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Pathoma KAM > CH8 - Cardiac Pathology > Flashcards

CH8 - Cardiac Pathology Flashcards

1
Q

What is ischemic heart disease (IHD)?

A

Group of syndromes related to myocardial ischemia

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2
Q

What is the leading cause of death in the US?

A

ischemic heart disease (IHD)

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3
Q

What is ischemic heart disease (IHD) usually due to?

A

atherosclerosis of coronary arteries, which decreases blood flow to the myocardium

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4
Q

What are the risk factors for IHD?

A

They are similar to those of atherosclerosis; incidence increases with age.

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5
Q

What is stable angina?

A

chest pain that arises with exertion or emotional stress.

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6
Q

What is stable angina due to?

A

atherosclerosis of coronary arteries with > 70% stenosis;

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7
Q

Why does stable angina arise with exertion?

A

decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion

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8
Q

What does stable angina represent?

A

reversible injury to myocytes (no necrosis)

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9
Q

How does stable angina present?

A

As chest pain lasting < 20 minutes that radiates to the left arm or jaw, diaphoresis, and shortness of breath

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10
Q

What does the EKG show in stable angina?

A

ST-segment depression due to subendocardial ischemia

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11
Q

What is stable angina relieved by?

A

rest or nitroglycerin

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12
Q

What is unstable angina?

A

chest pain that occurs at rest.

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13
Q

What is unstable angina usually due to?

A

rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery

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14
Q

What does unstable angina represent?

A

reversible injury to myocytes (no necrosis)

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15
Q

What does the EKG show in unstable angina?

A

ST-segment depression due to subendocardial ischemia

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16
Q

What is unstable angina relieved by?

A

Nitroglycerin

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17
Q

In unstable angina there is a high risk of what?

A

progression to myocardial infarction

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18
Q

What is prinzmetal angina?

A

episodic chest pain unrelated to exertion.

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19
Q

What is prinzmetal angina due to?

A

coronary artery vasospasm

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20
Q

What does prinzmetal angina represent?

A

reversible injury to myocytes (no necrosis)

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21
Q

What does the EKG for prinzmetal angina show?

A

ST-segment elevation due to transmural ischemia.

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22
Q

What is prinzmetal angina relieved by?

A

nitroglycerin or calcium channel blockers

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23
Q

What is myocardial infarction?

A

Necrosis of cardiac myocytes

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24
Q

What is myocardial infarction usually due to?

A

rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery

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25
Q

In addition to atherosclerotic plaque what are some other causes of myocardial infarction?

A

coronary artery vasospasm (due to Prinzmetal angina or cocaine use), emboli, and vasculitis (e.g., Kawasaki disease).

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26
Q

What are the clinical features for myocardial infarction?

A

include severe, crushing chest pain (lasting > 20 minutes) that radiates to the left arm or jaw, diaphoresis, and dyspnea; symptoms are not relieved by nitroglycerin.

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27
Q

In myocardial infarction what does the infarction usually involve?

A

the left ventricle (LV); right ventricle (RV) and both atria are generally spared.

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28
Q

What artery is most commonly involved artery in MI?

A

LAD; left anterior descending artery ? 45% of cases

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29
Q

What does occlusion of the left anterior descending artery (LAD) lead to?

A

infarction of the anterior wall and anterior septum of the LV

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30
Q

What does occlusion of right coronary artery (RCA) lead to?

A

infarction of the posterior wall, posterior septum, and papillary muscles of the LV;

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31
Q

What is the 2nd most commonly involved artery in MI?

A

RCA, right coronary artery

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32
Q

What does occlusion of the left circumflex artery lead to?

A

infarction of lateral wall of the LV.

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33
Q

What does the initial phase of infarction lead to?

A

subendocardial necrosis involving < 50% of the myocardial thickness (subendocardial infarction);

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34
Q

What does the EKG show for the initial phase of infarction?

A

(subendothelial infarction) ST-segment depression.

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35
Q

After the initial phase of infarction, what does continued or severe ischemia lead to?

A

transmural necrosis involving most of the myocardial wall (transmural infarction)

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36
Q

What does the EKG show in transmural infarction?

A

ST-segment elevation

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37
Q

What do the laboratory tests detect for myocardial infarction?

A

elevated cardiac enzymes.

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38
Q

What is the most sensitive and specific marker (gold standard) for Ml?

