addi'n to regular HyperTSH SSX . . . - exophthalmos - diffuse goiter w/o nodules - thyroid acropachy = hand swelling + finger clubbing - pretibial myxedema → that area of skin will have a discolored, waxy, + edematous appearance = SPECIFIC TO GRAVE'S ! - 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 . . . - 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 op'ns - Carbimazole for 12-18 months → side effect = neutropenia + agranulocytosis ∴ pt should tell u if they notice any infective SSX, especially a sore throat - Propylthiouracil (PTU) which ↓ convers’n of T4 to T3 - β blocker (propanolol) for adrenergic SSX i.e tachycardia / sweating / palpita'ns / tremor + for thyroid storm - Ttl thyroidectomy if above meds fail → these pts will require life long levothyroxine Complica’n = thyrotoxic crisis / thyroid storm → SSX = fever, tachycardia + delirium → only occurs in thyrotoxicosis due to HyperTSH * Know for OSCE *

Answer 106

"BLT KP" - breast (#2) - lung (#3) - thyroid - kidney - prostate (#1) ⚠️ All = osteoLYTIC metastases except prostate = osteoSCLEROTIC metastasis ! * Know for OSCE *

Answer 107

"CS yr PBL" - Colon - Stomach - Pancreas - Breast - Lung Liver metastases = common b/c of its rich vasculature i.e portal venous system

Answer 108

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 - 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 *

Answer 109

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 *

Answer 110

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 - side effects = muscle pain, abdo pain, nausea + diarrhea - C/I = pregnancy + don't take w/ grapefruit ⚠️ Must monitor LFTs before prescribing, @ 3 months + then again @ 12 months Statin dose = appropriate if we see a > 40% ↓ in NON-HDL cholesterol after 3 months of Tx Complica'n = CVD * Know for OSCE *

Answer 111

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 2. 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 *

Answer 112

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) - low Na + high K → 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) 1. Give pt Synacthen (synthetic ACTH) 2. Check blood cortisol 30 mins before + 60 mins after dose → synthetic ACTH will stimulate adrenal glands to produce cortisol → cortisol level won’t double as it normally should 2. 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 *

Answer 113

" 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 *

Answer 114

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 → high Na + low K - 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 or 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 *

Answer 115

- Pituitary adenomas = most common disease of the anterior pituitary = BENIGN tumors Types a) Func'nal pituitary tomurs = secrete a hormone - Prolactinomas = most common type of func'nal adenoma → secrete prolactin → 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 → secrete GH → will cause HAs / visual pbs (usually in men + post-menopausal women) + ACROMEGALY i.e thick hands + feet, protruding lower jaw, coarse facial appearance, larger tongue, excessive sweating, oily skin + ↑ in collar size ⟹ diagnostic Ix for acromegaly = OGTT ⟹ mortality rate = 2x that of normal popula'n b/c of LVH + CVD as a result of insulin resistance - TSH secreting adenomas → secrete TSH ∴ cause hyperthyroidism SSX → mortality rate = 2x that of normal popula'n b/c of LVH + CVD as a result of insulin resistance b) Non-func'nal = don't secret any hormones * Know for OSCE *

Answer 116

- 98.9% = skeleton - 1% = intracellular - 0.1% = extracellular (45% bound to albumin, 10% unbound as a free ion)

Answer 117

- 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

Answer 118

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 i.e MM / breast cancer / lung SCC / bone mets - 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 = 1L 0.9% NaCI over 4 hrs Complica’ns - pancreatitis - renal failure - kidney stones * Know for OSCE *

Answer 119

Def - low Ca Eti - Cancer - HypoPTH - PTH resistance - Acute pancreatitis - Toxic shock syndrome - Acute rhabdo - 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 +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 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 *

Answer 120

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 *

Answer 121

Def - ↑ in PTH as a response to HypoCa Eti = something causing HypoCa i.e . . . - aging - CKD - Vit D def (could be due to inadequate sunlight exposure, malbasorp’n, etc) Ddx = 1° HyperPTH Ix’s = serum Ca, ALP + PTH Complica’n = nephrolithiasis b/c excess Ca can precipitate + cause kidney stones * Know for OSCE *

Answer 122

Def - low PTH RFs - parathyroid Sx - HypoMg - thyroid gland Sx b/c parathyroid glands might have been removed accidentally SSX = complica'ns of HypoCa i.e dry hair + brittle nails Ddx - HypoMg - 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 *

Answer 123

1. Pre hepatic = due to excessive RBC breakdown → unconjugated bilirubinemia b/c = there is too much bilirubin for the liver to conjugate → normal urine color b/c only conjugated bilirubin makes urine dark → normal stool color b/c flow of bile to duodenum isn’t impaired ⟹ ex’s = SCD or other hemolytic condi’ns 2. Intra-hepatic = due to ↓ed hepatocyte func’n for whatever reason → mix of conjugated + unconjugated bilirubin in blood b/c liver = somewhat able to conjugate bilirubin but not fully → 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 3. Post-hepatic = caused by something obstructing flow of bile to duodenum → conjugated bilirubinemia b/c whatever the obstructive pb is, it's happening outside of the liver ∴ liver's ability to conjugate bilirubin ≠ affected → dark urine b/c of conjugated bilirubin → pale stool b/c bilirubin gives stool it’s brown color so if there’s something obstructing flow of bile to small intestine, stool will be pale b/c it doesn't contain any bilirubin ⟹ ex’s = gallstones, stricture, pancreatitis

Answer 124

- High ALT + AST = liver pb - High Gamma + ALP = bile flow pb

Answer 125

B/c zone 1 = closer to portal vessels

Answer 126

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 Max dose of paracetamol in 24 hrs = 4g ! → paracetamol 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 → Tx for paracetamol overdose . . . 1. Measure paracetamol [ ] if it’s been ≥ 4 hrs since ingest'n, if it hasn't been 4 hrs yet wait 2. If [ ] @ time since ingest'n lies on or above graph, then treat w/ IV N-acetylcysteine Addi'nal Mx for paracetamol overdose = psych assess'nt * Know for OSCE *

Answer 127

- drugs w/ constipating effects i.e opioids - drugs that ↓ K i.e loop + thiazide diuretics b/c HypoK ↑ ammonium - drugs w/ sedative effects i.e benzos / antihistamines such as chlorphenamine

Answer 128

Max of 14 units / wk spread evenly over ≥ 3 days + max of 5 units in a single day What's "1 unit" of alcohol ? - 1/2 a pint of cider or a weak beer - 1/2 a small glass of wine → larger / stronger vers'ns of the above = 3 units

Answer 129

- For men = > 8 units of alcohol in a single sess'n - For women = > 6 units of alcohol in a single sess'n

Answer 130

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

Answer 131

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 > 10.5 means there's advanced fibrosis < 10.5 means advanced fibrosis = unlikely (check this every 3 yrs in NAFLD pts) - 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

Answer 132

- tremor - slurred speech - bloodshot eyes - smelling of alcohol - telangiectasia i.e dilated capillaries on the face

Answer 133

≥ 1 of the following SSX . . . ("CT WPOC") - Compul'sn to drink - Tolerance - W/drawal SSX - Primacy - Ongoing use - Control loss

Answer 134

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 (seeing insects) = 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

Answer 135

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

Answer 136

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 - benzo (for w/drawal) - weight loss + smoking cessa'n - nutri'nal supplementa'n - influenza + pneumococcal vaccines - corticosteroids in severe alcoholic hepatitis Complica'ns - portal HTN - coagulopathy - renal failure - HCC - Wernicke-Korsakoff Syndrome (WKS) = Wernicke encephalopathy + Korsakoff syndrome

Answer 137

"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 ?

