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Flashcards in Cardiovascular System - Fung Deck (207):
1

What are the layers of a blood vessel?

1. the tunica intima
2. the tunica media
3. the tunica adventitia

2

How are the layers of a blood vessel related to the heart?

The major blood vessels that connect to the heart are continuous with the heart.
1. the intima becomes endocardium
2. the media is made up of cardiac myocytes
3. the adventitia becomes epicardium

3

What two characteristics of the heart are most important in heart pathology?

1. cardiac weight
2. ventricular wall thickness

4

What is the average weight of a female heart?

250-300 grams

5

What is the average weight of a male heart?

300-350 grams

6

What is the typical thickness of the ventricular wall in females?

0.3-0.5 cm

7

What is the typical thickness of the ventricular wall in males?

1.3-1.5 cm

8

How is cardiac muscle different from striated muscle?

It has centrally located nuclei.

9

Describe the functions of vascular endothelial cells?

1. maintain non-thrombogenic blood-tissue interface
2. modulate vascular resistance
3. metabolize hormones
4. regulate inflammation
5. regulate cell growth

10

Describe the function of smooth vascular smooth muscle cells?

1. synthesize collagen, elastin and proteoglycans
2. produce growth factors and cytokines

11

What are the components of of vascular extracellular matrix?

1. elastin
2. collagen
3. gycosaminoglycans

12

What are the two types of arteries?

1. elastic arteries
2. muscular arteries

13

What layer of vasculature contain smooth muscle cells?

The tunica media

14

Which cells of vasculature are responsible for homeostasis of the vessel?

The endothelial cells.

15

Does an artery have more smooth muscle in it's tunica media?

Yes. Arteries have to work under higher pressure than veins.

16

What is the vasa vasorum and why do we need it?

The vasa vasorum are tiny blood vessels that supply other larger vessels. We need them because nutrients and oxygen can only diffuse so far. The vasa vasorum supplies part of the tunica media and the tunica adventitia.

17

Which types of vessels have more elastic tissue?

Elastic arteries.

18

Do muscular arteries have elastic tissue?

Yes. They have elastic tissue in the internal and external elastic lamina. They have less elastic tissue than elastic arteries.

19

Give a couple examples of elastic arteries.

1. aorta
2. common carotids

20

Give a couple examples of muscular arteries.

1. radial artery
2. femoral artery

21

What are the two types of vascular systems?

1. blood vascular system
2. lymph vascular system

22

Do lymph vessels have muscular walls?

No. Lymph moves due to contraction of surrounding muscle.

23

Where does gas and nutrient exchange take place?

Capillaries.

24

Veins are not very muscular. How do they get blood back to the heart?

Contraction of skeletal muscle helps blood flow back to heart and one way valves keep the blood from flowing backwards.

25

Most cardiovascular disease results from….?

“a complex interplay of genetics and environmental factors that disrupt networks of genes and signaling pathways that control morphogenesis, myocyte survival and response to injury, biochemical stress responses, contractility or electrical conduction”

26

What are the six mechanisms of cardiac dysfunction?

1. failure of pump
2. obstruction of flow
3. regurgitant flow
4. shunted flow
5. disorders of cardiac conduction
6. rupture of the heart or a major blood vessel

27

Cardiovascular disease is most commonly related to what?

Atherosclerosis.

28

Describe the stereotypical response of blood vessels to injury.

1. recruitment of smooth muscle cells or smooth muscle precursor cells to the tunica intima
2. smooth muscle cells undergo mitosis and proliferation
3. elaboration of smooth muscle cell extracellular matrix
4. inflammation

29

Endothelial cell loss or dysfunction does what…?

Stimulates smooth muscle cell growth and extracellular matrix synthesis leading to intimal thickening.

30

What is hypertension?

Sustained increased blood pressure associated with increased risks.

31

Sustained increased blood pressure is associated with risk of...?

1. atherosclerosis
2. hypertensive heart disease
3. multi-infarct dementia
4. aortic dissection
5. renal failure

32

What is the normal blood pressure range?

less than 120/less than 80 mmHg

33

What is prehypertension?

Blood pressure between 120-139/ 80-89 mm Hg

34

What is the blood pressure range for hypertension?

greater than 140/greater than 89 mm Hg

35

What is the blood pressure range associated with malignant hypertension?

greater than 200/ greater than 120 mm Hg

36

What are some broad categories of causes of essential hypertension?

1. single gene defects
2. polymorphisms
3. vascular - vasoconstricion, structural changes
4. environmental factors

37

Single gene defects that cause essential hypertension are usually involved in what functions?

1. aldosterone
2. metabolism
3. sodium reabsorption

38

Polymorphisms associated with essential hypertension are usually involved with what systems?

