Chapter 7, Section 1 Cardiovascular Pathology : Flashcards

1
Q

What are the three functional layers of blood vessels ?

A

intima, media, adventitia

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2
Q

Intima

A

single layer of endothelial cells supported by a basement membrane.

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3
Q

What separates intima and media ?

A

Internal Elastic Lamina

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4
Q

What is the Internal Elastic Lamina ?

A

made up of an organized band of elastin fibers

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5
Q

Where are internal elastic lamina prominently visual ?

A

Muscular Arteries

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6
Q

What is the media compound of ?

A

Smooth Muscle Cells with circular orientation

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7
Q

Where is this layer best developed ?

A

Muscular Arteries

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8
Q

Which system demonstrates greatest variation ?

A

Media

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9
Q

Elastic fibers are prominent in ?

A

Media

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10
Q

What is the importance of elastic fibers ?

A

provide a cushioning effect that smoothes blood pressure during the cardiac cycle

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11
Q

What is adventitia composed of ?

A

Loose connective tissue with small blood vessels called vasa vasorum

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12
Q

Role of Vasa Vasorum ?

A
  • Penetrate the larger arteries to provide nutrition to the media.
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13
Q

What is the function of the venous system ?

A

functions as a low- pressure collecting system of the return of blood from capillary networks to the heart.

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14
Q

What type of flow happens in the veins ?

A

Laminar

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15
Q

What are the three layers of the heart ?

A

Endocardium, Muscular Wall, and Epicardium

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16
Q

What is endocardium ?

A

intima of blood vessels

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17
Q

What is the muscular wall made of ?

A

cardiac myocytes

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18
Q

What is epicardium ?

A

consisting of adipose tissue covered by mesothelium containing coronary arteries and veins.

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19
Q

What are cardiac valves composed of ?

A

Fibrous annulus to which are attached to valve leaflets

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20
Q

What are the valve leaflets made up of ?

A

Core collagen covered by endothelium

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21
Q

Where do the valves get their nutrition ?

A

luminal blood

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22
Q

What does arteriosclerosis mean?

A

hardening of the arteries and corresponds to three separate pathologic entities.

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23
Q

What are the three separate pathologic entities arteriosclerosis ?

A

Atherosclerosis, Monckeberg’s medical calcific sclerosis, and arteriolosclerosis

24
Q

Arteriolosclerosis is markedly accelerated in individuals with ?

A

hypertension or diabetes mellitus

25
What are the two forms of arteriosclerosis ?
Hyaline and Hyperplastic
26
What is hyaline arteriolosclerosis ?
is typical of diabetes and consists of the thickening of arterial walls by amorphous protein deposits
27
What does the hyaline arteriolosclerosis result from ?
leakage of plasma proteins into the blood vessel wall
28
Hyperplastic Arteriolosclerosis
characterized by hypertrophy/hyperplasia of smooth muscle cells in the media of small arteries
29
What does hyperplastic arteriosclerosis result in ?
concentric muscle layers with an "Onionskin" appearance
30
The process of hyperplastic arteriosclerosis is observed in ?
Kidneys in the setting of severe (malignant) hypertension
31
Where is Atherosclerosis almost universally present in ?
- larger arteries of Western population.
32
How are atherosclerosis characterized ?
progressive accumulation of lipid, inflammatory cells, smooth muscle cells, and connective tissue within intima of large and medium arteries.
33
What are the results of the accumulation of materials in atherosclerosis ?
Progressive luminal narrowing and predisposition to thrombosis, - end-organ ischemia and infarction
34
What is the essential lesion of atherosclerosis ?
atheroma (atherosclerotic plaque)
35
What does the atheroma (atherosclerotic plaque) develops as?
As an eccentric thickening of the arterial intima.
36
Atheromas are composed of
cellular, lipid, and extracellular matrix components
37
Reaction to Injury Hypothesis
the interaction of multiple types with each other and with chemical and inflammatory mediators drives the incremental growth of atherosclerotic plaques
38
What are form cells ?
the accumulation of macrophages with lipid droplets in their cytoplasm
39
What is the first step in atherogenesis ?
Foam cells
40
What are the fatty streaks ?
Whiteish yellow, non-raised longitudinal streaks on the endothelial surface of arteries
41
Fatty streaks appear to be precursors of ?
Atheromatous plaques
42
Endothelial Cells are key players in
events in atherosclerosis and - produce many mediators that direct plaque formation - attract or recruit key inflammatory cells and platelets from the blood
43
Endothelium
active tissue that maintains hemostasis, regulates vascular tone, and modulates leukocyte and platelet adhesion.
44
What does endothelial injury can result from ?
- mechanical shear stress - hyperlipidemia - Free radicals - Hyperhomocysteinemia
45
What cell are involved in the development of plaque?
monocytes/macrophages as well as T and B lymphocytes which are activated by cytokines.
46
What type of feedback drives plaque formation forward ?
- Positive feedback
47
How does HDL reduce plaque formation?
they carry cholesterol away to the liver for removal from the body
48
Nationally recommended levels for total blood cholesterol should not exceed
200 grams/dL
49
What do oxidized LDL and other chemotactic factors eventually stimulate ?
the migration of smooth muscle cells from the arterial media across the internal elastic lamina into the intima
50
When foam cells are stimulated from PDGF, FGF, and TGF-alpha they produce ?
produce collagen, elastin, and proteoglycans to form a "fibrous cap" over the lipid core of the mature atheroma
51
What causes the release of proangiogenic factors ?
Artheromas increase in size, hypoxia at their center
52
What causes neovascularization ?
release of proangiogenic factors
53
Episodes of hemorrhage contribute to ?
hemosiderin to the plaque core as well as additional lipid material and cholesterol, derived from erythrocyte, membranes
54
Enlargement of the plaque eventually results in ?
- significant obstruction to vascular flow with resultant end organ ischemia.
55
What are the major complications of atherosclerosis ?
- ischemic heart disease, myocardial infarction, stroke, and gangrene
56
What can initiate occlusive thrombosis or release of microthrombi ?
- formation of small platelet and fibrin thrombi on the surface of atheromas
57
What happens when the plaque ruptures ?
exposes highly thrombogenic components of the lipid core - stimulates the production of an occlusive thrombosis - release of atheroemboli (cholesterol crystals) into the coronary circulation.