Answer 138

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 1. Treat based on eti . . . - lifestyle Δs for NAFLD - antiviral drugs for hep C - immunosuppressants for autoimmune hepatitis 2. 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 - HCC - bleeding + thrombosis - ascites due to portal HTN → initial Tx = paracentesis + Tx for refractory ascites = TIPSS ⟹ complica'n of TIPSS = hepatic encepalopathy - spontaneous bacterial peritonitis due to ascites → Tx = IV Abx - malnutri'n b/c cirrhosis ↓ amt of protein liver produces + also disrupts liver's ability 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 adequately breaking down glycogen to make glucose - 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 → main SSX = asterixis → Tx = lactulose → PO4 enemas → stop diuretics if Na < 130mmol/L → avoid sedatives → consider IV broad spectrum Abx 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

Answer 139

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 *

Answer 140

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-suppressant such as azathioprine to control disease Complica’ns = side effects of long term corticosteroid use * Know for OSCE *

Answer 141

→ 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 HCC - CT + MRI for staging - Bx for histology Barcelona Staging - Stage 0 = single tumor < 2 cm + liver is working normally - Stage A = up to 3 tumors that are all < 3 cm + liver is working well - Stage B = > 3 tumors 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 *

Answer 142

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 instead if bleeding = 2° to endoscopy → w/ Glasgow-Blatchford score, score > 0 means pt = @ high risk for upper GI bleed U + E → elevated urea Emergency Tx = "ABATED" A = ABCDE's 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 for 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 *

Answer 143

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 + transfuse if pt is profusely bleeding * Know for OSCE *

Answer 144

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 SSX - N + V - dysphagia - abdominal pain - unwanted weight loss - Trosier’s sign (means there's mets) Ddx = peptic ulcer disease Ix’s - 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 *

Answer 145

- 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

Answer 146

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 - High 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 Mx of Barret's esophagus - no dysplasia = PPI + endoscopic surveillance - low grade dysplasia = either or - high grade dysplasia = endoscopic RFA + resec'n of visible les'ns GERD IN CHILDREN → usually occurs in babies < 2 months old SSX - NBNB emesis - chronic cough - hoarse cry - poor weight gain - reluctance to eat - distress after feeding - faltering growth Ddx of vomiting in children - overfeeding - appendicitis - gastroenteritis - Intestinal obstruc'n - pyloric stenosis (also presents w/ NBNB emesis) - infec'ns such as UTI / tonsillitis / meningitis Ix = clinical but refer them to pediatrician if pt is not responding to Tx or if it persists after 1 y/o Tx 1. Trial alginate therapy if baby = breastfed or thickened formula feeds if baby = bottle fed 2. 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 *

Answer 147

- 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

Answer 148

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 *

Answer 149

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) → AXR will show Rigler's sign i.e pneumoperitoneum → 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 *

Answer 150

- 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 !

Answer 151

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 *

Answer 152

RFs - alcohol - smoking - EBV - HPV - Betel nut - chewing tobacco Main SSX = neck lump Redflag SSX i.e require urgent ENT referral - weight loss - hoarse voice - dyshpahgia - odynophagia - u/l ear pain w/o explana'n - u/l blocked nose - unexplained mouth ulcer for ≥ 3 wks 1st line Ix = neck U/S * Know for OSCE *

Answer 153

Def - cancer of the esophagus → 2 main types = SCC + adenocarcinoma (glands + mucin) RFs for SCC - FHx - male - older age - SMOKING + alcohol RFs for adenocarcinoma - FHx - male - older age - smoking - GERD + obesity - hiatal hernia - Barrett’s esophagus 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 *

Answer 154

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

Answer 155

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

Answer 156

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 - EGD + Bx for diagnosis Tx = oral corticosteroids such as prednisolone + azathioprine to maintain remiss'n → can consider adding methotrexate 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") ⚠️ Admit IBD pt having flare up for high dose IV steroid if they are systemically unwell i.e have a fever > 38°C Complica'ns - stricture - perfora'n - colorectal cancer - massive lower GI bleed - 1° sclerosing cholangitis (PSC) → = diagnosed w/ MRCP which will show beaded appearance of CBD → presenta'n = RUQ pain, jaundice + hepato-splenogemaly - 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 *

Answer 157

→ 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

Answer 158

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 1. 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 → will be elevated 2. Duodenal Bx via endoscopy = gold std for diagnosis → 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 *

Answer 159

- adult w/ new diagnosis of T1D - child w/ FHx of celiac, autoimmune thyroiditis, T1D, juvenile chronic arthritis, Down, Turners' or selective IgA deficiency - 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 *

Answer 160

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 *

Answer 161

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 *

Answer 162

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 it should be

Answer 163

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 like they can't control their eating - Inappropriate compensatory behavior to prevent weight gain i.e diuretics / laxatives / vomiting - Above behaviors must occur ≥ once/wk for ≥ 3 months - disproportionate influence of weight + shape on their self-worth - disturbance should not occur exclusively during episodes of anorexia nervosa SSX - normal weight - dental eros'n - HypoK, HypoCl, HypoNa + metabolic 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

Answer 164

1. Anaphylactic rxn → SSX = urticaria, pruritus, wheezing, hypoTN, respiratory arrest, shock → Tx = STOP tranfus'n + NS +/- epi 2. Acute hemolytic transfus'n rxn = caused by giving incompatible blood to pt → SSX = fever, hypoTN, tachypnea, tachycardia, flank pain → Tx = STOP tranfus'n + NS 3. Febrile non-hemolytic transfus'n rxn → SSX = fever + chills but pt is otherwise well → Tx = SLOW tranfus'n + paracetamol 4. Transfus'n-associated circulatory overload → SSX = fluid overload SSX → Tx = SLOW tranfus'n + furosemide * Know for OSCE *

Answer 165

When pt's Hgb < 7

Answer 166

- Anticoagulant = prevents EXISTING clots from growing by inhibiting coagula'n cascade - Antiplatelet = inhibits FORM'AN OF NEW CLOTS by preventing platelets from aggregating - Thrombolytic drug = PROMOTES CLOT BREAKDOWN by stimulating fibrinolysis

Answer 167

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 - platelet count + fibrinogen will be low - PT + APTT + bleeding time will be prolonged - 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 *

Answer 168

- 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

Answer 169

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 1. Thromboxane (TXA2) binds to platelets + makes platelets aggregate at site of injury → forms loose platelet plug (platelets adhere to plug via vWF) 2. 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 * 3. 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 ! 1. CTPA to diagnose P.E but V/Q scan instead if pt has kidney pb or is allergic to contrast dye 2. Wells score to figure out if DVT = cause of P.E (Well’s score > 4 = DVT likely) 3. If Wells score = +ve do proximal leg vein U/S + if -ve do D-dimer + follow steps 4 + 5 4. 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 5. If D-dimer = +ve repeat U/S + if -ve it's NOT DVT ! 5. 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 1. 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" 2. Warfarin → must monitor via INR (goal INR = 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 - 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 ! 3. If pt already on warfarin has another VTE, ↑ target INR to 3-4 instead of 2-3 4. 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 5. Dalteparin if pt = pregnant * Know for OSCE *

Answer 170

- 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

Answer 171

- 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 *

Answer 172

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

Answer 173

- 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

Answer 174

- Stop all anti-platelets 1 wk prior to Sx - Stop Warfarin 5 days prior to Sx + give Vitamin K1 if on day prior to Sx INR ≥ 1.5

Answer 175

Short-acting depolarizing muscle relaxant ∴ can cause malignant hyperthermia in pt w/ any RFs

Answer 176

Vitals + ECG

Answer 177

- PE - infec'n - electrolyte abnormality i.e hypoglycemia / HypoNa

Answer 178

- 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

Answer 179

- ↓ in BP - resp. depress'n - painful sensa'n on injec'n - hypnosis

Answer 180

" 4 W's" Post op day 1-3 = "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

Answer 181

W/in the first 72 hrs after Sx

Answer 182

Amt of times woman has given birth to fetus that was ≥ 20 wks gesta'n

Answer 183

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 !

Answer 184

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 *

Answer 185

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 - easy bruising - epistaxis - excessive bleeding from minor wounds - menorrhagia i.e extremely heavy periods Ix’s - platelets + PT will be normal - vWF antigen (for diagnosis) → will be low - APTT + bleeding time will be prolonged Emergency Tx i.e in severe blood loss = platelet transfu’n Regular Tx = vWF containing concentrate

Answer 186

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 *

Answer 187

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 *

Answer 188

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 *

Answer 189

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

Answer 190

Palpable spleen, which means that spleen has enlarged > 2x its normal size

Answer 191

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

Answer 192

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 !

