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Pathoma > Chapter 8 cardiac pathology > Flashcards

Chapter 8 cardiac pathology Flashcards

1
Q

Define stable angina

A

chest pain that arises with exertion or emotional stress

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2
Q

How does stable angina present?

A

chest pain last less than 20 minutes that radiates tot he left arm or jaw, diaphoresis and SOB

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3
Q

EKG shows ST segment depression due to subendocardial ischemia in what two types of angina?

A

Stable angina and unstable angina

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4
Q

EKG shows ST segment elevation due to transmural ischemia in what type of angina?

A

Prinzmetal angina

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5
Q

Stable angina is relieved by what?

A

rest and nitroglycerin

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6
Q

Define unstable angina

A

chest pain that occurs at rest

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7
Q

unstable angina has a high risk of progressing to?

A

MI

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8
Q

unstable angina is usually due to?

A

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

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9
Q

Define prinzmetal angina

A

episodic chest pain unrelated to exertion

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10
Q

prinzmetal angina is due to?

A

coronary artery vasospasm

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11
Q

myocardial infarction is usually due to?

A

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

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12
Q

clinical features of MI include

A

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

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13
Q

MI usually involves what part of the heart?

A

left ventricle

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14
Q

occlusion of which coronary artery leads to infarction of the anterior wall and anterior septum of the LV

A

left anterior descending artery (LAD)

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15
Q

What is the most commonly involved artery in MI (45% of cases)?

A

left anterior descending artery (LAD)

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16
Q

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

A

right coronary artery

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17
Q

occlusion of which coronary artery leads to infarction of the posterior wall, posterior septum and papillary muscles of the LV?

A

right coronary artery

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18
Q

initial phase of the MI is characterized by?

A

subendocardial necrosis involving <50% of the myocardial thickness; EKG shows ST-segment depression

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19
Q

Continued or severe ischemia seen in MI is characterized by?

A

transmural necrosis involving most of the myocardial wall; EKG shows ST segment elevation

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20
Q

What is the most sensitive and specific marker for MI?

A

Troponin I; it is the gold standard!

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21
Q

How does troponin I levels change post MI?

A

levels rise 2-4 hours after infarction
peak at 24 hours
return to normal by 7-10 days

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22
Q

What is CK-MB useful for in regards to MI?

A

useful for detecting reinfarction that occurs days or after an initial MI

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23
Q

How do CK-MB levels change post MI?

A

levels rise 4-6 hours after infarction
peak at 24 hours
return to normal by 72 hours

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24
Q

explain contraction band necrosis

A

reperfusion of irreversibly-damaged cells results in calcium influx, leading to hypercontraction of myofibrils

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25
Q

explain reperfusion injury

A

return of oxygen and inflammatory cells may lead to free radical generation, further damaging myocytes

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26
Q

What changes and complications occur <4 hours post MI?

A

No gross changes; No microscopic changes; complications include cardiogenic shock, CHF, arrhythmia

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27
Q

What changes and complications occur 4-24 hours post MI?

A

Gross changes - dark discoloration
Microscopic changes - coagulative necrosis
Complications - arrhythmia

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28
Q

What changes and complications occur 1-3 days post MI?

A

Gross changes - Yellow pallor due to WBCs
Microscopic changes - Neutrophils
Complications - Fibrinous pericarditis, presents as chest pain with friction rub

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29
Q

What changes and complications occur 4-7 days post MI?

A

Gross changes - Yellow pallor due to WBCs
Microscopic changes - Macrophages
Complications - rupture of ventricular free wall (leads to cardiac tamponade), IV septum (leads to shunt) or papillary muscle (leads to mitral insufficiency)

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30
Q

What changes and complications occur 1-3 weeks post MI?

A

Gross changes - red border emerges as granulation tissue enters from edge of infarct
Microscopic changes - granulation tissue with plump fibroblasts, collagen and blood vessels
Complications - none

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31
Q

What changes and complications occur months post MI?

A

Gross changes - white scar
Microscopic changes - fibrosis
Complications - Aneurysm, mural thrombus or Dressler syndrome

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32
Q

What is Dressler’s syndrome?

A

pericarditis that occurs 6-8 weeks post MI; Ab is produced against the myocardium

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33
Q

Causes of left sided heart failure

A

ischemia, HTN, dilated cardiomyopathy, myocardial infarction, restrictive cardiomyopathy

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34
Q

Mainstay treatment of left sided heart failure

A

ACE inhibitor

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35
Q

Dyspnea, paroxysmal norturnal dyspnea, orthopnea and crackles seen in left sided heart failure is due to?

A

pulmonary congestion that leads to pulmonary edema

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36
Q

Heart failure cells seen in left sided heart failure are ?

A

hemosiderin laden macrophages

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37
Q

Decreased flow in the kidneys, which can happen in left sided heart failure leads to?

A

activation of the renin-angiotensin system => resultant fluid retention exacerbates CHF

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38
Q

What is the most common cause of right sided heart failure?