1. angiotensinogen locus
2. angiotensin receptor locus
3. renin-angiotensin system

39

What are some environmental factors associated with essential hypertension?

1. diet
2. stress
3. obesity
4. smoking
5. physical inactivity

40

Most commonly, the cause of essential hypertension is what?

Idiopathic

41

What are systems that if effected could cause secondary hypertension?

1. renal system
2. endocrine system
3. cardiovascular system
4. neurologic system

42

What kinds of conditions affecting the renal system could lead to secondary hypertension?

1. acute glomerulonephritis
2. chronic renal disease
3. polycystic disease
4. renal artery stenosis
5. renal vasculitis
6. renin-producing tumors

43

What kinds of conditions affecting the endocrine system could lead to secondary hypertension?

1. adrenocortical dysfunction
2. exogenous hormones
3. pheochromocytoma
4. acromegaly
5. hypothyroidism
6. hyperthyroidism
7. pregnancy-induced

44

What kinds of conditions affecting the cardiovascular system can lead to secondary hypertension?

1. coarctation of the aorta
2. polyarteritis nodosa
3. increased vascular volume
4. increased cardiac output
5. rigidity of aorta

45

What kinds of conditions affecting the neurologic system can lead to secondary hypertension?

1. psychogenic
2. increased intracranial pressure
3. sleep apnea
4. acute stress

46

Hyperplastic arteriosclerosis is associated with what type of hypertension?

Malignant hypertension.

47

What are atheromas?

Raised lesions that protrude into a vessel lumen. They consist of a sod yellow core of lipid and are covered by a fibrous cap.

48

What does a fibrous cap consist of?

1. smooth muscle cells
2. macrophages
3. foam cells
4. lymphocytes
5. collagen
6. elastin
7. proteoglycans
8. they are also neovascularized

49

What does the necrotic center of an atheroma consist of?

1. cell debris
2. cholesterol crystals
3. foam cells
4. calcium

50

Atheromas can cause…..?

1. obstruction of blood flow
2. they can rupture and cause vessel thrombosis
3. can lead to formation of an aneurysm

51

Does atherosclerosis start in childhood?

Yes.

52

What is one consequence of an atheroma?

Because they protrude out from the vessel wall and into the lumen, they increase the distance with which nutrients have to diffuse to get to the layers of the vessel wall.

53

What are the constitutional risk factors for atherosclerosis?

1. age
2. gender (male)
3. genetics

54

What are the modifiable risk factors for atherosclerosis?

1. hyperlipidemia
2. hypertension
3. smoking
4. diabetes

55

What are some other risk factors for atherosclerosis?

1. inflammation
2. hyperhomocysteinemia
3. metabolic syndrome
4. Lipoprotein A
5. hemostatic factors
6. sedentary life style
7. Type A personality/stress
8. obesity

56

What is the response to injury hypothesis of athersclerosis?

This theory states that atherosclerosis is a chronic inflammatory and healing response to arterial wall and endothelial injury.

57

What are the steps leading to atherosclerosis according to the injury response hypothesis?

1. endothelial injury
2. lipoprotein accumulation
3. monocyte adhesion and formation of foam cells
4. platelet adhesion
5. smooth muscle cell recruitment
6. smooth muscle cell proliferation and ECM production
7. lipid accumulation

58

What are the two main causes of endothelial injury?

1. hemodynamic disturbances
2. hyperlipidemia

59

What are some ways that endothelium can be injured?

1. mechanical denudation
2. immune complex deposition
3. irradiation
4. chemicals

60

What are some things that can cause endothelial dysfunction?

1. hemodynamic disturbances
2. hypercholesterolemia
3. hypertension
4. smoking
5. infectious agents
6. homocysteine

61

Where do atherosclerotic plaques tend to occur?

At areas of disturbed blood flow or areas of hemodynamic disturbance. Including - branch points, ostia of exiting vessels, and the posterior wall of the abdominal aorta.

62

What type of blood flow is protective against atherosclerosis?

Non-turbulent, laminar flow.

63

What are the dominant types of lipids in atherosclerotic plaques?

1. cholesterol
2. cholesterol esters

64

Describe the relationship between lipids and atherosclerosis.

1. Genetic hyperlipoproteinemia is associated with accelerated atherosclerosis
2. DM and hypothyroidism is associated with hypercholesterolemia
3. Lowering serum cholesterol slows the rate of atherosclerosis

65

What affect does lipid accumulation have on vessels?

It reduces their ability to dilate. Hyperlipidemia increases ROS production which then accelerates decay of nitric oxide so that vessels cannot vasodilate very well.

