UWorld Cardio I

Question 1

Person had myocardial infarction 1 year ago, you are given histo section of an enlarged ventricle. The type of collagen seen on the section is similar to the collagen found in what other tissue?
A. basement membrane
B granulation tissue
C. hyaline cartilage
D. nucleus pulposus
E. tendon

Answer 1

7d after an acute MI, you get type III collagen with granulation tissue. However, after that it is replaced by type 1 as infarct matures.

Type I- dermis, bone, tendons, ligaments, dentin, cornea, blood vessels & scar tissue- associated with osteo imperfecta

Type 2- cartilage, vitreous humor & nucleus pulposus

Type 3- skin, lungs, intestines, blood vessels, bone marrow, lymphatics & granulation tissue- associated with EDS types 3 & 4

Type 4- basement membrane- alport syndrome

Question 2

What kind of sugar can S aureus ferment?

Answer 2

Mannitol

Question 3

A girl comes in with short stature, short and thick neck, broad chest, shortened fourth metacarpals. What kind of heart anomaly do you expect to find? What is this condition?

Answer 3

Bicuspid aortic valve, Turner

• associated with coarctation of aorta
• nonstenotic bicuspid aortic valve- early systolic, high frequency click heard over right 2nd interspace- calcifies, progressive valvular dysfunction => aortic stenosis and associated murmurs
• very susceptible to infectious endocarditis due to abnormal leaflet and turbulent flow.

Question 4

List the murmurs heard with the following: ASD, VSD, Mitral Stenosis, PDA

Answer 4

ASD: fixed S2 split
VSD: holosystolic murmur at left lower sternal border
Mitral Stenosis: rheumatic heart isease, mid-diastolic, low-pitched, rumbling murmur begins with opening snap
PDA: continuous machinelike murmur systole and diastole; common in premature infants esp in those with respiratory distress syndrome, also with coarctation of aorta in infants

Question 5

child presents with cyanotic spells that improve with squatting, prominent right ventricular impulse, systolic murmur

Answer 5

Tetralogy of Fallot
-abnormal neural crest cell migration => anterior and cephalad deviation of infundibular septum during embryologic development => malaligned VSD and overriding aorta.

1. VSD
2. overriding aorta over right and left ventricles
3. right ventricular outflow tract obstruction
4. RVH

cyanosis from right to left shunt in patients with worsening of right ventricular outflow tract obstruction => harsh systolic ejection murmur over mid to left upper sternal border- subvalvular, pul valve stenosis or supravalvular narrowing in main pulmonary artery

squatting increases peripheral systemic vascular resistance = afterload => decrease right to left shunting, improving cyanosis

Question 6

Discuss the embryological origins of the following:

1. Transposition of Great Vessels
2. anomalous pulmonary venous return
3. Coarctation of aorta
4. ASD/VSD/Eisenmenger

Answer 6

1. abnormal leftward looping of primitive heart
2. blood from pulmonary and systemic venous systems flow into right atrium => right atrial and ventricular dilation, obligatory right to left shunting
3. Aortic arch constriction => coarctation of aorta, distal to left subclavian artery- juxtaductal; brachial femoral pulse delay and blood pressure discrepancy between upper and lower extremities
4. Failed fusion of superior and inferior endocardial cushions => AV septum and valve defects (mitral, tricuspid) => ASD/VSD, left to right shunting; increased right sided blood flow => pul HTN, reversal of blood flow through shunt, development of late cyanosis- Eisenmenger

Question 7

deposition of amyloid in cardiac atria, what is the amyloid made of?
A. calcitonin
B. prolactin
C. amylin
D. beta amyloid protein
E. immune globulin light chain
F. natriuretic peptide

Answer 7

localized amyloidosis confined to cardiac atria- isolated atrial amyloidosis = IAA = deposition of abnormally folded (beta pleated sheet conformation) ATRIAL NATRIURETIC PEPTIDE-derived proteins. incidence of this increased with age, >90% in ninth decade
*senile cardiac amyloidosis which may increase risk of afib