A

left sided heart failure

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39
Q

Clinical features of right sided heart failure are mainly due to ?

A

congestion

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40
Q

What are the clinical features of right sided heart failure?

A

jugular venous distension; painful hepatosplenomegaly with characteristic “nutmeg liver”; dependent pitting edema

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41
Q

Eisenmenger syndrome

A

increase pulmonary resistance from a left to right shunt leads to a reversal of the shunt causing late cyanosis with right ventricular hypertrophy, polycythemia and clubbing

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42
Q

When does cyanosis present in defects with right to left shunting?

A

shortly after birth

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43
Q

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

A

Ostium primum type

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44
Q

Atrial septal defect results in what type of shunt and what is heart on auscultation?

A

results in left to right shunt; split S2 heard on auscultation (increased blood in right heart delays closure of pulmonary valve)

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45
Q

What is an important complication of atrial septal defect?

A

paradoxical emboli

46
Q

Patent ductus arteriosus is associated with which congenital infection?

A

congential rubella

47
Q

What type of shunting results from a patent ductus arteriosus?

A

left to right shunting between the aorta and the pulmonary artery

48
Q

How does PDA present at birth?

A

asymptomatic with a holosytolic machine like murmur

49
Q

What is used to treat a PDA

A

Indomethacin - decreases PGE (PGE keeps the DA patent so decreasing it would cause closure)

50
Q

How does tetrology of fallot present on chest xray?

A

boot shaped heart

51
Q

What are the 4 characteristics of the tetrology of fallot?

A

stenosis of the right ventricular outflow tract; right ventricular hypertrophy; VSD; aorta that overrides the VSD

52
Q

patients with a tetrology of fallot engage in what action during a cyanotic spell

A

they learn to squat - this increases arterial resistance which decreases shunting from the right to the left and allows more blood to reach the lungs

53
Q

What is transposition of the great vessels characterized by?

A

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

54
Q

What condition is transposition of the great vessels associated with?

A

maternal diabetes

55
Q

What is required for survival in patients with transposition of the great vessels?

A

A PDA in order for the circuits to mix

56
Q

Name the four congenital defects that can cause early cyanosis?

A

tetrology of fallot; transposition of the great vessels; truncus arteriosus; tricuspid atresia

57
Q

What type of shunting generally presents as cyanosis shortly after birth?

A

right to left shunting

58
Q

What characterizes truncus arteriosus?

A

a single large vessel arising from both ventricles

59
Q

What characterizes tricuspid atresia?

A

tricuspid valve orifice fails to develop; RV is hypoplastic; often associated with ASD

60
Q

What characterizes the infantile form of coarctation of the aorta?

A

associated with PDA; coarctation lies after the aortic arch but before the PDA

61
Q

How does the infantile forms of coarctation of the aorta present?

A

lower extremity cyanosis, often at birth

62
Q

Infantile form of coartation of the aorta is associated with what condition?

A

Turner syndrome

63
Q

What characterizes the adults form of coarctation of the aorta?

A

is not associated with PDA; coarctation lies after the aortic arch

64
Q

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

A

HTN in the upper extremities; hypotension with weak pulses in the lower extremities; collateral circulation develops across intercostal arteries causing notching on ribs

65
Q

Coarctation of the aorta in adults is associated with what type of valve abnormality?

A

bicuspid aortic valve

66
Q

What evidence indicates prior group A beta hemolytic streptococcal infection

A

elevated ASO or anti-DNase B titers

67
Q

Major criteria of acute rheumatic fever

A

migratory polyarthritis; pancarditis; subcutaneous nodules; erythema marginatum; sydenham chorea

68
Q

Myocarditis caused by acute Rheumatic fever is characterized by what components?

A

Aschoff bodies (foci of chronic inflammation); Anitschkow cells (reactive histiocytes with slender, wavy nuclei); giant cells and fibrinoid material

69
Q

Chronic rheumatic heart disease is characterized by?

A

valve scarring; stenosis with a classic “fish mouth” appearance; almost always involves MITRAL VALVE

70
Q

Aortic stenosis is usually due to?

A

fibrosis and calcification from “wear and tear”; presents late in adulthood (>60)

71
Q

What can increase risk of aortic stenosis?

A

bicuspid aortic valve; normally there are 3 cusps, fewer cusps result in increased wear and tear

72
Q

Aortic stenosis can cause what to be heard during auscultation?

A

systolic ejection click followed by crescendo - decrescendo murmur

73
Q

What is aortic regurgitation?

A

back flow of blood from the aorta into the LV during diastole

74
Q

Aortic regurgitation causes hyperdynamic circulation due to increased pulse pressure b/c?

A

diastolic pressure decreases due to regurgitation while systolic pressure increases due to increased stroke volume

75
Q

How does hyperdynamic circulation seen in aortic regurgitation present?

A

bound pulse; pulsating nail bed (Quincke pulse); head bobbing

76
Q

What is mitral valve prolapse?

