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Cardiovascular Module > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

Atherosclerosis

A

Degenerative disease of medium and large arteries
Lipid deposition in arterial wall
Fibrosis and chronic inflammation
Formation of asymmetric obstructive fibre-fatty plaques

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2
Q

Atheroma/atheromatous/ fibrofatty plaque

A

Elevated lesion made of
lipid core
Fibrous cap
Forms into intimal layer of artery

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3
Q

Is the progression of atherosclerosis slow or fast

A

Slow

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4
Q

Etiology of Atherosclerosis

A

Ischemic heart disease is an indicator of the incidence of atherosclerosis

Factors increasing IHD and therefore AS:

Increasing Age because of increasing to causative factors

Male gender

Genetic factors ( familial predisposition)

Hyperlipidemia, hypertension, diabetes, Cigarettes ==> most important causes

fatty diet
low birth weight
sedentary lifestyle

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5
Q

Hyperlipidaemia

A

Higher level of blood LDL cholesterol predisposes to atherosclerosis

High levels of HDL cholesterol associated with lower risk of atherosclerosis

LDL/HDL ratio very important

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6
Q

Hypertension in atherosclerosis

A

The higher the blood pressure the greater the risk of atherosclerosis

Synergistic with other factors

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7
Q

At what age is hypertension a stronger risk factor to develop a atherosclerosis then hyper cholesterolemia

A

Above 45

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8
Q

Can antihypertensive reduce his incidence of atherosclerosis related diseases

A

Yes

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9
Q

Diabetes mellitus in atherosclerosis

A

Gives 2 fold increase in risk of ischemic heart disease

A lot of them have hypercholesteroleamia
A lot of them are hypertensive , low HDL
Increased platelet adhesiveness
Increased response to aggregating agents

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10
Q

Level of HDL in type two diabetes patients

A

Reduced HDL level

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11
Q

Metabolic syndrome / syndrome X

A

Cluster of conditions that increase risk of heart disease
Associated with diabetes and hypertension

Major risk factor for coronary heart disease

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12
Q

Component of insulin resistance

A

Hyperinsulinemia

Glucose intolerance

Reduced HDL

Hypertriglyceridemia

Central obesity

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13
Q

Factor with the Strongest epidemiological association with high incidence of atherosclerosis

A

Smoking

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14
Q

How is smoking related to the incidence of atherosclerosis

A

Directly correlated with the number of cigarettes smoke per day

Decreased smoking also decrease his risk of complication in atherosclerosis

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15
Q

Possible mechanism of effect of smoking on developing atherosclerosis

A

Decreased endothelial PGI2 synthesis

Increased platelet aggregation

Increased fibrinogen

Decreased HDL level

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16
Q

Smocking one or more packs of cigarette a day increases risk of death from IHD by …

A

200%

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17
Q

How does diet impact risk of AS

A

High diet in saturated fatty acid and cholesterol—> high plasma level of cholesterol, LDL, VLDL

