UWorld Cardio I Flashcards

Question

``` Transient myocardial ischemia -> myocardial cells increase in size. Due to what? A. Intracellular K+ accum B. Intracellular Ca2+ accum C. High cellular HCO3- content D. Cascade protein phosphorylation E. Net cellular solute loss ```

Answer 1

Cardiac myocytes transition from aerobic to anaerobic metabolism when blood flow cannot meet myocardial demands -> can't maintain proper intracellular ATP levels -> ADP, AMP, adenosine accumulate -> Na+/K+ ATPases and sarcoplasmic reticulum Ca2+ ATPases fail -> increased intracellular Na+ and Ca2+, increased intramitochondrial Ca2+ -> attract free water -> cellular and mitochondrial swelling Failure of SR to resequester Ca2+ -> cessation of contraction within ischemic zones of myocardium A. Na/K pump normally brings K+ INTO cell, in exchange for Na+ OUT. So intracellular K+ would be DECREASED C. Anaerobic met -> elevated lactic acid, decrease in pH -> tissue CO2 (cons acid of HCO3-) elevated in ischemic myocardium D. Protein phosphorylation- second messenger signaling, regulation of apoptosis. Response to ischemia does not cause swelling this way E. Ischemia causes net solute GAIN within cardiac myocytes; elevated concentrations of Na+ and Ca2+ draw in free water -> edema

Answer 2

Cerebrovascular event- TIA, stroke, in setting of known venous thromboembolic disease suspicious for paradoxical embolism; originate in venous circulation and enter systemic arterial circulation via intracranial or intrapulmonary shunt -> patent for amen ovals, ASD, VSD, large pulm AVM ASD, L->R shunting -> wide and fixed splitting, no change in respiration, of S2; will also have mid-systolic ejection murmur over left upper sternal border resulting from increased flow across pulmonic valve and mid-diastolic rumble due to increased flow across tricuspid valve Paradoxical embolism can occur even in net left to right shunting due to transient reversal of shunt during periods of elevated right-sided pressure- early ventricular systole, straining during coughing or defecation A. Early diastolic decrescendo murmur- aortic regurgitate; inhaled amyl nitrite -> vasodilation -> reduce systemic arterial pressure and regurgitant flow B. Systolic ejection murmur increases in intensity with standing- patients with hypertrophic cardiomyopathy- decrease in left ventricular outflow tract size; murmur of valvular aortic stenosis decreases in intensity upon standing C. Mitral or tricuspid valve stenosis- diastolic murmur with pre systolic accentuation due to atrial contraction. Mild stenosis, murmur may only be audible during accentuation phase in late diastole; afib may cause murmur to disappear completely D. Wide splitting of S1 accentuated by inspiration- delay closure of tricuspid valve- patients with RBBB or tricuspid stenosis

Answer 3

Dyspnea, Orthopnea, bibasilar crackles -> high pulmonary venous pressure and pulmonary edema in deep lung. Holosystolic murmur over cardiac apex suggestive of mitral regurgitation S3 gallop reflects increased left ventricular filling rate during mid diastole- consequence of mitral regurg Txt with diuretic reduces LV preload -> decreases LVEDV; patient's murmur and gallop disappeared after this, MR most likely functional, due to transient hemodynamics factors causing LV dilatation and/or papillary muscle ischemia rather than due to fixed mitral valve lesion. Acute LV dilatation can sufficiently separate otherwise normal mitral valve leaflets to permit functional regurg. Most common anatomical abnormality producing mitral regurg is myxomatosis degeneration (MVP); after load reduction with vasodilator decrease average intraventricular systolic pressure required to generate a given stroke volume and tends to reduce MR due to any cause A. Thickened and deformed mitral valve cusps fixed anatomical lesions, chronic rheumatic heart disease. Usually found in older individuals who may not have had access to antibiotics when younger, resulting in mitral stenosis B. Mitral annular calcification- degenerative calcification deposits in fibrous ring of mitral valve, does not impair valvular function. Associated