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Pathology > CVS Pathology II > Flashcards

CVS Pathology II Flashcards

1
Q

Ischemic heart disease (IHD) results from an imbalance of the _______ and ______ of the heart

A

Blood supply and oxygen demand

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2
Q

Name modifiable risk factors of IHD

A

Diet, hyperlipidemia, hypertension, DM, cigarette smoking

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3
Q

Name non-modifiable risk factors of IHD

A

Age, gender (male), familial dispostion

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4
Q

Factors associated with a decreased risk in IHD

A

Alcohol (red wine), regular exercise, high HDL, estrogen, folate

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5
Q

Causes of IHD

A

Fixed stenosing atherosclerosis, Fissure/rupture/ulceration/hemorrhage, Coronary artery thrombosis, Coronary artery vasoconstriction/vasospasm (no plaque), Critical stenosis

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6
Q

At what percentage is stenosis considered critical? Why?

A

> 70%; at this fixed level of obstruction compensatory mechanisms areinsufficient to meet moderate increases in myocardial O2 demand

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7
Q

Acute plaque changes are associated with

A

Acute coronary syndromes (unstable angina, AMI, Sudden cardiac death)

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8
Q

Name some acute plaque changes

A

rupture/fissuring, erosion/ulceration, hemorrhage into atheroma

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9
Q

What is the underlying cause of a typical angina pectoris

A

Fixed coronary obstruction, causing transient myocardial ischemia that falls short of infarction

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10
Q

Occlusive thrombus is associated with…

A

acute transmural myocardial infarction

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11
Q

Name some atheromatous Coronary arterial occlusions

A

embolism, dissecting aneurysm, vasospasm, congenital anomaly, trauma

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12
Q

Inflammation plays a role in later stages of IHD by…

A

secretion of metalloproteinases by macrophages

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13
Q

Inflammation plays a role in the initial stages of IHD by…

A

interaction of endothelial cells and circulating leukocytes

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14
Q

IHD syndromes are _____ manifestations of coronary atherosclerosis

A

late

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15
Q

What are the syndromes of IHD

A

1) Angina Pectoris
2) Acute MI
3) Chronic Ischemic heart disease (Ischemic cardiomyopathy)
4) Sudden Cardiac death

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16
Q

Angina pectoris is cause by increased myocardial demand with decreased perfusion d/t:

A

Chronic stenosing coronary atherosclerosis, disrupted atherosclerotic plaques, vasospasm, thrombosis, coronary artery embolization

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17
Q

3 types of Angina Pectoris

A

Stable, Prinzmetal, Unstable

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18
Q

In stable angina, chest pain is precipitated by _______ and relieved by _______

A

exertion and emotion, rest and vasodilators

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19
Q

Prinzmetal Angina Pectoris is d/t and ECG changes are suggestive of _____

A

Vasospasm; transmural ischemia (ST segment elevation)

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20
Q

In Prinzmetal angina pectoris, there is episodic pain at _____ that responds to _____

A

Rest; nitroglycerin, Ca-channel blockers, vasodilators

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21
Q

% vessel blocked in Unstable Angina Pectoris

A

90%

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22
Q

In unstable angina, pain __________ in frequency and duration and occurs _______

A

progressively increases; at rest

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23
Q

Unstable angina pectoris is associated with

A

Acute plaque change with superimposed partial thrombosis or vasospasm

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24
Q

In MI, coronary obstruction produces what kind of cardiac muscle necrosis?

A

coagulative

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25
Q

Major risk factors of AMI

A

HTN, cigarette smoking, DM, hyperlipidemia

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26
Q

Minor risk factors of AMI

A

Obesity, sex, age, stress, physical inactivity

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27
Q

What is the hallmark myocardial change in AMI? In what region and what type of progression?

A

Ischemic coagulative necrosis; Subendocardial region; wavefront progression

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28
Q

Biochemical changes in AMI

A

Anaerobic glycolysis, ATP and creatinine phosphate reduction, lactic acidosis (increase muscle death)

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29
Q

Ultrastructural changes in AMI

A

mitochondrial swelling, myofibrillar relaxation, glycogen depletion, sarcolemmal membrane damage

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30
Q

In AMI, irreversible myocardial damage is seen in sever ischemia lasting from _____ or longer

A

20-40 minutes (another part says 10 minutes is the window period)

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31
Q

The patient may present with arrhythmia if the obstruction occurs in the _____

A

Anterior descending coronary artery

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32
Q

A rapid rate of occlusion development is mosre severe than a slow one b/c…

A

there is no time for collateral vessels to form

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33
Q

Types of infarction; Describe the difference in terms of wall thickness affected

A

Transmural (full thickness), Subendocardial (limited to inner 1/3 or 1/2 of ventricle)

