Step 1 - CV from Uworld

denniskwinn's version from 2015-04-25 16:29


Question Answer
ANP/BNP from ventriclesHappens in both hypertrophy and volume overload
Reperfusion injuryfrom generation of oxygen-free radicals
QRS complex phase in ventricular myocyte action potentialphase 0
Drug induced lupus syndromeProcainamide, hydralazine, isoniazid
Cardiac drug combination leading to severe bradycardia and hypotensionNon-dihydropiridine Ca blockers (verapamil, diltiazem) and β blockers (atenelol)
major determinant of the ratio of forward·to-regurgitant left ventricular (LV) output in patients with mitral regurgitation (MR) is LV afterload
Arterial vasodilator SE (hydralazine, minoxidil)reflex sympathetic activation (tachy, edema) to counteract these effects, give with sympatholytics and diuretics
NO and like drugs mechanismincreases cGMP, decreases intracellular calcium and myosin dephosphorylation
Chi squared to compareproportions - 2x2 table may be used to compare the observed values w/expected
Pulsus paradoxus seen inacute cardiac tamponade, constrictive pericarditis, severe obstructive lung disease(including acute asthma), restrictive cardiomyopathy
BNP/ANP effects/mechanismcauses vasodilation and diuresis - activate guanylate cyclase which induces an increase of intracellular cGMP
Antiarrhythmic that bind ischemic myocardiumLidocaine - binds to rapidly depolarizing and depolarized cells - use in post MI arrhythmias or for prevention - but amiodarone is used for Vtach
Congenital heart problems b/c of neural crest cellsTetralogy of Fallot, transposition of great vessels and truncus arteriosus - all can be caused by abnormal migration of these cells through the primitive truncus arteriosus and bulbus cordis
Abnormal primitive heart tube looping causessevere cardiac malformations - misplaced inflow and outflow tracts
Acute cardiac transplant rejectionprimarily a cell-mediated histo show a dense mononuclear lymphocytic infiltrate with cardiac myocyte damage
Organ susceptibility to infarct after occlusion of feeding artery greatest to leastCNS, myocardium, kidney, spleen, liver (dual blood supply)
Treatment of coag - staphvanco with or without rifampin or gentamicin due to widespread antibiotic resistance of s. Epidermidis
Bacterial endocarditis vegetationsfibrin and platelet deposition at site of colonization
Afib conductionirregular, chaotic electrical activity within atria - while some of the impulse are transmitted to ventricles most are not due to AV nodal refractory period
K sparing diuretics act in thecollecting duct
Acetazolamide acts in thePCT - carbonic anhydrase inhibitor (blocks bicarb reabsorption in kidney)
Furosemide, bumetanide, torsemide, ethacrynic acid site of actionthick ascendinlng limb of loop of henle
Thiazide diuretics site of actionDCT
Down syndrome cardiac defect associationsendocardial cushion defect, ASD, regurgitant AV valves
Digeorge syndrome cardiac associationstetralogy of fallot and aortic arch anomalies
Friedrichs’ ataxia cardiac associationshypertrophic cardiomyopathy
Marfan syndrome cardiac associationscystic medial necrosis of aorta
Tuberous sclerosis cardiac associationsvalvular obstruction due to rhabdomyomas
Turners syndrome cardiac associationscoarctation of aorta
Type I error occurs when researchers reject the null hypothesis when the null hypothesis is really true
Alpha (a)maximum probability of making a type I error a researcher is willing to accept It corresponds with the p value, or the probability of making a type I error, The a is typically set at p" 0,05, meaning that researchers accept a 5% possibility that a difference perceived as true is actually due to chance,
Type II error occurs when researchers fail to reject the null hypothesis when it is truly false, It causes investigators to miss true relationships, An example would be a study finding that aspirin does not affect platelet function when, in fact, it does,
Beta is the probability of committing a type II error, Thus, if it is set at 0.2, the powerwill be 80%; there will be an 80% chance rejecting a null hypothesis when it is truly false
Genetic Hypertrophic cardiomyopathyoften presents as sudden cardiac death in a young athlete. Almost all cases are due to autosomal dominant mutations in cardiac sarcomere proteins. The most common protein involved is beta· myosin heavy chain.
Genetic dilated cardiomyopathy1/3 of cases - majority due to autosomal dominant mutations of cardiac myocyte cytoskeletal proteins (dystrophin) or mitochondrial enzymes.