regurg/stenosis in rare instances. Most common in women older than 60, individuals with history of myxomatosis degeneration of mitral valve, individuals with chronically elevated LV pressures- radius is fixed in patients with a calcified mitral valve annulus, so murmur would not have gone away after diuretics C. Increased rate of flow through aortic valve -> functional aortic stenosis -> systolic ejection type murmur heard over aortic area D. Chordate tendineae rupture produces severe MR complication of bacterial endocarditis; papillary muscle or chordate rupture occurs in association with MI, usually an early complication of MI within 10 days

Answer 4

Left sided CHF- dyspnea on exertion, Orthopnea (dyspnea while lying flat), paroxysmal nocturnal dyspnea (waking up from sleep gasping for air) Right sided CHF- lower extremity edema and hepatomegaly CHF- progressive decrease in myocardial contractility- systolic dysfunction, inability of heart to relax to accommodate incoming blood in diastole- diastolic dysfunction. Ultimately both CHFs -> decreased cardiac output and inadequate oxygen delivery to tissues. Decreased perfusion of peripheral tissues -> RAAS -> decreased GFR activates macula dense -> increase renin.. Angiotensin II 1. Sodium retention 2. Aldosterone production 3. VASOCONSTRICTION Vasoconstriction ->increase arterial resistance and after load Failing heart unable to pump blood against increased after load induced by angio II -> tissue perfusion decreases and more renin.. Vicious cycle Aldosterone -> increase circulating blood volume (preload) further exacerbate CHF Increase symp output stimulated by baroreceptors sense decreased perfusion -> epinephrine and norepinephrine increase heart rate and contractility, also increase peripherall arterial resistance -> increase after load A. Cardiac output decreased in both systolic and diastolic HF B. Decreased perfusion of viscera, includes kidneys d. Less arterial blood delivered to peripheral tissues- contact of tissues with venous blood is increased - uptake of oxygen from venous is higher -> mixed venous oxygen content decreased E. Increased pressure in pulm circulation -> transmutation of fluid into lung interstitial and air spaces -> decrease lung compliance and oxygen diffusion

Answer 5

E. Collecting duct Patient had hypokalemia secondary to CHF med- prob a K+ wasting such as a loop diuretic (furosemide) normal treatments for CHF- positive ino tropes- digoxin, beta blockers, ACE inhibitors, diuretics (loop, K+ sparing) Physician added a K+ sparing diuretic to regimen -> act primarily antagonizing effects of aldosterone on late distal tubule and cortical collecting ducts Amiloride and triamterene- directly blocking epithelial sodium channels (ENaCs) in apical membrane of principal cells spironolactone and eplerenone competitively inhibit aldosterone receptor -> down reg of ENaCs and basolateral Na/K Eplerenone- more specific receptor antagonist than spironolactone with fewer side effects preferred in patients with heart failure- prevent deleterious effects of aldosterone-induced cardiac remodeling A. Carbonic anhydrase inhibitor acetazolamide- PCT B. Mannitol- osmotic diuretic- PCT and descending limb of Henle D. Loop diuretic- furosemide, bumetanide, torsemide, ethacrynic acid- thick ascending limb of Henle E. Thiazide diuretics early DCT- would exacerbate hypokalemia All diuretics EXCEPT K+ sparing => HYPOKALEMIA => increasing volume delivered to collecting duct => aldosterone attempts to reclaim additional volume at expense of K+; K+ sparing act on late distal tubule and CD to antagonize effects of aldosterone

Answer 6