A- abnormally folded calcitonin derived peptides- localized amyloidosis of thyroid gland in patients with medullary carcinoma of thyroid
B- prolactin derived proteins- pituitary gland
C- amylin = islet amyloid protein, patients with localized pancreatic amyloidosis; >90% patients with type II diabetics in pancreatic islets
D- beta amyloid core of cerebral plaques of Alzheimer’s; localized amyloid deposits in walls of cerebral blood vessels of Alzeimer’s patients and those with cerebral amyloid angiopathy
E- lamba-light chains and their fragents- primary systemic amyloidosis- monoclonal b cell proliferations like multiple myeloma => SYSTEMIC (not local) amyloid deposition involving heart, skin, tongue, GI tract, kidney, peripheral nerves; bence jones proteins may also be found in serum or urine

Question 8

Pathway of arteries regarding the iliac and lower

Answer 8

Internal and external iliac arteries
exteral iliac –> inferior epigastric artery, takes off immediately proximal to inguinal ligament; once external iliac passes the inguinal ligament, it becomes the common femoral artery
inferior epigastric artery –> superioly and medially up abdomen, blood supply to lower anterior abdominal wall
external iliac –> deep circumflex iliac artery –> more lateral, supplies lower abdomina lwall

Question 9

Formulae for cardiac output (there are 3 of them)

Answer 9

CO = SV*HR
CO = O2 consumption/arteriovenous O2 difference
CO = (135*BSA)/[(13*Hb)*(SaO2-SvO2)]

Question 10

What is the region called where the frontal, parietal, temporal, sphenoid bones meet, and what artery (and what does it branch off of) comes from it?

Answer 10

Pterion- thin in this region, huge risk of fractures with trauma
middle meningeal artery => epidural hematoma => increased intracranial pressure/Cushing reflex, brain herniation (uncal with CN III palsy), death

branch of maxillary artery, which itself isa terminal branch of the external carotid artery- enters the skull at he foramen spinosum, supplies dura mater and periosteum

Question 11

Discuss the facial, occipital, sphenopalatine branches of the external carotid artery.

Answer 11

Facial- mandible anterior to the insertion of masseter to supply oral, nasal, buccal regions
Occipital- opposite facial artery from external carotid- courses posteriorly- posterior scalp, SCM muscles
Sphenopalatine- branch of third part of maxillary artery, nasal mucosa; anastomoses with branches of ophthalmic and facial within anterior prat of nasal septum- Kiesselbach’s plexus- nosebleeds

Question 12

Discuss EKG localizations with the following ST elevations in the leads:
V1-V2
V3-V4
V5-V6
I, aVL
II, III, aVF
V7-V9/V1-V3, R waves

Answer 12

V1-V2- LAD- anterioseptal
V3-V4- anteroapical (distal LAD)
V5-V6- Anterolateral- (LAD or LCX)
I, aVL- LCX, lateral
II, III, aVF- RCA, inferior
V7-V9/ST depression in V1-V3, tall R waves- posterior, PDA

Question 13

23 yo recurrent severe nosebleeds, has pink spider like lesions on oral and nasal mucosa, face,arms. Patient most likely has what?

Answer 13

Osler-Weber-Rendu = hreditary hemorrhagic telangietasia- aut dominat inheritance of congenita ltelangiectasias to skin and mucous membranes- lips, oronasopharynx, respiratory tract, GI, urinary; rarely do these occur in the brain, liver, spleen
rupture of telangectasias => epistaxs, GI bleeding, hematuria

Question 14

Discuss characteristics of the following diseases:
Von Recklinghausen's
Neurofibromatosis Type II
Sturge-Weber
Von Hippel-Lindau
Tuberous Sclerosis

Answer 14

1. Von Reck- NF-1- inherited peripheral tumor syndrome; neruofibromas, optic nerve gliomas, lisch nodules (pigmented nodules of iris), cafe au lait spots- hyperpigmented cutaneous macules
2. NF-2- aut dom bilateral cranial nerv VII schwannomas and multiple meningiomas
3. Sturge-Weber- encephalotrigeminal angiomatosis- cutaneous facial angiomas, leptomeningeal angiomas- mental retardation, seizures, hemiplegia, skull radiopacities; skull radiographs show tram-track calcifications
4. VHL- rare aut dom - capillary hemangioblastomas in retina and/or cerebellum, congenital cysts or neoplasms in kidney, liver, pancreas; increased risk for potentially bilateral renal cell carcinoma
5. Tuberous sclerosis- kidney, liver,pancreatic cysts, CNS involvement manifests as cortical and subependymal hamartomas; aut dom- cutaneous angiofibromas- adenoma sebaceum, visceral cysts, variety of other hamartomas, renal angiomyolipomas nadcardiac rhabdomyomas; seizures major complication

