CVS Pathology II Flashcards Preview

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Flashcards in CVS Pathology II Deck (122):
1

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

Blood supply and oxygen demand

2

Name modifiable risk factors of IHD

Diet, hyperlipidemia, hypertension, DM, cigarette smoking

3

Name non-modifiable risk factors of IHD

Age, gender (male), familial dispostion

4

Factors associated with a decreased risk in IHD

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

5

Causes of IHD

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

6

At what percentage is stenosis considered critical? Why?

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

7

Acute plaque changes are associated with

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

8

Name some acute plaque changes

rupture/fissuring, erosion/ulceration, hemorrhage into atheroma

9

What is the underlying cause of a typical angina pectoris

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

10

Occlusive thrombus is associated with...

acute transmural myocardial infarction

11

Name some atheromatous Coronary arterial occlusions

embolism, dissecting aneurysm, vasospasm, congenital anomaly, trauma

12

Inflammation plays a role in later stages of IHD by...

secretion of metalloproteinases by macrophages

13

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

interaction of endothelial cells and circulating leukocytes

14

IHD syndromes are _____ manifestations of coronary atherosclerosis

late

15

What are the syndromes of IHD

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

16

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

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

17

3 types of Angina Pectoris

Stable, Prinzmetal, Unstable

18

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

exertion and emotion, rest and vasodilators

19

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

Vasospasm; transmural ischemia (ST segment elevation)

20

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

Rest; nitroglycerin, Ca-channel blockers, vasodilators

21

% vessel blocked in Unstable Angina Pectoris

90%

22

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

progressively increases; at rest

23

Unstable angina pectoris is associated with

Acute plaque change with superimposed partial thrombosis or vasospasm

24

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

coagulative

25

Major risk factors of AMI

HTN, cigarette smoking, DM, hyperlipidemia

26

Minor risk factors of AMI

Obesity, sex, age, stress, physical inactivity

27

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

Ischemic coagulative necrosis; Subendocardial region; wavefront progression

28

Biochemical changes in AMI

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

29

Ultrastructural changes in AMI

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

30

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

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

31

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

Anterior descending coronary artery

32

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

there is no time for collateral vessels to form

33

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

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

34

Transmural Infarctions are associated with

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

35

Subendocardial infarctions are associated with

Diffuse stenosing coronary atherosclerosis WITHOUT thrombosis and acute plaque change

36

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

Transmural; Subendocardial

37

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

unstained area

38

Gross & microscopic findings 0-18 hours post MI

no gross change; wavy myocyte fibers

39

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

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

40

Gross & microscopic findings 7-28 days post MI

Central pallor with a red border; granulation tissue

41

Gross & microscopic findings 1-7 days post MI

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

42

Gross & microscopic findings months post MI

White firm scar; fibrotic scar

43

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

1-3 days

44

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

3-7 days

45

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

7-10 days

46

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

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

47

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

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

48

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

Scarring complete; Dense collagenous scar

49

What is the most effective way to rescue ischemic myocardium?

Reperfusion

50

Give complications of reperfusion

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

51

Reperfusion beyond _____ does not appreciable reduce myocardial infarct size

6 hours

52

Symptoms of AMI

Rapid weak pulse , diaphoresis

53

In AMI, cardiac troponins I and T are ______

elevated

54

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

Absence of change

55

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

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

56

Lab increase of ______ is found EARLIEST post MI

troponin

57

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

1-3 days

58

Treatment for AMI

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

59

Complications of AMI

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

In AMI, prognosis and complications are dependent on

Infarct size, site, fractional thickness of myocardial wall damaged

61

Types of infarct modifications

Thrombolysis, Angioplasty, Stent, CABG,

62

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

Chronic Ischemic Heart Disease (Ischemic cardiomyopathy)

