MKSAP Flashcards
Acute pericarditis dx
1) Pleuritic chest pain
2) Friction rub (squeaky, scratchy, high pitched)
3) Diffuse concordant ST elevation (PR depression)
Also: worse lying down
Aortic dissection presentation
Sudden onset severe chest pain radiating to back
BP difference between R and L arms
Murmur of AR
Widened mediastinum on CXR
RV MI
Findings: hypotension, clear lungs, elevated CVP (JVD)
Tx with normal saline then IV dobutamine if still hypotension after 1L saline
ST elevation in II, III, aVF but also V4
Medical therapy for chronic stable CAD
Antianginal: beta blockers, CCBs, nitrates
Vascular-protective therapy: aspirin, ACE inhibitors, statins
Workup of CAD
Exercise stress test is best
Adenosine nuclear perfusion stress test should NOT be done in asthma pts
Dobutamine stress echo should NOT be done in those that can exercise or those that are hypertensive
V-tach
After structural damage such as MI
Wide QRS (>0.12 sec)
Cannon waves (large a waves) suggest v-tach or heart block (AV dissociation)
Complications after MI
Papillary muscle rupture –> severe MR (several days later)
Ventricular free wall rupture –> CV collapse, tamponade, PEA, sudden hypotension then death (1-4 days later)
VSD –> systolic murmur, hypotension, resp distress, thrill (2-7 days after)
LV aneurysm –> intractable v-tach, septic emboli, heart failure (much later)
CHADS2
Whether or not pt with a-fib should be on warfarin
INR 2-3 decreases stroke risk 62%
3 or more points means YES warfarin
CHF
HTN
Age > 75
DM
Stroke (2) or TIA (1)
Digoxin use
Used in patients with CHF for SYMPTOMS (no mortality benefit)
Use low doses (0.5-0.8 ng/mL)
Treatment of heart failure
All stages of systolic heart failure: beta blocker
NYHA Class III or IV: beta blocker, ACE inhibitor, spironolactone
How to treat HTN or angina in pt with CHF already on beta blocker and ACE inhibitor
CCBs that aren’t bad in CHF: amlodipine, felodipine
Antibiotic endocarditis prophylaxis
Prosthetic valve
Hx infective endocarditis
Cardiac transplant with valve abnormality
Unrepaired cyanotic congenital heart disease
Complex congenital heart disease w/residual abnormalities
Chronic pancreatitis
Clinical presentation: mid-epigastric pain, diarrhea after eating, DM 2/2 pancreatic endocrine insufficiency
Malabsorption occurs when 80% of pancreas destroyed
Serum to ascites albumin gradient (SAAG)
Serum albumin - ascites albumin
>1.1 means ascites is due to chronic liver disease: cirrhosis, RHF, Budd-Chiari
<1.1 means due to infection, inflammation, cancer, TB, nephrotic syndrome
Hepatic encephalopathy triggers and treatment
Triggers: infection (SBP), dehydration, GI bleeding, diet, medications
Treatment: lactulose to 2-3 BM per day at pH < 6
Precipitants of hepatorenal syndrome
Hepatorenal syndrome: renal failure in pt with liver disease after r/o prerenal azotemia, renal parenchymal disease, obstruction
Precipitants: SBP, vigorous diuretics, paracentesis w/o volume expansion, GI bleeding
Treatment: liver transplant
Goals for patient with sepsis
Central venous oxygen saturation of at least 70%
Central venous pressure of 8-12
MAP of 65
Urine output of 0.5 mL/kg/hr
Early goal directed therapy: give 5-6L fluids within first 6 hours
When to use activated protein C (drotrecogin alpha activated)
APACHE II score >25
Septic shock requiring vasopressors
Sepsis-induced ARDS requiring mechanical ventilation
2+ sepsis induced organ dysfunctions
Do NOT use if: platelets < 30, active bleeding, surgery <12 hours agowha
Glomerular vs nonglomerular hematuria
Glomerular hematuria: dysmorphic RBCs, RBC casts, proteinuria; do kidney biopsy to eval glomeruli
Nonglomerular hematuria: do cystoscopy to eval for malignancy if increased risk for bladder cancer (male, >50, smoking, exposure to cyclophosphamide/radiation, etc)
HUS
Presents as AKI, thrombocytopenia, MAHA (schistocytes on smear), bloody diarrhea
Caused by shiga toxin producing E. coli: shiga toxin binds platelets, glomerular capillary endothelial cells, mesangial cells, and glomerular and tubular epithelial cells, causes platelet aggregation, can also cause release of large vWF multimers from endothelial cells causing more platelet aggregation
Caused by familial deficiency of factor H: factor H is complement component that usually protects cells from damage by alternative complement system so when deficient, C3 potentiates damage to glomerular cells and exposes subendothelium which causes activation of platelets and coagulation
Indications for chest tube drainage of parapneumonic effusion
Loculated
pH <7.2
Glucose <60
LDH >1000
Positive gram stain or culture
Pus
When to intubate in asthma exacerbation
Resp acidosis
Hypoxemia
Fatigue
Wells criteria for PE
Cancer w/tx within 6 months or palliative
Paralysis or recent cast
Recent immobilization or surgery
Tenderness along deep veins
Swelling
Greater than 3cm circumference difference
Pitting edema
Collateral superficial veins
-2 if suspect a different dx
Urine anion gap
UAG = Na + K - Cl
Should be 30-50
If very negative, have increased urine ammonium secretion and extrarenal cause of metabolic acidosis (GI, pancreatic, biliary, ureter losses)
If positive UAG, have decreased urine ammonium secretion and kidney cause of metabolic acidosis (RTA)