Question 15

Add cortisol alone, nothing happens in the blood vessels. Add cortisol and norepinephrine, and there is an increased effect (as compared to norepi without cortisol). What term best describes this response to cortisol?
A. additive effect
B. altered metabolism
C. permissiveness
D. synergistic effect
E. tachyphylaxis

Answer 15

permissiveness- one hormone allows another to exert its maximal effect- cortisol upregulates alpha 1 adrenergic receptors on vascular smooth muscle; low glucocorticoid levels can contribute to hypotensive crisis by decreasing vascular responsiveness to angiotensin II and norepi.
A and D- combo of 2 drugs with similar actions- synergistic or additive
B- certain drugs inhibit P450 cyt ox syste => decrease metabolism of other drugs that are metabolized this way => additive or synergistic responses
E- decreased drug responsiveness in short period following one or more doses- rapidly developing tolerance

Question 16

Repeated episodes of palpitations that start and stop abruptly. abnormal conduction pathway bypasses AV node. which part of the EKG most likely affected during normal sinus rhythm?

Answer 16

Recurrent temporary arrhythmias, bundle of Kent- recurent temporary tachyarrhythmias due to atrioventricular re-entry circuit involving AV node and pathway- Wolff-Parkinson-White pre-excitation syndrome, most common re-entry circuit responsible for paroxysmal, narrow QRS complex tachycardia [supraventricular]
- accessory pathway pre-excites ventricles ahead of normal conduction pathway- pre-excitation => shortened PR interval (

Question 17

62 yo patient HTN had sinus bradycardia, PR interval prolongation. What medication would be most effective in lowering HTN without worsening ECG?

Answer 17

Nifedipine- dihydropyridine- arterial smooth muscle, vasodilation WITH LITTLE OR NO EFFECT NO CARDIAC CONDUCTION OR CONTRACTILITY
Non-dihydropyridines- verapamil, diltiazem- affect myocardium- slow heart rate and reduce contractility
dihydropyridines –> reflex tachycardia in response to peripheral vasodilation, HTN with resting bradycardia
Verapamil- nondihydropyridine- depressive effect on cardiac conduction
Diltiazem- myocardium, peripheral arterial beds; both of the nondihydropyridines can worsen bradycardia and AV block
Metoprolol- cardioselective beta blocker with negative chronotropic and dromotropic (decreased AV conduction) effects
Sotalol- class III antiarrhythmic drug with significant beta blocking properties- worsen bradycardia and AV conduction defects

Question 18

Discuss the effects of the different Class I A, B, C antiarrhythmics.

Answer 18

Class IA: quinidine, procainamide, disopyramide- intermediate strength in inhibiting phase 0 depolarization- prolonged AP length

IB: lidocaine, mexiletine- weak inhibition of phase 0 depol, shortened AP length

IC: flecainide, propafenone- strong inhibition of phase 0 depol, no change in AP length
lidocaine: block sodium channels in depolarized cardiac myocytes. shorten phsae 3 repol => decrease action potential duration

Question 19

Discuss the following drugs: Adenosine, Digoxin, Propranolol

Answer 19

Adenosine- activate K+ channels, increases conductance K+ via interaction with A1 receptors on surface of cardiac cells => membrane hyperpol => transient slowing of sinus rate, increase in AV nodal conduction delay; Adenosine does NOT modulate ventricular myocyte action potential

Digoxin- increasing vagal output to AV node and conduction system- slowing conduction; does not alter ventricular myocyte action potential, but can increase intracell calcium in ven myocytes => increased cardiac contractility

Propranolol: beta adrenergic blocking agent slows conduction through AV node and prolongs phase 4 depol in cardiac pacemaker cells; do not affect ventricular myocyte AP; primary site on AV node, with automaticity

Question 20

A 65 yo man has isolated diastolic heart failure. What would be expected of:
Left ventricular end-diastolic volume
Left ventricular end-diastolic pressure
Left ventricular ejection fraction
(increased/decreased/normal)?