66

Lipid accumulation increases the production of what type of cells?

Foam cells. The ROS's oxidize LDL which is then ingested by macrophages through a scavenger receptor. Also, oxidized LDL increases release of growth factors, cytokines and chemokines that lead to monocyte recruitment.

67

LDL is cytotoxic to what?

Endothelial cells and smooth muscle cells of the vessel wall. This injures the endothelium and leads to plaque formation.

68

Atherosclerotic lesions cause what?

Chronic inflammation with T-cell proliferation. It also leads to release of chemokines and growth factors that promote smooth muscle cell proliferation and ECM synthesis.

69

What are the major consequences of atherosclerosis?

1. MI
2. cerebral infarction
3. aortic aneurysm
4. peripheral vascular disease

70

Atheroma's project into the lumen of a vessels and cause….?

Stenosis.

71

What percentage of stenosis of a vessel is critical and causes chronically decreased perfusion?

70%

72

Chronically decreased perfusion leads to…..?

1. bowel ischemia
2. chronic ischemic heart disease
3. ischemic encephalopathy
4. intermittent claudication

73

Unstable atherosclerotic plaques can undergo what changes?

1. they can rupture, fissure, erode or ulcerate
2. if any of the above happen then thrombogenic plaque contents or the thrombogenic sub endothelial basement membrane is exposed to blood and can lead to thrombus formation
3. plaques can also hemorrhage

74

Describe the progression of atherosclerosis.

Pre-clinical phase - usually younger age:
1. lesion prone areas start to form fatty streaks or undergo endothelial injury or dysfunction
2. endothelial injury/dysfunction leads to formation of plaques
3. over time plaques remodel and grow and may become unstable
Clinical phase - usually middle age to elderly:
1. plaques/atheroma's begin to cause clinical symptoms
2. They can cause thrombosis, emboli and vessel wall weakening leading to aneurysm and rupture
3. atheroma's can rupture, erode, hemorrhage leading to thrombus formation and occlusion
4. atheroma's can grow and cause critical stenosis

75

Describe ischemic heart disease.

This term is a generic designation for a group of pathologically related syndromes resulting from myocardial ischemia.

76

What is myocardial ischemia?

An imbalance between the supply and demand of the heart for oxygenated blood.

77

Ischemic heart disease is also called what?

Coronary artery disease.

78

Ischemic heart disease results from what?

1. a greater than 90% obstructive atherosclerotic lesion in the coronary arteries
2. coronary emboli
3. blockage of coronary arteries
4. severe hypotension

79

What are some results of ischemic heart disease?

1. tachycardia
2. myocardial hypertrophy
3. hypoxemia

80

Name some ischemic heart diseases?

1. angina pectoris
2. MI
3. chronic ischemic heart disease with heart failure
4. sudden cardiac death (usually due to arrythmias)

81

Describe angina pectoris.

1. Paroxysmal and recurrent attacks of substernal and precordial chest discomfort
2. Caused by transient myocardial ischemia that falls short of inducing myocyte necrosis

82

What are the variants of angina pectoris?

1. stable (most common)
2. prinzmetal
3. unstable (crescendo)

83

Describe Stable angina.

1. Caused by an imbalance of perfusion (75% occlusion) relative to myocardial demand
2. Physical activity, emotional excitement or increased cardiac workload
3. Relieved by rest or vasodilators

84

Describe Prinzmetal angina.

1. Caused by coronary artery spasm unrelated to physical activity, heart rate or BP
2. Relieved by vasodilators and calcium channel blockers

85

Describe Unstable angina.

1. Pattern of increasingly frequent pain of prolonged duration that is precipitated at low levels or activity or at rest
2. Seen in artery occlusion of 90% or greater
3. Caused by:
Acute plaque change with superimposed thrombosis/embolism or vasospasm
4. Warning of impending acute MI

86

What is MI?

Myocardial infarction - death of cardiac muscle due to prolonged severe ischemia.

87

Describe the typical sequence of an MI.

1. Acute change of an atheromatous plaque exposes very thrombogenic contents
2. Platelets adhere to the exposed plaque and degranulate and initiate vasospasm
3. Tissue factor activates the coagulation cascade adding to the bulk of the thrombus
4. Thrombus completely occludes the lumen of the vessel

88

What is the time frame in which ischemia may occur but in which myocardium can still be saved?

Transient myocardial ischemia can last for about 20-30 minutes. After this time there will be myocardial death and an MI has occurred.

89

90% of MI's are caused by what?

Atherosclerosis. The other 10% occur without accompanying coronary vascular pathology.

90

What are some ways for MI to occur without vascular pathology?

