PATH Lab 2 Flashcards

1
Q

What other complications are encountered in infective endocarditis?

A

The complications of infective endocarditis may be cardiac or extracardiac. Cardiac complications include valve insufficiency, myocardial abscesses (ring abscesses), suppurative pericarditis, and, rarely, a hemopericardium. Embolic complications include infarcts and abscesses. Their location depends on whether the right-side or left-side valves are affected. Renal complications include, in addition to infarcts and abscesses, focal glomerulonephritis (due to microemboli) and diffuse glomerulonephritis due to antigen-antibody complex formation.

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2
Q

Is the cardiac dysfunction in patients with ARF attributable to valve dysfunction or myocardial damage?

A

Myocardial damage.

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3
Q

Why are the patient’s (with hyaline arteriolosclerosis) serum BUN and creatinine elevated? Why does she have progressive loss of renal function?

A

Elevation of serum BUN and creatinine reflects progressive loss of renal function. The kidneys of this patient showed changes of severe arteriolar nephrosclerosis. Small vessels revealed hyaline arteriolar sclerosis, and there were many globally sclerotic or partially sclerotic glomeruli. As the glomeruli are lost, the distal nephron components atrophy, so there is tubular atrophy. These changes are responsible for the loss of renal function.

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4
Q

What is the etiology of these inflammatory lesions (Aschoff bodies)?

A

A hypersensitivity reaction induced by group A streptococci. Following a streptococcal infection (pharyngitis), antibodies to streptococcal M proteins develop. These antibodies cross-react with cardiac glycoprotein antigens.

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5
Q

Why is pulmonary hypertension less common in patients with ASD than VSD?

A

ASDs present an increased volume load to the pulmonary circulation, but at lower pressures than VSDs, and are therefore better tolerated by the pulmonary vasculature.

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6
Q

What is a possible explanation for the episode of syncope and temporary unilateral blindness in this patient, with rheumatic heart disease?

A

Atrial thromboemboli are a major potential complication of mitral stenosis. The episode of syncope and temporary unilateral blindness was probably an embolic event, the embolus arising from a left atrial thrombus.

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7
Q

Are there other types of cardiomyopathy? What must the clinician do before the term cardiomyopathy is applied?

A

The three main categories of cardiomyopathy are hypertrophic, dilated, and restrictive. Before the term cardiomyopathy can be applied, the clinician must rule out cardiac disease due to coronary artery disease, valvular heart disease, or congenital malformations of the heart.

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8
Q

What are some renal diseases that can cause hypertension? Are some of these associated with activation of the renin-angiotensin axis? What can be done for these patients?

A

Renal diseases that can cause hypertension include pyelonephritis, glomerulonephritis, polycystic kidney disease, renin-producing renal tumors, and others. Many of these are associated with activation of the renin-angiotensin axis. Angiotensin-converting enzyme inhibitors are sometimes used to treat hypertension.

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9
Q

In hyperplastic arteriolosclerosis, smooth muscle cells are proliferating and undergoing hypertrophy in an attempt to cope with rapidly rising ____________.

A

blood pressure

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10
Q

What are the components of a vegetation? What are the predisposing conditions for their formation?

A

A vegetation is an intracardiac thrombus. They often form on the valves. They form when the valves are hemodynamically abnormal and/or there is injury to the endocardium. This may occur due to diseases such as rheumatic fever, lupus, or congenital heart diseases. Hypercoagulable states sometimes associated with chronic illnesses can also predispose to cardiac vegetations.

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11
Q

What does the heart look like in dilated cardiomyopathy? What is the physiology of dilated cardiomyopathy?

A

The heart in dilated cardiomyopathy is large but dilated and flabby. The physiology of dilated cardiomyopathy is that of ineffective contraction. Patients present with progressive congestive heart failure symptoms.

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12
Q

Why would a patient with aortic stenosis have chest pain?

A

He has chest pain because the pressure in his aorta is not adequate to fill his intramyocardial coronary arteries during diastole. Hypoperfusion of subendocardial zones leads to ischemia, cardiac dysfunction, and angina. The problem is made worse by his left ventricular hypertrophy and elevated left ventricular diastolic pressure. Left ventricular hypertrophy in response to the elevated pressure load means the heart has to work harder and uses more oxygen. Elevated left ventricular diastolic pressure also limits blood flow, particularly to the endocardial zone.