Answer 193

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

Answer 194

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

Answer 195

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

Answer 196

1. 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 2. 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

Answer 197

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 = "CRAB HI" - HyperCa SSX - Renal impairment - Anemia b/c bone marrow crowding suppresses erythropoiesis - bleeding + bone pain + ↑ed risk of fractures due to lytic les'ns - Hyperviscoity → causes HAs, dizziness + blurry vis'n - ↑ed risk of infec'n due to ↓ in Ig produc'n 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 - FBC → will show thrombocytopenia due to bone marrow crowding ∴ ↑ing risk of bleeding - X ray → will show lytic les'ns due to bone marrow infiltra'n by plasma cells + osteoclast overactivity Tx = chemo Complica'ns → leukopenia → recurrent infec'ns → fracture of vertebral bodies → myeloma cast nephropathy = forma’n of casts in renal tubes from free Ig light chains = most common cause of renal failure in MM pts

Answer 198

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

Answer 199

Def - oncological emergency where tumor cells release their contents into bloodstream after chemo → HyperK → HyperPhos → Hyperuricemia b/c of released nucleic acids → High urea b/c of renal dysfunc'n → 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

Answer 200

Eti = recently started chemo Tx = broad spectrum IV Abx

Answer 201

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

Answer 202

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

Answer 203

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

Answer 204

Def - anemia due to underlying disease Eti - RA - SLE - HIV - GCA - malaria - liver disease - renal failure - cancers like lymphoma or myeloma

Answer 205

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

Answer 206

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 (screening test) → 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 *

Answer 207

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 → jaundice W/IN first 24hrs of life = pathological ! 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 HypoTSH as a 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

Answer 208

Def - when Rh -ve pregnant woman carries Rh +ve baby during 2nd pregnancy 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 SSX - neonatal jaundice in 1st 24hrs after birth - pallor due to anemia - hepatosplenomegaly Ix's - Maternal blood group - Direct Coombs test in baby → will be +ve Antenatal Tx = anti-D immunoglobulin ppx @ 28 wks + w/in 72 hrs of deliver Post-natal Tx = phototherapy for baby, exchange transfus'n in severe anemia or hyperbilirubinemia + IVIG Complica'ns - hydrops fetalis - intrauterine death - kernicterus

Answer 209

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

Answer 210

= 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

Answer 211

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 *

Answer 212

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 1. Progressive, symmetrical, proximal muscle weakness 2. Muscle Bx shows necrosis / phagocytosis / regenera'n / inflamma'n 3. Elevated CK or Aldolase 4. Electromyography typical findings 5. 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 - rhabdo - statin use - strenuous exercise Ix’s - muscle Bx - CK + 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

Answer 213

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

Answer 214

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 *

Answer 215

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

Answer 216

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 = Nifedipine Mx - keeping hand warms - avoiding stress + triggers - smoking cessa'n - should avoid β blockers b/c can make their SSX worse Complica'n = ischemic digit

Answer 217

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 → check FBC, kidney + liver func'n before starting pt on a DMARD - avoiding smoking - regular emollients - avoiding cold triggers (for Raynaud’s) - gentle skin stretching to maintain good ROM Complica'ns - skin ulcers - hypoTSH - heart / lung / kidney involv'nt * Know for OSCE *

Answer 218

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 to check for IBD Tx = supportive b/c usually resolves spontaneously w/in 6 wks - rest - leg eleva'n - NSAIDs → K iodide → intrales'nal corticosteroid injec'n

Answer 219

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

Answer 220

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 *

Answer 221

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 SSX onset Complica'ns - otitis media - sinusitis - bronchitis - encephalitis - viral pneumonia - febrile convuls'ns (in pediatric pts) * Know for OSCE *

Answer 222

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 = immunsuppress'n < 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 - 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) → 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 * Know for OSCE *

Answer 223

- Tx - full screening for other STIs - contact tracing - advice about avoiding sexual activity until STI = treated - educa'n on importance of practicing safe sex

Answer 224

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 * Know for OSCE *

Answer 225

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 ! * Know for OSCE *

Answer 226

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 * Know for OSCE *

Answer 227

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 * Know for OSCE *

Answer 228

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 * Know for OSCE *

Answer 229

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 Tx for severe = admit for IV Abx → switch to oral Abx once pt can tolerate PO intake ⚠️ Don't wait for swab reuslts to start Tx ! 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) → SSX = RUQ pain that might radiate to shoulder + fric'n rub on ausculta'n * Know for OSCE *

Answer 230

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 - 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 * Know for OSCE *

Answer 231

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 pregnant pt * Know for OSCE *

Answer 232

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 * Know for OSCE *

Answer 233

→ 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 * Know for OSCE *

Answer 234

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 *

Answer 235

→ 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 r/o 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 * Know for OSCE *

Answer 236

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 * Know for OSCE *

Answer 237

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 3 wks → 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 *

Answer 238

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 *

Answer 239

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 1. Classic FUO - fever > 38.3°C - dura’n of > 3wks - no diagnosis after > 2 outpt visits or 3 days of hospital Ix 2. Nosocomial /Health-care associated) = fever > 38.3°C on several occas'ns 3. Neutropenic (immune-deficient) - fever > 38.3°C - neutrophil count < 500 - no diagnosis after 3 days of hospital Ix 4. HIV-related FUO - fever > 38.3°C - dura’n of > 3 wks for outpts + > 3 days for inpts * Know for OSCE *

Answer 240

B/c Abx killed healthy gut flora as well → if diarrhea = smelly ≠ due to Abx → if diarrhea ≠ smelly = due to Abx

Answer 241

" 4 C's" - cipro - cephalosporins i.e CTX - clindamycin - co-amoxiclav Tx = oral vancomycin

Answer 242

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, caused 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 *

Answer 243

Def - parasitic infec’n caused by protozoa of the genus Plasmodium = transmitted to humans by being bitten by infected female Anopheles mosquito 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 female Anopheles mosquito 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 *

Answer 244

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 (erythema 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 *

Answer 245

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 dwelling - 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 use microscopy to detect eggs or scyballa (fecal pellets) Tx = permethrin 5% cream → malathion 0.5% cream ⟹ permethrin cream should be applied on entire body when skin is cool + should be left on for 8 -12 hrs + then wash it off + repeat process for 1 more wk to kill hatched eggs that survived 1st round * Know for OSCE *

Answer 246

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 for 8 days → should be left on hair for 8 hours i.e overnight + then washed off Mx = detec'n combing to check if Tx was successful * Know for OSCE *

Answer 247

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 / MRSA folliculitis = clindamycin Tx for gram -ve folliculitis = topical benzyl peroxide * Know for OSCE *

Answer 248

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 *

Answer 249

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 but h 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 2. Vascular dementia → SSX = stepwise ↓ in cognitive ability w/ late onset memory impair'nt + pt has RFs such as HTN + T2D 3. Lewy body dementia → SSX = Parkinsonism, progressive cognitive decline, visual hallucina'ns, delus'ns, fluctuating levels of conciousness + REM sleep disorders ⚠️ Regular Parkinson's can also have Lewy bodies ! 4. Fronto temporal dementia → 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 *

Answer 250

- fluctuates v.s progresses - days ~ wks v.s permanent - reversible v.s NOT reversible

Answer 251

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 Staging 1 = just erythema 2 = partial thickness i.e shallow open ulcer 3 = full thickness tissue loss → subq fat may be visible, but not tendon, bone or muscle 4 = exposed bone, tendon or muscle +/- slough or eschar Ppx for pressure ulcers = pressure reducing aids + frequent reposi'ning 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 *

Answer 252

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 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, ↓ed PO intake + lymphadenopathy → Tx = aciclovir * Know for OSCE *

Answer 253

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 → isn't immune mediated like allergic contact dermatitis RFs - 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 *

Answer 254

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 for fungal infec'n Complica'ns - eros'n - ulcera'n - candida infec'n - cellulitis

Answer 255

Def - diffuse erythema + scaling involving ≥ 90% of skin surface area = dermatological emergency ! Eti - eczema - psoriasis - drugs such as NSAIDs, penicillins, anti-epileptics + anti-malarial drugs SSX - warm psoriatic les'ns - fever - malaise - tachycardia - hypoTN - 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 *

Answer 256

- head + neck = 9% - each arm = 9% - torso = 18% - back = 18% - each leg = 18% - groin area = 1% * Know for OSCE *

Answer 257

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 tissue → SSX = eschar, charred, lack of sensa'n * Know for OSCE *

Answer 258

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

Answer 259

Aggressive IV fluid resucita'n using Parkland formula → escharotomy → urgent transfer to burn center

Answer 260

- 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)

Answer 261

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

Answer 262

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 !

Answer 263

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 !