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34
Q

Transmural Infarctions are associated with

A

CHRONIC atherosclerotic obstruction, acute plaque change, superimposed complete occlusive thrombosis

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35
Q

Subendocardial infarctions are associated with

A

Diffuse stenosing coronary atherosclerosis WITHOUT thrombosis and acute plaque change

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36
Q

What infarcts are referred to as ST elevation infarcts? Non-ST elevation infarcts

A

Transmural; Subendocardial

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37
Q

In the gross morphology of AMI, using triphenyl tetrazollium chloride stain, the infarct will show as _______

A

unstained area

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38
Q

Gross & microscopic findings 0-18 hours post MI

A

no gross change; wavy myocyte fibers

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39
Q

Dark mottling is seen _____ hours after AMI; What are the microscopic changes related this?

A

12-24 hours; coagulation necrosis, pyknosis of nuclei, myocytehypereosinophilia, marginal contraction band with beginning neutrophilic infiltrate

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40
Q

Gross & microscopic findings 7-28 days post MI

A

Central pallor with a red border; granulation tissue

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41
Q

Gross & microscopic findings 1-7 days post MI

A

Yellow pallor; Coagulative necrosis (4-24 hours), neutrophilic infiltrate (1-4 days), macrophages (4-7 days)

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42
Q

Gross & microscopic findings months post MI

A

White firm scar; fibrotic scar

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43
Q

Mottling with yellow-tan infarct center is seen _____ days post MI

A

1-3 days

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44
Q

Hyperemic border with a central yellow-tan softening is seen ____ days post MI

A

3-7 days

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45
Q

Maximally yellow-tan and soft with depressed red-tan margin margins seen _____ days post MI

A

7-10 days

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46
Q

10-14 days post MI, what are the gross features and microscopic features

A

red-gray depressed infarct borders; well-established granulation tissue WITH new blood vessels and collagen deposition

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47
Q

2-4 weeks post MI, what are the gross features and microscopic features

A

Gray-white scar progressive from border toward core of infarct; Increased collagen deposition with DECREASED cellularity

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48
Q

> 2 months post MI, what are the gross features and microscopic features

A

Scarring complete; Dense collagenous scar

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49
Q

What is the most effective way to rescue ischemic myocardium?

A

Reperfusion

50
Q

Give complications of reperfusion

A

arrhythmias, myocardial hemorrhage with contraction bands, irreversible cell damage superimposed on the original ischemic injury, mircovascular injury, prolonged ischemic dysfunction

51
Q

Reperfusion beyond _____ does not appreciable reduce myocardial infarct size

A

6 hours

52
Q

Symptoms of AMI

A

Rapid weak pulse , diaphoresis

53
Q

In AMI, cardiac troponins I and T are ______

A

elevated

54
Q

_______ in levels of CK, CKMB troponin I in the 1st 2 days following chest pain essentially EXCLUDES a diagnosis of MI

A

Absence of change

55
Q

CK-MB is sensitive and specific for MI (T/F)

A

False; it is sensitive but NOT specific b/c it is found in other muscles

56
Q

Lab increase of ______ is found EARLIEST post MI

A

troponin

57
Q

Time frame for use of SGOT and LDH as markers of AMI

A

1-3 days

58
Q

Treatment for AMI

A

Aspirin and heparin, oxygen, nitrates, beta adrenergic blockers, ACE Inhibitors

59
Q

Complications of AMI

A

Contractile dysfunction, Arrhythmias, Myocardial rupture, Pericarditis, R-ventricular infarct, Infarct extension, Infarct expansion, Mural thrombus, Ventricular aneurysm, Papillary muscle dysfunction, Progressive late heart failure

60
Q

In AMI, prognosis and complications are dependent on

A

Infarct size, site, fractional thickness of myocardial wall damaged

61
Q

Types of infarct modifications

A

Thrombolysis, Angioplasty, Stent, CABG,

62
Q

It is the development of progressive heart failure as a result of chronic ischemic myocardial damage

A

Chronic Ischemic Heart Disease (Ischemic cardiomyopathy)

63
Q

In Ischemic cardiomyopathy, postinfarct decompensation is d/t

A

exhaustion of compensatory hypertrophy of non-infarcted viable myocardium

64
Q

Describe the gross morphology of the heart in ischemic cardiomyopathy

A

Large and heavy d/t L-ventricular dilation and hypertrophy, Moderate to severe stenosing atherosclerosis, Mural endocardium may have patchy fibrous thickenings and mural thrombi

