UWorld Questions

Question 1

What are the causes for dilated cardiomyopathy (dilatation of all 4 cardiac chambers, resultant decrease in contractility, systolic dysfunction)?

Answer 1

• viral myocarditis (Coxsackie B)
• peripartum cardiomyopathy
• alcohol abuse
• chronic supraventricular tachycardia
• cardiotoxic drugs – doxorubicin
• thiamine deficiency (wet beriberi)

Question 2

0-4 hours after a MI

Answer 2

no visible changes

Question 3

4-12 hours after a MI

Answer 3

early coag necrosis, wavy fibers with long, elongated myocytes

Question 4

12-24 hours after a MI

Answer 4

early coag necrosis, myocyte hypereosinophilia with pyknotic nuclei

Question 5

1-3 days after a MI

Answer 5

coagulation necrosis (loss of nuclei and striations), prominent neutrophilic infiltrate

Question 6

3-7 days after a MI

Answer 6

• disintegration of dead neutrophils and myofibers,
• macrophage infiltration

LV rupture is likely to occur because coagulative necrosis, neutrophil infiltration, and enzymatic lysis have substantially weakened the infarcted myocardium (10% of cases)

Question 7

7-10 days after a MI

Answer 7

• robust phagocytosis of dead cells by macrophages

- beginning formation of granulation tissue

Question 8

10-14 days after a MI

Answer 8

well-developed granulation tissue with neovascularization

death at this point is most likely due to ventricular arrhythmia

Question 9

2 weeks to 2 months after a MI

Answer 9

progressive collagen deposition and scar formation

Question 10

What is the pathogenesis of Syndenham chorea as it relates to the heart?

Answer 10

• 1-8 months after infection by Group A Strep
• caused by anti-streptococcal antibodies that cross react with the basal ganglia
• restlessness and involuntary jerking
• high risk of chronic valvular disease

Question 11

What disorder is associated with early onset dementia

Answer 11

Trisomy-21

Question 12

Most common cause of death in a patient hospitalized for MI

Answer 12

ventricular failure (cardiogenic shock)

Question 13

Most frequent complication of fibrinolytic therapy for an MI?

Answer 13

bleeding, the most dangeous being intracranial hemorrhage

Question 14

Presentation and risk factors for having a LV rupture post MI?

Answer 14

presentation - the free wall rupture causes cardiac tamponade which greatly restricts ventricular filling during diastole; as the pressure increases in the pericardial cavity venous return to the heart is reduced leading to systemic hypotension

female, >60, pre-existing hypertension, absence of LV hypertrophy; rupture is more likely if this is the patients first MI – previous MIs are protective because of the fibrosis

Question 15

What is a complication of coarctation of the aorta

Answer 15

CoA can also present with berry aneurysms which are susceptible to rupture (intracranial hemorrhage) because of the high pressures proximal to the coarc

Question 16

What is a complication of ASDs and VSDs?

Answer 16

parodoxical embolism as a result of late onset right to left shunt can lead to thromboembolism

Question 17

What is the role of active peripheral inflammation in atherosclerosis?

Answer 17

Activated macrophages in an atheroma contribute to collagen degradation by secreting metalloproteases which can destabilize the mechanical integrity of the plaque – potentially promote rapid coronary occlusion

Statins decrease this inflammation

Question 18

S. aureus in IV drug users?

Answer 18

acute right-sided bacterial endocarditis with septic embolization to the lungs

Question 19

Signs of left-sided heart failure?

Answer 19

SPECIFIC: orthopnea - supine dyspnea that is relieved by sitting up

non-specific: exertional wheezing (cardiac asthma - exercise increases venous return, but failing left heart can’t keep up), productive cough (pink frothy sputum is due to the rupture of the bronchial veins), and chest tightness

Question 20

Mediators of coronary artery vasodilation and where they act?

Answer 20

Large arteries and pre-arteriolar vessel: NITRIC OXIDE; synthesized from arginine and oxygen (by eNOS) in endothelial cells causing relaxation of smooth muscle by increasing the levels of cGMP by acting on guanylyl cyclase

small coronary arterioles: ADENOSINE as a byproduct of ATP metabolism

Question 21

Conditions of histamine being a vasodilator?

Serotonin?

Answer 21

released primarily from mast cells when there is tissue damage; increasing cap permeability causing edema

produced by gut neuroendocrine cells, platelets, and serotonergic neurons in the CNS; has both constrictor and vasodilator effects

Question 22

Nitroprusside’s effect on the heart

Answer 22

NP is a arterial and venous vasodilator - it decreases the preload and the afterload; but it is balanced and the stroke volume is maintained; contractility is unchanged

Question 23

Signs of aortic regurgitation and the etiology?

Answer 23

“water-hammer pulse” caused by a widened pulse pressure; increased LV stroke volume

• head bobbing (de Musset sign)
• carotid and femoral pulsations

Question 24

What happens to the carotid pulse with aortic stenosis?

Answer 24

pulsus parvus et tardus –> delayed, prolonged carotid pulse

Question 25

What is the mechanism of ivabradine?

Answer 25

Ivabradine selectively inhibits the funny sodium channels prolonging phase 4 and slowing the SA node firing rate; no effect on contractility