5 star topics Flashcards
Valves open during systole
Aortic, pulmonic
Valvular lesions producing systolic murmurs
MR, TR, AS, PS, Mitral valve prolapse
Valves open during diastole
mitral, tricuspid
Valvular lesions producing diastolic murmurs
MS, TS, AR, PR
Murmurs and sounds heard best with patient in left lateral decubitus position
Mitral murmurs
Left sided S3, S4 heart sounds
Cardiac auscultation findings considered benign when there is no evidence of disease
Split S1
Split S2 on inspiration
S3 under 40 yo
early, quiet systolic M
Causes of aortic stenosis
Congenital bicuspid valve - about 40 yo
Senile calcifications - over 60 yo
Rheumatic heart disease
Tertiary syphilis - aortitis (tree barking of aorta and dilation of aortic root -> AS, AR, dissection)
Presentation of aortic stenosis
Dyspnea (CHF)
Syncope
Angina
-all with exertion
Physical exam findings with aortic stenosis
Ejection click
Systolic ejection murmur “crescendo-decrescendo” heard at RUSB
Murmur radiates to neck/carotids
Valsalva will decrease the murmur
Peripheral pulses are weak and prolonged/delayed “pulsus parvus et tardus”
Next step: ECHO
Treatment of aortic stenosis
aortic valve replacement if symptomatic
Causes of Mitral regurgitation
MV prolapse Rhematic heart disease infective endocarditis papillary muscle rupture LV dilation (from ischemic heart disease or dilated cardiomyopathy)
Presentation of MR
often asx
Fatigue
Exertional dyspnea
A fib with LA dilation
Physical exam findings of MR
holosystolic murmur heard at apex, may radiate to axilla
Next step ECHO
Treatment of MR
Vasodilators for LV dysfunction
Anticoagulate patients with Afib or hx of rheumatic heart disease
Mitral valve repair
Mitral valve prolapse
Large billowy leaflets into atrium
Midsystolic click with late systolic crescendo murmur
Causes of aortic regurgitation
Infective endocarditis
Rheumatic heart disease
Tertiary syphilis - aortitis (tree barking of aorta and dilation of aortic root -> AS, AR, dissection)
Presentation of Aortic regurgitation
usually asx until severe
Dyspnea, heart failure
Physical exam findings of aortic regurgitation
Wide pulse pressure - normal SBP, DBP way off
Bounding pulses
de Musset sign - rhythmic bobbing of head
Rumbling, early diastolic murmur heard at RUSB or Left side of sternum
Treatment of aortic regurgitation
Medical management of HF - ACE-i, Bb, spironolactone
Aortic valve replacement
Causes of mitral stenosis
Mainly rheumatic heart disease
Presentation of mitral stenosis
Dyspnea and CHF - may be exacerbated by pregnancy 2/2 expended blood volume, increased HR and SV -> increased CO
Afib d/t dilation of LA
Most patients have concomitant mitral and/or tricuspid regurgitation
Physical exam findings of mitral stenosis
Opening snap after S2
Rumbling, late diastolic murmur at apex
Treatment of mitral stenosis
Balloon valvuloplasty
diruetics for CHF sxs prior to valvulopasty
Anticoagulation pts with Afib
Presentation of shock
Hypotension \+/- tachycardia \+/- cool, clammy, cyanotic skin Decreased urine output - monitor closely AMS - monitor closely Metabolic acidosis - d/t anaerobic metabolism - check lactic acid level and BMP for anion gap
Mechanisms, causes, and treatment for Hypovolemic shock
Mech: decreased intravascular volume
Cause: hemorrhage - trauma, GI bleed; burns; GI losses - prolonged V/D
Tx: IVF, blood transfusion, tx underlying cause
Mechanisms, causes, and treatment for Cardiogenic shock
Mech: pump failure
Cause: acute MI, dilated CM, arrhythmia, ruptured septum, papillary muscle rupture
Tx: Dobutamine (beta 1 effect); intra-aortic balloon pump
Caution IVF can lead to pulmonary edema
Mechanisms, causes, and treatment for Obstructive shock
Mech: Extracardiac causes of pump failure; decreased venous return and decreased preload
