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Pathophysiology Loyola > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1. To know the definition of atherosclerosis 2. To understand changes in SMC and endothelial cells during inflammation. 3. To know the origin and progression of the disease 4. To know the pathogenesis of atherosclerosis 5. To know the difference between vulnerable and stable plaques 6. To know which factors induce SMC proliferation 7. To understand the complications of atherosclerosis 8. To know the clinical manifestations of atherosclerosis 9. To know the prevalence of atherosclerosis 10. To u

1
Q

Define atherosclerosis

A

Characterized by fibrous thickening of the arterial wall associated with lipid-infiltrated plaques that may eventually calcify

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2
Q

What size of arteries are usually affected by atherosclerosis?

A

Mid to large

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3
Q

Which areas in arteries are most likely to suffer from lesions?

A

Areas of turbulent flow and increased shear stress

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4
Q

Why are compliance and flow affected by atherosclerosis?

A

Atherosclerosis reduces the diameter of the artery

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5
Q

What is the first step in progression of atherosclerosis?

A

LDL cholesterol adhesion and infiltration - LDL binds cholesterol and penetrates the intima layer due to leaky endothelium

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6
Q

What happens in atherosclerosis progression after LDL adhesion and infiltration?

A

LDL oxidation via ROS

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7
Q

What happens after LDL oxidation in the progression of atherosclerosis?

A

Monocyte infiltration, production of chemokines, macrophage infiltration

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8
Q

What happens in the progression of atherosclerosis after macrophage infiltration?

A

Scavenger receptor recognition of altered LDLs, stimulating inflammation.

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9
Q

Does foam cell formation happen before or after SMC migration in the progression of atherosclerosis?

A

Before

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10
Q

What happens in the progression of atherosclerosis after SMC migration

A

Apoptosis, necrosis, calcification and subsequent formation of thrombi and clots

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11
Q

What is the function of endothelial cells

A

Serve as a physical barrier, protective, anti-inflammatory, vasodilatory, non-thrombogenic

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12
Q

How is an endothelial cell activated by inflammation changed?

A

Increase permeability, increase inflammatory cytokines, increase leukocyte adhesion molecules, decrease vasodilatory molecules, decrease antithrombotic molecules

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13
Q

How is a smooth muscle cell changed in diseased states (atherosclerosis)?

A

Increased inflammatory cytokines, increased extracellular matrix synthesis, increased migration and proliferation into subintima

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14
Q

Where are SMC normally located?

A

Contained in the medial layer

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15
Q

What molecules promote vasodilation in normal endothelial cells?

A

NO, prostacyclin, endothelin

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16
Q

What molecules resist thrombosis in normal endothelial cells?

A

Heparan sulfate, thrombomodulin, plasminogen factors

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17
Q

Where do LDLs infiltrate in atherosclerosis?

A

Into subendothelial region

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18
Q

How does oxidized LDL impact vasodilation?

A

It blocks NO synthase, therefore there cannot be vasodilation

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19
Q

How does calcification impact plaque stability?

A

Decreases it

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20
Q

Describe the make up of a “vulnerable” plaque?

A

Thin fibrous cap, large lipid pool, many inflammatory cells

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21
Q

Describe the make up of a “stabilized” plaque

A

Small lipid pool, thick fibrous cap, preserved lumen

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22
Q

Describe the make up of a healed ruptured plaque

A

Narrow lumen, may entirely occlude blood flow; fibrous intima

23
Q

What 2 things favor thrombosis?

A

Procoagulant (tissue factor) and antifibrinolytic (PAI-1, stabilizes clot)

24
Q

What 2 things resist thrombus accumulation?

A

Anticoagulants (thrombomodulin, protein S, protein C, heparin-like molecules) and profibrinolytics (tPA, uPA)

25
Q

What is a major causative factor in clinical sequelae of atherosclerosis?

A

Intravascular thrombosis

26
Q

How does aspirin resist thrombus formation?

A

Inhibits thromboxane production by platelets

27
Q

In the clinical sequelae of atherosclerosis, what specifically causes embolic stroke?