A

troponin I

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39
Q

What are the troponin I levels after 2-4 hours?

A

Levels rise 2-4 hours after infarction

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40
Q

When do troponin I levels peak?

A

at 24 hours

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41
Q

When do troponin I levels return to normal?

A

By 7-10 days.

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42
Q

What is CK-MB is useful for?

A

detecting reinfarction that occurs days after an initial MI

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43
Q

When do creatine kinase MB (CK-MB) levels rise?

A

4 - 6 hours after infarction

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44
Q

When does creatinine kinase MB levels peak?

A

They peak at 24 hours

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45
Q

When does creatinine kinase MB levels return to normal?

A

by 72 hours.

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46
Q

What does treatment for myocardial infarction include?

A

1) Asprin 2) Supplemental O2 3) Nitrates 4) beta-blockers 5) ACE inhibitor 6)Fibrinolysis or angioplasty

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47
Q

How does aspirin and/or heparin help treat MI?

A

limits thrombosis

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48
Q

How does supplemental 02 help treat MI?

A

minimizes ischemia

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49
Q

How do nitrates help treat MI?

A

vasodilate coronary arteries

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50
Q

How does beta-blockers help treat MI?

A

slows heart rate, decreasing O2 demand and risk tor arrhythmia

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51
Q

How does ACE inhibitors help treat MI?

A

decreases LV dilation

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52
Q

How does fibrinolysis or angioplasty help treat MI?

A

opens blocked vessel

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53
Q

What happens in fibrinolysis or angioplasty post-MI?

A

it opens bloced vessel; 1) contraction band necrosis 2) reperfusion injury

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54
Q

What is contraction band necrosis?

A

After fibrinolysis or angioplasty post-MI there is reperfusion of irreversibly damaged cells resulting in calcium influx, leading to hypercontraction of myofibrils

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55
Q

What is reperfusion injury?

A

After fibrinolysis or angioplasty post-MI, the return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes

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56
Q

< 4 hours from time of infarction what are the gross and microscopic changes?

A

No gross changes, and no microscopic changes

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57
Q

What are the complications < 4 hours from time of infarction?

A

Cardiogenic shock (massive infarction), congestive heart failure, and arrhythmia

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58
Q

4-24 hours from time of infarction what are the gross and microscopic changes?

A

[Gross] Dark discoloration and [microscopic] Coagulative necrosis

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59
Q

What are the complications from 4-34 hours from the time of infarction?

A

arrhythmia

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60
Q

1-3 days from time of infarction what are the gross and microscopic changes?

A

[gross] Yellow pallor, [microscopic] Neutrophils

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61
Q

What are the complications for 1-3 days from time of infarction?

A

Fibrinous pericarditis presents as chest pain with friction rub

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62
Q

What does fibrinous pericarditis present as?

A

chest pain with friction rub

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63
Q

4-7 days from time of infarction, what are the gross and microscopic changes?

A

[gross] Yellow pallor, [Microscopic] Macrophages

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64
Q

What are the complications 4-7 days from time of infarction?

A

Rupture of ventricular free wall, interventricular septum, or papillary muscle

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65
Q

What does rupture of ventricular free wall lead to?

A

cardiac tamponade

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66
Q

What does rupture of interventricular septum lead to?

A

shunt,

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67
Q

What does rupture of papillary muscle lead to?

A

mitral insufficiency

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68
Q

1-3 weeks from time of infarction, what are the gross and microscopic changes?

A

[gross] Red border emerges as granulation tissue enters from edge of infarct, [microscopic] Granulation tissue with plump fibroblasts, collagen, and blood vessels

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69
Q

Months from time of infarction, what are the gross and microscopic changes?

A

[gross] White scar, [microscopic] Fibrosis

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70
Q

What are the complications for 1 Month from the time of infarction?

A

Aneurysm, mural thrombus, or Dressier syndrome

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71
Q

What is sudden cardiac death?

A

Unexpected death due to cardiac disease, occurs without symptoms or <1 hour after symptoms arise

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72
Q

What is sudden cardiac death usually due to?

A

fatal ventricular arrhythmia

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73
Q

What is the most common etiology for sudden cardiac death?

A

acute ischemia; 90% of patients have preexisting severe atherosclerosis.

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74
Q

What are the less common causes for sudden cardiac death?