Cause: Tension PTX -> decreased preload; hemothorax; PE; cardiac tamponade
Tx: Tx underlying cause; pericardiocentesis for tamponade; chest tube for PTX
Mechanisms, causes, and treatment for Septic shock
Mech: peripheral VASODILATION due to infection
Cause: infection
Tx: IVF, NE if IVF fails, Abx
Mechanisms, causes, and treatment for Anaphylactic shock
Mech: peripheral VASODILATION due to severe type 1 hypersensitivity reaction
Cause: allergic reaction
Tx: Epi - vasoconstrict, increase CO = increased BP, airway dilation; IVF; airway management - O2, ET; diphenhydramine, H2 blocker
Mechanisms, causes, and treatment for Neurogenic shock
Mech: peripheral VASODILATION and BRADYCARDIA due to autonomic dysregulation
Cause: CNS injury
Tx: IVF, vasopressors, atropine for brady
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for hypovolemic shock
MAP - low - hypotension
SVR - increased
HR - increased
PCWP - low
PCWP after fluid challenge: unchanged or increased
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for cardiogenic shock
MAP - low - hypotension
SVR - increased
HR - variable
PCWP - increased
PCWP after fluid challenge: higher, not volume issue
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Obstructive shock d/t lung cause (tension PTX, hemothorax, PE)
MAP - low - hypotension
SVR - increased
HR - increased
PCWP - low or normal
PCWP after fluid challenge: unchanged or increased
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Obstructive shock d/t cardiac tamponade
MAP - low - hypotension
SVR - increased
HR - increased
PCWP - increased
PCWP after fluid challenge: increased
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Septic shock
MAP - low - hypotension
SVR - low - vasodilation
HR - increased
PCWP - normal
PCWP after fluid challenge: increased
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Anaphylactic shock
MAP - low - hypotension
SVR - low - vasodilation
HR - increased
PCWP - normal
PCWP after fluid challenge: increased
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Neurogenic shock
MAP - low - hypotension
SVR - low - vasodilation
HR - increased
PCWP - normal
PCWP after fluid challenge: increased
Normal PR interval
conduction delay through AV node
less than 1 large box (200 ms)
P wave
atrial depolarization
QRS
ventricular depolarization
normal 3 small boxes - less than 120 ms = narrow
ST segment
ventricles depolarized
T wave
Ventricular repolarization
Peaked - hyperkalemia
flat - hypokalemia
U wave
papillary or purkinje repolarization
prominent in hypo/hyperkalemia, hyperthyroidism
First degree block
PR greater than 0.2sec (large box)
Causes: AV node disease, increased vagal tone, drugs increasing refractory time of AV node (b-blockers, CCB, digoxin)
Tx: usually asx, not needed
Second degree Mobitz type I block (Wenckebach)
Progressively lengthened PR interval until blocked QRS occurs then resets
normal, athletes, older, other heart dz
Causes: AV node disease, drugs
Tx: adjust medications, pacemaker for symptomatic bradycardia - usually asx
Second degree Mobitz type II block
Cause: infra nodal conduction problem - bundle of His, Purkinje fibers
randomly blocked QRS without PR interval changes
Can progress to third degree AV block
Tx: pacemaker - usually asx
Third degree block
Absence of conduction between atrium and ventricles
Dizziness, syncope, hypotension
Avoid B-blockers, CCB, digoxin
Tx: ventricular pacemaker
Paroxysmal supraventricular tachycardia
HR >100, arising from atria or av junction
Narrow QRS
D/t re-entry anomaly
young patients
- palpitations
- CP
- sudden tachy
- SOB
- syncope
Tx: carotid massage, valsalva, IV adenosine, CCB, B-blocker, cardioversion, catheter ablation
Multifocal atrial tachycardia (MAT)