1. cocaïne abuse can cause vasospasm
2. A-fib, infective endocarditis with vegetations, left sided mural thrombus, paradoxical right sided emboli can all cause occlusion via an emboli
3. vasculitis, sickle cell disease, amyloid deposition, vascular dissection and hypotensive shock can all cause MI without atherosclerosis or thrombosis

91

Describe when irreversible and reversible injury occur during ischemia/MI.

1. reversible injury occurs when ischemia lasts no more than 20-30 minutes
2. irreversible injury occurs with severe and prolonged ischemia (longer than 30 minutes) leading to myocyte necrosis

92

Necrosis after an MI is complete within……?

6 hours

93

What happens to cardiac myocytes during ischemia?

1. within seconds there will be cessation of aerobic metabolism
2. there will be loss of contractility within 60 seconds

94

The morphologic features of an MI depend on what factors?

1. Location and severity of the atherosclerosis
2. Size of the vascular bed perfused by the obstructed vessel
3. Duration of the occlusion
4. Oxygen demands of the affected myocardium
5. Extent of collateral circulation
6. Heart rate, cardiac rhythm and 7. O2 saturation

95

Myocardial ischemia proceeds….?

From the endocardium outward.

96

Name two types of infarctions.

1. transmural infarction
2. subendocardial infarction

97

Describe a transmural infarction.

1. Necrosis involves the full thickness
2. Associated with chronic atherosclerosis, acute plaque change, superimposed thrombus
3. ST elevation infarcts

98

Describe subendocardial infarction.

1. Necrosis limited to the inner 1/3-1/2 of the ventricular wall
2. Due to any reduction in coronary flow: plaque disruption with lysed thrombus, global hypotension
3. Non-ST elevation infarcts

99

The LAD supplies what areas of the heart?

1. apex
2. anterior wall of the left ventricle
3. anterior 2/3 of the ventricular septum

100

The Right coronary artery supplies what areas of the heart?

1. posterior 1/3 of the septum
2. free wall of right ventricle
3. posterolateral wall of the left ventricle

101

The left circumflex artery supplies what area of the heart?

The myocardium of the left ventricle.

102

Describe some of the changes that occur in myocardium after an MI.

1. in the first two days there will be coagulative necrosis
2. in 3-4 days there is recruitment of acute inflammatory cells and the myocardium begins healing
3. in 1-2 weeks granulation tissue, lots of macrophages and new blood vessels will be present
4. eventually there will be scarring and once there is scarring you cannot tell when the MI occurred

103

What are the clinical features of an MI?

1. rapid, weak pulse
2. diaphoresis
3. dyspnea
4. can also be asymptomatic

104

Name three cardiac markers in the blood.

1. myoglobin
2. CK-MB
3. Troponin I and T

105

When does Myoglobin appear in the blood after an MI?

0-2 hours and it peaks at about 6-8 hours.

106

Is the myoglobin marker specific and/or sensitive for an MI?

No. It can be found in the blood after cardiac or skeletal muscle injury.

107

When does CK-MB appear in the blood after an MI?

2-4 hours and it peaks at about 24 hours.

108

Is the CK-MB marker specific and/or sensitive for an MI?

It is sensitive but not specific. It is mainly found in cardiac muscle but can be found in some skeletal muscle.

109

When does Troponin appear in the blood after an MI?

2-4 hours and it peaks at about 48 hours. Levels persist for 7-10 days post MI.

110

Is the Troponin marker specific and/or sensitive for an MI?

It is both sensitive and specific. It is more sensitive than CK-MB.

111

What is given to treat MI's?

Aspirin
Heparin
Oxygen
Nitrates
Beta-adrenergic inhibitors
ACE inhibitors
Reperfusion

112

How does repercussion help treat an MI?

1. Rescues ischemic myocardium and limits infarct size and can be done via:
Thrombolysis
Angioplasty
Stent placement
Coronary artery bypass graft (CABG)

2. Is limited by:
Rapidity of alleviating the obstruction
Extent of the correction and the underlying causal lesion

113

What are some adverse complications that can occur after reperfusion?

1. Arrhythmias
2. Myocardial hemorrhage with contraction bands
3. Irreversible cell damage superimposed on the original injury (reperfusion injury)
4. Microvascular injury
5. Prolonged ischemic dysfunction (myocardial stunning)

114

What are some complications of an MI?

Contractile dysfunction
Arrhythmias
Myocardial rupture
Pericarditis
Right ventricular infarctionInfarct extension
Infarct expansion
Mural thrombus
Ventricular aneurysm
Papillary muscle dysfunction
Progressive late heart failure

115

Describe chronic ischemic heart disease.

