Robbins Heart Flashcards

1
Q
  1. What predicts the severity of the clinical presentation of Tetralogy of Fallot?
A

degree of pulmonary stenosis (with smaller one, you just have the equivalent of a VSD; with enough of one, you could get cyanosis and right heart failure

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2
Q
  1. A large ventricular aneurysm could result from
A

weakening of the ventricular wall at the site of a previously healed MI

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3
Q
  1. Most common mutations in inherited forms of hypertrophic cardiomyopathy are
A

those affecting beta-myosin heavy chain

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4
Q
  1. Clinical features are those of
A

pericarditis with effusion, and most common causes of hemorrhagic pericarditis are metastatic carcinoma and TB

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5
Q
  1. Mitral annular calcification is
A

often an incidental finding on chest radiograph, echocardiograph, or at autopsy; larger accumulations of Ca in the mitral ring can impinge on the conductive system and perhaps cause arrhythmias or disrupting endocardium and can provide focus for thrombus formation or infective endocarditis

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6
Q
  1. Most common toxin producing DCM is
A

alcohol (lead to R and L heart failure)

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7
Q
  1. When pulmonary HTN and right heart failure are secondary to lung disease,
A

it is called cor pulmonale and caused most often by pulmonary emphysema and other obstructive lung diseases; restrictive lung diseases can lead to cor pulmonale

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8
Q
  1. Mitral valve prolapse, when symp, can lead to
A

fatigue, chest pain, and arrhythmias

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9
Q
  1. Cyanosis at an early age suggests
A

right-left shunt like truncus arteriosus, and cerebral lesion suggests an abscess as a consequence of septic embolization from infective endocarditis, which can complicate congenital heart disease

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10
Q
  1. Patient with fibrinous pericarditis, most common cause of which is
A

uremia resulting from renal failure

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11
Q
  1. PND is a feature of
A

left-sided CHF, and rheumatic heart disease most often involves the mitral, aortic, or both valves

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12
Q
  1. Extensive iron deposition signifies
A

hemochromatosis, markedly reducing ventricular compliance, resulting in restrictive cardiomyopathy

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13
Q
  1. Dynamic LV outflow obstruction suggests; valvular insufficiency of mitral and tricuspid valvues suggests; lack of diastolic expnasion suggests
A

hypertrophic cardiomyopathy; dilated cardiomyopathy (also reduces contractility and EF);
constrictive pericarditis

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14
Q
  1. Subendocardial/marantic vegetations may occur on
A

any cardiac valve, but tend to be small and won’t damage valves; have a tendency to embolize and can occur with hypercoagulable stages that accompany certain malignancies, especially mucin-secreting adenocarcinomas (Trousseau syndrome)

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15
Q
  1. What here is an indicator of coagulative necrosis?
A

Deeply eosinophilic myocardial fibers with loss of nuclei;
look for the deeply staining transverse bands called contraction bands, and here there are neutrophils infiltrating, meaning an MI occurred about 24-48 hrs ago

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16
Q
  1. Findings compatible with
A

hypoplastic left heart syndrome, with varying degrees of severity; blood returns from LA and shunted across foramen ovale back to lungs, increasing pulmonary flow and decreasing oxygenation; unoxygenated blood exiting RV can shunt through ductus arteriosus to aorta to supply systemic circulation