A

mitral valve prolapse, cardiomyopathy, and cocaine abuse

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75
Q

What is chronic ischemic heart disease?

A

Poor myocardial function due to chronic ischemic damage (with or without infarction);

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76
Q

What does chronic ischemic heart disease progress to?

A

congestive heart failure (CHF)

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77
Q

What is congestive heart failure?

A

Pump failure; divided into right- and left-sided failure

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78
Q

What are the causes of left-sided heart failure?

A

ischemia, hypertension, dilated cardiomyopathy, myocardial infarction, and restrictive cardiomyopathy

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79
Q

What are the clinical features for left-sided heart failure due to?

A

decreased forward perfusion and pulmonary congestion.

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80
Q

What are the clinical features for left-sided heart failure?

A

1) decreased perfusion and pulmonary congestion 2) activation of rennin angiotensin system

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81
Q

In left-sided heart failure what does pulmonary congestion lead to?

A

pulmonary edema.

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82
Q

In left-sided heart failure why is there paroxysomal nocturnal dyspnea?

A

Its due to increased venous return when lying flat

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83
Q

In left-sided heart failure, pulmonary edema results in what?

A

dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles

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84
Q

How can left-sided heart failure lead to intra-alveolar hemorrhage?

A

Small, congested capillaries may burst, leading to intraalveolar hemorrhage

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85
Q

In left-sided heart failure what is intra-alveolar hemorrhage marked by?

A

hemosiderin-laden macrophages (heart-failure cells)

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86
Q

In left sided heart failure how are the kidneys involved?

A

Decreased flow to kidneys leads to activation of renin-angiotensin system

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87
Q

In left sided heart failure does the kidney affect the rennin angiotensin system?

A

Fluid retention exacerbates CHF

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88
Q

What is the main treatment for left sided heart failure?

A

treatment is ACE inhibitor.

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89
Q

What is right-sided heart failure most commonly due to?

A

left-sided heart failure;

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90
Q

Aside from left sided heart failure what are some other important causes for right sided heart failure?

A

Left to-right shunt and chronic lung disease (cor pulmonale)

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91
Q

What are the clinical features for right sided heart failure due to?

A

congestion

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92
Q

What are the clinical features for right sided heart failure?

A
  1. Jugular venous distension 2. Painful hepatosplenomegaly with characteristic nutmeg liver; may lead to cardiac cirrhosis 3. Dependent pitting edema
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93
Q

In right sided heart failure what is the dependent pitting edema due to?

A

increased hydrostatic pressure

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94
Q

What are the congenital heart defects?

A

Arise during embryogenesis

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95
Q

When do congenital heart defects usually arise?

A

usually weeks 3 through 8

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96
Q

In what percentage of live births do you see congenital heart defects?

A

seen in 1% of live births

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97
Q

Most congenital heart defects are?

A

sporadic.

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98
Q

Congenital heart defects often result in?

A

shunting between left (systemic) and right (pulmonary) circulations.

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99
Q

Defects with left-to-right shunting

A

may be relatively asymptomatic at birth, but the shunt can eventually reverse

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100
Q

What does increased flow through the pulmonary circulation result in?

A

hypertrophy of pulmonary vessels and pulmonary hypertension.

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101
Q

What does increased pulmonary resistance eventually result in?

A

reversal of shunt

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102
Q

What does the reversal of shunt in congenital defects with left to right shunt lead to?

A

late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia, and clubbing.

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103
Q

What do defects with right-to-left shunting usually present as?

A

cyanosis shortly after birth.

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104
Q

What is ventricular septal defect (VSD)?

A

Defect in the septum that divides the right and left ventricles

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105
Q

What is the most common congenital heart defect?

A

ventricular septal defect (VSD)

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106
Q

What is ventricular septal defect (VSD) associated with?

A

fetal alcohol syndrome

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107
Q

What does ventricular septal defect (VSD) result in?

A

left-to-right shunt,

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108
Q

What determines extent of shunting in ventricular septal defect (VSD)?

A

size of defect and age at presentation

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109
Q

What happens with small defects in ventricular septal defect (VSD)?

A

they are often asymptomatic

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110
Q

What happens with large defects in ventricular septal defect (VSD)?

A

can lead to Eisenmenger syndrome

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111
Q

What is the treatment for ventricular septal defect (VSD)?