Nesiritide - recombinant form of BNP- used in patients with decompensated LV dysfunction -> CHF HF, esp systolic dysfunction -> increased blood volume within heart -> stretching of atria and ventricles beyond appropriate stretch to cause maximal contraction by Frank-Starling -> release of natriuretic peptides from walls of atria (ANP) and ventricles (BNP)- both activate guanylate Cyclase, induces increase of intracellular cyclic GMP. Natriuretic peptides cause vasodilation, diuresis/natriuretic, decrease in blood pressure ANP/BNP counteract endothelin, symp effects and angio II A. Endorphin- endogenous morphine- same receptors as narcotic analgesics; released by hypothalamic-pituitary axis, does not play a role in diuresis or vasodilation; synthesized in and released from primarily corticosteroid cells in ant pit B. TGF-beta- synthesized by most cells in body -arrest of cell cycle- tumor suppressing agent -promotion of angiogenesis- allowing tumor metastasis after resistant to TGF -stim of fibroblasts to lay down extracellular matrix proteins => atherosclerosis and fibrotic diseases D. Bradykinin- produced by kidney where adrenergic and RAAS stim; locally constrict veins and dilate arterioles to increase renal perfusion; metabolized by ACE, implicated as a cause of angio edema E and F. Endothelin, Angio II- POTENT VASOCONSTRICTORS- increase after load which failing heart has to pump against in setting of heart failure Endothelin mediated by angio II; ACE-I class of drugs useful in treating Heart failure BNP- lab test in clinical setting to determine if patient suffering from CHF exacerbation Released by ventricles when stretched (CHF from systolic dysfunction)

Answer 7

headaches and epistaxis collaterals arterial circulation to region of aorta distal to coarctation Radio graphic exam- notching of ribs as result of enlarged tortuous intercostal arteries D. L->R shunt of isolated PDA usually doesn't result in poor exercise tolerance until persistent pulmonary HTN -> pulmonary vascular sclerosis and shunt flow reversal- Eisenmenger; wouldn't find epistaxis or enlarged intercostal arteries e. TOF could decrease exercise tolerance via increased R->L shunting and hypoxemia in response to vasodilation in active skeletal muscles. Would NOT expect epistaxis or enlarged intercostal arteries in these patients

Answer 8

Cardiac myocytes- depol -> L type calcium channels on plasma membrane open, allow influx of extracellular calcium -> binds and activates sarcoplasmic RyR2 -> release of calcium from SR (calcium induced calcium release) -> binds troponin -> allows actin and myosin to interact Vascular smooth muscle- similar, but instead of calcium-troponin, uses calcium-calmed Union to facilitate interaction between actin and myosin Skeletal- L type calcium channel DIRECTLY interacts with RyR1 Ca2+ channels to cause release of calcium from SR. No significant influx of Ca2+ across plasma membrane L type calcium channel -> PHYSICAL INTERACTION between 2 channels -> SR Ca2+ release -> calcium-troponin -> myosin and actin interact Skeletal muscle not dep on extracellular calcium b/c of L-type Ca2+ channel-Ryr mechanical coupling, so calcium channel blockers like verapamil do not affect troponin C's affinity to intracellular calcium

Answer 9

Interaction between nitrates and phosphodiesterase inhibitors used in erectile dysfunction- tadalafil, sildenafil, vardenafil** Nitrates -> nitric oxide by vascular smooth muscle cells, nitric oxide -> increased intracellular cGMP as 2nd messenger Increased cGMP -> Vascular smooth muscle relaxation CGMP metabolized within cells by phosphodiesterase; phosphodiesterase inhibitors --> increased intracellular cGMP Both => profound hypotension due to extreme vasodilation when drugs used together A. Receptor down reg/tachyphylaxis- topical glucocorticoids, opiates, L-dopa, etc. Body develops tolerance to drugs on cellular level, not cause of hypotension in patient who took nitrates together with PDE inhibitor B. Gs protein phosphorylation -> Gs; no role in cGMP affected by nitrates and PDE inhibitors D. Tyrosine kinase over activity- exaggeration of effects on insulin or insulting-like growth factor. No effect regarding nitrates or PDE inhibitors on vascular smooth muscle E. Enhanced phospholipid metabolism -> increase in production of prostaglandins (diacylglycerol) and IP3 (Ca2+ release from endoplasmic reticulum); mediates effects of alpha1, angio II, oxytocin, vascular vasopressin; not involved with nitrates or PDE inhibitors F. Tolerance- need for larger dose of drug to achieve same clinical effect achieved previously with smaller dose of drug; change in cellular response to drug (dec receptors, dec response to receptor stimulation), increased rate of drug elimination by the body.