Answer 264

Types - acute = allergic rxn - chronic = idiopathic autoimmune rxn Eti for acute - allergy to food, medica'n or animal - contact w/ latex or some other chemical - 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, drowsiness * Know for OSCE *

Answer 265

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

Answer 266

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 Eti - Abx - NSAIDs - allopurinol - anti-epileptics → Infec'n Eti - HIV - HSV - CMV - Mycoplasma pneumonia SSX chronology 1. non-specific SSX of fever, cough, sore throat, sore mouth, sore eyes + itchy skin 2. Pt develop purple or red rash that spreads across skin + starts to blister 3. 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 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 *

Answer 267

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 - excis'n Bx to determine Breslow tumor thickness = best indicator of prognosis → < 1 mm = low chance of metastasis - sentinel lymph node Bx for staging Staging - Stage 1 = ≤ 1mm thick - 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 ⟹ however thick les'n is, take that thickness in cm as margins Tx for resectable stage 3 or 4 = pembrolizumab + Sx Tx for non-resectable stage 3 or 4 = nivolumab + ipilimumab or talimogene laherparepvec Ppx = avoiding UV light * Know for OSCE *

Answer 268

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 immuno-compromised pts = oral retinoid * Know for OSCE *

Answer 269

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 smooth pearly white or pink papulo-nodules varying in size 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 * Know for OSCE *

Answer 270

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 * Know for OSCE *

Answer 271

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 IgG deposits on keratinocyte surface + histology will show keratinocyte acantholysis Regular Tx = long term rituximab Tx for severe = IV Ig or IV corticosteroid ⚠️ Pemphigus = fragile, superficial blisters v.s bullous pemphigoid = deep + tense blisters * Know for OSCE *

Answer 272

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 * Know for OSCE *

Answer 273

Def - inflammatory rheumatological condi’n in pts > 50 y/o that causes pain + stiffness in neck, shoulders + pelvis 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 / prolonged 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 → urine dipstick → CK to r/o myositis → serum protein electrophoresis to r/o MM → rheumatoid factor to r/o RA Tx = PO corticosteroid i.e 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 effects of long term corticosteroid use

Answer 274

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 - u/l HA around temple or forehead - scalp tenderness - auditory SSX such as tinnitus or hearing loss - 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 that is 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 - CT PET scan b/c will show large vessel inflamma’n which is useful for quantifying extent of disease 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

Answer 275

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) 1. Methotrexate normally but hydroxychloroquine instead if pt = pregnant 2. 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 3. 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 ! Complica'ns - Raynaud - ↑ed risk of CVD - pleural effus'ns / pulm. fibrosis - Felty syndrome i.e neutropenia + spleno-megaly * Know for OSCE *

Answer 276

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 jts i.e hip + knee Ddx - RA - PA - gout X ray findings ("LOSS") - Loss of jt space - Osteophyte forma'n - Subchondral cyst - Subchondral sclerosis Tx 1) Weight loss if applicable 2) Topical NSAIDs such as ibuprofen gel → C/I of ibuprofen = 3rd trimester of pregnancy b/c can cause premature closure of ductus arteriosus 2) Oral NSAIDs such as ibuprofen or naproxen → side effect of naproxen = ankle edema 3) IA corticosteroid injec'ns 4) Jt replac’nt Sx (requires ortho referral + PT before + after Sx to optimize outcomes) * Know for OSCE *

Answer 277

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 colchicine + then 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 *

Answer 278

Def - crystal arthropathy caused by Ca pyroPO4 crystals collecting in jt RF = low Mg 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 *

Answer 279

- 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

Answer 280

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 * Know for OSCE *

Answer 281

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 + tender, swan neck / boutonniere deformity OA - bony PA - pencil in cup deformity on X-ray Gout - swollen, red, hot + 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 due to subq uric acid accumula'n

Answer 282

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 * Know for OSCE *

Answer 283

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 1. Topical adapalene w/ benzoyl peroxide, or topical tretinoin w/ clindamycin 2. For mild - moderate = topical benzoyl peroxide w/ clindamycin 3. For moderate - severe = topical adapalene w/ benzoyl peroxide w/ doxycycline Complica'ns - scarring - hyperpigmenta'n - self image issues * Know for OSCE *

Answer 284

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 - HyperTSH 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 but can start female pt > 75 y/o who had a fragility fracture on aldendronate Tx 1) Bisphosphonates for pre-menopausal women + denosumab 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 denosumab = monoclonal antibody RANK-L inhibitor → monoclonal antibodies end in "MAB" or "NIB" 2) Raloxifene instead for post menopausal pt if denosumab = contraindicated → MOA of raloxifene = selective estrogen receptor modulator (SERM) Complica'n = Wedge fracture * Know for OSCE *

Answer 285

Def - chronic bone disordered characterized by ↑ed bone remodelling → usually just 1 site = affected i.e just the hip or just the femur for ex 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) LOCALIZED bone pain Ddx = osteomalacia ⚠️ muscle weakness + DIFFUSE bone pain = more consistent w/ osteomalacia Ix’s - X ray - ALP → > 20x elevated due to ↑ed osteoblast activity - normal Ca + PO4 v.s in osteomalacia both = low 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 * Know for OSCE *

Answer 286

- 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 - diffuse bone pain + tenderness (usually in back and/or pelvis) - Low Vit D - Low Ca + low PO4 - High PTH (compensa'n mechanism in response to low Ca) - High ALP (due to ↑ed osteoblast activity i.e body = trying to reBuild bone) 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) * Know for OSCE *

Answer 287

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 ↓ in ROM (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 vanc 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 4. Rehab once SSX resolve Complica'ns - osteomyelitis - destruc'n of that jt * Know for OSCE *

Answer 288

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 * Know for OSCE *

Answer 289

"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

Answer 290

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 *

Answer 291

Def - Joint synovitis 1-4 wks after an 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 ⚠️ Poor prognosis in pts diagnosed @ 16 y/o or earlier * Know for OSCE *

Answer 292

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 *

Answer 293

- Dog bites can lead to osteomyelitis - Tx of human bite wound requires Abx

Answer 294

Lactate > 2 + base excess > -2 (i.e more -ve)

Answer 295

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 *

Answer 296

Def - when gas or passage of food through intestines = blocked = surgical emergency ! Eti - hernias - malignancy (Tx in this case = urgent surgical resec'n) - adhes'ns 2° to 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 a 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's 2. Drip + suck i.e IVF + NG tube for decompress'n 3. Exploratory laparotomy if NG tube decompress'n ≠ successful after 72 hrs ⚠️ Keep these pts NPO to ↓ risk of aspira'n + in case they need to go to the OR for ex. lap Complica'ns - sepsis - multi organ failure - bowel ischemia - bowel necrosis

Answer 297

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 *

Answer 298

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

Answer 299

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 *

Answer 300

- lipase for fat digest'n - proteases for B12 + protein absorp'n

Answer 301

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 *

Answer 302

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 *

Answer 303

→ 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 *

Answer 304

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 *

Answer 305

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 *

Answer 306

- 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)

Answer 307

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 *

Answer 308

Def - autoimmune disease where the pt's immune system attacks the small bile ducts in their liver → will cause obstructive jaundice RF = women aged 40-60 y/o SSX - jaundice - pale, greasy stools - dark urine - abdominal pain Ix’s - LTFs → raised ALP - Anti-mitochondrial antibodies (AMA) for diagnosis → will be +ve Tx = ursodeoxycholic acid → liver transplant if needed Complica’ns - liver cirrhosis - deficiency in fat soluble vitamins * Know for OSCE *

Answer 309

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 *

Answer 310

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 *

Answer 311

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 → twist 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 → 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 + embryo sign in cecal 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 *

Answer 312

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 = Sx + post-op chemo → D = Sx (hemi-colectomy if descending colon + beyond = involved) + 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 op days 3-5 ⟹ Tx = IV Abx if pt = septic + then send back to OR * Know for OSCE *

Answer 313

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 → AXR will show Rigler's sign i.e pneumo-peritoneum 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 *

Answer 314

1. Get all ur equipment 2. Posi'n pt + bed as u want 3. Palpate fluctuence of abscess i.e where u would "pop it" 4. Put cover around it 5. 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) 6. 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 7. make a straight incision 1cm deep across fluctuence 8. Cut an ellipse around that 9. Use kelly to open + close inside that cavity in all direc'ns to drain it 10. Flush that cavity with saline as many times as u need to 11. Pack it w/ iodoform in all direc'ns + leave a tail so pt can pull it out 12. Tape it w/ ABD dressing

Answer 315

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 *

Answer 316

Stimulant + osmotic laxative

Answer 317

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 or retracted testicle - absent cremasteric reflex - abnormal testicular lie - rota'n i.e epididymis ≠ in its 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 *

Answer 318

Cyst w/in scrotum, feels like a bag of worms

Answer 319

= 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

Answer 320

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 *

Answer 321

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 for visualiza'n + Bx = 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 *

Answer 322

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 1. Radical inguinal orchiectomy (for any suspicious testicular mass irregardless of stage + type) 2. 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 3. For metastasis (irregardless of it’s seminoma or non seminoma) = combina’n chemo post orchiectomy 4. For relapse (irregardless of it’s seminoma or non seminoma) = salvage chemo Complica’n = infertility * Know for OSCE *

Answer 323

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

Answer 324

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"

Answer 325

- Hypertrophy = ↑ in SIZE of cells which causes ↑ size of tissue/organ - Hyperplasia = ↑ in # of cells which also causes ↑ size of tissue/organ