A

involves surgical closure; small defects may close spontaneously

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112
Q

What is atrial septal defect?

A

Defect in the septum that divides right and left atria;

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113
Q

What is the most common type of atrial septal defect?

A

It is ostium secundum (90% of cases)

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114
Q

What type of atrial septal defect is type is associated with Down syndrome?

A

Ostium primum

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115
Q

What does atrial septal defect result in?

A

left-to-right shunt and split S2 on auscultation

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116
Q

Why is there split S2 on auscultation in atrial septal defect?

A

increased blood in right heart delays closure of pulmonary valve

117
Q

What is an important complication of atrial septal defect?

A

Paradoxical emboli

118
Q

What is patent ductus arteriosus?

A

Failure of ductus arteriosus to close

119
Q

What is patent ductus arteriosus associated with?

A

congenital rubella

120
Q

What does patent ductus arteriosus result in?

A

left-to-right shunt between the aorta and the pulmonary artery

121
Q

During development what does the ductus arteriosus normally do?

A

shunts blood from the pulmonary artery to the aorta, bypassing the lungs

122
Q

What are the symptoms for patent ductus arteriosus?

A

Asymptomatic at birth with holosystolic machine-like murmur; may lead to Eisenmenger syndrome, resulting in lower extremity cyanosis

123
Q

What does the treatment for patent ductus arteriosus involve?

A

indomethacin, which decreases PGE2 resulting in PDA closure

124
Q

What is the effect of PGE on patent ductus arteriosus?

A

PGE maintains patency of the ductus arteriosus

125
Q

What is tetralogy of fallot?

A

It is characterized by (1) stenosis of the right ventricular outflow tract, (2) right ventricular hypertrophy, (3) VSD, and (4) an aorta that overrides the VSD

126
Q

In tetralogy of fallot what does the right-to-left shunt lead to?

A

early cyanosis;

127
Q

In tetralogy of fallot what determines the extent of shunting and cyanosis?

A

the degree of stenosis

128
Q

In tetralogy of fallot what patient behavior is observed?

A

they learn to squat in response to a cyanotic spell

129
Q

In tetralogy of fallot why does squatting help with the cyanotic spell?

A

increased arterial resistance decreases shunting and allows more blood to reach the lungs.

130
Q

What is seen on x-ray in tetralogy of fallot?

A

Boot-shaped heart on x-ray

131
Q

What is transposition of the great vessels characterized by?

A

pulmonary artery arising from the left ventricle and aorta arising from the right ventricle

132
Q

What is the transposition of the great vessels associated with?

A

maternal diabetes

133
Q

What does transposition of the great vessels presents with?

A

early cyanosis; pulmonary and systemic circuits do not mix.

134
Q

In transposition of the great vessels what is required for survival?

A

creation of shunt (allowing blood to mix) after birth is required for survival.

135
Q

What is the effect of PGE in transposition of the great vessels?

A

can be administered to maintain a PDA until definitive surgical repair is performed.

136
Q

What does transposition of the great vessels result in?

A

hypertrophy of the right ventricle and atrophy of the left ventricle

137
Q

What is truncus arteriosus?

A

Characterized by a single large vessel arising from both ventricles 1. Truncus fails to divide.

138
Q

What does truncus arteriosus present with?

A

early cyanosis

139
Q

Why is there early cyanosis in truncus arteriosus?

A

deoxygenated blood from right ventricle mixes with oxygenated blood from left ventricle before pulmonary and aortic circulations separate

140
Q

What is tricuspid atresia?

A

Tricuspid valve orifice fails to develop; right ventricle is hypoplastic.

141
Q

What is tricuspid atresia often associated with?

A

ASD, resulting in a right-to-left shunt; presents with early cyanosis,

142
Q

What is coarctation of the aorta?

A

Narrowing of the aorta,

143
Q

What is coarctation of the aorta classically divided into?

A

infantile and adult forms

144
Q

What is the infantile form of coarctation of the aorta associated with?

A

a PDA

145
Q

In the infantile form of coarctation of the aorta where is the coarctation located?

A

after (distal to) the aortic arch, but before (proximal to) the PDA

146
Q

What does the infantile form of the coarctation of the aorta present as?

A

lower extremity cyanosis in infants, often at birth

147
Q

What is the infantile form of coarctation of the aorta associated with?

A

Turner syndrome

148
Q

What is the adult form of coarctation of the aorta associated with?

