cardio Flashcards
HDL is too high, what is a cardioprotective drug?
statins. don’t focus on HDL or triglycerides, give HMGCoA inhibitor
recently pregnant mother with symptoms of heart failure, dx?
Peripartum dilated cardiomyopathy
how does heart failure after doxorubicin affect the LVEDV and the RA pressure?
increases both. doxorubicin is dilated cardiomyopathy which is most common cardiomyopathy, systolic HF. LVEDV increases because EF decreases, and RA because of RV being affected as well as back up from left heart failure
constipation and AV block
verapamil and diltiazem (class IV)
complete heart block on ECG, what is mechanism of pathology?
degenerative changes in AV node (ischemia, infection with spirochetes, infiltrative)
how does nitrates work?
release of cGMP and dephyosphorylation of myosin, smooth muscle relaxation
S3 S4 explain
S3 is atrial kick, rapid ventricular filling in compliant LV wall, S4 is stiff wall, blood hitting it in restrictive cardiomyopathy/diastolic heart failure
AFib, heart failure patient with visual difficulties, GI disturbances, hyperkalemia, drug?
digoxin- similar to amiodarone SE profile but with hyperkalemia
atenolol affects what receptors how?
selective B1 antagonist, affects heart and kidney, not vascular sm muscle.
myxomatous changes with pooling of proteoglycans in the media is due to what condition and cause?
aortic dissection, Marfan’s
what collagen type after MI?
type I, bone + tendon
Inferior MI, RCA occlusion, chest and lung clear, what is cardiac output, PCWP, CVP? up or down
down, down, up
blue baby with PDA, Echo shows anterior aorta, dx and what is the embryological process that went wrong?
transposition of the great arteries, spiraling. if septation then it is truncus arteriosus
viagra, NO work similarly to what substance in body?
ANP,BNP, via cGMP level increase
ejection fraction equation and stroke volume equatino
SV/LVEDV, EDV-ESV
fatigue, dyspnea, orthopnea with TTN gene or beta myosin gene, what is the dx for both?
DCM and HCM
increased pressure requred for the same amount of volume in the EDV, what is diagnosis? and cause?
diastolic heart failure due to restrictive/infiltrative cardiomyopathy caused by transthyretin deposition (in amyloidosis)
where is great saphenous vein harvested from in CABG?
near the pelvic triangle, inferiorlateral to pubic tubercle
elevation of homocysteine increases risk of what?
thrombosis
potassium efflux is prolonged, what class of drugs and mnemonic?
Class 3, AIDS (amiodarone, ibutilide, dofetilde, sotalol)
femoral cannulation above the inguinal ligament leads to?
retroperitoneal bleeding
common site for AFlutter? how about AFib?
cavotricuspid isthmus, pulmonary vein ostia (where it enters)
severe AS, decreased cardiac output, 90/60, pulmonary edema, no changes on ECG except atrial fibrillation, diagnosis and mechanism?
AS causing LVH and atrial fibrillation, which prevents atrial contraction into ventricles, lowering cardiac output = sudden decrease in cardiac left ventricular preload
how do bb help in a patient with thickened intervententricular septal hypertrophy?
because of HOCM, outflow tract obstruction which is worse with decreased preload, so bb help increase preload by slowing heart and reducing contractility
which chamber is closest to esophagus
LA
septic shock- what is CVP, PCWP, Cardiac index, SVR, SvO2(mixed venous return), temperature?
low low high low high, low or high
endocarditis, gram pos cocci, catalase negative, bile and sodium 6.5% resistant, what is procedure that leads to this guy being introduced?
cystoscopy (enterococcus -faceium/faecalis)
hemosiderin in lungs, what is pathology?
LV failure, causing backup of blood in lungs
aortic stenosis due to calcifciations, what type of calcification and mechanism?
dystrophic calcification, damaged, necrosed tissue acts as nidus for calcification
beck’s triad for what?
hypotension, elevated JVP, muffled heart sounds, for cardiac tamponade
MI heart suddenly regains some function after PCI, why?
hibernating myocardium
RHF symptoms, CT scan shows thickened pericardiumm, dx?
constrictive pericarditis
inferior MI, bradycardia, mechanism? what drug do you give?
inferior MI leads to nodal ischemia because RCA provides the nodes. give atropine, because anticholinergic effect will counter the bradycardia and the increased vagal tone
QRS prolongation drug, not much effect on QT interval, which part of depolarization does it effect and what class of drug?
class IC, phase 0 (depolarization, opening of sodium channels)
trastuzumab effect on heart
blocks HER2 which protects heart from oxidative stress, so reduced cardiac contractility with no fibrosis
esmolol given, which part of PQRST does it affect and how?