supra ventricular origin
Older patients - COPD exacerbations
Several foci initiating signals
-> P waves with variable morphology, at least 3 different
Tachycardia
Tx: CCB - verapamil, diltiazem; b-blockers, correct hypokalemia above 4, correct hypomagnesemia over 2, catheter ablation
Bradycardia
less than 50 ppm (up to 60)
Caused by increased vagal tone or nodal disease
MC: elderly, hx of CAD, b-blockers, CCB
asx or weakness, syncope, fatigue
Tx: stop precipitating medications, pacemaker - sxs frequent or severe
AV nodal re-entry
fast and slow conduction system at AV node
Fast goes quick to ventricles and retrograde through slow pathway to AV node -> conduction loop
AV re-entry (WPW syndrome)
separate accessory conduction path
MC - Bundle of Kent
Return to AV node
WPW associated with delta wave - upstroke prior to QRS
-tachycardia, narrow QRS
Common causes of upper GI bleeding
proximal to the ligament of trietz
MC: PUD - gastric more likely to bleed than duodenum
Esophagitis
Esophageal varices
Mallory-Weiss tears
Gastritis
Gastric/duodenal cancers
Common cases of lower GI bleeding
Distal to ligament of trietz
Vascular malformations - angiodysplasia, AVM
mesenteric ischemia
Meckel’s diverticulum (secretes gastric acid)
Colon CA
Diverticular disease
UC
Hemorrhoids
Signs of Upper GI bleed
hematemesis - ongoing
coffee ground emesis
melena
+/- BRBPR - laxative effect
Signs of lower GI bleed
hematochezia - rapid or heavy
BRBPR
Melena
Hemodynamic instability
S/S: hypotension, tachycardia
Start IVF right away
Substantial loss -> anemia
Can have stable Hct d/t loss of both RBC and plasma
Steps in management of acute upper GI bleed
assess hemodynamic stability
Admit to ICU - NPO
Type and screen 2 units RBC
Labs: CBC, PT/PTT, BUN, Cr - hypovolemic/reabsorption of bili elevates BUN -> >20:1
-give FFP if PT/PTT elevated
If bleeding source uncertain consider NG lavage
Medications:
IV PPI
If variceal bleeding - octreotide - decreases splanchnic blood flow to GI tract
EGD
Steps in management of acute lower GI hemorrhage
Assess hemodynamic stability - usually stable
Type and screen 2 units of PRBCs
Labs: CBC, PT/PTT, BUN, Cr
NG lavage and/or EGD to r/o massive upper GI bleed prn
Colonoscopy up to terminal ileum
-if not diagnostic or not feasible - too much bleeding and bleeding persists ->
-angiogram (AVM)
-Radionuclide scan - “tagged RBC scan” to localize to quadrant
-Capsule endoscopy
Main risk factors for colorectal cancer
adenocarcinoma
Adenomatous colon polyps hereditary syndromes FHx of colon cancer Previous colon cancer UC > Crohns AA - younger Low fiber/high fat diet etOH Smoking DM
Familial adenosis polyposis
Hundreds of adenomatous colon polyps - shag carpet
Mutation Adenomatous Polyposis Coli (APC) gene
tumors: stomach/duodenal polyps osteomas fibromas lipomas medulloblastomas
Tx: ppx subtotal colectomy before 25
Hereditary nonpolyposis colon cancer (HNPCC) aka Lynch syndrome
cancers arise from basically normal appearing colonic mucosa - not polyps
cancers develop early 40s-50s
Cancers form in proximal colon - right side
Peutz Jegher’s syndrome
hamartomas in GI tract
Pigmented lesions on lips and oral mucosa
Colon cancer screening guidelines
Average risk: - start t 50 yo
colonoscopy q10 yr
Flex sig q 5 yr
Fecal occult blood test annually
CT colonography if positive -> colonoscopy
Screening stops when patient’s life expectancy is less than 5 years or age 75 whichever comes first
If polyps - screen 3-5 yr with colonoscopy
FHx - age 40 or 10 yr before age of family member
S/S of colon cancer
GI bleeding:
hematochezia - left sided cancer
Melena - right sided cancer
Iron def. anemia
Change in stool caliber - left sided
-pencil thin or flat ribbon like
Bowel obstruction - constipation, abdominal distension, N/V