1. Progressive heart failure as a consequence of ischemic myocardial damage
2. Also referred as ischemic cardiomyopathy
3. Appears due to function decompensation of hypertrophied noninfarcted myocardium

116

Sudden cardiac death can be caused by what?

Congenital structural or coronary arterial abnormalities
Aortic valve stenosis
Mitral valve prolapse
Myocarditis
Cardiomyopathies
Pulmonary hypertension
Drug abuse (cocaine, meth)
Hereditary or acquired cardiac arrhythmias
Systemic metabolic and hemodynamic alterations
Catecholamines

117

What are some hereditary or acquired arrhythmias that can cause sudden cardiac death?

1. long QT
2. short QT
3. WPW
4. sick sinus syndrome
5. catecholamine polymorphic VT

118

Sudden cardiac death can also be caused by what complication of atherosclerosis and ischemia?

1. formation of a lethal arrhythmia such as Asystole or V-fib
2. arrhythmia normally occurs at a site distant from the conduction system such as adjacent to scars of previous MI's

119

Heart failure occurs when….?

1. Heart is unable to pump blood sufficiently to meet the demands of the tissue
2. Heart can only pump blood sufficiently at elevated filling pressures

120

Heart failure develops due to….?

1. Chronic or acute valve disease
2. Long standing hypertension
3. Ischemic heart disease with myocardial infarction
4. Fluid overload

121

Heart failure is characterized by….?

1. Forward failure: decreased cardiac output and tissue perfusion (often associated with left-sided heart failure)
2. Backward failure: pooling of blood in the venous system (pulmonary and/or peripheral edema and liver congestion) - often associated with right sided heart failure

122

The body adapts to heart failure by what types of adaptive mechanisms?

1. Frank-starling mechanism - dilation and increased filling pressure
2. ventricular remodeling such as hypertrophy (with or without dilation)
3. neurohormonal mechanisms

123

Describe some neurohormonal mechanisms of adaption to heart failure.

1. Norepinephrine release to increase the heart rate
2. Activation of renin-angiotensin-aldosterone system to adjust filling volumes and pressures
3. Release of atrial natriuretic peptide to adjust filling volumes and pressures

124

What is hypertrophy in relation to heart failure?

Increased mechanical work due to pressure or volume overload or due to trophic signals causes the myocytes to increase in size.

125

How do myocytes increase in size during hypertrophy?

1. Protein synthesis to increase sarcomeres
2. Mitochondria increased to gain more energy
3. Nuclear size increased due to ploidy

126

Describe pressure overload hypertrophy.

1. Cardiac weight is increased
2. Sarcomeres increase in parallel to the long axes of cells, there is concentric increase in wall thickness
3. ventricular chamber size is normal

127

Describe volume overload hypertrophy.

1. Cardiac weight is increased
2. Sarcomeres increase in series with existing cells
3. Ventricle wall thickness may be increased, normal or less than normal
4. ventricles may dilate so that the ventricular chamber is increased in size

128

Adaptive changes of heart muscle in response to heart failure may themselves contribute to heart failure. By what mechanisms?

1. Hypertrophy isn’t accompanied by increase in capillaries
2. Change in myocardial metabolism
3. Alteration in intracellular handing of calcium ions
4. Apoptosis of myocytes
5. Reprogramming of gene expression

129

Left sided heart failure is caused by……?

Ischemic heart disease
Hypertension
Aortic and valvular diseases
Myocardial diseases

130

Describe the systolic and diastolic failure associated with left sided heart failure.

1. Systolic failure caused by insufficient cardiac output (basically pump failure)
2. Diastolic failure caused by stiff ventricles that cannot expand to increase output

131

What are the symptoms of left sided heart failure?

Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Renal failure
Loss of attention span, restlessness

132

Symptoms develop because of what in left sided heart failure?

Congestion of pulmonary circulation
Stasis of blood in left chambers
Hypoperfusion of tissues

133

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

Left sided heart failure.

134

Right sided heart failure (Cor Pulmonale) is caused by what?

1. Left sided heart failure and its causes
2. Pulmonary hypertension resulting from:
Parenchymal disease of the lung
Pulmonary vasculature disorders
Pulmonary thromboembolism
Hypoxic conditions

135

What are the symptoms of right sided heart failure?

Systemic and venous congestion dominate and cause:

Hepatosplenomegaly
Peripheral edema
Pleural effusions
Ascites
Abnormal mental function
Renal failure

136

Patients with heart failure frequently present with what?

Biventricular heart failure with symptoms of both right and left sided heart failure.

137

What meds are used to treat heart failure?

1. Diuretics
2. Renin-angiotensin-aldosterone blockers (ACE inhibitors)
3. β-blockers (lower adrenergic tone)

138

Hypertensive heart disease results from….?

