UWorld Questions Flashcards
What are the causes for dilated cardiomyopathy (dilatation of all 4 cardiac chambers, resultant decrease in contractility, systolic dysfunction)?
- viral myocarditis (Coxsackie B)
- peripartum cardiomyopathy
- alcohol abuse
- chronic supraventricular tachycardia
- cardiotoxic drugs – doxorubicin
- thiamine deficiency (wet beriberi)
0-4 hours after a MI
no visible changes
4-12 hours after a MI
early coag necrosis, wavy fibers with long, elongated myocytes
12-24 hours after a MI
early coag necrosis, myocyte hypereosinophilia with pyknotic nuclei
1-3 days after a MI
coagulation necrosis (loss of nuclei and striations), prominent neutrophilic infiltrate
3-7 days after a MI
- 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)
7-10 days after a MI
- robust phagocytosis of dead cells by macrophages
- beginning formation of granulation tissue
10-14 days after a MI
well-developed granulation tissue with neovascularization
death at this point is most likely due to ventricular arrhythmia
2 weeks to 2 months after a MI
progressive collagen deposition and scar formation
What is the pathogenesis of Syndenham chorea as it relates to the heart?
- 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
What disorder is associated with early onset dementia
Trisomy-21
Most common cause of death in a patient hospitalized for MI
ventricular failure (cardiogenic shock)
Most frequent complication of fibrinolytic therapy for an MI?
bleeding, the most dangeous being intracranial hemorrhage
Presentation and risk factors for having a LV rupture post MI?
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
What is a complication of coarctation of the aorta
CoA can also present with berry aneurysms which are susceptible to rupture (intracranial hemorrhage) because of the high pressures proximal to the coarc
What is a complication of ASDs and VSDs?
parodoxical embolism as a result of late onset right to left shunt can lead to thromboembolism
What is the role of active peripheral inflammation in atherosclerosis?
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
S. aureus in IV drug users?
acute right-sided bacterial endocarditis with septic embolization to the lungs
Signs of left-sided heart failure?
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
Mediators of coronary artery vasodilation and where they act?
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
Conditions of histamine being a vasodilator?
Serotonin?
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
Nitroprusside’s effect on the heart
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
Signs of aortic regurgitation and the etiology?
“water-hammer pulse” caused by a widened pulse pressure; increased LV stroke volume
- head bobbing (de Musset sign)
- carotid and femoral pulsations
What happens to the carotid pulse with aortic stenosis?
pulsus parvus et tardus –> delayed, prolonged carotid pulse
What is the mechanism of ivabradine?
Ivabradine selectively inhibits the funny sodium channels prolonging phase 4 and slowing the SA node firing rate; no effect on contractility