Answer 10

Acute MI- use beta blockers to reduce heart rate, cardiac output, myocardial oxygen demand- reduce short-term morbidity, minimize infarct size, improve long term survival. Contraindications to beta blockers include bradycardia or heart block, hypotension, overt heart failure (Pulm edema) Do NOT use non-cardio selective beta blockers (propranolol, nadolol) => could trigger broncospasm in patients with underlying obstructive lung disease- asthma, COPD USE CARDIOSELECTIVE BETA BLOCKERS with predominant action on beta 1 receptors (metoprolol, atenolol, bisoprolol, nebivolol)- safe in patients with stable obstructive lung disease Combined beta and alpha receptor blockers- carvedilol, labetalol also well tolerated A. Ibutilide- class III antiarrhythmic acute termination of atrial flutter or atrial fib E. Sotalol- class III antiarrhythmic with beta blocker properties- treatment of atrial and ventricular arrhythmias, not used in acute MI

Answer 11

Dihydropyridine calcium channel blockers- amlodipine, nifedipine, mono therapy or in combo with others. Major side effect- headache, flushing, dizziness, PERIPHERAL EDEMA- because of preferential dilation of pre capillary vessels (arteriolar dilation) -> increased capillary hydrostatic pressure and fluid extravasated not into interstitium ACE inhibitors or ARBs- post capillary venodilation- normalize increased cap hydrostatic pressure- reduces risk of peripheral edema in patients taking calcium channel blockers B. Eplerenone- aldosterone antag, K+ sparing diuretic; most frequent side effects are hyperkalemia, increased creatinine, gynecomastia (less so than in those using spironolactone) C and E. Thiazides and loop diuretics (torsemide)- electrolyte abnormalities- hypokalemia, hyponatremia, hypomagnesemia, do NOT cause peripheral edema D and F. ACE inhibitors (ramipril) and ARBs (Valsartan)- cough, hypotension, hyperkalemia, angio edema. Much lower risk of cough and angio edema in those with ARBs. Do not cause peripheral edema

Answer 12

D. increased cAMP in cardiac myocytes the lady probably overosed on beta blocker meds => non-selective blockade of peripheral beta adrenergic receptors => depression of myocardial contractility, bradycardia, varying degrees of AV block. => low cardiac output state. Glucagon for beta blocker overdose. Gs => increase in cAMP => increase intracellular Ca2+ durng muscular contraction => increases heart rate and cardiac contractility

Answer 13

C. atorvastatin and gemfibrozil Statins are first line therapy for most patients with hypercholesterolemia, primary and secondary prevention of acute coronary events. inhibit HMG-CoA reductase- lower total cholesterol, LDL, triglyceride levels primary side effects- myopathy and hepatitis =Statin-associated myopathy- mild muscular pain, resolves with discontinuation of meds. some patients can develop severe myopathy striking elevations in creatine kinase and aoccasional rhabdomyolysis. increased risk with fibrates (gemfibrozil particularly) => impair hepatic clearance of statins => excessive blood levels -can also occur with statin + niacin or +ezetimibe, but to a lesser extent

Answer 14

D. Tolerance development around the clock nitrate administration in any form rapidly results in DEVELOPMENT OF TOLERANCE to nitrates => need an interval of nitrate free time in patients that use daily nitrates. possibly due to decreased vascular sensitivity to nitrates, increased sensitivity to endogenous vasoconstricting agents. usually nitrate free period when least cardiac work (when you sleep) example of pharm drug intxn- rifampin increases metabolism and elimination of warfarin by inducing Cytochrome P450 drug antagonism- labetalol alpha1 and beta => prevents binding of catecholamines to these receptors beta adrenergic blockers prescribed with nitrates to prevent reflex tach, decreased cardiac work differently from how nitrates do that withdrawal- alcohol, opiates, benzos, stimulants, antidepressants

Answer 15