Answer 20

LVEDP- increased
LVEDV- normal
LVEF- normal

Diastolic heart failure- common cause of acute decompensated HF.
-normal LVEF >50%, normal EDV, in presence of INCREASED LV filling pressures
-this occurs whenever you have REDUCED LV COMPLIANCE
Ex. Impaired myocardial relaxation from ischemia, increased intrinsic ventricular wall stiffness from amyloid deposition
Patient prob had long-standing HTN -> LV wall hypertrophy -> impair myocardial relaxation and INCREASE INTRINSIC WALL STIFFNESS

LV diastolic pressure- blood volume in LV cavity AND COMPLIANCE of LV
AT A GIVEN LVEDV -> reduced ventricular compliance -> increased LVEDV
Shift in pressure-volume curve -> upward and to the left

Worsening of diastolic dysfunction -> decompensation when LVEDP -> pulmonary edema and dyspnea; cardiac reserves diminish as stiffened ventricle less effective at accommodating increased blood volumes

Question 21

Talk briefly about systolic heart failure.

Answer 21

The pressure volume curve for systolic HF completely shifts to the right
Caused by primary decrease in myocardial contractility than compliance –> reduced LVEF (

Question 22

12 mo boy has temp 101F, bp 92/45, pulse 110, resp 25/min; erythema and swelling of nasal mucosa and nasal discharge- normal upper resp infection. Cardiac auscultation findings at left sternal border. Most likely diagnosis (this was audio)
A. Aortic aneurysm
B. Aortic coarctation
C. ASD
D. MVP
E. PDA

Answer 22

Audio showed continuous murmur with inspirations splitting of S2. Symptoms of PDA relate to degree of L->R shunting
Patient prob has small PDA since detected incidentally.
Continuous murmur best heard in the left infraclavicular region with max intensity at S2
Greatest risk for PDA are those prematurely born and those with cyanosis congenital heart disease
A. Ascending aortic aneurysm- aortic regurgitate -> early diastolic murmur as opposed to continuous murmur
B. Coarctation of aorta- continuous murmur because of large collaterals vessels, but much less common than PDA; would also see differing blood pressure or pulse delay between upper and lower extremities, would be evident on physical exam.
C. Small ASD can cause continuous murmur in rare instances, only when associated with mitral valve obstruction due to elevated pressure gradient across atria = Lutembacher syndrome. Less common than PDA
D. MVP- mid systolic click and mid-to-late systolic murmur

Question 23

53 yo man has progressive dyspnea, increased antelopes terror diameter of his chest. Auscultation shows decreased breath sounds, scattered wheezes throughout lungs. Dilation of right ventricle and increased CVP. Absence of peripheral edema via what compensatory mechanism?
A. Dec capillary perm
B. Dec circulating aldosterone levels
C. Dec interstitial fluid pressure
D. Inc plasma oncotic pressure
E. Inc tissue lymphatic drainage

Answer 23

E. Inc tissue lymphatic drainage
Person prob has COPD caused by emphysema
RV dilation and inc CVP –> Cor pulmonale 2ary to COPD
Excess accum of transduction fluid in interstitial tissues:
1. Elevated cap hydrostatic pressure- dihydropyridine calcium channel blockers [abnormal arteriolar dilation], impairments in venous return [venous thrombosis and right sided heart failure]
2. Dec plasma oncotic pressure- reduces interstitial fluid returning to circulation via capillary bed venules; decreased albumin- nephrotic syndrome- liver disease and malnutrition
3. sodium and water retention- increase in intravascular volume- increase cap hydrostatic pressure; salt and water retention with acute kidney injury, chronic kidney disease, congestive heart failure
4. Lymphatic obstruction- impairing removal of excess interstitial fluid; filariasis, invasive malignancies, iatrogenic- surgical lymph node dissection and radiation therapy
Moderate increases in cap fluid transduction can be offset by compensatory increase in tissue lymphatic drainage that occurs due to increased interstitial fluid pressure