Apple core lesion on barium enema
Staging colon cancer
CT chest, abd, pelvis
No LN involvement - stage I, II
-> resect
Regional LN involved - Stage III
-> resect, adjuvant chemo
Distant mets - IV
-> palliative chemo
MC mets - liver, lung
MC chemo - 5-FU
Post-treatment surveillance for colon cancer
CEA - q3-6 mo for at least 3 years
CT Chest/Abd q1 yr for at least 3 years - pelvis iv rectal CA
Colonoscopy at 1 yr, then q3-5 yr depending on findings
Iron deficiency anemia iron studies Serum iron Transferrin (TIBC) % transferrin saturation Ferritin
Serum iron low
Transferrin (TIBC) high
% transferrin saturation low less than 12 %
Ferritin low
Anemia of chronic disease Serum iron Transferrin (TIBC) % transferrin saturation Ferritin
Serum iron low
Transferrin (TIBC) low normal
% transferrin saturation normal >18%
Ferritin normal or high
Lead poisoning Serum iron Transferrin (TIBC) % transferrin saturation Ferritin
Serum iron normal or elevated
Transferrin (TIBC) normal of low
% transferrin saturation normal
Ferritin normal or high
Sideroblastic anemia Serum iron Transferrin (TIBC) % transferrin saturation Ferritin
Serum iron high
Transferrin (TIBC) low
% transferrin saturation normal or high
Ferritin high
Hemochromatosis Serum iron Transferrin (TIBC) % transferrin saturation Ferritin
Serum iron high
Transferrin (TIBC) low
% transferrin saturation high
Ferritin high - if normal r/o hemochromatosis
Thalassemia Serum iron Transferrin (TIBC) % transferrin saturation Ferritin
Serum iron normal or high
Transferrin (TIBC) normal
% transferrin saturation normal
Ferritin normal or high
Tension headache
MC type of headache
Associated with fatigue and stress
Typically bilateral, band squeezing
Frontal or occipital location, may involve neck
No aura, photophobia, phonophobia, or nausea/vomiting
no testing
Tx:
NSAIDs
Second line: dihydroergotamine or sumatriptan
-vasoconstrictors - avoid in CAD, Prinzmetal angina, pregnant
Migraine headache
Young adult female
Triggered by: fluctuations in estrogen, OCP’s, tyramine or nitrate rich foods (chocolate, cheese, processed meats, aged foods, old bananas)
Throbbing unilateral headache
Nausea/vomiting
Photophobia and/or phonophobia
Visual aura - streaks of light or blurring (increased risk of stroke)
Tx: Mild: NSAID or acetaminophen Mod-Sev: -PO tryptan (sumatripin) + naproxen Dihydroergotamine (DHE 45) Antiemetics - chlorpromazine, prochlorperazine, metoclopramide
Migraine prophylaxis
TCAs - amitriptyline, nortriptyline B-blocker - propranolol, metoprolol Anticonvulsant - valproic acid, topiramate, gabapentin Verapamil Naproxen
Cluster headache
Young male smokers
Headache occurs same time daily for weeks, may stop for several months
Severe unilateral periorbital headache
Conjunctival injection
Lacrimation
Nasal congestion +/- nasal discharge
Partial Horner syndrome - ptosis and miosis without anhydrosis
Tx: 100% O2 - 6+L/min on nonrebreather for 20+ min
Sumatriptan (or other triptan)
Dihydroergotamine (DHE 45)
Headache features suspect of brain tumor
Mild headache progressively worsening over days to weeks
New onset after age 50
Papilledema
Associated seizures, confusion, altered mental status
Abnormal neurologic signs and symptoms - numbness, weakness
Disturb sleep or presents immediately upon awakening
Vomiting proceeds headache
known systemic illness - cancer, HIV, or collagen vascular disorder
idiopathic intracranial hypertension (IIH)
Young obese female
Daily pulsatile headache - worse at night or early morning
Nausea/vomiting
Retroocular pain worsened by eye movement
Papilledema and elevated ICP
Most worrisome sequelae is vision loss
CT normal
CSF: elevated pressure (over 200 in nonobese, over 250 in obese)