PR interval because Bb slow down AV node conduction
fever, joint pain, rash, ANA positive. what drug?
procainamide and hydralazine isoniazid also (drug induced lupus)
smoker, raynauds, vasculitis, dx and histo features?
buerger’s disease; segmental vessel vasculitis extending to contiguous veins and nerves
chronic COPD leading to chronic heart failure, what compensatory change prevents development of edema?
increased lymphatic uptake
one sided swelling of face and arms from a smoker, where is the blockage?
brachiocephalic. SVC on one side only
corrigan and duzeiz sign, what is relative aortic and LV systolic and diastolic pressures?
aortic = elevated systolic, low diastolic. LV= elevated systolic, increased diastolic
what is viscious cycle components (2) in heart failure?
sympathetic activation due to baroreceptors and RAAS activation
Pharyngeal arches mnemonic
Gambling if you don't study these: 1 man Fucked 2 Strippers In 3 Great Styles but don't tell 4 always remember to say That what happens in vagus recurs in vagus
CVP is high, PCWP is low, patient with recent MI with syncope. causes?
Right ventricular failure
25mmHg and 2 mmHg –> 25 mmHg and 10 mmHg, where are the measurements being taken
RV and PA
what causes BNP release and what two things does it do?
stress of ventricular wall, vasodilation and diuresis
constrictive pericarditis, what sign do you expect to see?
kussmaul’s sign (rise in JVP during inspiration), pulsus paradoxus (drop in SBP during inspiration)
what is behind the esophagus in thorax?
descending aorta
norepinephrine effects and mechanism/second messenger
a1 and a2 stimulation, using IP3, causing vasoconstriction; and B1 stimulation, using increased cAMP, causing cardiac heart rate increase
AV fistulas lead to what kind of pressure volume loop?
high EDV, lower afterload (load ventricle has to pump against)
dobutamine moa and effect
Gs protein adenylate cyclase activation leading to rise in cAMP, and Ca++ in heart, and vasodilation. increases contractility
phenoxybenzoamine uses, mechanism
pheochromocytoma, a blocker as irreversible inhibitor
prinzmetal trigger and treatment
dihydroergotamine or triptans, treatment is CCB or nitrates
continuous murmur in child, palpable thrill below clavicle, what embryological origin is the structure?
sixth aortic arch (PDA)
young woman with a stroke, and on oral contraceptives, bubble study shows patent foramen ovale, what is dx?
paradoxical embolism to the brain, from PFO with patient on oral contraceptives
fever, joint pain, rash, ANA positive. what drug?
procainamide and hydralazine isoniazid also (drug induced lupus)
clubbing and cyanosis in the toes, childhood heart condition, dyspnea now. dx and differential?
PDA, ddx coarctation (the infant form) where coarctation lies after subclavian but before PDA
what is pathophysiology of AAA? how about aortic dissection in marfans? and thoracic aneurysm in syphillis?
chronic transmural inflammation because atherosclerotic plaques increase diffusion barrier for O2 and cause inflammation, which means MMP and elastase are secreted by inflammatory cells to destroy ECM and weaken wall/ cystic degeneration of media, syphillis is vasa vasorum endarteritis
what is made by endothelial cells to oppose platelet aggregation, and what does it specifically oppose? and what does kallikrein do?
Prostacyclin–> TXA2. kallikrein- turns kininogen to bradykinin. maybe plays a role in fibrinolytic pathway
death 5 days after MI, what is most likely cause a=nd symtpoms and time frame?
Left ventricular free wall rupture, chest pain, tamponade, shock, severe hypotension in 5-14 days after AMI
prolonged QRS interval on treadmill test, with preserved QTc, what is drug? what is use-dependence?
flecainide, class 1C, use-dependence means the faster a heart is beating the more effect the drug will have
dyspnea, edema, =======fistula between aortacough with recent hoarseness, cause?
ortner’s syndrome, LA enlargement causing neurapraxia (failure of nerve conduction due to blunt injury to nerve)
mechanism of prinzmetal variant angina?
hyperreactivity of coronary artery smooth muscle because defective production of NO by endothelial cells, which means vagal tone (acetylcholine) takes over and vasoconstricts
what drug increases cardiac contractility and decreases TPR?
isoretinoin- B1 equals B2,
fistula between aorta and RV, when does blood flow and where?
aorta to RV, continuously. because 120/80 in aorta, 25/5 in RV, 25/10 in PCWP
polyarteritis nodosa, what vessels does it spare?, appearance on histo?
pulmonary, string of pearls
dobutamine effect on normal myocardium and on a patient with angina? and what is mechanism of pathology?
