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54 Cards in this Set
- Front
- Back
- 3rd side (hint)
what drug given in pt with known CAD to reduce risk of MI/stroke?
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statins, esp pravastatin and simvastatin
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target LDL value
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0-1 RF: <160; 2+ RF: <130; CAD/DM/PAD/AAA: <100, maybe <70
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how to convert hba1c to average FSG
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HbA1c * 33 - 86
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causes of secondary hypertriglyceridemia (4)
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DM, Hypothyroidism, alcohol abuse, estrogen use
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None
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tx for hypertriglyceridemia
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if secondary, treat 1' disorder; if 1', use NIACIN, fibric acid derivatives (?fibrates), or omega-3 fatty acids; also, lifestyle changes
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use of bile acid sequestrants in hyperTG
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contraindicated -- can actually increase TG
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what TG level confers risk for pancreatitis?
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>1000 (?>500)
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classification of TG levels
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<150: normal; 150-199: borderline; 200-499: high; >500: very high
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what is total chol the sum of?
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LDL + HDL + vLDL
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what is the non-HDL cholesterol goal?
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non-HDL chol = totalchol - HDL = vLDL + LDL; non-HDL cholesterol goals are LDL goals + 30;
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what risk with statin-fibrate combo?
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myositis
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what to do if LDL not adequately controlled on max dose statin?
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add bile acid sequestrant or ezetimibe (as long as no hTG)
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max dose simvastatin
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40mg/d
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criteria for metabolic syndrome
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>= 3 risk factors (ABCDeFG): 1) Abdominal obesity; 4) BP > 130/85; 3) Cholesterol -- HDL<50 in women; 2) TG>150; 5) fasting glucose > 110
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what drugs elevate HDL and decrease TG? Which to use with statin?
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niacin and fibrates; niacin-statin preferred b/c of fibrate-statin risk of myositis
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dosage of niacin
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titrate up to 1500-2000 mg/d, depending on tolerance
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ecg findings in pericarditis
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diffuse pr depression, st elevation
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mgmt of symptomatic aortic stenosis
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valve replacement (3-5yr prognosis is poor)
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symptoms of chronic pericarditis
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dyspnea, signs of R-sided HF; no chest pain
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PTCA vs CABG in diabetics
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CABG shown to have better long-term mortality
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which murmurs increase in intensity with valsalva?
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MVP and HOCM
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4 causes of CP that can quickly lead to death
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1) MI; 2) Aortic dissection; 3) Tension pneumothorax; 4) PE
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best rapid diagnostic test for aortic dissection
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TEE
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when to do echo/nuclear imaging vs electrocardiography in stress testing?
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if baseline ECG is abnormal, difficult to interpret ECG changes
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risk of thromboembolus with cardioversion in afib? how to avoid?
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if afib < 48hrs, cardioversion usu safe; else, need anticoag first; TEE if need to confirm absence of thrombus formation
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None
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common causes of pleuritis in young people
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viral pleurisy; also autoimmune dzs (SLE, RA), drug-induced lupus
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VQ scan vs PECT for r/o PE
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according to MKSAP, VQ unless high risk pt (not sure this is still true)
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which drugs have mortality benefit in CAD?
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beta blockers and ACEi (independent of effects on BP and LV function)
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what change in heart sounds with WPW?
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paradoxically split S2
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P-P interval in mobitz I
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constant
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pathophys of mobitz II
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usu a/w L or R BBB; dropped beat when the remaining branch suffers intermittent block
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detecting MI in pt with LBBB
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cannot assess ST depression in presence of LBBB ==> need to do nuclear imaging
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use of class Ia antiarrythmics in pts with frequent PVCs
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contraindicated -- proarrythmic effects of class Ia drugs outweighs benefit
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in-hospital mortality of cardiogenic shock
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50%
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most important intervention in cardiogenic shock due to acute MI
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restore patency of vessel - angiography/angioplasty
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what immediate intervention in acute STEMI?
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angioplasty (not thrombolysis)
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what does persistent ST elevation very late after acute MI indicate? (3)
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1) persistent myocardial injury; 2) ventricular aneurysm formation; 3) localized MI-related pericarditis
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what is isosorbide mononitrate?
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venous and arterial vasodilator used to tx angina
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tx of choice for preventing post-MI remodeling
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ACEi (improves LV function, reduces short- and long-term mortality, reduces incidence of heart failure, reduces incidence of recurrent reinfarction)
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which cardiac pts benefit most from ACEi tx?
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anterior wall MI, systolic dysfunction, or clinical evidence of CHF
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when do most post-MI VSDs occur?
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2-7 days after infarction (same timing as post-MI papillary rupture)
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acute hypotension and bradycardia in setting of acute MI -- whats the cause?
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vagal reaction
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which vessels usu involved in RV infarction?
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right coronary artery proximal to RV marginal branch
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what can cause triad of hypotension, elevated JVP, and clear lung fields? (2)
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RV infarct or tamponade
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None
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what kind of arrythmia a/w RV infarct?
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bradycardia (from SA or AV node ischemia)
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therapy for RV infarct
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standard MI tx + volume loading, avoid diuretics/venodilators (eg nitrates), ?pacing
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survival rate 24hrs after large VSD/papillary muscle rupture
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25% with medical therapy
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tx of post-MI VSD
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nitroprusside or intra-aortic balloon pump
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where does free wall rupture typically occur after MI?
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at juncture of infarcted myocardium with normal myocardium; less often in ccenter of infarct
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when does free wall rupture occure post MI?
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1-4d, rarely up to 3wks after MI
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coronary angiography before discharge for which patients?
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pts with angina or residual ischemia (at rest or with exertion) after successful thrombolysis; for pts w/o angina/ischemia, stress test sufficient for discharge
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what leads involved in lateral MI?
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I, aVL, V5, V6
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presentation of posterior MI on ecg
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prominent R waves + ST depression in precordial leads, often a/w inferior MI
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vtach vs vfib
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arbitrary distinction based on cycle length; both are fatal if not corrected
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