65
Q

Describe the microscopic morphology of the heart in ischemic cardiomyopathy

A

gray-white scars of healed infarcts, myocardial hypertrophy, diffuse subenedocardial vacuolization

66
Q

In sudden cardiac death, there is unexpected death in _______ patients or those with symptoms less than _______

A

Asymptomatic; 1 hour

67
Q

Major cause of sudden cardiac death

A

Atherosclerosis

68
Q

Non-atherosclerotic causes of sudden cardiac death

A

Congenital structural or coronary arterial abnormalities, AV stenosis, MV prolapse, dilated or hypertrophic cardiomyopathy, myocarditis, Pulmonary HTN, Hereditary or acquired abnormality of cardiac conduction system, isolated hypertrophy

69
Q

(T/F) In sudden cardiac death, there will be no apparent changes in morphology of the heart

A

true

70
Q

A consistent finding in patients with sudden cardiac death is _____

A

Marked coronary atherosclerosis involving 1 or more major vessels and severe chronic ischemia is commonly seen

71
Q

2 types of hypertensive heart disease

A

Systemic (left-side) and Pulmonary (right-sided)

72
Q

What is the adaptive response of the heart in systemic hypertensive heart disease

A

CONCENTRIC left ventricular hypertrophy

73
Q

What is the adaptive response of the heart in pulmonary hypertensive heart disease

A

Right ventricular dilation

74
Q

What are the diagnostic criteria for What is the adaptive response of the heart in systemic hypertensive heart disease

A

Left ventricular hypertrophy, Hitory or pathologic evidence of HTN, Absence of other CVS lesions that may induce hypertrophy (ex valvular disease)

75
Q

In systemic hypertensive heart disease, papillary muscles and the intraventricular septum are ________ and there is stiffness and impairment of ________

A

thick, diastolic filling

76
Q

In systemic hypertensive heart disease, there is an increase in the ________ diameter of the myocytes with ______ nuclei

A

transverse, enlarged

77
Q

Pulmonary hypertensive heart disease is characterized by

A

RV hypertrophy, dilation and potentially failure d/t increased pulmonary resistance

78
Q

Different types of pulmonary hypertensive heart disease

A

Acute cor pulmonale; Chronic cor pulmonale

79
Q

How do you differentiate between acute and chronic cor pulmonale?

A

Acute = RV dilation WITHOUT hypertrophy; Chronic = RV dilation WITH hypertrophy

80
Q

Why is there no hypertrophy in acute cor pulmonale?

A

Because there is no time for adaptation (hypertrophic change)

81
Q

What kinds of disorders predispose you to chronic cor pulmonale?

A

Diseases of pulmonary parenchyma, pulmonary vessels, affecting chest movements, inducing pulmonary arterial constriction

82
Q

Name diseases of pulmonary parenchyma

A

COPD, diffuse pulmonary interstitial fibrosis, Pneumoconiosis, Cystic fibrosis, Bronchiectasis

83
Q

Name diseases of Pulmonary vessels

A

Recurrent pulmonary thromboembolism, primary pulmonary hypertension, extensive pulmonary arteritis, drugs, extensive pulmonary tumor microembolism

84
Q

Name diseases affecting chest movement

A

kyphoscoliosis, marked obesity, neuromuscular disease,

85
Q

Name diseases inducing pulmonary arterial constriction

A

hypoxemia, metabolic acidosis, chronic altitude sickness, obstruction to major airways, idiopathic alveolar hypoventilation

86
Q

Gross morphology of the heart in cor pulmonale

A

Compression of LV or tricuspid thickening and regurgitation

87
Q

Microscopic changes of the heart in cor pulmonale

A

Loss of fat in wall with myocytes aligned circumferentially (normally haphazard)

88
Q

Different kinds of myocardial disease

A

Inflammatory disorders, Immunologic and systemic metabolic disorders, genetic abnormalities

89
Q

4 types of cardiac myopathies (CMP)

A

Dilated, Hypertrophic, Restrictive, Arrhythmogenic Right Ventricular Dysplasia

90
Q

What is the most common type of cardiomyopathy

A

Dilated

91
Q

Ejection fraction in dilated cardiomyopathy

A

Low

92
Q

In dilated cardiomyopathy, death is usually attributable to

A

progressive heart failure or arrhythmia

93
Q

(T/F) The heart is hypocontracting in dilated cardiomyopathy

A

True

94
Q

S/S of dilated cardiomyopathy

A

(Manifestations of progressive CHF) SOB, easy fatigability, poor exertional capacity