A

Its not associated with a PDA

149
Q

Where is the coarctation for the adult form of coarctation of the aorta?

A

coarctation lies after (distal to) the aortic arch

150
Q

How does the adult form of coarctation of the aorta present?

A

as hypertension in the upper extremities and hypotension with weak pulses in the lower extremities; classically discovered in adulthood

151
Q

In the adult form of coarctation of the aorta what is seen on x-ray?

A

Notching of ribs

152
Q

Why is there notching of the ribs seen on x-ray for the adult form of coarctation of the aorta?

A

Collateral circulation develops across the intercostal arteries; engorged arteries cause notching of ribs on x-ray

153
Q

What is the adult form of coarctation of the aorta associated with?

A

bicuspid aortic valve

154
Q

What is the purpose of heart valves?

A

To prevent back flow

155
Q

What are the has four valves of the heart?

A

tricuspid, pulmonary, mitral, and aortic

156
Q

What does valvular lesions generally result in?

A

stenosis (decreased caliber of the valve orifice) or regurgitation (backflow)

157
Q

What is acute rheumatic fever?

A

Systemic complication of pharyngitis due to group A beta-hemolytic streptococci

158
Q

Who does acute rheumatic fever affect?

A

children 2-3 weeks after an episode of streptococcal pharyngitis strep throat

159
Q

What is acute rheumatic fever caused by?

A

molecular mimicry, bacterial M protein resembles proteins in human tissue

160
Q

What is diagnosis of acute rheumatic fever based on?

A

Jones criteria.

161
Q

What evidence is needed for the Jones Criteria?

A

Evidence of prior group A beta-hemolytic streptococcal infection with the presence of major and minor criteria

162
Q

What would indicate prior group A beta-hemolytic streptococcal infection?

A

Elevated ASO or anti-DNase B titers

163
Q

What is the minor Jones criteria?

A

Minor criteria are nonspecific and include fever and elevated ESR.

164
Q

What is the major Jones criteria?

A

1) migratory polyarthritis 2) pancarditis 3) subcutaneous nodules 4) erythema marginatum 5) Sydenham chorea

165
Q

What is Migratory polyarthritis?

A

In Jones criteria, swelling and pain in a large joint (e.g., wrist, knees, ankles) that resolves within days and migrates to involve another large joint

166
Q

What is Pancarditis?

A

a) endocarditis b) myocarditis c) pericarditis

167
Q

In endocarditis which valve is involved more commonly?

A

Mitral valve is involved more commonly than the aortic valve.

168
Q

How is endocarditis characterized?

A

by small vegetations along lines of closure that lead to regurgitation

169
Q

What is myocarditis in pancarditis?

A

its with Aschotf bodies that are characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material

170
Q

What is the most common cause of death during the acute phase?

A

myocarditis

171
Q

What is pericarditis in pancarditis lead to?

A

friction rub and chest pain

172
Q

What is involved with erythema marginatum in the major criteria of Jones criteria

A

annular, nonpruritic rash with erythematous borders, commonly involving trunk and limbs

173
Q

What is Sydenham chorea in the major criteria of Jones criteria?

A

It is rapid, involuntary muscle movements

174
Q

What usually happens to an acute attack of rheumatic fever?

A

usually resolves, but may progress to chronic rheumatic heart disease;

175
Q

What does repeat exposure to group A beta-hemolytic streptococci result in?

A

relapse of the acute phase of rheumatic fever and increases risk for chronic disease.

176
Q

What is chronic rheumatic heart disease?

A

Valve scarring that arises as a consequence of rheumatic fever

177
Q

What does chronic rheumatic heart disease result in?

A

stenosis with a classic fish mouth appearance

178
Q

What does chronic rheumatic heart disease almost always involve?

A

the mitral valve

179
Q

What does the involvement of the mitral valve in chronic rheumatic heart disease lead to?

A

thickening of chordae tendineae and cusps

180
Q

What does chronic rheumatic heart disease occasionally involve?

A

the aortic valve

181
Q

What does the involvement of the aortic valve in chronic rheumatic heart disease lead to?

A

fusion of the commissures

182
Q

What do complications in chronic rheumatic heart disease include?

A

infectious endocarditis

183
Q

What is aortic stenosis?

A

Narrowing of the aortic valve orifice

184
Q

What is aortic stenosis usually due to?