B1 agonists, mimics exercise, so transient increase in heart rate and contractility, which means ejection fraction also increases. in patient with angina, OXYGEN SUPPLY AND DEMAND MISMATCH leads to decreased EF
Mechanism of alteplase and why it’s risky
binds fibrin and converts plasmin to plasminogen, risky because of intracerebral hemorrhage risk
mitral valve calcification and vegetation but no bacterial organism, what is dx and common causes?
NBTE non-bacterial thrombotic endocarditis, caused commonly by advanced malignancy (hypercoagulable state and proinflammatory state) and SLE
2 SE of ACEi therapy
first dose hypotension and reduced GFR
what exacerbates S3? and why?
end expiration, because it decreases lung volume and brings heart closer to chest, and also cause left-sided murmurs are worse on expiration because it causes return of blood from lungs to left atrium
JVP on cardiac cycle stages
a,c,x,v,y (atrial contraction, RV contraction and tricuspid bulging into RA, x descent is tricuspid going down, v is right atrial villing, and y descent is RA emptying into RV
two places that bear the greatest atherosclerotic burden?
coronary and lower abdominal aorta
beta blocker toxicity, what do you give and how does it work?
glucagon, cAMP, raises Ca release, increases heart rate and contractility
lipofuschin what is it aresult of?
lipid peroxidation
aortic dissection two prereqs and histological feature
tear in intima, preexisting weakness in media. cystic degeneration of media, being replaced by MMP
chest pain, dysphagia and hoarsenss, and dies of hypotension later, dx?
ruptured thoracic aortic anueyrsm
where is SA and AV node located?
SA- junction of SVC and RA, AV- septal cusp of tricuspid valve
eccentric and concentric hypertrophy, explain and give example
eccentric- adding in series (dilated cardiomyopathy, systolic HF), concentric- adding in parallel (HFpEF, HOCM)
describe the carotid sinus reflex, what is afferent/efferent limb?
arterial stetch–> afferent- glossopharyngeal, efferent –>vagus, lowers BP and CO
highest predisposing factor to IE in developed, developing countries?
mitral valve prolapse/rheumatic heart disease
major determining factor for symptom severity in TOF?
pulmonary stenosis, because that determines cyanosis or not
HLD drugs moa- fibrates, ezetimibe, statins, omega 3
fibrates and omega 3- decrease VLDL production by activating PPAR-a and increase HDL by activating LPL. ezetimibe blocks intestinal absorption of cholesterol. statins inhibit HMG CoA, blocking production of cholesterol in liver,
person treated for systolic HF, nausea, vomiting, stomach upset, dizziness, anorexia, visual distrubance, what is causing and what is complication?
digoxin, arrhtyhmia
post MI drug that exacerbates ischemia? what do you not give in a specific MI context?
arterial vasodilator (adenosine, dipyridamole) that leads to coronary steal syndrome. also don’t give nitrates in inferior MI (RV is dependent on preload)
what are conditions that can cause pulsus paradoxus?
COPD and asthma, because lungs are so compliant, drop is significant
loading dose and maintenance dose equation
Vd x Cpss, CL x Cpss (divide by bioavailability if not intravenous
why is class 1b good for ischemic heart? and 1c bad for ischemic heart?
because ischemic heart has delayed transition to resting state, so 1b drugs bind preferentially to those areas. 1c has strong use dependence, strongly binds, so can lead to arrhythmic events
in AF, what determines rate of ventricular contraction?
AV node refractory period. AF is atrium firing like crazy but does not all reach ventricle because of AV node refractory period
what cells help in development of atheroma?
platelet, activated macrophages, endothelial cells
irreversible sign of cell injury?
vacuolizaition onf mictrochondria
what structures blocks outflow in HOCM
mitral valve and septal hypertrophy
mvmt of calcium in contraction and relaxation
L-type Ca open, enteres, RyR senses Ca and opens sarcoplasmic reticulum gate to send. then SERCA and Na/Ca exchanger promotes outflow of Ca into SR and extracelluarly
hematuria, ischemic stroke, lactate is high, CT of abdo shows lucency in kidney, dx?
renal infarct
murmur best heard on leaning forward, crescendo-decrescendo- where is the murmur loudest?
AR is loudest right after closure of aortic valve, when pressure difference is the highest