Question 24

57 yo dies 30min after severe chest pain while driving to ED. He had been complaining of intermittent short lived episodes of chest pain over last 2 mo. HTN, type 2 diabetes [insulin dep], Hypercholesterolemia, patient not compliant with meds or follow up. Strong family history of heart disease and type 2 diabetes mellitus. Autopsy shows occlusion of mid right coronary artery. What most likely caused his death?
A. A fib
B. Cardiac free wall rupture
C. Embolic stroke
D. Severe contractile dysfunction
E. V fib
F. Ventricular septal rupture

Answer 24

Coronary artery disease causes acute MI due to thrombotic occlusion of RCA- large atheromatous plaque, significant stenosis with superimposed thrombosis -> lumen occlusion

SUDDEN CARDIAC DEATH- abrupt cessation of organized cardiac activity with hemodynamics collapse- inability to maintain adequate tissue perfusion- malignant ventricular arrhythmia a- sustained ventricular tachycardia/fibrillation- related to coronary heart disease in ~70% patients
V fib most frequent mechanism of SCD in first 48hrs after acute MI electrical instability due to lack of perfusion in ischemic myocardium
A. A fib- can occur in acute MI, but does NOT lead to SCD
B and F. Ventricular septal rupture- most common with LAD occlusion; cardiac free wall rupture- mechanical complications of acute MI- cardio genie shock and/or sudden death- 3-7d after initial MI episode; autopsy- hemopericardium, perforating wound in wall of left ventricle
C. Embolism stroke- LV mural thrombus from area of infarct end and a kinetic myocardium- usually takes several days to form, does not lead to SCD
D. LV contractile dysfunction ->cardiogenic Shock with multi organ systemic failure and death- large anterior MI due to abrupt occlusion of proximal LAD >50% myocardium, VF leading cause of SCD in these patients

Question 25

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 25

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

Question 26

46 yo with 30 pack year smoking history develops right leg pain and swelling, diagnosed with lower extremity DVT, started on IV heparin, develops right sided weakness and facial droop. CT shows left MCA stroke- what would you expect to see on physical examination?
A. Diastolic decrescendo murmur decreases following amyl nitrite inhalation
B. Ejection type systolic murmur increases on standing
C. Pre systolic murmur disappears with atrial fib
D. Split of S1 accentuated on inspiration
E. Split of S2 that does not change with respiration

Answer 26

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

Question 27

63 yo presents with severe dyspnea, Orthoptera, fatigue, had MI 6mo ago, not compliant with meds since. 170/100, 100bpm, auscultation- crackles at lung bases, S3 gallop, II/VI holosystolic murmur over apex. Treated with diuretics and vasodilator a, patient’s condition improves significantly. No appreciable gallops or murmurs heard the next morning. Murmur prob explained by what?
A. Thickened and deformed mitral valve cusps
B. Heavily calcified mitral annulus
C. Increased flow rate through aortic valve
D. Ruptured chords tendineae
E. Functional mitral regurgitation

Answer 27

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

Question 28

67 yo history of progressive dyspnea. Orthopnea, swelling of ankles, does not smoke or consume alcohol. PMH significant Hypercholesterolemia and recurrent chest pain. What would be increased?
A. Cardiac output
B. Renal perfusion
C. Arteriolar resistance
D. Mixed venous oxygen content
E. Lung compliance

Answer 28

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

Question 29

71 yo woman with history CHF, fatigue and muscle weakness. 3wks ago, started on med to treat heart failure. Lab veal shows serum K+ of 2.2 mEq/L (normal is 3.5-5). Physician adds another med, fatigue and muscle weakness resolve. New med acts on which nephron segment?
A. PCT
B. Descending limb Henle
C. Thick ascending Henle
D. DCT
E. Collecting duct

Answer 29

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

Question 30

new drug developed for CHF, dilates arterioles and veins, promotes diuresis. Most likely an analog to which of the following?
A. Endorphin
B. TGF-beta
C. Brain Natriuretic peptide
D. Bradykinin
E. Endothelin
F. Angiotensin II

Answer 30

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)

Question 31

10 yo Caucasian male complains occasional headaches, nose bleeds, difficulty walking or running uphill due to muscle weakness. Pulsatile vessels palpable along patient's ribs. Most likely suffers from:
A. Primal-type ASD
B. Secundum-type ASD
C. VSD
D. PDA
E. Coarctation of aorta
F. Tetralogy of Fallot