A

fibrosis and calcification from wear and tear

185
Q

When does aortic stenosis present?

A

in late adulthood (> 60 years)

186
Q

What does a bicuspid aortic valve increase the risk for?

A

aortic stenosis and hastens disease onset.

187
Q

How many cusps does a normal aortic valve have?

A

three cusps,

188
Q

What is the effect of fewer cusps on the aortic valve?

A

it results in increased wear and tear on each cusp

189
Q

What is the relationship between aortic stenosis and chronic rheumatic fever?

A

aortic stenosis may arise as a consequence of chronic rheumatic valve disease;

190
Q

What distinguishes rheumatic disease from wear and tear in aortic stenosis?

A

coexisting mitral stenosis and fusion of the aortic valve commissures

191
Q

In aortic stenosis what happens during cardiac compensation?

A

it leads to a prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur is heard

192
Q

What does the complications of aortic stenosis include?

A

1) Concentric left ventricular hypertrophy 2) angina and syncope with exercise 3) microangiopathic hemolytic anemia

193
Q

In aortic stenosis what does concentric left ventricular hypertrophy lead to?

A

It may progress to cardiac failure

194
Q

In aortic stenosis what does angina and syncope with exercise lead to?

A

Limited ability to increase blood flow across the stenotic valve leads to decreased perfusion of the myocardium and brain

195
Q

In aortic stenosis what does microangiopathic hemolytic anemia lead to?

A

RBCs are damaged (producing schistocytes) while crossing the calcified valve

196
Q

In aortic stenosis what does treatment involve?

A

valve replacement after onset of complications.

197
Q

What is aortic regurgitation?

A

Backflow of blood from the aorta into the left ventricle during diastole

198
Q

Aortic regurgitation arises due to what?

A

aortic root dilation (syphilitic aneurysm and aortic dissection) or valve damage (infectious endocarditis)

199
Q

What is the most common cause of aortic regurgitation?

A

isolated root dilation

200
Q

What are the clinical features for aortic regurgitation?

A
  1. Early, blowing diastolic murmur 2. Hyperdynamic circulation due to increased pulse pressure
201
Q

What is pulse pressure?

A

it is the difference between systolic and diastolic pressures

202
Q

What is the relationship between pressure and aortic regurgitation?

A

Diastolic pressure decreases due to regurgitation, while systolic pressure increases due to increased stroke volume

203
Q

How does aortic regurgitation present?

A

with bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse), and head bobbing

204
Q

What does aortic regurgitation result in?

A

LV dilation and eccentric hypertrophy (due to volume overload)

205
Q

What is the treatment for aortic regurgitation?

A

valve replacement once LV dysfunction develops

206
Q

What happens in mitral valve prolapse?

A

Ballooning of mitral valve into left atrium during systole

207
Q

What is the incidence of mitral valve prolapse in US adults

A

Seen in 2-3% of US adults

208
Q

What is mitral valve prolapse due to?

A

myeloid degeneration (accumulation of ground substance) of the valve, making it (loopy)

209
Q

What is the etiology for mitral valve prolapse?

A

Unknown

210
Q

What might mitral valve prolapse be seen in?

A

Marfan syndrome or Ehlers-Danlos syndrome

211
Q

What does mitral valve prolapse present with?

A

an incidental mid-systolic click followed by a regurgitation murmur that is usually asymptomatic

212
Q

With mitral valve prolapse, when does the mid-systolic click get louder?

A

Click and murmur become louder with squatting

213
Q

Why does squatting make the mid-systolic click get louder in mitral valve prolapse?

A

increased systemic resistance decreases left ventricular emptying

214
Q

What are the complications for mitral valve prolapse?

A

they are rare, but include infectious endocarditis, arrhythmia, and severe mitral regurgitation.

215
Q

What is the treatment for mitral valve prolapse?

A

valve replacement.

216
Q

What is mitral regurgitation?

A

Reflux of blood from the left ventricle into the left atrium during systole

217
Q

Mitral regurgitation usually arises as a complication of what?

A

mitral valve prolapse

218
Q

Aside from mitral valve prolapse, what are some other causes of mitral regurgitation?

A

Left ventricular dilatation (left-sided cardiac failure), infective endocarditis, acute rheumatic heart disease, and papillary muscle rupture after a myocardial infarction.