``` C. pulmonary Polyarteritis Nodosa (PAN) segmental, transmural, necrotizing inflammation of MEDIUM-TO-SMALL sized arteries in any organ. kidneys, heart, liver, GI MOST COMMONLY INVOLVED ``` PAN usually spares pulmonary arteries, rarely involves bronchial arteries. inflammation of arteries => ischemia, infarction, hemorrhage bead-like aneurysm formation esp in mesenteric 1/3rd patients cutaneous manifestations- livedo reticularis- purplish network patterned discoloration, palpable purpura (small 1-1.5cm infarcts, sometimes with ulceration)

Answer 16

C. carvedilol patient has decompensated systolic heart failure due to nonischemic cardiomyopathy from chemo. after initial stabilization, patients should be started with beta blockers (carvedilol, metoprolol) with left ventricular systolic dysfunction to improve survival. beta blockade decreases cardiac work by slowing ventricular rate. reduces peripheral resistance (afterload) by decreasing circulating vasoconstricting hormones (norepinephrine, renin, endothelin). do not give beta blockers in those with UNSTABLE HF, introduc beta blockers slowly to avoid impairing cardiac output. other drugs to use: ACE inhibitors, ARBs, aldosterone antagonists- spironolactone, eplerenone ``` A. amiodarone- class III antiarrhythmic, supraventricular and ventricular arrhythmias B, E- calcium channel blockers do not provide any benefit or improve survival in patients with HF from LV systolic dysfunction D- digoxin adjunctive therapy in patients with HF and systolic dysfunction, improves and reduces rate of hospitalization for HF, not shown to improve overall survival F- flecainide, class IC antiarrhythmic, ocasionally for supraventricular arrhythmias in patients with structurally normal heart. doesn't even go here wrt HF G- diuretics (furosemide) first line agents for rapid symptoms contrl in patients with acute congestive HF, not shown to improve long-term survival ```

Answer 17

B. slow diastolic depol cardiac pacemkaer cells undergo DIASTOLIC DEPOL during phase 4 due to slow, inward sodium current. latter parts of phase 4, augmented by transient inward calcium currents. once membrane potential reaches threshold, opening of additional calcium channels triggered => increase in calcium influx begins phase 0 depol verapamil is calcium channel blocker and class IV, treatment of angina, HTN, supraventricular tachyarrhythmias. blocking SA and AV calcium channels, verapamil slows depol tha occurs in phase 0 and later phase 4 => decreases rate of SA node fring and slows AV node conduction ``` A. class I and IV anti arrhythmics raise threshold potential of cardiac fast and slow response tissues respectively (threshold potential is amount of depol needed to initiate action potential) C. Class IB antiarrhythmic- lidocaine, tocainide, mexiletine shorten action potential. mild sodium channel blocking activity and dissociate from sodium channel more rapidly than other class i drugs D. verapamil increase refractory period in nodal tissues by reducing calcium influx, slowing recovery of inactivated calcium channels. Class IA (quinidine) and III (amiodarone) prolong repol and increase refractory period due to K+ blocking E. verapamil decrease intracell calcium available for excitation-contraction coupling within cardiomyocytes => reduce myocardial contractility - harmful in patients with impaired ventricular function tracing shows pacemaker cells, not cardiac muscle cells ```