A

ballooning of the mitral valve into the LA during systole

77
Q

What causes MV prolapse?

A

myxoid degeneration (accumulation of ground substance) of the valve making it floppy

78
Q

MV prolapse is seen in what two conditions?

A

Marfan syndrome and Ehlers-Danlos syndrome

79
Q

How does MV prolapse present on auscultation?

A

mid-systolic click followed by crescendo murmur

80
Q

What action increases the click and murmur heard on auscultation with MV prolapse?

A

squatting - increases systemic resistance decreases left ventricular emptying

81
Q

What is mitral regurgitation?

A

reflux of blood from the LV into the left atrium during systole

82
Q

What can be heard on auscultation for mitral regurgitation?

A

holosystolic blowing murmur - louder with squatting due to increased systemic vascular resistance decreases ventricular emptying and expiration due to increase return to LA

83
Q

How does mitral stenosis present on auscultation?

A

opening snap followed by diastolic rumble

84
Q

What is the most common cause of endocarditis overall?

A

Strep viridans - low virulence organism that infects previously damaged valves

85
Q

What is the laboratory profile of strep viridans?

A

alpha hemolytic; bile esculin negative; optochin resistant

86
Q

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

A

Staph aureus

87
Q

What valve is most commonly affected by staph aureus?

A

tricuspid valve

88
Q

Endocarditis as a result of staph aureus infection causes what kind of vegetation?

A

results in large vegetations that destroy the valve

89
Q

Endocarditis as a result of strep viridans infections causes what kind of vegetation?

A

results in small vegetations that do not destroy the valve

90
Q

Endocarditis from prosthetic valves is associated with what bacteria?

A

Staph epidermidis

91
Q

Strep bovis is associated with endocarditis in patients with what underlying condition?

A

colorectal carcinoma

92
Q

Clinical features of bacterial endocarditis?

A

Janeway lesions (nontender lesions on palms, soles); Osler nodes (tender lesions on fingers, toes); splinter hemorrhages on nail bed

93
Q

What is Libman Sacks endocarditis?

A

sterile vegetations that arise in association with SLE; vegetations are present on the surface AND undersurface of the mitral valve and cause mitral regurgitation

94
Q

What is the most common form of cardiomyopathy?

A

dilated cardiomyopathy

95
Q

dilated cardiomyopathy is characterized by?

A

dilation of all four chambers of the heart

96
Q

the most common cause of dilated cardiomyopathy is?

A

idiopathic (also associated with alcohol use, pregnancy and doxorubicin)

97
Q

What is hypertrophic cardiomyopathy?

A

massive hypertrophy of the LV

98
Q

what is the most common cause of hypertrophic cardiomyopathy?

A

genetic mutations in sarcomere proteins; most commonly AD

99
Q

biopsy of hypertrophic cardiomyopathy will show what?

A

myofiber hypertrophy with disarray

100
Q

What are the clinical features of hypertrophic cardiomyopathy?

A

decreased CO b/c LV hypertrophy leads to diastolic dysfunction where ventricle cannot fill; sudden death; syncope with exercise

101
Q

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

A

hypertrophic cardiomyopathy

102
Q

What is restrictive cardiomyopathy?

A

decreased compliance of the ventricular endomyocardium that restricts filling during diastole

103
Q

What are some causes of restrictive cardiomyopathy?

A

amyloidosis, sarcoidosis, hemochromatosis, endocardial fibroelastosis, Loeffler syndrome (associated with eosinophilia)

104
Q

How does restrictive cardiomyopathy present?

A

as congestive heart failure

105
Q

What is a classic finding on low voltage EKG that indicates restrictive cardiomyopathy?

A

diminished QRS amplitude

106
Q

Name the cardiac tumor — benign mesenchymal tumor with a gelatinous appearance and abundant ground substance, most common primary cardiac tumor in adults; forms a pedunculated mass in the LA

A

Myxoma

107
Q

Name the cardiac tumor — benign hemartoma of cardiac muscle; most common primary cardiac tumor in CHILDREN; associated with TUBEROUS SCLEROSIS; usually in ventricle

A

Rhabdomyoma

108
Q

T/F metastatic tumors are more common in the heart than primary tumors

A

T

109
Q

Metastasis to the heart most commonly affect which part?

A

pericardium - results in pericardial effusion

110
Q

What are some common metastases to the heart?

A

breast and lung carcinoma, melanoma, lymphoma

111
Q

Risk for free wall rupture is greatest after how many days post MI and why?

A

After 5-10 days; macrophages have degraded important structural components as they replace neutrophils, the heart is maximally soft and prone to rupture

112
Q

When is the heart at greatest risk for undergoing a ventricular aneurysm post MI and why?

A

around 7-8 weeks; dense type I collagen replaces the primitive type III collagen, this puts the heart at risk for undergoing a ventricular aneurysm as the scar tissue has diminished contractile properties it can become weak

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