Sustained increased hypertension that causes pressure overload and ventricular hypertrophy.

139

How is hypertensive heart disease (HHD) classified?

1. Left-sided (systemic) HHD
2. Right-side (cor pulmonale or pulmonary) HHD

140

What is the diagnostic criteria for Systemic HHD?

1. Left ventricular hypertrophy without any other cardiovascular pathology
2. History or pathologic evidence of hypertension

141

Describe pulmonary HHD.

1. Characterized by right ventricular hypertrophy and dilation
2. Can be acute (pulmonary embolism) or chronic

142

What is stenosis in relation to valvular heart disease?

1. Failure of a valve to open completely, which impedes flow
2. Leads to pressure overload

143

What is insufficiency/regurgitation in relation to valvular heart disease?

1. Failure of a valve to close completely, allowing reversed flow
2. Leads to volume overload
3. Functional regurgitation - failure in another component that then effects the valves

144

What causes mitral stenosis?

Rheumatic heart disease.

145

What are some causes of mitral regurgitation?

1. Rheumatic heart disease
2. infective endocarditis
3. mitral valve prolapse
4. drugs
5. rupture of papillary muscles
6. papillary muscle dysfunction
7. rupture of chordae tendineae
8. LVH
9. calcification

146

What are some causes of aortic valve stenosis?

1. rheumatic heart disease
2. senile calcifications
3. calcification of a congenitally deformed valve

147

What are some causes of aortic regurgitation?

1. rheumatic heart disease
2. infective endocarditis
3. marfan syndrome
4. degenerative aortic dilation
5. syphilitic aortitis
6. ankylosing spondylitis
7. rheumatoid arthritis

148

Describe Calcific aortic stenosis.

1. Due to normal wear and tear
2. Normally presents in the seventh to ninth decades of life
3. Obstruction results in pressure overload and LVH
4. the calcium that is deposited is made in fibroelastic cells of the valve itself

149

Describe calcific stenosis of a congenitally bicuspid aortic valve.

1. Most frequent congenital cardiovascular malformation
2. Due to normal wear and tear
3. Presents in the fifth to seventh decades of life, presents earlier in those with a bicuspid aortic valve because there are two cusps instead of three so wear and tear occurs faster

150

Describe mitral annular calcification.

1. Calcifications in the peripheral fibrous ring - NOT in valve itself
2. Does not affect valvular function or become clinically important
3. Rare complications include:
Regurgitation
Stenosis
Arrhythmias and sudden cardiac death

151

Describe mitral valve prolapse.

1. Mitral valve leaflets are floppy and prolapse into the left atrium during systole
2. Histologic change is myxomatous degeneration by an unknown mechanism
3. Most patients are asymptomatic and associated with a midsystolic click

152

What are some rare complications of mitral valve prolapse?

Infective endocarditis
Mitral insufficiency
Stroke
Arrhythmias

153

Describe Rheumatic fever.

1. Acute, immunologically mediated multisystem inflammatory disease that occurs a few weeks after group A streptococcal pharyngitis (antibodies to Group A strep attack antigens in heart that are similar in structure to Group A strep antigens)
2. Acute rheumatic carditis is a frequent consequence

154

What are the clinical features of Rheumatic fever?

Migratory polyarthritis of large joints
Pancarditis
Subcutaneous nodules
Erythema marginatum of the skin
Sydenham chorea

155

How is Rheumatic fever diagnosed?

The Jones criteria - According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection: elevated or rising antistreptolysin O titre or DNAase"

156

What are the major criteria in Jones criteria?

1. polyarthritis
2. carditis
3. erythema marginatum
4. sydenham's chorea
5. subacute nodules

157

What are the minor criteria in Jones criteria?

1. fever
2. arthralgia
3. leukocytosis
4. abnormal ECG
5. previous episodes of rheumatic fever
6. raised erythrocyte sedimentation rate of C-reactive protein

158

Acute rheumatic heart disease is characterized by…..?

1. Aschoff bodies (can be found in any layer - called pancarditis)
2. vegetations with underlying fibrinoid necrosis
3. MacCallum plaques within the left atrium

159

What types of cells are included in Aschoff bodies?

Aschoff bodies are granulomatous nodules found in the heart with Rheumatic disease, they are caused by inflammation and contain:
1. lymphocytes
2. plasma cells
3. Anitschkow cells ( are enlarged macrophages called Caterpillar cells because of the appearance of their chromatin)

160

Describe chronic Rheumatic heart disease.

1. A deforming fibrotic valvular disease
2. Only cause of mitral stenosis
3. Other valves can be involved
4. Aschoff bodies not identified

161

What happens to the mitral valve in chronic Rheumatic heart disease?