Answer 18

E. reducing hepatic VLDL production patient's elevated triglyceride level => increased risk of cardiovascular disease LPL hydrolyze triglycerides in chylomicrons and VLDL => release free fatty acids => energy or converted back to triglycerides for storage in adipose tissue. Facilitatestransfer of triglycerides fro lipoproteins to HDL fibrates activate peroxisome proliferator-aactivated receptor alpha [PPAR-alpha] => decrease hepatic VLDL, increase LPL => decrease triglyceride leves by 25-50% and increase HDL by 5-20%. fish oil supplementation high concentrations of omega-3 fatty acids decrease VLDL production an inhibit synthesis of apoB these supplementations lower triglycerides, alternative treatment for patients with moderate hypertriglyceridemia A,C,E- Ezetimibe block intestinal cholesterol absorption. Bile acid-binding resins increase fecal loss of cholesterol derivatives binding bile acids in intestine and disrupting enterohepatic bile acid circulation. PCSK9 (proprotein convertase subtilisin kexin 9) inhibitors monoclonal antibodies that reduce LDL receptor degradation in liver. used in patients with elevated cholesterol, but minimal effect on triglyceride levels B- statins decrease hepatic cholesterol synthesis by inhibiting HMG-CoA reductase. statins have modest effect on triglyceride levels, recommended for patients with mild to moderate hypertriglyceridemia

Answer 19

E. Mitral valve prolapse infective endocarditis complicated by embolic cerebrovascular accident. irregular mass prob vegetation, source of embolus into left MCA. Mitral valve most commonly involved with infective endocarditis. Mitral valve prolapse most common underlying valvular disease predisposing to endocarditis => 25-30% of cases. Microscopic deposits of platelets and fibrin spontaneously in individuals with valvular disease secondary to endocardial injury from turbulent blood flow. deposits colonized by microorganisms during bacteremia episodes (dental extraction) A. bicuspid aortic valve, VSD,PDA, unrepaired tetralogy of fallot. isolated ASD not commonly associated with increased risk of IE => low-pressure dfferential between atria and absence of high-velocity intracardiac flow jets that can damage endocardium B. coronary heart disease => ischemic papillary musle dysfunction with resultant mitral regurg. however, clinical presentation and autopsy most consistent with MVP and IE C. IE rare complication of hypertrophic cardiomyopathy, almost always seen in patients with outflow obstruction. asymmetric ventricular hypertrophy => reduced left ventricular cavity size D. Mitral annular calcification- degeneration and progressive calcium deposition involving fibrous annulus of mitral valve. usually in older adults, annulus not common location for IE F. Rheumatic heart disease historically considered predisposing factor for IE; however, MVP, valvular sclerosis, mechanical valves now more frequent causes in developed nations. on the other hand, rheumatic heart disease most important form of acquired heart disease in children and young adults in developing countries.

Answer 20

C. mitral regurg the wave that was represented was the "v" wave on left atrial pressure tracing, which is left atrial filling. patient presents with nonspecific heart failure symptoms: exertional dyspnea and fatigue (inability to increase cardiac output) and orthopnea- elevated pulm circulation pressures and resulting pulm edema. increase in left atrial systolic pressure- characteristic for mitral regurg "v" wave is normally aboaut 10mm Hg increase due to passive filling of left atrium. if you have mitral regurg, abnormal retrograde blood flow through mitral valve => increases filling of left atrium during systole => elevation of peak v wave, earlier upswing than normally seen A. aortic regurg- elevated LVEDP, decreased aortic diastolic pressure b/c regurg flow from aorta to left ventricle B. aortic stenosis- abnormal pressure gradient to form across aortic vlave due to obstruction blood flow from left ventricle to aorta during systole => left ventricular systolic pressure >> arotic systolic pressure D. mitral stenosis - increase left atrial pressure during diastole due to primary obstruction of left ventricular filling E. tricuspid regurg- increased right atrial and jugular venous pressure; left heart pressures not affected. signs of right heart failure- ascites, increased jugular venous pressure and increased peripheral edema