Answer 326

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 *

Answer 327

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 *

Answer 328

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 *

Answer 329

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 . . . 1. Stage = most important prognostic factor in all cancers not just breast Ca 2. Grade 3. Histological subtype 4. Vascular invas'n 5. Whether or not all margins can be excised 6. 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 *

Answer 330

Lumpectomy

Answer 331

Eti - shortening + widening of mammary ducts → most commonly affects elderly women SSX - b/l nipple retrac'n - b/l green or white nipple discharge * Know for OSCE *

Answer 332

- 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

Answer 333

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

Answer 334

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 *

Answer 335

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 (legs affected 1st) - peripheral neuropathy - ↓ed or absent reflexes 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 before normalizing - spirometry every 6 hrs to check FVC since resp. failure = major complica'n + these pts can deteriorate quickly 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 → Tx = admit them to ICU for intuba'n + ventila'n * Know for OSCE *

Answer 336

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 *

Answer 337

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 *

Answer 338

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 1. Carbamazepine (anti-convulsant) → MOA = Na channel blocker (just like Na valproate) 2. Gabapentin or pregabalin = for neuropathic pain 3. Ablative Sx for idiopathic + microvascular decompress'n for classical * Know for OSCE *

Answer 339

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 1. acetazolamide → MOA - ↓ CSF produc'n → side effect = tingling of fingers + toes 2. shunt to drain CSF Complica'n = vis'n loss

Answer 340

Dexamethasone

Answer 341

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

Answer 342

- 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

Answer 343

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 ⟹ +ve if pt has rotary 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 → 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 happen in episodes 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 *

Answer 344

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

Answer 345

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 *

Answer 346

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 *

Answer 347

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 - viral mainly - if bacterial = caused by strep pneumoniae, Hib 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 → tympanic membrane will be be bulging + opacified instead of pearly-grey translucent as it should be Tx = Tylenol / ibuprofen for pain / fever b/c otitis media = usually viral in etiology ∴ will self-resolve in 3-7 days → 5-7 days of PO amoxicillin for those who are systemically unwell, have otorrhea, or if pt is < 2 y/o + has 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 *

Answer 348

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 + keeping ear dry Tx for severe = combined Abx + steroid drops + keeping ear dry Tx for fungal = clotrimazole otic drops * Know for OSCE *

Answer 349

- 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 - 4 in 1 preschool booster (diphtheria, pertussis, polio, tetanus) - MMR dose 2/2 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

Answer 350

- Live vaccines if pt = pregnant or immunocompromised - anaphylactic rxn to previous dose or vaccine component

Answer 351

= the 4 diseases in children that pneumoccoccal vaccine protects against - Meningitis - Otitis media - Pneumonia - Sinusitis

Answer 352

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 Main complica'n = splenic rupture → SSX = fever, lympha-denopathy, hepato-splenomegaly + guarding * Know for OSCE *

Answer 353

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 *

Answer 354

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

Answer 355

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 *

Answer 356

→ 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 *

Answer 357

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 *

Answer 358

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 *

Answer 359

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 1. 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 2. CPAP - also involves using sealed nasal cannula but delivers much higher + more controlled pressures 3. 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 *

Answer 360

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

Answer 361

Painful red eye = all the "itis" except episcleritis + conjunctivitis - 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)

Answer 362

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 *

Answer 363

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

Answer 364

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, HA, N+V - hazy cornea - ↓ed visual acuity - seeing halos around lights 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 ⚠️ Must be done in both eyes even if other eye is asymptomatic ! ⟹ 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 1. 360° selective laser trabeculoplasty → 2nd procedure may be needed later on but this will at least delay or prevent need for eye drops 2. 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) 3. Other eye drops to ↓ aqueous humor produc'n such as CA inhibitor or timolol = β blocker 4. Trabulectomy Complica'n = vis'n loss * Know both for OSCE *

Answer 365

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 *

Answer 366

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 *

Answer 367

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

Answer 368

- CRVO - CRAO → sudden vis'n loss + afferent pupillary defect - retinal detach'nt → shadow in vis'n - AMD → gradual central vis'n loss, scotoma, metamorphopsia

Answer 369

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 *

Answer 370

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 *

Answer 371

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 perfus'n 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 *

Answer 372

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 - fluctua'n in visual acuity i.e some days their vis'n is just fine 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 = yellow deposits of proteins + lipids ⟹ small amt of Drusen = normal in older pts but large amt = suggestive of AMD - slit lamp exam Tx for wet = ophtho referral → anti-VEGF intravitreal injec'ns once / month * Know for OSCE *

Answer 373

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 steroid 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 - glares from bright lights - colors becoming more faded or more yellow or brown 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 → SSX = pain + ↓ed vis'n in operated eye + hypopyon → can lead to vis'n loss → Tx = intravitreal Abx * Know for OSCE *

Answer 374

Def - visual hallucina'ns in who is legally blind or visually impaired ⚠️ These pts have insight i.e they know what they're seeing isn't real Tx = nothing just reassure pt

Answer 375

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 *

Answer 376

Abscess in eyelash follicle = painful

Answer 377

- 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

Answer 378

- 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 *

Answer 379

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

Answer 380

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 1. 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" 2. 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

Answer 381

- 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

Answer 382

- 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 w/ high risk of commiting suicide

Answer 383

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

Answer 384

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 *

Answer 385

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 for 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 ⚠️ Do not stop Li abruptly ! Complica’n = suicide * Know it for OSCE *

Answer 386

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 *

Answer 387

Def - persistent obsess’n / compuls'n that takes > 1 hr / day RF = FHx Ix = clinical diagnosis Tx = psychotherapy Complica’n = suicidal idea’n

Answer 388

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

Answer 389

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 = individual trauma focused CBT

Answer 390

Persistent delus'n for ≥ 1 month that DOESN'T impact their daily func'ning

Answer 391

≥ 1 of the following SSX for 1 wk - 1 month max . . . - delus'ns - hallucina'ns - disorganized speech

Answer 392

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

Answer 393

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 (w/o insight), 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 1. Typical / 1st genera'n anti-pyschotics 2. Switch to diff typical / 1st genera'n anti-pyschotics OR atypical / 2nd genera'n that isn't clozapine 3. 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 rhabdo - Rhabdo = 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 *

Answer 394

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 HAs / stomach aches in stressful situa'ns Schizoid - limited emo'nal express'n - prefer solitary activities - little to no interest in forming close connec'ns - prefer activities that involve little to no social interac'n

Answer 395

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 1. 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) 2. 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 3. 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 ! 4. CT Angiography to identify blocked vessel + locate source of bleed 5. ECG to r/o arrhythmias 6. 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 *

Answer 396

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 1. 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 r/o a subarachnoid hemorrhage ! 2. 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 ! 3. CT angiography after confirming diagnosis to locate where bleed is coming from Tx = neuroSx referral + nimodipine to prevent vasospasms * Know it for OSCE *

Answer 397

- blood thinners - drugs that cause drowsiness i.e sleep drugs, TCAs, benzos, opioids

Answer 398

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 *

Answer 399

Unconsciousness or ↓ed GCS that persists for > 4 wks after injury

Answer 400

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 - fundoscopy → will show pale optic disc Tx = methylprednisolone SSX Mx - 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 *

Answer 401

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 *

Answer 402

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 = Abx Complica'ns - death - seizures - hydrocephalus

Answer 403

Types a) Frontal lobe tumors → SSX = Δs in personality and/or behavior b) Gliomas = tumor in glial cells → astrocytoma (most common + also most aggressive form = glioblastoma) → oligodendroglioma → ependymoma c) Meningiomas = tumors from meninges → usually benign but can take up space + hence cause an ↑ in ICP d) Pituitary tumors → if they grow large enough can press on optic chiasm + hence cause bitemporal hemianopia e) 2° metastases ("My Little BRother") → melanoma → lung → breast → RCC Ix = Brain MRI + Bx

Answer 404

If seizure lasts > 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'nts 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 + irritable - 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 - 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 rule 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 - tonic clonic = Na valproate OR lamotrigine / levertiracetam in women of child-bearing age → side effects of Na valproate . . . - hair loss - teratogenic - tremor - live damage - ↓ed fertility - atonic = Na valproate OR lamotrigine in women of childbearing ag - myoclonic = Na valproate or levetiracetam in women of childbearing age ⟹ Na valproate only for children - partial / focal seizures → levetiracetam or lamotrigine in adults → lamotrigine or carbamazapine in children ⟹ side effects of carbamazepine = aplastic anemia + agranulocytosis Seizure advice for parents - showers over 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 *