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13
Q

What are some of the clinical manifestations associated with the presence of an unstable atheromatous plaque?

A

Unstable angina, acute myocardial infarction, sudden cardiac death.

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14
Q

__________ and ___________ are common in reperfused infarcts.

A

Hemorrhage; contraction bands

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15
Q

What factors determine infarct size? What factors determine the risk for post-MI complications?

A

The factors that determine eventual infarct size and the factors that determine the risk for complications are nearly identical. They include: Size of the myocardial bed at risk and its metabolic/oxygen needs, duration of coronary artery obstruction, coronary artery anatomy, dominance/collaterals, site of coronary artery obstruction, severity of obstruction, rate at which obstruction developed.

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16
Q

What was the cause of the diastolic murmur in the infant with the ventricular septal defect?

A

The diastolic murmur in the infant with the VSD was the result of the large volume of blood produced by the left-to-right shunt returning from the lungs to the left atrium and flowing across the mitral valve.

17
Q

What are some endocrine diseases that can cause hypertension?

A

Endocrine diseases that can cause secondary hypertension include a diverse group of adrenal diseases: pheochromocytoma (neoplasm of the adrenal medulla), Cushing disease and syndrome, adrenal neoplasms with hyperaldosteronism, and congenital or hereditary adrenogenital syndromes.

18
Q

What is the significance of atrial fibrillation in this patient, wiht rheumatic heart disease?

A

Atrial fibrillation is a dire consequence in patients with aortic as well as mitral stenosis. In the normal heart, left atrial contraction contributes little to left ventricular filling. In the case of mitral stenosis, the left atrium has a major responsibility for pumping blood across the tiny mitral orifice and filling the left ventricle. Atrial fibrillation takes away almost all of the beneficial effects of atrial contraction during diastole; cardiac output can acutely drop, precipitating acute pulmonary edema. Atrial fibrillation also predisposes to the formation of thrombi, as seen in the previous image.

19
Q

Which test is more sensitive for myocardial injury, CK or CK-MB?

A

CK.

20
Q

Is myocardial necrosis necessary to get arrhythmias?

A

Irreversible myocardial damage is not necessary to get arrhythmias. The majority of survivors of sudden death resuscitated early in the course of events do not develop myocardial infarction. After a region of myocardium becomes ischemic, there is a change to anaerobic glycolysis within seconds. Over the following several minutes, myocardial pH drops, and high-energy phosphates are depleted. Myocardial function is lost within minutes, and myocardial ionic pumps become unstable, leading to arrhythmias.

21
Q

At what time after infarction are patients at the greatest risk for rupture of an acute MI?

A

During the first four to seven days.

22
Q

How much myocardium must a patient lose before signs and symptoms of cardiogenic shock are manifest? What does this indicate about prognosis?

A

Signs and symptoms of severe pump failure/cardiogenic shock generally occur with large infarcts (> 40% of the left ventricle involved). Cardiogenic shock indicates a poor prognosis (70% mortality) and accounts for 2/3 of hospital deaths.

23
Q

Define myocarditis and list some common etiologic agents.

A

Myocarditis is characterized by inflammation and the consequent degeneration and necrosis of myocardial fibers. The most common causes in North America are viruses, especially enteroviruses such as coxsackie, echo, and influenza. The most important cause in South America is Chagas disease. In addition, myocarditis can also be caused by immune-mediated reactions (eg, rheumatic fever, drug hypersensitivities) or unknown causes (eg, giant cell myocarditis).

24
Q

The aortic wall in most cases of aortic dissection is weakened by ___________.

A

cystic medial necrosis

25
Q

Hypertension-associated acute CNS hemorrhage often begin where?

A

in the deep grey matter of the cerebral hemispheres (putamen, thalamus), in the pontine tegmentum, or cerebellar hemispheres.

26
Q

What is the clinical evidence for aortic dissection?

A

The clinical evidence for aortic dissection includes the presenting symptom of sharp, severe, tearing chest pain. Uneven pulses and a widened mediastinum are also an important clue. The left pleural effusion is probably blood in the pleural space.

27
Q

Ventricular wall aneurysms may also cause ___________ and ___________

A

congestive heart failure and dangerous arrhythmias.