63

In Ischemic cardiomyopathy, postinfarct decompensation is d/t

exhaustion of compensatory hypertrophy of non-infarcted viable myocardium

64

Describe the gross morphology of the heart in ischemic cardiomyopathy

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

Describe the microscopic morphology of the heart in ischemic cardiomyopathy

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

66

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

Asymptomatic; 1 hour

67

Major cause of sudden cardiac death

Atherosclerosis

68

Non-atherosclerotic causes of sudden cardiac death

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

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

true

70

A consistent finding in patients with sudden cardiac death is _____

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

71

2 types of hypertensive heart disease

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

72

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

CONCENTRIC left ventricular hypertrophy

73

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

Right ventricular dilation

74

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

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

75

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

thick, diastolic filling

76

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

transverse, enlarged

77

Pulmonary hypertensive heart disease is characterized by

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

78

Different types of pulmonary hypertensive heart disease

Acute cor pulmonale; Chronic cor pulmonale

79

How do you differentiate between acute and chronic cor pulmonale?

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

80

Why is there no hypertrophy in acute cor pulmonale?

Because there is no time for adaptation (hypertrophic change)

81

What kinds of disorders predispose you to chronic cor pulmonale?

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

82

Name diseases of pulmonary parenchyma

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

83

Name diseases of Pulmonary vessels

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

84

Name diseases affecting chest movement

kyphoscoliosis, marked obesity, neuromuscular disease,

85

Name diseases inducing pulmonary arterial constriction

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

86

Gross morphology of the heart in cor pulmonale

Compression of LV or tricuspid thickening and regurgitation

87

Microscopic changes of the heart in cor pulmonale

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

88

Different kinds of myocardial disease

Inflammatory disorders, Immunologic and systemic metabolic disorders, genetic abnormalities

89

4 types of cardiac myopathies (CMP)

Dilated, Hypertrophic, Restrictive, Arrhythmogenic Right Ventricular Dysplasia

90

What is the most common type of cardiomyopathy

Dilated

91

Ejection fraction in dilated cardiomyopathy

Low

92

In dilated cardiomyopathy, death is usually attributable to

progressive heart failure or arrhythmia

93

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

True

94

S/S of dilated cardiomyopathy

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

95

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

True

96

Causes of Dilated cardiomyopathy

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

97

4 Criteria for diagnosis of dilated cardiomyopathy

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

98

Gross morphology in dilated cardiomyopathy

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

99

What is the most important finding in Hypertrophic cardiomyopathy

Myocardial hypertrophy

100

Differentiate Dilated and Hypertrophic cardiomyopathy in terms of chamber and contraction

DCM --> flabby and HYPOcontracting
HCM --> muscular and HYPERcontracting

101

Differentiate Dilated and Hypertrophic cardiomyopathy in terms of abnormalities

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

102

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

False. Only diastolic dysfunction, systolic dysfunction is preserved

103

What 2 diseases must be distinguished clinically from HCM

Amyloidosis, Hypertensive heart disease

104

Clinical features of HCM

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

105

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

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

106

What are the major clinical problems in HCM

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

107

Describe the gross morphology of the heart in HCM

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

108

Describe the microscopic morphology of the heart in HCM

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

109

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

Decrease

110

What are the causes of Restrictive cardiomyopathy

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

111

Gross morphology in Restrictive cardiomyopathy

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

112

What are the other types of RCM

Endomyocardial fibrosis, Leoffler endomyocarditis, Endocardial fibroelastosis

113

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

Arrhythmogenic Right ventricular cardiomyopathy

114

Heart morphology in Arrhythmogenic Right ventricular cardiomyopathy

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

115

Arrhythmogenic Right ventricular cardiomyopathy with hyperkeratosis of plantar palmar skin surfaces

Naxos syndrome

116

Defect in Arrhythmogenic Right ventricular cardiomyopathy

Cell adhesion proteins in desmosomes that link adjacent cardiac myocytes

117

Major causes of myocarditis are related to

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

118

Type of myocarditis with an aggressive clinical course

Giant cell myocarditis

119

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

Hypersensitivity myocarditis

120

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

Methyldopa

121

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

Beefy red; flabby and mottled by focal hemorrhagic lesions

122

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

Beefy red; flabby and mottled by focal hemorrhagic lesions