A

Peripheral emboli

28
Q

In the clinical sequelae of atherosclerosis, what specifically causes thrombotic stroke?

A

plaque ulceration or rupture and intraplaque hemorrhage

29
Q

In the clinical sequelae of atherosclerosis, what specifically causes aneurysms?

A

Weakening of vessel wall

30
Q

In the clinical sequelae of atherosclerosis, what specifically causes claudication (PAD)

A

Narrowing of vessel by fibrous plaque

31
Q

In the clinical sequelae of atherosclerosis, what specifically causes Limb ischemia?

A

narrowing of vessel by fibrous plaque and peripheral emboli (skin ulceration, gangrene)

32
Q

In the clinical sequelae of atherosclerosis, what specifically causes myocardial ischemia?

A

Narrowing of vessel by fibrous plaque

33
Q

In the clinical sequelae of atherosclerosis, what specifically causes unstable angina

A

Plaque ulceration or rupture and intraplaque hemorrhage

34
Q

In the clinical sequelae of atherosclerosis, what specifically causes myocardial infarction

A

Plaque ulceration or rupture and intraplaque hemorrhage

35
Q

How does the following condition accelerate the progression of atherosclerosis: Male gender and females after menopause

A

Lack of LDL-lowering effect of estrogens, estrogens probably act by increasing the number of LDL receptors in the liver

36
Q

How does the following condition accelerate the progression of atherosclerosis: Primary HLD

A

Inherited disorders cause lipoprotein lipase deficiency, defective LDL receptors, abnormal apoprotein E, deficiency of apoprotein C, or unknown cause

37
Q

How does the following condition accelerate the progression of atherosclerosis:: secondary HLD

A

Increased circulating triglycerides produced by diuretics, beta adrenergic blocking drugs, excess alcohol intake

38
Q

How does the following condition accelerate the progression of atherosclerosis: Cigarette smoking

A

Probably CO induced hypoxic injury to endothelial cells

39
Q

How does the following condition accelerate the progression of atherosclerosis: HTN

A

increased shear stress with damage to endothelium

40
Q

How does the following condition accelerate the progression of atherosclerosis: Diabetes

A

Decreased hepatic removal of LDL from circulation; increased glycosylation of collagen, which increases LDL binding to vessel walls

41
Q

How does the following condition accelerate the progression of atherosclerosis: obesity, particularly abdominal obesity

A

Alters endothelial function and inflammatory state

42
Q

How does the following condition accelerate the progression of atherosclerosis: hypothyroidism

A

Decreased formation of LDL receptors in the liver

43
Q

What are lipid modifying drugs?

A

HMG-CoA reductase inhibitors (Statins), niacin, fibric acid derivatives, cholesterol intestinal absorption inhibitors, bile-acid binding agents

44
Q

What is the desirable amount of total cholesterol?

A

Less than 200 mg/dL

45
Q

What is the optimal amount of LDL cholesterol

A

Less than 100 mg/dL

46
Q

What is the cardioprotective amount of HDL cholesterol?

A

240 mg/dL

47
Q

What is the mechanism by which the following drug treats atherosclerosis: Statins

A

Inhibit cholesterol synthesis, anti-inflammatory

48
Q

What is the mechanism by which the following drug treats atherosclerosis: Niacin (nicotinic acid)

A

Inhibits fat breakdown in adipose tissue and increases HDL cholesterol, anti-inflammatory

49
Q

What is the mechanism by which the following drug treats atherosclerosis: Aspirin

A

Inhibits platelet aggregation

50
Q

What is the mechanism by which the following drug treats atherosclerosis: B-blockers

A

Antihypertensive

51
Q

What is the mechanism by which the following drug treats atherosclerosis: ACE inhibitors

A

Antihypertensive

52
Q

What is the mechanism by which the following drug treats atherosclerosis: Maraviroc (CCR5 antagonist)

A

Blocks CCR5 (decreases inflammation)

53
Q

Why is estrogen beneficial in atherosclerosis?

A

Increases NO production and promotes cholesterol removal by the liver

Pathophysiology Loyola (7 decks)

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