1. Leaflet thickening
2. Commissural fusion and shortening
3. Thickening and fusion of tendinous cords

162

Describe infective endocarditis.

1. Serious condition characterized by colonization or invasion of the heart valves or mural endocardium by a microbe
2. Vegetations composed of thrombotic debris and organisms
3. Acute or subacute forms

163

How is infective endocarditis diagnosed?

Via the Duke criteria which has pathologic, major and minor criteria. To diagnose you must have pathologic criteria, 2 major criteria, 5 minor criteria or 1 major plus three minor criteria.

164

What is the pathologic criteria of the Duke criteria?

1. vegetation or intracardiac abscess present - confirmed by histology
2. bacteria demonstrated by culture or histology in a vegetation, a emboli zed vegetation or an intracardiac abscess

165

What is the major criteria of the Duke criteria?

1. supportive lab evidence - such as typical bacteria for infective endocarditis in two separate blood cultures or community acquired enterococci in the absence of a primary focus.
2. evidence of endocardial involvement such as an echocardiogram
3. new valvular regurgitation - increase or change in pre-existing murmur not sufficient

166

What is the minor criteria of the Duke criteria?

1. predisposing heart condition or IV drug use
2. Fever greater than 38.0 C
3. vascular phenomenon such as a major arterial emboli
4. immunologic phenomena such as glomerulonephritis
5. positive blood culture that does not meet criterion of the major criteria.

167

What are two types of infective endocarditis?

1. acute
2. subacute

168

Describe acute infective endocarditis.

1. Previously normal heart valve by a highly virulent organism
2. Necrotizing, ulcerative, destructive lesions
3. Difficult to cure with antibiotics - especially because valves are not very vascular

169

Describe subacute infective endocarditis.

1. Insidious infections of deformed valves by organisms of lower virulence
2. Less destructive lesion
3. Cures produced with antibiotics

170

List some organisms that can cause infective endocarditis.

1. S. viridans effects mainly
native but previously damaged or abnormal valves
2. S. aureus effects mainly
healthy or deformed valves
3. S. epidermis (coagulase (-) Staph) effects mainly
prosthetic valves
4. HACEK - (Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
5. Enterococci
6. Gram negative bacilli
7. Fungi

171

What are the two most common organisms causing infective endocarditis?

1. Staph aureus
2. S. viridans

172

What can cause non-infective endocarditis?

1. Systemic Lupus - called Libman-Sacks endocarditis
2. non-bacterial vegetations

173

Describe non-bacterial thrombotic endocarditis.

1. Previously referred as marantic endocarditis
2. Characterized by deposition of small sterile thrombi on the leaflets of cardiac valves
3. Vegetations are thrombi that do not invade or elicit an inflammatory reaction
4.May be the source of systemic thrombi
5. Occurs in patients with cancer (mucinous adenocarcinoma), sepsis or hypercoagulable state

174

Describe Libman-Sacks endocarditis.

1. Patients have systemic lupus erythematosus
2. Vegetations located:
mitral and tricuspid valves,
valvular endocardium, chords, or
mural endocardium of the atria
3. Vegetations composed of finely granular, fibrinous eosinophilic material with hematoxylin bodies
2. Intense valvulitis with fibrinoid necrosis of the valve

175

What are some possible complications of receiving artificial heart valves?

Thromboembolism
Infective endocarditis with ring abscess
Structural deterioration

176

Describe Carcinoid heart disease.

1. Cardiac manifestation of carcinoid syndrome
2. Lesions are firm plaque-like endocardial fibrous thickenings and the tricuspid and pulmonary valves
3. Due to carcinoids that occur outside the portal system that empty directly into the IVC

177

What are primary cardiomyopathies?

Heart muscle disorders classified as dilated (most common), hypertrophic or restrictive.

178

What are secondary cardiomyopathies?

Heart muscle disorders that are components of a systemic or multi-organ disorder.

179

Describe dilated cardiomyopathy.

Characterized by progressive cardiac dilation and contractile or systolic dysfunction

180

Describe hypertrophic cardiomyopathy.

1.Characterized by myocardial hypertrophy, poorly compliant LV myocardium leading to abnormal diastolic filling and intermittent ventricular outflow obstruction
2. Leading cause of unexplained LVH

181

Describe restrictive cardiomyopathy.

Characterized by primary decreased ventricular compliance resulting in impaired filling during diastole

182

What are some causes of dilated cardiomyopathy?

Genetic
Myocarditis
Alcohol abuse
Childbirth
Chronic anemia
Medications
Hemochromatosis

183

What causes hypertrophic cardiomyopathy?

Genetics.

