Atherosclerosis Flashcards

1
Q

what is atherosclerosis?

A

its hardening of the walls of blood vessels. its deposition of fat in large elastic arteries and large and medium sized muscular arteries.

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2
Q

what is atherosclerosis characterized by?

A

characterized by lesions in the tunica intima called atheromas (also called atherosclertoic plaques) which protrudes into vessel lumens and narrow them

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3
Q

what are the non-modifiable risk factors of atherosclerosis?

A

1 Genetics: family history (most important risk factor)
2 Age (dominant factor) development of atherscelrotic plque is a progressive process. it does not usually become clincically manifested until lesions reach a critical threshhold in middle age or later)
thus between ages 40 and 60, the incidences of myocardial infraction increases five fold
3 Male gender
estrogen is a protective factor against eschemic heart disease so after menopause the incidence of atherosclerosis and related diseases increases in women

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4
Q

What are the risk factors- modifiable?

A

Hyperlipidemia, Hypertension, cigaretter smoking, diabetes mellitus
(most important risk factor is hyperlipidemia and more specifically hypercholesterolemia is a major risk even isn absence of other risk factors, hypercholesterolemia is sufficcient to initiate lesion development)

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5
Q

What is hypercholesterolemia?

A

Elevated low density lipoproteins LDL which takes the cholesterol to tissue (bad cholesterol)
low High density lipoprotein (HDL) which mobilzies cholesterol from the periphery and transport to liver for excertion in the bile
obesity and smoking lowers HDL levels
Exercise raise HDL levels
Diabetes mellitus induces hypercholesterolemia

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6
Q

what is the “response to injury” hypothesis?

A

according to this hypothesis, atherosclerosis is a chronic inflammatory and healing response of the arterial wall to endothelial injury.
Endothelial cell injury is the corner stone of the response-to-injury hypothesis

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7
Q

What are sequence of event in atherosclerosis in response to injury hypothesis?

A
  1. endothelial injury
  2. accumulation of lipoproteins
  3. monocyte adhesion
  4. platelet adhesion
  5. factor released from activated platelets and macrophages inducing smooth muscle cell recruitment
  6. smooth muscle cell proliferation, extracellular matrix production and recruitment of t cells
  7. lipid accumulation
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8
Q

what are fatty streaks?

A

are the earliest lesions and are composed of lipid filled foamy macrophages begins as multiple small flat yellow spots coalesce into elongated streaks

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9
Q

what are atherosclerotic plaque?

A

The key processes in atherosclerosis are intimal thickening and lipid accumulation which forms plaques.
Atheromatous plaques are white / yellow and encroach on the lumen of the artery.

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10
Q

atherosclerotic plaques have 3 principle components, what are they?

A

(1) Fibrous cap (smooth muscle cells, macrophages, collagen and T cells)
(2) Shoulder (macrophages, T cells, and smooth muscle cells)
(3) Necrotic lipid core.
intracellular and extra cellular lipid (cholesterol and cholesterol esters).

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11
Q

what are the changes to a plaque that can occur?

A

Rupture, ulceration, or erosion 
become organized and incorporated 
Hemorrhage into a plaque
Athero embolism
Aneurysm formation

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12
Q

what is rupture ulceration or erosion change in atherosclerosis

A

Rupture, ulceration, or erosion of the surface of atheromatous plaques exposes highly thrombogenic substances and leads to thrombosis which occludes the vessel lumen

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13
Q

what is organized and incorporated change in atherosclerosis

A

If the patient survives, the clot may become organized and incorporated into the growing plaque.

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14
Q

what is hemmorrhage into a plaque change in atheroscelerosis

A

Hemorrhage into a plaque - Rupture of the overlying fibrous cap or of the thin-walled vessels.

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15
Q

what is athero embolsim

A

Athero embolism - Plaque rupture can discharge atherosclerotic debris into the bloodstream, producing microemboli.

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16
Q

what is aneurysm formation

A

Aneurysm formation - Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes weakness and potential rupture.