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Pathology > Chapter 7, Section 1 Cardiovascular Pathology : > Flashcards

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
Q

What are the two forms of arteriosclerosis ?

A

Hyaline and Hyperplastic

26
Q

What is hyaline arteriolosclerosis ?

A

is typical of diabetes and consists of the thickening of arterial walls by amorphous protein deposits

27
Q

What does the hyaline arteriolosclerosis result from ?

A

leakage of plasma proteins into the blood vessel wall

28
Q

Hyperplastic Arteriolosclerosis

A

characterized by hypertrophy/hyperplasia of smooth muscle cells in the media of small arteries

29
Q

What does hyperplastic arteriosclerosis result in ?

A

concentric muscle layers with an “Onionskin” appearance

30
Q

The process of hyperplastic arteriosclerosis is observed in ?

A

Kidneys in the setting of severe (malignant) hypertension

31
Q

Where is Atherosclerosis almost universally present in ?

A
  • larger arteries of Western population.
32
Q

How are atherosclerosis characterized ?

A

progressive accumulation of lipid, inflammatory cells, smooth muscle cells, and connective tissue within intima of large and medium arteries.

33
Q

What are the results of the accumulation of materials in atherosclerosis ?

A

Progressive luminal narrowing and predisposition to thrombosis,
- end-organ ischemia and infarction

34
Q

What is the essential lesion of atherosclerosis ?

A

atheroma (atherosclerotic plaque)

35
Q

What does the atheroma (atherosclerotic plaque) develops as?

A

As an eccentric thickening of the arterial intima.

36
Q

Atheromas are composed of

A

cellular, lipid, and extracellular matrix components

37
Q

Reaction to Injury Hypothesis

A

the interaction of multiple types with each other and with chemical and inflammatory mediators drives the incremental growth of atherosclerotic plaques

38
Q

What are form cells ?

A

the accumulation of macrophages with lipid droplets in their cytoplasm

39
Q

What is the first step in atherogenesis ?

A

Foam cells

40
Q

What are the fatty streaks ?

A

Whiteish yellow, non-raised longitudinal streaks on the endothelial surface of arteries

41
Q

Fatty streaks appear to be precursors of ?

A

Atheromatous plaques

42
Q

Endothelial Cells are key players in

A

events in atherosclerosis and

  • produce many mediators that direct plaque formation
  • attract or recruit key inflammatory cells and platelets from the blood
43
Q

Endothelium

A

active tissue that maintains hemostasis, regulates vascular tone, and modulates leukocyte and platelet adhesion.

44
Q

What does endothelial injury can result from ?

A
  • mechanical shear stress
  • hyperlipidemia
  • Free radicals
  • Hyperhomocysteinemia
45
Q

What cell are involved in the development of plaque?

A

monocytes/macrophages as well as T and B lymphocytes which are activated by cytokines.

46
Q

What type of feedback drives plaque formation forward ?

A
  • Positive feedback
47
Q

How does HDL reduce plaque formation?

A

they carry cholesterol away to the liver for removal from the body

48
Q

Nationally recommended levels for total blood cholesterol should not exceed

A

200 grams/dL

49
Q

What do oxidized LDL and other chemotactic factors eventually stimulate ?

A

the migration of smooth muscle cells from the arterial media across the internal elastic lamina into the intima

50
Q

When foam cells are stimulated from PDGF, FGF, and TGF-alpha they produce ?

A

produce collagen, elastin, and proteoglycans to form a “fibrous cap” over the lipid core of the mature atheroma

51
Q

What causes the release of proangiogenic factors ?

A

Artheromas increase in size, hypoxia at their center

52
Q

What causes neovascularization ?

A

release of proangiogenic factors

53
Q

Episodes of hemorrhage contribute to ?

A

hemosiderin to the plaque core as well as additional lipid material and cholesterol, derived from erythrocyte, membranes

54
Q

Enlargement of the plaque eventually results in ?

A
  • significant obstruction to vascular flow with resultant end organ ischemia.
55
Q

What are the major complications of atherosclerosis ?

A
  • ischemic heart disease, myocardial infarction, stroke, and gangrene
56
Q

What can initiate occlusive thrombosis or release of microthrombi ?

A
  • formation of small platelet and fibrin thrombi on the surface of atheromas
57
Q

What happens when the plaque ruptures ?

A

exposes highly thrombogenic components of the lipid core

  • stimulates the production of an occlusive thrombosis
  • release of atheroemboli (cholesterol crystals) into the coronary circulation.

Pathology (1 decks)

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