184

What are some causes of restrictive cardiomyopathy.

Idiopathic
Amyloidosis
Radiation induced
Fibrosis

185

Describe Arrhythmogenic right ventricular cardiomyopathy.

1. Inherited (autosomal dominant, variable penetrance) disease of the cardiac muscle causing:
Right ventricular failure
Various rhythm disturbances (ventricular tachycardia, ventricular fibrillation)
2. Right ventricular wall is severely thinned due to:
loss of myocytes, fatty infiltration and fibrosis
4. Disease is related to defective cell adhesion proteins in the desmosomes that link adjacent myocytes

186

What is myocarditis?

Infectious or inflammatory processes that cause myocardial injury.

187

What types of organisms cause myocarditis?

1. Viruses:
Coxsackie A/B (most common), Enterovirus, HIV, CMV
2. Bacteria:
Chlamydia, Neisseria, Borrelia, Rickettsia
3. Fungus
4. Protozoa (Tyrpanosoma)
5. Helminths

188

What are some immune mediated causes of myocarditis?

1. Post-viral
2. Poststreptococcal
3. SLE
4. Drug hypersensitivity:
Methyldopa
Sulfonamides
5. Transplant rejection

189

What else can cause myocarditis?

Sarcoidosis
Giant cell myocarditis

190

What do you see with myocarditis?

1. chronic inflammatory reaction/infiltration - histologically
2. punctate hemorrhages grossly

191

What are some types of pericardial diseases?

1. Pericardial effusion: pericardial space distended by serous fluid
2. Hemopericardium: pericardial space distended by blood
3. Purulent pericarditis: pericardial space distended by pus

192

The normal pericardial space contains how much fluid?

30-50 mL of thin, serous fluid. With chronic pressure there can be up to 500 mL of effusion and with rapid effusion - up to 200-300 mL.

193

Name the types of acute pericarditis.

Serous pericarditis
Fibrinous/serofibrinous pericarditis
Purulent pericarditis
Hemorrhagic pericarditis
Caseous pericarditis

194

Name the types of chronic pericarditis.

Adhesive pericarditis
Constrictive pericarditis

195

Describe serous acute pericarditis.

1. Produced by non-infectious inflammatory diseases
2. Mild lymphocytic infiltrate in the epipericardial fat

196

Describe fibrinous/Serofibrinous pericarditis.

1. Most frequent type with a loud pericardial friction rub
2. Composed of serous fluid mixed with fibrinous exudate
3. Associated with acute MI, postinfarction syndrome, uremia, chest radiation, RF, SLE, trauma

197

Describe acute purulent pericarditis.

1. Caused by invasion of microbes into the pericardial space by:
Direct extension
Seeding from the blood
Lymphatic extension
Introduction during craniotomy
2. Acute inflammatory reaction that can produce a mediastinopericarditis
3. Organization and scarring usual outcome with constrictive pericarditis

198

Describe acute hemorrhagic pericarditis.

1. Blood with a fibrinous or suppurative effusion
2. Most commonly caused by a metastatic malignant neoplasm
3. Also found in TB and bacterial infections and post-cardiac surgery

199

Describe acute caseous pericarditis.

1. Rare
2. Almost always due to TB by direct spread, but sometimes fungus
3. Leads to a disabling, fibrocalcific, chronic constrictive pericarditis

200

Describe chronic adhesive pericarditis.

1. Follows infectious pericarditis, cardiac surgery, radiation
2. Pericardial sac is obliterated and pericardium adheres to surrounding structures

201

Describe chronic constrictive pericarditis.

1. Heart is encased in a fibrous/ fibrocalcific scar that limits diastolic expansion and cardiac output
2. Mimic restrictive cardiomyopathy
3. Heart sounds are muffled or distant

202

What is a myxoma?

A cardiac tumor. The most common primary cardiac tumor in adults.

203

Describe Myxomas.

1. Benign neoplasm with abnormalities of chr 12 & 17
2. Arise from primitive multipotent mesenchymal cells
3. Most often in the atria, but can arise in any chamber
4. 10% associated with Carney complex

204

What is a rhabdomyoma?

A cardiac tumor. The most frequent primary cardiac timor in children. Is considered a harmartoma.

205

What disease are rhabdomyoma's associated with?

Tuberous sclerosis.

206

What are Lipomas?

Benign tumors of mature adipose tissue. Can occur in heart - most often in LV, RA or atrial septum.

207

What are papillary fibroelastoma's?

Benign neoplasm often discovered at autopsy. Resembles a Lambl excrescence (filiform fronds that occur at sites of valve closure. They originate as small thrombi on endocardial surfaces (where the valve margins contact) and have the potential to embolize to distant organs).