When low fat diets and cholesterol , low plasma cholesterol too

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18
Q

Is alcohol a dependent or an independent risk factor in a AS

A

Independent

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19
Q

Is obesity a dependent or independent risk factor in

atherosclerosis

A

Independent

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20
Q

HDL level in obesity

A

Low

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21
Q

How can oral contraceptive lead to AS

A

Impact BP, plasma lipids, and coagulation

Decreases HDL

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22
Q

Impact of regular physical exercise in atherosclerosis

A

Decrease risk of IHD

23
Q

Impact of stress and behavior on AS

A

Increase risk

24
Q

Based on behavior and stress , what patient are most at risk of AS

A

Ambitious, aggressive, impatient, short tempered individual

25
Homocystinuria in As
Patient with high homocystine in blood and urine have premature vascular disease
26
Coagulation factors that can help predict risk of AS
High serum fibrinogen ( high risk of IHD) High Factor VII high plasminogen activitor inhibitor 1
27
If you have 2 major risk factors how much does your risk of AS increases
4 folds
28
If you have 3 major risk factors how much does your risk of AS increases
7
29
Can atherosclerosis develop in the absence of any apparent risk factors
Yes
30
AS pathogenesis : thrombogenic/ encrustations theory of rokitansky
Atheroma formed from repeated mural thrombi Mural thrombi gets replaced by fibrous tissue and covered by endothelium Plaque formed in intima
31
AS pathogenesis : theory of virchow
``` Atheroma formed by : Injury to intima Insudation of plasma into injured area Fibrosis Fatty degeneration ```
32
Cause of injury to endothelium leading to atherosclerosis
Hyperlipidemia oxidized LDL produced by macrophage derived free radicals hemodynamic factors which can determine the focal distribution of atheroma Hemodynamics stress which can lead to severe atheroma
33
How can response to endothelial injury leads to atherosclerosis
Injury —> increased permeability to plasma constituents (with lipids , LDL, cholesterol ). —> monocyte and platelet adherence enhanced
34
Mediators of cell injury
Mechanical shear stress in HPT BIOCHEMICAL abnormalities Immunological factors Inflammation Genetic alteration
35
LDL oxidation mechanism to be taken up by macrophages
Free radicals from inflammatory cells Glycation in diabetes
36
Impact of LDL oxidative
More readily ingested by macrophages through the scavenger receptors on macrophages ( form foamy macrophages)
37
What happens at site of injury
There migrate there Become macrophages and express gene for GF GF Released and make smooth muscle cells migrate, accumulate and proliferate in intima Prolifération of SM cells + synthesis of extra cellular matrix components —> accumulation of collagen, proteoglycans, uptake of lipids —> foam cells
38
How do you see subsequent accumulation of foam cells microscopically
Fatty streaks
39
Chronic injury impact
Lymphocyte and macrophage interaction stimulate Gf macrophages and endothelium stimulate GF, smooth muscle Loss of endothelial covering allowing platelet adherence
40
Morphology of AS
Principal : Fatty streak Fibrofatty plaque Complicated lesion Major : Fatty dots Intermediate lesions Fibroatheroma
41
Fatty streak
Ubiquitous lesion found in arterial tree at all ages When low does not cause anything Tiny, multiple, yellow, flat spots and form linear elevations/ streaks
42
Where are fatty streaks more obvious
Aorta
43
Progression of fatty streak
Some can become fibrous plaque Some can regress and disappear Some stay same
44
Fibrous plaque/ fibrolipid/ fibrofatty/ lipid plaque
White / whitish yellow Elevated lesions Variable sizes Impinge lumen of artery Fibrous cap (firm and white) on superficial part of luminal surface Deep part is yellow to white and soft Atheroma in middle of large plaque with yellow porridge like debris
45
Histology of AS
Fibrous cap ( thick band of collagen rich connective tissue , numerous smooth muscles, macrophages endothelium in lumen side) Under cap ( varying number of smooth muscles , macrophages, with deposit of lipids) Beneath ( rich number of macrophages full of lipids (foam cells), t lymphocytes, necrosis ( mass of lipid material, cholesterol clefts, cellular debris. Lipid laden foam cells )
46
Main arteries with plaques
Origin aorta ( mostly below origin of renal arteries) Coronary arteries Popliteal arteries Descending thoracic artery Internal carotid Circle of Willis
47
Vessels generally spared by As
Upper extremities vessels Mesenteric artery Renal arteries
48
Complicated lesions components
Calcification - make arteries rigid and eggshell brittle Plaque rupture , fissuring or ulceration - exposure of subendothelial collagen and thrombus formation —> rupture leads to discharge of content of plaque into blood causing cholesterol emboli —> intra plaque hemorrhage at vasa vasorum
49
Superimposed thrombosis cause and consequence
Thrombosis and intraplaque hemorrhage accumulation Can lead to occlusion of medium sized muscular arteries
50
Clinical manifestations of AS - Slow, insidious narrowing of vascular lamina —> ischemia of tissues leads to
Angina , Chronic IHD with risk of cardiac failure Peripheral vascular disease, dry gangrene , intermittent claudication Atherosclerotic cerebral atrophy, dementia Carotid atheroma with transient ischemic attacks Renal artery stenosis with risk of secondary hypertension Mesenteric artery occlusion with risk of ischaemic enteritis / colitis
51
Clinical presentation of Sudden occlusion of lumen by superimposed thrombosis or intraplaque hemorrhage ( thrombosis )
Myocardial infarction Peripheral gangrene Infarctive stroke Gangrenous bowel
52
Clinical presentation of emboli | Due to superimpose md thrombi
Transient ischemic attack Cerebral infarction Renal infarct Mesenteric artery occlusion + gangrenous bowel
53
Clinical presentation of aneurysm
``` Severe cases Ischaemic atrophy Loss of elastic tissue Weakness of vessel wall Rupture Cause death ```

Cardiovascular Module (21 decks)

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