95
Q

(T/F) Cardiac transplantation is recommended in dilated cardiomyopathy

A

True

96
Q

Causes of Dilated cardiomyopathy

A

Idiopathic, Previous viral or complicated myocarditis, alcohol abuse, Pregnancy, Genetic, Malnutrition (B12, B1), Cobalt (added to beer), Adriamycin therapy

97
Q

4 Criteria for diagnosis of dilated cardiomyopathy

A

NEGATIVE CRITERIA:

1) NO major CAD
2) NO valvular disease
3) NO systemic HTN
4) NO shunts within or outside the heart

98
Q

Gross morphology in dilated cardiomyopathy

A

Generalized chamber dilation (flabby), mural thrombi common, regurgitation d/t annular ring dilation, abnormal release of blood flow, increased weight, global enlargement

99
Q

What is the most important finding in Hypertrophic cardiomyopathy

A

Myocardial hypertrophy

100
Q

Differentiate Dilated and Hypertrophic cardiomyopathy in terms of chamber and contraction

A

DCM –> flabby and HYPOcontracting

HCM –> muscular and HYPERcontracting

101
Q

Differentiate Dilated and Hypertrophic cardiomyopathy in terms of abnormalities

A

DCM –> cytoskeleton; HCM –> mutations of proteins in sarcomere

102
Q

(T/F) HCM causes both diastolic and systolic dysfunction

A

False. Only diastolic dysfunction, systolic dysfunction is preserved

103
Q

What 2 diseases must be distinguished clinically from HCM

A

Amyloidosis, Hypertensive heart disease

104
Q

Clinical features of HCM

A

Decreased diastolic filling, reduced chamber size, reduced SV and CO, increased pulmonary venous pressure, exertional dyspnea; Harsh systolic ejection murmur

105
Q

In HCM, what is the cause of the harsh systolic ejection murmur

A

Ventricular outflow obstruction as the anterior mitral leaflet moves toward the ventricular septum during systole

106
Q

What are the major clinical problems in HCM

A

A.fib with mural thrombosis, infective endocarditis of MV, Intractable cardiac failure, Ventricular arrhythmias, Sudden death

107
Q

Describe the gross morphology of the heart in HCM

A

Massive myocardial hypertrophy WITHOUT ventricular dilation, Asymmetric septal hypertrophy, Banana-like ventricular cavity, endocaridal thickening, anterior mitral valve thickening

108
Q

Describe the microscopic morphology of the heart in HCM

A

Extensive myocardial hypertrophy, Haphazard myocardial fiber disarray (Most important), Interstitial fibrosis

109
Q

In restrictive cariomyopathy there is a ______ in cardiac compliance, ventricular filling during diastole and ejection fraction

A

Decrease

110
Q

What are the causes of Restrictive cardiomyopathy

A

Idiopathic, Amyloidosis, radiation fibrosis, sarcoidosis, immune, metabolic, metastatic tumors, deposition of metabolites d/t inborn errors of metabolism

111
Q

Gross morphology in Restrictive cardiomyopathy

A

Normal or slightly enlarged heart with non-dilated stiff ventricles; BI-ATRIAL DILATION

112
Q

What are the other types of RCM

A

Endomyocardial fibrosis, Leoffler endomyocarditis, Endocardial fibroelastosis

113
Q

Autosomal dominant Inherited cardiomyopathy that causes right ventricular failure and various rhythym disturbances (v.tach)

A

Arrhythmogenic Right ventricular cardiomyopathy

114
Q

Heart morphology in Arrhythmogenic Right ventricular cardiomyopathy

A

Severely thinned R-ventricular wall d/t loss of myocyte with extensive fatty infiltration and fibrosis

115
Q

Arrhythmogenic Right ventricular cardiomyopathy with hyperkeratosis of plantar palmar skin surfaces

A

Naxos syndrome

116
Q

Defect in Arrhythmogenic Right ventricular cardiomyopathy

A

Cell adhesion proteins in desmosomes that link adjacent cardiac myocytes

117
Q

Major causes of myocarditis are related to

A

Infections, Immune-mediated reactions, can be unknown, drugs

118
Q

Type of myocarditis with an aggressive clinical course

A

Giant cell myocarditis

119
Q

Myocarditis associated with ADR, with little or no necrosis, granulomas

A

Hypersensitivity myocarditis

120
Q

ADR of what drug is most of the time related to hypersensitivity myocarditis

A

Methyldopa

121
Q

In myocarditis, the heart is _______ d/t vascular congestion and the ventricular myocardium is _____

A

Beefy red; flabby and mottled by focal hemorrhagic lesions

122
Q

In myocarditis, the heart is _______ d/t vascular congestion and the ventricular myocardium is _____

A

Beefy red; flabby and mottled by focal hemorrhagic lesions

Pathology (7 decks)

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