Answer 405

Def - seizure + high fever (i.e > 38°C) in child btw 6 months + 5 y/o Eti = viral infec'n usually Type → simple seizure = generalized tonic clonic seizure that lasts < 15 min (only occurs once during a single febrile illness) → complex seizure = ≥ 1 of the following . . . - 15 min long - focal seizure - recurs w/in 24 hrs / single febrile illness When to get pediatric assess'nt for seizure in pediatric pt . . . < 18 months old - 1st seizure - complex seizure - focal neurological deficit 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 seizure 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 *

Answer 406

Seizure = confus'n / amnesia AFTER regaining consciousness i.e post-ictal state Syncope = amnesia only lasts as long as person is blacked out

Answer 407

Def - ↓ in SBP by ≥ 20 mmHg + drop in diastolic by ≥ 10 mmHg when going from sitting to standing Eti - Dehydra'n / electrolyte / metabolic disturbance - Neurogenic → T2D → Parkinson's - Cardiac → MI → aortic stenosis → arrthymias → FBC + U + E to r/o electrolyte abnormality - Medica'ns → diuretics (especially in older pts) → anti hypertensives → tamsulosin → insulin → levodopa → TCAs SSX - dizziness - confus'n - blurry vis'n - syncope Ix's - BP - ECG to r/o cardiac causes Tx 1. Lifestyle Δs - ↑ing fluid intake - avoiding sudden sitting to standing or prolonged standing - wearing compress'n stockings 2. Fludrocortisone or midorine → C/Is of fludrocortisone = CHF, ascites + CKD → C/I of midorine = urinary rete'n

Answer 408

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

Answer 409

1. Neglect 2. Emo'nal abuse 3. Multiple i.e > 1 type 4. Physical abuse 5. Sexual abuse

Answer 410

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 *

Answer 411

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 AXR will show double bubble sign

Answer 412

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

Answer 413

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

Answer 414

- IV fluids - anti emetics - thiamine b/c hyperemesis can cause encephalopathy

Answer 415

- every 4 wks up to wk 28 - every 2 wks from wk 28-wk 36 - every wk from wk 36 onwards 1. 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 2. 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 3. 16 wks = AFP for spina bifida, pertussis vaccine 4. 20 wks = anatomy U/S 5. 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 6. 28 wks = HIV + syphilis again, blood group + Rh antibody status again 7. 30 wks 8. 32 wks 9. 34 wks 10. 36 wks = Group B strep, fetal presenta'n = assessed @ very visit from here onwards 11. 37 wks 12. 38 wks 13. 39 wks 14. 40 wks if it gets to that

Answer 416

- 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

Answer 417

- 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

Answer 418

1. Mammogenesis - estrogen + progesterone↑ to ↑ # ducts/lobules/alveoli 2. 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 3. Galactokinesis - suckling triggers oxytocin which triggers milk expuls'n 4. Galactopoiesis - maintenance of milk = due to prolactin, which surges every time baby suckles

Answer 419

Period from delivery till 42 days after delivery

Answer 420

- prophylactic Abx = always given - bladder = always catheterized - reg'nal anesthesia = preferred over general anesthesia - post op TED stockings - not all women will be NPO

Answer 421

Most will have successful vaginal delivery !

Answer 422

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 *

Answer 423

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 *

Answer 424

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 fasting glucose - women w/ existing diabetes should ↓ their insulin doses b/c of physiological postnatal hypoglycemia * Know it for OSCE *

Answer 425

- 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 *

Answer 426

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

Answer 427

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

Answer 428

< 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

Answer 429

" 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

Answer 430

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 *

Answer 431

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 *

Answer 432

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 *

Answer 433

Def - when anterior shoulder of baby becomes stuck behind pubic symphysis of pelvis after head has been delivered = obstetric emergency ! Emergency Tx = " HELPRR" 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. 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 *

Answer 434

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 *

Answer 435

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 *

Answer 436

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 *

Answer 437

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 *

Answer 438

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 *

Answer 439

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 *

Answer 440

1. 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 2. 6 wk post natal visit . . . - 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 *

Answer 441

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 *

Answer 442

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 if there's sepsis, hemorrhage or mom has pre-e) - expectant Mx → moms must be closely monitored - induc'n of labor w/ mifepristone + vaginal or oral misoprostol * Know for OSCE *

Answer 443

Can be performed legally @ ANY POINT during 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

Answer 444

Def - rare but serious psychosis in woman who 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 *

Answer 445

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 *

Answer 446

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 1. Estrogen / COCP 2. 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 3. Hysterectomy * Know for OSCE *

Answer 447

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 *

Answer 448

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 *

Answer 449

- PCOS - Cushing's syndrome - hyperprolactinemia - androgenic drugs * Know for OSCE *

Answer 450

Prolonged menstrual cycle i.e > 21-32 days

Answer 451

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 *

Answer 452

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 *

Answer 453

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 1. Speculum + equipment called colposcope = used to magnify cervix 2. Acetic acid causes abnormal cells to appear white = called acetowhite (probably CIN or cancer) 3. Schiller’s iodine test - cervical cells = stained w/ iodine solu'n → normal cells = brown stain → abnormal areas will NOT stain 4. 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 *

Answer 454

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 *

Answer 455

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 1. TRUS to asses endomtrical thickness → normally shoudl be < 4 mm in post menopausal women 2. 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 *

Answer 456

1. 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, lasts 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 5 yrs) - releases hormones which change the womb to make it unfavorable for pregnancy, causes period 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 ⟹ Cu IUD (lasts 5-10 yrs) - 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. Takes effect immediately if started w/in 5 days of period but if started after, must use alternative contracep'n for 7 days 2. 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 2. IRREVERSIBLE = male + female steriliza'n → male = vasectomy + female = tubal liga'n or tubal occlusive device 3. 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 *

Answer 457

Ectopic pregnancy + ovarian tors'n - ectopic pregnancy = life threatening - ovarian tors'n = pt can lose ovary

Answer 458

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 detect 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 → might show adnexal mass ⟹ 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 op'ns - expectant Mx = for low risk i.e . . . → no pain → hemodynamically stable → serum β hCG < 1500 → adnexal mass < 35 mm → no visible fetal heartbeat → able to return for f/u - methotrexate for moderate risk = same indica'ns as above but pt has moderate pain + tenderness - surgical extrac'n via laparoscopic salpingectomy for rupture or if . . . → pt = in significant pain → hemodynamically unstable → serum β hCG ≥ 5000 → adnexal mass ≥ 35 mm → visible fetal heartbeat → pt ≠ able to return for f/u Complica'ns - recurrence - maternal death due to rupture of implanta'n site + intraperitoneal hemorrhage

Answer 459

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

Answer 460

- 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

Answer 461

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

Answer 462

Sperm motility b/c sperm has to be able to reach egg !

Answer 463

- anti mitotic drugs - breast reduc'n w/ nipple transplant - any radioactive substance (diagnostically or therapeutically)

Answer 464

1. Dry, stimulate + wrap in warm towel 2. AIRWAY - check for obstruc'n, meconium + intubate if very premature or HR = low 3. BREATHING - if not breathing by 90 secs, do 5 infla'n breaths w/ bag + then O2 mask ventila'n 4. CIRCULA'N - if chest is moving + airway is ≠ obstructed but pt is still bradycardic start chest compress'ns 5. DRUGS - if none of the above worked give adrenaline / Na bicarb / dextrose

Answer 465

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

Answer 466

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

Answer 467

1. 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 2. 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 3. 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 1. Dry 2. A, B, C 3. Drugs a) antenatal steroids to mom such as dexamethasone → speeds up surfactant produc'n in lungs b) exogenous surfactant 4. 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

Answer 468

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 * Know for OSCE *

Answer 469

Def - non progressive permanent neurological problems resulting from damage to brain @ 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 Common SSX = drooling → treat w/ glycopyrronium bromide 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 * Know for OSCE *

Answer 470

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

Answer 471

1. Lifestyle Δs i.e not drinking too much before bed + setting alarm to pee @ certain time 2. Desmopressin b/c ↓ nighttime urine produc'n

Answer 472

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 1. 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 2. Liver transplant in end stage liver disease Complica'ns - fibrosis - cirrhosis - portal HTN - GI bleed - deficiency in fat soluble vitamins * Know for OSCE *

Answer 473

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 * Know for OSCE *

Answer 474

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 * Know for OSCE *

Answer 475

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 * Know for OSCE *

Answer 476

Toddler's diarrhea → usually resolves by age 5

Answer 477

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) * Know for OSCE *

Answer 478

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 * Know for OSCE *

Answer 479

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 * Know for OSCE *

Answer 480

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 - episodes of apnea @ night - snoring - always tired - daytime somnolence - morning HAs - poor [ ] 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 Scoring w/ STOP-bang score or Epworth sleepiness scale 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 * Know for OSCE *