R/O other pathology with CT and MRI DC inciting agents - excess Vit A, Accutane, long term tetracyclines Weight loss acetazolamide - first line Invasive treatment options: Serial LP Optic nerve sheath decompression Lumboperitoneal shunting - CSF shunt
Trigeminal neuralgia
Compression of the trigeminal nerve root
Lightning like unilateral facial pain
Worsened by any stimulation
Not associated with neurological defects
Carbamazepine - first line
Other options: oxcarbazepine, lamotrigine, baclofen
Surgical decompression or rhizotomy
Epidural hematoma
Laceration of middle meningeal artery
Presentation:
Trauma -> lucid interval -> lethargy, confusion, or obtundation
Headache
Vomiting
People abnormalities
Focal neurological deficits - hemiparesis, seizures
CT head w/o contrast - biconvex (Lens shaped) hematoma
Avoid LP - risk herniation
Tx:
Lower ICP - elevate head of bed to 30, hyperventilate, mannitol
Craniotomy to drain hematoma
Subdural hematoma
Rupture of bridging veins
Presentation:
Headache - gradually worsens over days to weeks
Mental status changes
somnolence
CT w/o contrast - Crescent shaped hematoma
Tx:
Craniectomy and surgical drainage - if deteriorating
Supportive care monitoring - if stable
Subarachnoid hemorrhage - presentation causes
Causes:
Rupture of arterial saccular aneurysm - berry aneurysm
-Assoc with ADPKD and Ehler’s Danlos
-MC location - anterior communicating a. and posterior communicating a.
Rupture of AVM
Trauma
Presentation:
“worst headache of my life” - thunderclap, sudden
Preceded by sentinel headache - severe recurrent headaches in weeks prior to major hemorrhage
Neck pain, nausea/ vomiting, +/- fever
CT w/o contrast - blood in CSF
LP - bloody
-Xanthochromia (yellow CSF) - recent bleeding
MRA or angiography to identify site of bleeding
Subarachnoid hemorrhage - management
Stop all anticoagulants, reverse anticoagulation
Keep SBP less than 150 if cognitive function intact until aneurysm is clipped or coiled to prevent replating
- if cerebral perfusion not adequate, lowering BP Will increase risk of infarction
- Labetalol preferred
- avoid nitroprusside and nitroglycerine - can increase ICP
Nimodipine (CCB) - prevent vasospasm
Prevent physiologic derangements that may worsen brain injury:
- avoid hypoxia and hyperglycemia
- maintain normal pH, euvolemia and normothermia
Definitive treatment: surgical clipping/ coiling
Parenchymal brain hemorrhage
MC caused by hypertension
Brain tumors, AVMs, anticoagulation
Drugs- cocaine, amphetamines
Presentation: Focal motor/sensory deficits Headache Nausea/vomiting Seizures Mental status changes
CT w/o contrast - bleeding within brain parenchyma
MRA or CTA - identify site of bleed
Tx: Supportive Control ICP Maintain SBP less than 200 Surgical decompression only for large hemorrhages with elevated ICP to prevent uncal herniation
Major risk factors of breast cancer
Female FHx BRCA 1/2 Estrogen exposures -early menarche -late menopause -fewer pregnancies -less time breastfeeding -older age at first live birth Obesity Advanced age
Clinical features suggesting breast cancer
Fixed, immobile breast mass Peau d'orange New nipple retraction Dimpling Axillary LAD MC - upper outer quadrant
Mammo - hyperdense regions and/or microcalcifications
Most common sites of breast cancer mets
bone, liver, lungs, brain
Ductal carcinoma in situ
arises from ductal hyperplasia
Malignant cells fill the duct lumen but do not penetrate the BM
eventually -> invasive ductal carcinoma
Tx: lumpectomy +/- radiation
consider mastectomy in high risk
Lobular carcinoma in situ
Arises from lobules but does not penetrate BM
LCIS high risk for invasive cancer than DCIS
ALWAYS ER and PR positive (more treatable)
Tx: observation + tamoxifen if low risk of invasion, no change in survival
consider ppx b/l mastectomy