219
Q

What are the clinical features for Mitral regurgitation?

A
  1. Holosystolic [blowing] murmur;
220
Q

In mitral regurgitation why is the holosystolic murmur louder with squatting?

A

increased systemic resistance decreases left ventricular emptying and expiration, increased return to left atrium

221
Q

What does mitral regurgitation result in?

A

Volume overload and left-sided heart failure

222
Q

What is mitral stenosis?

A

Narrowing of the mitral valve orifice

223
Q

What is mitral stenosis usually due to?

A

chronic rheumatic valve disease

224
Q

What are the clinical features for mitral stenosis?

A
  1. Opening snap followed by diastolic rumble 2. Volume overload leads to dilatation of the left atrium
225
Q

In mitral stenosis what does the dilation of the left atrium leading to volume overload result in?

A

i. Pulmonary congestion with edema and alveolar hemorrhage ii. Pulmonary hypertension and eventual right-sided heart failure iii. Atrial fibrillation with associated risk for mural thrombi

226
Q

What is endocarditis?

A

Inflammation of endocardium that lines the surface of cardiac valves

227
Q

What is endocarditis usually due to?

A

bacterial infection

228
Q

What is the most common overall cause of endocarditis?

A

Streptococcus viridans

229
Q

What is streptococcus viridans?

A

it is a low virulence organism that infects previously damaged valves (chronic rheumatic heart disease and mitral valve prolapse).

230
Q

What does streptococcus viridans result in?

A

small vegetations that do not destroy the valve (subacute endocarditis)

231
Q

How does streptococcus viridans affect the endocardial surface?

A

develops thrombotic vegetations (platelets and fibrin) on damaged endocardial surface, transient bacteremia leads to trapping of bacteria in the vegetations, prophylactic antibiotics decrease risk of endocarditis.

232
Q

What is the most common cause of endocarditis in IV drug users?

A

Staphylococcus aureus

233
Q

What is Staphylococcus aureus?

A

High-virulence organism that infects normal valves, most commonly the tricuspid.

234
Q

What does Staphylococcus aureus result in?

A

large vegetations that destroy the valve (acute endocarditis)

235
Q

What is Staphylococcus epidermidis associated with?

A

endocarditis of prosthetic valves

236
Q

What is Streptococcus bovis associated with?

A

endocarditis in patients with underlying colorectal carcinoma

237
Q

What are HACEK organisms associated with?

A

are associated with endocarditis with negative blood cultures.

238
Q

HACEK

A

Haemophilus, Actinobacius, Cardiobacterium, Eikenella, Kingella

239
Q

What are the clinical features of bacterial endocarditis?

A

1) Fever 2) Lesions 3) Janeway lesions 4) anemia of chronic disease

240
Q

What is the fever in bacterial endocarditis due to?

A

bacteremia

241
Q

What is the murmur in bacterial endocarditis due to?

A

vegetations on heart valve

242
Q

What are the Janeway lesions, splinter hemorrhages in nail bed and osier nodes in bacterial endocarditis due to?

A

embolization of septic vegetations

243
Q

What are Janeway lesions?

A

erythematous nontender lesions on palms and soles.

244
Q

What are Osier nodes?

A

tender lesions on fingers or toes

245
Q

What is anemia of chronic disease due to?

A

chronic inflammation

246
Q

What are the laboratory findings for endocarditis?

A
  1. Positive blood cultures 2. Anemia of chronic disease 3. Transesophageal echocardiogram is useful for detecting lesions on valves
247
Q

What are the general lab findings of anemia of chronic diseae?

A

low Hb, low MCV; high ferritin, low TIBC, decreased serum iron, and decreased l% saturation

248
Q

What is the transesophageal echocardiogram useful for?

A

detecting lesions on valves

249
Q

What is non-bacterial thrombotic endocarditis due to?

A

sterile vegetations that arise in association with a hypercoagulable state or underlying adenocarcinoma.

250
Q

What does non-bacterial thrombotic endocarditis result in?

A

Vegetations arise on the mitral valve along lines of closure and result in mitral regurgitation.

251
Q

What is Libman-Sacks endocarditis due to?

A

sterile vegetations that arise in association with SLE.

252
Q

What does Libman-Sacks endocarditis result in?

A

Vegetations are present on the surface and undersurface of the mitral valve and result in mitral regurgitation

253
Q

What is cardiomyopathy?