Answer 481

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 * Know for OSCE *

Answer 482

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 * Know for OSCE *

Answer 483

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 ("young, fat boy") - 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 * Know for OSCE *

Answer 484

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 remodelling as bone heals RFs = " thin little boy" i.e 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 * Know for OSCE *

Answer 485

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)

Answer 486

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 1. 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 2. Surgical interven'n if Ponsetti fails, if there's recurrence or if there are residual deformities

Answer 487

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 *

Answer 488

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

Answer 489

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's - 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

Answer 490

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 *

Answer 491

Def - exotoxin-mediated infectious disease associated w/ group A strep infec'n (tonsillitis usually) = NOTIFIABLE DISEASE ! Eti - strep pyogenes usually 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 *

Answer 492

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 *

Answer 493

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

Answer 494

Def - when ≥ 1 testes hasn't descended yet → testes have to descend for optimal sperm produc'n + to avoid cancer ! RFs - FHx - SGA - prematurity - birth weight < 2.5 kg - 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 (i.e higher risk) - testicular tors'n - infertility - testicular cancer

Answer 495

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 or any activity requiring [ ] - inability to focus - thoughtless mistakes in schoolwork or assignments Hyperactive SSX - squirms when seated - constantly fidgets w/ hands or feet - marked restlessness that is difficult to control - always on the go - can't play quietly - overly talkative - can't stay seated in class Impulsive SSX - can't wait for their turn - interrupts or intrudes conversa'ns / 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 Classfica'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 *

Answer 496

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 making + understanding 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 hyporesponse to visual or sensory input Diagnostic criteria = impaired social interac'n SSX + ≥ 2 repetitive behavior SSX + SSX must have started in childhood Ix = autism questionnaire Tx 1. behavioral interven'n 2. early interven'n 3. family support + educa'n * Know for OSCE *

Answer 497

"FedBiL" Fe = duodenum → side effect of Fe supplement = constipa'n B12 = ileum B9 = jejunum

Answer 498

- Anterior → ACTH- stimulates adrenal glands to produce hormones → LH → FSH → GH → TSH → Prolactin - Posterior → ADH → Oxytocin

Answer 499

"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

Answer 500

= membranous covering of brain + spinal cord w/ 3 layers . . . (from superficial to deep) - dura mater - arachnoid mater - pia mater

Answer 501

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

Answer 502

- Lordosis = swayback - Kyphosis = hunchback (think "knotre dame") - Scoliosis = curved left or right ⚠️ We naturally have cervical lordosis, thoracic kyphosis + lumbar lordosis

Answer 503

- asymptopmatic - normal CXR - non-contagious

Answer 504

CSF microscopy + culture

Answer 505

Neisseria mengitidis

Answer 506

Sputum culture → +ve means active TB

Answer 507

Neutrophils

Answer 508

Peripheral arterial disease

Answer 509

- 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

Answer 510

Abnormal kidney where inferior kidney poles of kidneys = fused hence result = U shaped kidney located lower than it normally would be → pts = asymptomatic

Answer 511

B/c pt will have suboptimal immune response due to maternal antibodies still present

Answer 512

12 pairs - 7 pairs of true ribs - 3 pairs of false ribs - 2 floating ribs

Answer 513

1. Initia'n of abduc'n i.e up to 15° = supraspinatus 2. Abduc'n of 15-90° = deltoid 3. Abduc' beyond 90° = trapezius + serratus anterior 4. Adduc'n = pec minor/major + lat dorsi + teres major 5. Extens'n = lat dorsi + teres major + long head of triceps + posterior fibers of deltoid 6. Flex'n = pec major + biceps brachii + coracobrachialis + anterior fibers of deltoid 7. 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) 8. Lateral/External rota'n = teres minor + posterior fibers of deltoid + infraspinatus 9. Circumduc'n = pec major + lat dorsi + teres major/minor + deltoid + subscapularis + biceps brachii + coracobrachialis + long head of triceps + supraspinatus + infraspinatus

Answer 514

Axillary nerve

Answer 515

Weakness in arm flex'n + sensory loss in lateral forearm

Answer 516

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

Answer 517

brachial artery + median + radial nerve

Answer 518

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 *

Answer 519

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 *

Answer 520

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 for pt to find comfortable sleeping posi'n * Know for OSCE *

Answer 521

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 = Abx 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 *

Answer 522

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 - 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 *

Answer 523

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 - pallor - pain (very severe) - paresthesia (in chronic compartment syndrome) - perishingly cold (body loses ability to auto regulate temp = late sign) - pulseless (late sign) - paralysis (late + worrying 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. elevate leg to heart level 4. keep pt normotensive Complica'ns - tissue necrosis if left untreated - limb loss * Know for OSCE *

Answer 524

RFs - old age - female - osteoporosis - frequent falls - low BMI Eti = trauma or 2° to osteoporosis 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 Ix's if fracture = 2° to fall . . . - FBC to check for anemia - U + E to check for electrolyte abnormalities - ECG to check for arrhythmias / MI - BNP to check for CHF - CT to check for stroke Types + Tx for each a) 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 displac'nt i.e trabeculae are @ an angle Grade IV = full displac'nt 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 + pt can walk independently = ttl hip replac'nt Tx for Grade 3 or 4 but pt has lots of co-morbidities or limited mobility = hemiarthroplasty i.e replacing femoral head but leaving acetabulum in place b) 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 Complica'ns - avascular necrosis - half of pts become less independent after a hip fracture * Know for OSCE *

Answer 525

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 *

Answer 526

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 max 3 steps ⚠️ Rapid swelling in knee injury = suggestive of hemarthrosis !

Answer 527

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 *

Answer 528

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 *

Answer 529

Def - when ball of shoulder i.e head of humerus comes entirely out of its 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 - palpable bulge on humeral head 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 *

Answer 530

" SITS AEI “ - Supraspinatus → abducts arm - Infraspinatus → externally rotates arm - Teres minor → externally rotates arm - Subscapularis → internally rotates arm * Know for OSCE *

Answer 531

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 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 *

Answer 532

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) 1. painful phase i.e shoulder pain (worse @ night) 2. 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 3. 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 *

Answer 533

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 . . . 1. Intrales'nal collagenase injec'ns 2. 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 *

Answer 534

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 throughout the day . . . - painful + tender finger (usually around MCP jt on palm side of hand) - finger that doesn't move smoothly - finger that makes clicking / popping 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 *

Answer 535

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 *

Answer 536

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

Answer 537

Median nerve + 9 flexor tendons

Answer 538

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 *

Answer 539

Fracture of scaphoid bone

Answer 540

- wrist drop i.e wrist + fingers are flexed + can't be extended

Answer 541

- Eti = medial epicondyle injury - SSX = claw hand deformity

Answer 542

Def - condi'n where abductor pollicis longus (APL) + extensor pollicis brevis (EPB) tendon sheaths in wrist = swollen + inflamed → = 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 *

Answer 543

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

Answer 544

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) +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 pt = immobilized - ice - eleva'n - analgesia

Answer 545

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)

Answer 546

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 a lump in their shoe - burning / numbness / tingling 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 - avoiding high heels - analgesia - using insoles - weight loss if applicable - steroid injec'ns - RFA - surgical excis'n of neuroma

Answer 547

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

Answer 548

Contralateral - pain - temp - crude touch - pressure Ipsilateral - vibra'n - propriocep'n

Answer 549

= stroke in basilar artery ∴ causing ttl body paralysis including difficulty breathing + swallowing → all they can move is their eyes

Answer 550

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, Bell's palsy, Ramsay Hunt + spinal muscular atrophy Both UMN + LMN can have weakness + paralysis

Answer 551

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 !

Answer 552

("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

Answer 553

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 consciousness ⟹ 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 1. 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 2. 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 3. MAO-B inhibitors → MOA - inhibit breakdown of epinephrine → side effects = HA, dyskinesia + psychological disorders → end in "GILINE" 4. 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 *

Answer 554

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 tremor 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 *

Answer 555

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 !

Answer 556

Procyclidine HCl

Answer 557

“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

Answer 558

- 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 *

Answer 559

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

Answer 560

- 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)

Answer 561

Ipsilateral

Answer 562

"DANISH" D - Dysdiadochokinesia, Dysmetria (past-pointing), dysarthria A - Ataxia N - Nystagmus + N/V I - Inten'n tremor S - Slurred staccato speech H - Hypotonia + Headache

Answer 563

1. Corpus striatum = caudate nucleus + lentiform nucleus (putamen + globus palidus internis + externis, separated from caudate nucleus + thalamus by internal capsule) = in base of each hemisphere 2. Subthalamic nucleus = in diencephalon 3. Substantia nigra = in midbrain

Answer 564

- Direct = initiates motor activity - Indirect = inhibits unwanted motor activity

Answer 565

Melatonin produc’n from serotonin → = stimulated by darkness + inhibited by light

Answer 566

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 !