Answer 31

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

Question 32

55 yo HTN coronary artery disease, adding verapamil to regimen, verapamil can be used in patients with systemic HTN due to vasodilator you properties, also affects cardiac contractility but minimal effect on skeletal muscle. What property of skeletal muscle is responsible for resistance to med?
A. Calmodulin-independent excitation-contraction coupling
B. Decreased troponin C affinity to intracellular calcium
C. Elaborate T-tubular system
D. No dependence on extracellular calcium influx
E. No internal automaticity

Answer 32

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

Question 33

50 yo man brought to ER with severe dizziness and confusion. Episode of chest pain and took several tablets of nitroglycerin. Meds: daily aspirin for heart attack prevention, occasional acetaminophen for headaches, tadalafil for erectile dysfunction. BP 50/20, HR 120. Which cellular change most likely responsible for patient's symptoms?
A. Receptor down reg
B. Gs protein phosphorylation
C. Cyclic GMP accumulation
D. Tyrosine kinase over activity
E. Enhanced phospholipid metabolism
F. Tolerance development

Answer 33

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.

Question 34

60 yo man comes in with chest pain, intermittent squeezing substernal pain over last 3 days, now sustained. Moderate COPD, bp 145/90, pulse 93, pulse ox 98%; no heart murmurs, lungs clear to auscultation. ECG- sinus rhythm with 2mm St elevation in leads II, III, aVF, cardiac troponin I levels elevated. Most appropriate treatment?
A. Ibutilide 
B. Metoprolol
C. Nadolol
D. Propranolol
E. Sotalol

Answer 34

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

Question 35

Relatively healthy 77 yo man comes in, has high blood pressure and no other problems. Started on bp med that causes bilateral leg swelling, 2+ pitting lower extremity edema. Everything else is fine. Which drug was likely prescribed?
A. Amlodipine
B. Eplerenone
C. Hydrochlorothiazide
D. Ramipril
E. Torsemide
F. Valsartan

Answer 35

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

Question 36

40 yo female history depression and hypertension brought to ER, hypotensive and bradycardic, she’s given IV glucagon, her condition improves. What intracellular change responsible for her improvement?
A. increased syn release of glutamate
B. decreased cAMP in vascular smooth muscle
C. decreased DAG in vascular smooth muscle
D. increased cAMP in cardiac myocytes
E. increased IP3 in cardiac myocytes

Answer 36

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

Question 37

68 yo 6 week history of muscle pain and fatigue. achy pain not related to activity. nothing has helped. history significant for HTN, mixed hyperlipidemia, coronary artery disease with acute MI 2 years ago. diffuse tenderness in proximal muscles of upper and lower extremities. Serum creatine kinase activity elevated. what drug combo most likely responsible for patient's condition?
A. Atorvastatin and cholestyramine
B. Atorvastatin and ezetimibe
C. Atorvastatin and gemfibrozil
D. Gemfibrozil and ezetimibe
E. Niacin and ezetimibe
F. Niacin and gemfibrozil

Answer 37

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

Question 38

60 yo Caucasian male diagnosed with exertional angina. Metoproloo, isosorbide dinitrate, aspirin. He takes dinitrate early in morning and again in afternoon, but he does not take an evening dose. does this to decrease what?

A. Pharmacokinetic drug interaction
B. Pharmacodynamic drug antagonism
C. Effect potentiation
D. Tolerance development
E. Withdrawal symptoms
F. Drug noncompliance

Answer 38

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

Question 39

32 yo Caucasian has polyarteritis nodosa, which of the following arteries would be spared?
A. renal
B. coronary
C. pulmonary
D. mesenteric
E. cutaneous
F. hepatic

Answer 39

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)

Question 40

68 yo several weeks of progressive exertional dyspnea and lower extremity edema. PMH non-Hodgkin lymphoma, in remission after 8 years of chemo. BP 126/76, pulse 88/min. bibasilar lung crackles, 1+ bilateral lower extremity edema. biventricular dilation, left ventricular ejection fraction of 35%. stress myocardial perfusion scan negative for inducible ischemia. after initial stabilization, long term use of which med would improve survival in patient?
A. amiodarone
B. amlodipine
C. carvedilol
D. digoxin
E. diltiazem
F. flecainide
G. furosemide