A

Group of myocardial diseases that result in cardiac dysfunction

254
Q

What are the types of cardiomyopathy?

A

Dilated cardiomypathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy

255
Q

What is dilated cardiomyopathy?

A

Dilation of all four chambers of the heart

256
Q

What is the most common form of cardiomyopathy?

A

Dilated cardiomyopathy

257
Q

What does dilated cardiomyopathy result in?

A

Results in systolic dysfunction (ventricles cannot pump),

258
Q

What does the systolic dysfunction resulting from dilated cardiomyopathy lead to?

A

biventricular CHF

259
Q

What are the complications of dilated cardiomyopathy?

A

mitral and tricuspid valve regurgitation and arrhythmia.

260
Q

What is the most common cause of dilated cardiomyopathy?

A

Its idiopathic

261
Q

What are some other causes of dilated cardiomyopathy?

A
  1. Genetic mutation (usually autosomal dominant) 2. Myocarditis (usually due to coxsackie A or B) 3. Alcohol abuse 4. Drugs (doxorubicin) 5. Pregnancy
262
Q

In pregnancy, when is dilated cardiomyopathy?

A

Its seen during late pregnancy or soon (weeks to months) after childbirth

263
Q

What characterizes myocarditis leading to dilated cardiomyopathy?

A

characterized by a lymphocytic infiltrate in the myocardium

264
Q

What does dilated cardiomyopathy from myocarditis result in?

A

chest pain, arrhythmia with sudden death, or heart failure. Dilated cardiomyopathy is a late complication.

265
Q

What is the treatment for dilated cardiomyopathy?

A

heart transplant.

266
Q

What is hypertrophic cardiomyopathy?

A

Massive hypertrophy of the left ventricle

267
Q

What is hypertrophic cardiomyopathy usually due to?

A

genetic mutations in sarcomere proteins; most common form is autosomal dominant

268
Q

What are the clinical features for hypertrophic cardiomyopathy?

A
  1. Decreased cardiac output 2. Sudden death due to ventricular arrhythmias 3. Syncope with exercise
269
Q

How does hypertrophic cardiomyopathy lead to syncope with exercise?

A

Subaortic hypertrophy of the ventricular septum results in functional aortic stenosis

270
Q

What is a common cause of sudden death in young athletes?

A

hypertrophic cardiomyopathy

271
Q

In hypertrophic cardiomyopathy what does the decreased cardiac output lead to?

A

Left ventricular hypertrophy leads to diastolic dysfunction (ventricle cannot fill).

272
Q

In hypertrophic cardiomyopathy, what does biopsy show?

A

myofiber hypertrophy with disarray

273
Q

What is restrictive cardiomyopathy?

A

Decreased compliance of the ventricular endomyocardium that restricts filling during diastole

274
Q

What are the causes of restrictive cardiomyopathy?

A

amyloidosis, sarcoidosis, hemochromatosis, endocardial fibroelastosis (in children), and Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia).

275
Q

What does restrictive cardiomyopathy present as?

A

congestive heart failure;

276
Q

What is the classic finding in restrictive cardiomyopathy?

A

low-voltage EKG with diminished QRS amplitude.

277
Q

What are the cardiac tumors?

A

Myxoma, rhabdomyoma

278
Q

What is myoxma?

A

Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology

279
Q

What is the most common primary cardiac tumor in adults?

A

myxoma

280
Q

What does myxoma usually form?

A

a pedunculated mass in the left atrium

281
Q

What does the pedunculated mass in the left atrium due to myxoma cause?

A

syncope due to obstruction of the mitral valve

282
Q

What is rhabdomyoma?

A

Benign hamartoma of cardiac muscle

283
Q

What is the most common primary cardiac tumor in children?

A

rhabdomyoma

284
Q

What is rhabdomyoma associated with?

A

Tuberous sclerosis

285
Q

Where does rhabdomyoma usually arise?

A

in the ventricle

286
Q

Which type of tumors are more common in the heart?

A

Metastatic tumors more than primary tumors

287
Q

What does common metastases to the heart include?

A

breast and lung carcinoma, melanoma, and lymphoma

288
Q

What does metastatic tumors in the heart most commonly involve? What does this result in?

A

the pericardium, resulting in a pericardial effusion

Pathoma KAM (19 decks)

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