Answer 21

A. beta myosin heavy chain sudden cardiac death,uncle died of it too => hypertrophic cardiomyopathy. aut dom genetic disorder, mutations in one of several sarcomere genes encoding myocardial contractile proteins- commonly, single-pont missense mutation in genes for beta-myosin heavy chain, myosin-binding protein C. B. dystrophin- X-linked familial dilated cardiomyopathy, Duchenne, Becker C. Marfan- aut dom defect of glycoprotein fibrillin-1 in connective tissue => disproportionaly telong extremities, pectus deformity, scoliosis, eyes (lens dislocation), cardiovascular system- aortic root dilation, aortic regurg D. K+ channels- congenital long QT syndrome; decrease in repolarizing K+ current => prolongation of QT interval => predisposes to torsades de pointes, sudden cardiac death. septal hypertrophy is NOT feature of congenital LQTS E. transthyretin- hereditary form of cardiac amyloidosis. amyloid deposition in myocardium => infiltrative cardiomyopathy- adults with progressive dyspnea, peripheral edema, ascites

Answer 22

A. extensive valve calcification aortic valve stenosis- heart unable to adequately increae cardiac output during exercise => pulm vascular congestion aand reduced mean arterial pressure => dyspnea and lightheadedness chronically lower cardiac output, increased tendency toward fatigue in general AS murmur usually harsh ejectiontype systolic murmur best heard at base of heart in aortic area with radiation to carotid. S2 diminished due to reduced mobility of aortic leaflets calcific degeneration of trileaflet aortic valve most common cause of valvular AS in developed nations. rheumatic heart disease => AS in developing nations, fusion of valve commissures due to repetitive inflammation- usually presents at earlier age, involves mitral valve too hypertrophy of basal IV septum with subaortic obstruction => hypertrophic cardiomyopathy; harsh crescendo-decrescendo murmur over apex and lower sternal border; does NOT radiate to neck, S2 normal infective endcarditis => AR due to inadequate coaptation of aortic leaflets. AR murmur early, decresendo, high pitched, blowing diastolic murmur begins immediately after A2. best heard along left sernal border at 3rd & 4th intercostal spaces myxomatous deg of mitral valve leaflets => mitral valve prolapse => non-ejection click and mid-to-late systolic murmur of mitral regurg

Answer 23

B. glossopharyngeal patient prob has carotid sinus hypersensitivity- pressure on carotid sinus by tight shirt collar carotid sinus baroreceptors important in bp control, arterial wall stretch as indicator of systemic bp. carotid sinu reflex- afferent limb from barorecepors in sinus, travels to medullary centers via Hering nerve- branch of CN IX => increase in parasymp output, withdrawal of symp output to heart and peripheral vasculature => decreased bpperipheral vasodilation) and decreased cardiac output [decreased contractility/stroke volume and heart rate]. in sensitive individuals = severe bradycarda, hypotension, sncope. A,C,D- XI, XII, V; XI- SCM and trapezius; XII- muscles of tongue; V- facial sensation, muscles of mastication E- X afferent limb for aortic arch baroreceptors, efferent limb for carotid sinus reflex

Answer 24

B. LCX coronary domiance- whatever supplies PDA RCA- right dom LCX- left dom both-codom distal embolization => AV block (AV node) AV nodal artery arises from posterior descending artery- person has left dominant => LCX A. LAD anterior interventricular groove, supplies anterior part of septum, and anterior wall of left ventricle, does not supply AV node C. Left diagonal- LAD, supplies lateral wall of left ventricle D. RCA- in patients with right dom or codom circulation e. right marginal- from right coronary artery and supplies blood to free wall of right ventricle

Answer 25

C. tricuspid right sided endocarditis involving the tricuspid valve commonly occurs in IV drug users, mostly due to staph aureus. tricuspid regurg => early systolic murmur heard over left lower sternal border accentuated by inspiration