Answer 40

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

Question 41

EKG tracing shows cardiac pacemaker cell. Which effect would verapamil most likely have on these cells?
A. lower threshold potential
B. slow diastolic depol
C. shorten action potential
D. reduce refractory period
E. decrease excitation and contraction coupling

Answer 41

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

Question 42

36 yo man abnromal lipid panel during employee wellness testing. no prior medical problems, no meds. sotware technician, sedentary lifestyle. he eats mostly fast foods, rarely exercises, drinks 2-3 cans of beer daily. BMI 31 kg/m^2. results:
total cholesterol: 290 mg/dL [ref: 150-240]
HDL: 45 mg/dL [30-70]
LDL 110 mg/dL [

Answer 42

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

Question 43

36 yo woman brought to ED with sudden-onset right-sided weakness and speech difficulty. last 3 weeks, experienced progressive fatigue, malaise, low-grade fevers. dental extraction 5 weeks ago which was uncomplicated. patient’s PMH insignificant. she works as receptionist at legal foirm, never traveled outside country. does not use tobacco, alcohol or illicit drugs. dies 2 hrs later. gross autopsy shows large, irregular mass attached to atrial surface of a valve. which underlying condition most likely predisposed patient to presenting disease?

A. ASD
B. CAD
C. Hypertrophic cardiomyopathy
D. Mitral annular calcification
E. Mitral valve prolapse
F. Rheumatic heart disease

Answer 43

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.

Question 44

54 yo woman exertional dyspnea an dfatigue, short of breath walking 2 blocks, troublebreathing at night ad needs to sleep using 2-3 pillows. left heart catheterization, findings show increased left atrial pressures peaking around the dicrotic notch. what is the most likely diagnosis?

A. aortic regurg
B. aortic stenosis
C. mitral regurg
D. mitral stenosis
E. tricuspid regurg

Answer 44

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&raquo_space; 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

Question 45

16 yo suddenly collapses and dies despite resuscitation. no sig med history, but his family history significant for uncle who died suddenly at age 20. autopsy shows left ventricular hypertrophy predom affecting IV septum. no valvular abnormalities. if boy died of an inherited condition, which protein was most likely affected by relevant mutation?

A. beta myosin heavy chain
B. dystrophin
C. fibrilin-1
D. IK membrane K+ channel
E. Transthyretin

Answer 45

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

Question 46

75 yo worsening dyspnea and fatigue on exertion over last 6 mo. severe lightheadedness during physical activity. harsh, ejection-type systolic murmur at base of heart, radiating to neck. S2 diminished in intensity. S4 heard at cardiac apex. which of the following most likely causing patient’s heart condition?

A. extensive valve calcification with impaired leaflet mobility
B. fusionof valve commissures due to repetitive inflammation
C. hypertrophy of basal IV septum with subaortic obstruction
D. infectious vegetations attached to valve cusps
E. myxomatous valve degeneration with leaflet prolapse

Answer 46

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

Question 47

65 yo multiple episodes of lightheadedness, during 2 episodes he passed out; bp 70/40, pulse 45/min. HTN, diet-controlled diabetes mellitus. lifetime nonsmoker, drinks alcohol on social occasions. normal physican exam shows 125/72 and 76/min. stim of afferent sensory fibers in which nerve most likely responsible for patient’s symptoms?

A. accessory
B. glossopharyngeal
C. hypoglossal
D. trigeminal
E. vagus

Answer 47

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

Question 48

66 yo man sudden onset chest pain and dyspnea. ST elevation MI, left and right coronary arteries- left dominant circulation with normal left main coronary artery. stenotic region identified in one of the other coronary vessels. percutaneous intervention on culprit lesion, small thromus detaches and moves forward => obstruction of artery supplying AV node. atherosclerosis of which artery most likely caused MI?

A. LAD
B. LCX
C. Left diagnoal
D. RCA
E. Right marginal

Answer 48

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

Question 49

33 yo smokes and uses IV drugs => blood cultures staph aureus. what valve is most likely affected/where can it be auscultated?

A. aortic
B. pulmonic
C. tricuspid
D. mitral

Answer 49

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