Answer 567

Aphasia = pb w/ speech or language → Broca's aphasia or expressive aphasia = pb w/ language produc'n ∴ sentence forma'n = impaired but their comprehens'n = intact → 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 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

Answer 568

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

Answer 569

- 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 !

Answer 570

- 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

Answer 571

FSH = injected to stimulate ovaries to produce eggs ∴ instead of just letting follicles die we force them to become ovulatory follicle

Answer 572

NO b/c will die after 1st wk

Answer 573

Cord lengthening b/c once placenta separates it falls into cavity

Answer 574

- 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 of normal pressure hydrocephalus = dementia, urinary incontinence + gait pb

Answer 575

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

Answer 576

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 !

Answer 577

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

Answer 578

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

Answer 579

1. 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 . . . - 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 2. 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

Answer 580

1. 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 2. 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 3. 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

Answer 581

Answer 582

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

Answer 583

"RII" - Rectus abdominis (medial border) - Inferior epigastric vessels (lateral border) - Inguinal ligament (inferior border)

Answer 584

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 for inguinal hernias - asymptomatic = nothing - symptomatic = Sx → open repair w/ mesh for u/l + 1st hernia repair → laparoscopic repair w/ mesh for b/l or recurrence of hernia 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

Answer 585

SSX - pain when pt sits down - visible tender anal mass (usually @ 2 o' clock posin) Ix = clinical diagnosis RFs for recurrent perianal abscess - diabetes - immunocompromised pts - hidradenitis Tx = incis'n + drainage Complica'n = sepsis * Know for OSCE *

Answer 586

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 *

Answer 587

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 *

Answer 588

= "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

Answer 589

1. 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 2. 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 3. 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

Answer 590

1. Central zone = 25% of prostate = where BPH mainly occurs 2. Peripheral zone = 75% of prostate = where prostate cancer mainly occurs

Answer 591

@ Meiosis I + then again @ Meiosis II until fertiliza'n occurs

Answer 592

- Follicular phase = days 1-13 - Ovula'n = day 14 - Luteal phase = days 15-28 1. Hypothalamus secretes GnRH 2. GnRH stimulates anterior pituitary to release FSH + LH 3. 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 ↓ 4. 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) 5. LH converts Graafian follicle into corpus luteum + causes egg to unpause from being stuck in meiosis I so it can be released 6. Egg = released into peritoneal cavity 24-36hrs after LH surge (released egg is now called ovum) * ovula’n from both ovaries will make twins * 7. 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) 8. 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) 9. 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 10. If pregnancy does occur, hCG secreted by embryo is what is keeping CL alive + in that case CL will eventually become placenta

Answer 593

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 1. C/Is . . . - VTE - pregnancy - liver disease - breast cancer - uncontrolled HTN - active angina or MI - endometrial hyperplasia or cancer - undiagnosed abnormal bleeding 2. 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) 3. Ways we ↓ those risks . . . - adding progesterone to HRT for women w/ a uterus - using patches rather than pills to ↓ risk of VTE 4. 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 5. Inform pt that it can be ↓ed gradually or stopped abruptly

Answer 594

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

Answer 595

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 *

Answer 596

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 1. 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 2. 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 *

Answer 597

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 1. 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 2. 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 *

Answer 598

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

Answer 599

- 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 halos in vis'n, N+ V, bradycardia w/ reverse tick sign on ECG ⟹ this is why plasma digoxin should be measured 8-10 days after starting Tx ⟹ pts will also have to do periodic renal func'n monitoring b/c poor renal func'n predisposes to digoxin toxicity - 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 ⟹ Tx = IVF

Answer 600

"L GDP" - Li - Gentamicin, vancomycin + amikacin - Digoxin - Phenytoin

Answer 601

Jt that only allows mov'nt in 1 direc'n → ex = knee jt b/c only does flex'n + extens'n

Answer 602

B/c can cause avascular necrosis

Answer 603

Anterior = loss of sharp angle Posterior = shoulder has light bulb appearance

Answer 604

“ VIIC + CC ” - Vagus nerve - Internal jugular vein - Internal carotid artery - Common carotid artery

Answer 605

DROOLING / SECRE'NS - glycopyrronium bromide - hyoscine RESTLESSNEESS / ANXIETY = Midazolam NAUSEA + VOMITING - metoclopramide → good for late chemo/radia'n vomiting → side effects = extrapyramidal SSX + prolonged QT interval - ondansetron → good for immediate chemo / radia'n vomiting → side effects = prolonged QT interval + constipa'n → very expensive - cyclizine → good for neuro related causes of vomiting i.e vestibular / ↑ed ICP → side effects = dry mouth + urinary reten'n → C/I = renal failure

Answer 606

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

Answer 607

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

Answer 608

"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

Answer 609

N2 = converted to urea by liver + excreted by kidneys via urine

Answer 610

- acetone, acetoacetate + β-hydroxybutyrate → urine dipstick CAN'T DETECT β-hydroxybutyrate !

Answer 611

- 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

Answer 612

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

Answer 613

7 hrs ∴ if u do FBC @ 7am + then again @ 3pm u might get diff neutrophil results

Answer 614

= compensa'n mechanism b/c ↑ in TIBC leads to ↑ in Fe binding spots ∴ more Fe can bind

Answer 615

- 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

Answer 616

- Palliative care = SSX Mx for pt w/ chronic condi'n - Hospice = for pts who have < 6 months to live

Answer 617

- 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

Answer 618

= 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

Answer 619

- court order - pt gives their consent - pt or someone else's life is directly threatened

Answer 620

- IQ < 70 - Onset @ birth - Impaired social adapta'ns

Answer 621

- 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

Answer 622

- Non-directed = person offers to donate organ to anyone who might benefit - Directed = person offers to donate organ to a specific person or group

Answer 623

Pt = deemed to have capacity if are able 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

Answer 624

- Sec’n 2 = ADMISS'N FOR ASSESS'NT for up to 28 days → pt must be suffering from a mental disorder of a nature or ° warranting admiss'n for assesss'nt + must be in the interests of their own health or safety or for the protec'n of others - Sec’n 3 = ADMISS'N FOR TX for up to 6 months but is renewable @ 6 months + then every 12 months → 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 - Sec’n 4 = EMERGENCY ADMISS'N for up to 72 hrs → pt must be suffering from a mental disorder + there must be urgent need → recommenda'n must be made by 1 Dr (Dr doesn't have to be a specialist but should know pt) - Sec'n 5.4 = DETAINING PT FROM LEAVING

Answer 625

- 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

Answer 626

- 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

Answer 627

- 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

Answer 628

Yes as long as they saw pt ≥ 14 days before they died

Answer 629

- 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

Answer 630

Tracheal tube

Answer 631

1. Paracetamol 2. Weak opiate i.e codeine / tramadol / hydrocodone 3. Strong opiate i.e morphine / oxycodone / methadone / fentanyl / hydromorphone → morphine = renally cleared so don't give this to pts w/ renal failure → oxycodone = hepatically metabolized so = fine to give to pts w/ renal dysfunc'n

Answer 632

MSK pain ⚠️ Ibuprofen = NSAID, so always co-prescribe a PPI w/ it !

Answer 633

0 = ambulatory + can do all ADLs w/o any help at all 1= ambulatory but has a hard time w/ strenuous activity 2 = ambulatory + can do self-care but needs help w/ most everyday tasks 3 = spends majority day in bed or in a chair but isn't completely bedridden 4 = fully confined to bed or chair all day

Answer 634

Purpose = to help provider determine if they should break confidentiality for pt < 16 y/o seeking to start contracep'n Steps 1. Does pt meet ALL of the following criteria . . . - Pt has sufficient intelligence + maturity to understand implica'ns of desired Tx - Pt cannot be persuaded to inform parents or have dr inform parents - Pt is very likely to begin or continue having intercourse regardless - Pt's physical or mental health is likely to suffer w/o this Tx - Tx is in the pt's best interest 2. If yes then don't break confidentiality + start Tx w/o informing parents 3. If no, then inform pt that parental consent must be obtained

Answer 635

- sweating - shivers - tremors - retching - dilated pupils

Answer 636

Spironolactone

Answer 637

> 60 yo OR < 50 y/o but have rectal bleeding

Answer 638

Ileostomy v.s colostomy - stoma bag = in RIF v.s LIF - stoma contents = liquid v.s solid - spouted (b/c contents are more irritant to skin) v.s flushed

Answer 639

- optic neuritis - papilloedema - CRVO - malignant HTN