Invasive ductal carcinoma
75-80%
arises from ducts, penetrates the BM, invades adjacent tissue
Rock-hard breast mass with sharp margins, fixed, immobile
Stellate border on mammo or bx
Tx: early focal - lumpectomy and radiation
Multifocal - mastectomy
Sentinel LN bx
Mets or large tumor >1 cm - chemo
Invasive lobular carcinoma
arises from breast lobule and invades adjacent tissue - less fibrotic response
often multifocal and/or b/l
Slower growing, slower to met
Signet ring cells or single-file rows of cells
Tx: early focal - lumpectomy and radiation
Multifocal - mastectomy
Sentinel LN bx
Mets or large tumor >1 cm - chemo
Inflammatory carcinoma
invasion of dermal lymphatics -> inflammatory changes
erythema, wamth, pain, peau d’orange, nipple retraction, dimpling
Rapid growing, poor prognosis
mimics mastitis - often treated for first and refractory
Signet ring cells
Kruckenburg tumors - GI adenocarcinoma - mets to ovary
Invasive lobular carcinoma
Paget disease of breast
form fo ductal carcinoma - malignant cells infiltrate the epidermis
Eczema-like patches on nipple and areola
may indicate underlying cancer in breast parenchyma
Bx: cells interspersed - surrounded by clear halo
Mammo/US -> bx
Treatment considerations in breast cancer
ER and PR positive - treat with tamoxifen
Over expression of HER2 - treat with trastuzumab (herceptin) - get baseline ECHO - causes reversible cardiotoxicity
BRCA mutations - b/l ppx mastectomy and oophorectomy recommended
-60-80% risk of cancers
ddx for p-ANCA
eosinophilic granulomatosis with polyangiitis
Pauci immune rapidly progressive glomerulonephritis
microscopic polyangiitis
ulcerative colitis
primary sclerosing cholangitis (PSC)
Physiologic jaundice
Increased RBCs at birth and fragile fetal RBCs -> increased heme breakdown and increased bilirubin
Natural deficiency of UDP glucuronosyltransferase -> decreased conjugation of bilirubin
Increased enterohepatic circulation of bilirubin
Bilirubin rises between 48-96 hours to 7-9
decreases around day 10
Breast milk jaundice
enzyme in breast milk
increased intestinal absorption of bilirubin
bilirubin does not go down after 2 weeks
breastfeeding failure jaundice
Not feeling well or not producing milk
Baby dehydrated
No bowel movements
-> no bilirubin excreted in bile
Hemolytic disease causing hyperbilirubinemia
Isoimmune-mediated hemolysis - ABO or Rh incompatability
Maternal antibodies attack fetal RBCs causes hemolysis
More severe hyperbilirubinemia -> kernicterus
Treatment of hyperbilirubinemia
benign causes - no treatment, correct feeding issues
Pathologic:
phototherapy - converts bilirubin to lumirubin
IVIG for ABO or Rh incompatability
Exchange transfusion
Crigler-Najjar types 1 and 2
Type 1 - no activity of UDP glucuronosyltransferase, needs phototherapy and liver transplant
Type 2: milder - no treatment or phenobarbital to stimulate UDPGT
Gilbert syndrome
Decreased production of UDP glucuronosyltransferase
Jaundice during times of stress
No Treatment
Biliary atresia
No bilirubin excretion
conjugated hyperbilirubinemia
Characteristics of Pathological newborn jaundice
Any jaundice in the first 24 hours
Rising total bilirubin by more than 0.5/hr
Rise in total bilirubin more than 5/day
Direct (conjugated) bilirubin >20% of total bilirubin or >1.5
Total bilirubin higher than 13 in term neonates
Jaundice appearing after 2-3 weeks of age
Diagnostic criteria for major depressive disorder
At least 5 of 9 in 2 weeks with impaired ability to function:
1 of these required:
Depressed mood
Interest diminished “anhedonia”
Guilt or worthlessness Sleep disturbance Concentration impairment Appetite or wt changes Psychomotor agitation or retardation Energy loss (fatigue) Suicidal ideation (recurrent thoughts of death)
“DIGSCAPES”
