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NancyMEDSCI203 > Lecture 20: Atherosclerosis > Flashcards

Lecture 20: Atherosclerosis Flashcards

0
Q

What is atherosclerosis?

A

A disease affecting innermost layer of large and medium sized arteries

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1
Q

How many deaths does atherosclerosis contribute in the western world?

A

> 50%

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2
Q

What does atherosclerosis appear as?

A

Thickenings called plaques

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3
Q

What are plaques?

A

Deposits of fibrous tissues and lipids

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4
Q

What is the difference between arteriosclerosis and atherosclerosis ?

A

Arteriosclerosis is the general term for hardening of arteries

Atherosclerosis is a type of arteriosclerosis

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5
Q

What does atherosclerosis affect?

A

Arteries

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6
Q

How many layers does an arterial wall consist of?

A

Three layers

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7
Q

What is the inner most layer called?

A

Tunica intima

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8
Q

What is the middle layer called?

A

Tunica media

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9
Q

What is the outer layer called?

A

Tunica adventitia

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10
Q

Where do the plaques causing atherosclerosis form?

A

In the tunica intima

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11
Q

What makes up the tunica intima?

A

Tunica intima consists of Endothelial cells lying on a basement membrane

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12
Q

What are endothelial cells?

A

Flattened cells separated by tight junctions

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13
Q

What is the function of endothelial cells?

A 
Many functions
Containment of blood
Selective transport of fluids, gases, ions and proteins into tissues
Control of clotting
Control of blood pressure
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14
Q

What does the tunica media consist of?

A

Two layers of elastic laminae with vascular smooth muscle cells in between them

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15
Q

What are vascular smooth muscle cells?

A

Fascinating cells which contract to regulate vessel diameter

And regulate function and fate of other cells in the vessel wall by secreting cytokines and growth factors

They also lay down extracellular matrix.

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16
Q

What does the tunica adventitia consist of.

A

Connective tissue

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17
Q

Why do different cell types within vessel walls have to continually communicate

A

So they can regulate one another’s state and function

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18
Q

What does the exact structure of arteries depend on?

A

Their size.

Large arteries like aorta and carotid are exposed to high pulsatile pressures so they have prominent elastic laminae hence called elastic arteries

Medium sized arteries like coronary arteries are classified as muscular arteries as their media is composed largely of smooth muscle cells.

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19
Q

What are the four major positive risk factors for atherosclerosis?

A

Hyperlipidaemia
Cigarette smoking
Hypertension
Diabetes mellitus

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20
Q

What are the other additional positive risk factors for atherosclerosis?

A 
Advancing age
Family history
Make gender 
High saturated fat diet
Stressful sedentary lifestyles
Obesity
Excess alcohol consumption
Low birth weight
Low socioeconomic status
Infections - chlamydia organisms
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21
Q

What are the three main negative risk factors of atherosclerosis ?

A

High levels of circulating HDLP (high density lipoproteins)
Moderate alcohol consumption (2 units per day)
Cardiovascular fitness

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22
Q

Why are lipoproteins important?

A

They are powerful risk modifiers for atherosclerosis

23
Q

What are lipoproteins?

A

They consist of a lipid core (e.g. Triglycerides, cholesterol, cholesterol esters, phospholipids) surrounded by a protein coat

24
Q

What are the proteins in the protein coat of lipoproteins called?

A

Apolipoproteins

25
Q

Why are lipoproteins risk modifiers?

A

High density lipoproteins are the good type of cholesterol that take lipids away from the liver, therefore they lower the risk of atherosclerosis

26
Q

What does the initiation of atherosclerosis involve?

A

Endothelial cell knjury

27
Q

What is the progression of atherosclerosis following initial EC injury an example of?

A

Chronic inflammation

28
Q

Outline the pathogenesis of atherosclerosis?

A

Endothelial cell injury
Leukocyte migration
Smooth muscle cell activation and migration
Lipoprotein filtration

29
Q

What is atherogenesis?

A

The pathogenesis of atherosclerosis

30
Q

What can endothelial cell injury be caused by?

A

A combination of
Haemodynamic force of blood (hypertension, branch points)
Chemical insults (cigarette smoke, lipids)
Cytokines

31
Q

What can damage of endothelial cells lead to?

A

Altered permeability, > lipid infiltration
Adhesion of leukocytes (due to enhanced expression of chemokines and adhesion molecules)
Activation of thrombosis

32
Q

What is leukocyte migration into the anterosclerotic plague a type of?

A

Chronic inflammation which is a hallmark of atherosclerosis

33
Q

What do circulating monocytes on other leukocyte types adhere to? And what do they enter?

A

Endothelial cells. They enter the atherosclerotic leison

34
Q

What happens when circulating monocytes and other leukocyte types enter the atherosclerotic leison?

A

They ingest large amounts of oxidised lipoproteins

This gives them a foamy appearance

They are called foam cells

35
Q

What other cells also play an important role?

A

T lymphocytes and dendritic cells

36
Q

Recently, what have neutrophils and mast cells been for to perform?

A

Important functions during atherogenesis

37
Q

Which cells produce growth factors that activate vascular smooth muscle cells?

A

Macrophages, platelets, and endothelial cells

38
Q

What do smooth muscle cells do once activated by growth factors?

A

Proliferate and migrate from tunica media to the tunica intima

39
Q

What is the migration of smooth muscle cells into the tunica intima likely to be caused by?

A

Damage or incomplete development of internal elastic lamina.

But this is not certain

40
Q

What other roles do smooth muscle cells play in atherosclerotic plaques?

A

They lay down extracellular matrix which contributes to a fibrous cap

This may later be degraded by matrix degrading protease enzymes

Vascular smooth muscle cells also ingest lipids, and interact with other cell types in the plaque through adhesion molecules present on their surface and growth factors which they secrete.

41
Q

What happens to lipoproteins in plaques?

A

They become oxidised

42
Q

What do oxidised lipoproteins attract?

A

Monocytes and stimulate several cell types in the plaque to release cytokines and growth factors,

43
Q

What do the oxidised lipoproteins cause?

A

Dysfunction and apoptosis in smooth muscle cells, macrophages and endothelial cells

44
Q

What do these changes (EC cell injury, leukocyte migration, smooth muscle cell activation and migration, lipoprotein infiltration) together result in ?

A

A spectrum of leisons

45
Q

Which leisons are clinically silent?

A

Type I initial lesion in isolated macrophage foam cells

Type II fatty streak lesion mainly due to intracellular lipid accumulation

Type III intermediate lesion due to type II changes and small extracellular lipid pools

46
Q

What are the clinically silent or overt lesions?

A

Type Iv atheroma lesion due to type II changes and core of extracellular lipid

Type V fibroatheroma lesion due to lipid core and fibrotic layer or multiple lipid cores and fibrotic layers, or mainly calcific or mainly fibrotic

Type VI complicated lesion due to surface defect, hematoma-haemorrhage, thrombus

47
Q

What are the types of lesions in sequence progression?

A

Type I initial lesion

Type II fatty streak lesion

Type III intermediate lesion

Type IV atheroma lesion (can lead straight to type VI complicated leison)

Type V fibroatheroma lesion

Type VI complicated lesion

48
Q

What do lesion type I, II, III and IV have in common?

A

They are all grown mainly by lipid accumulation

49
Q

What is type V lesion’s main growth mechanism?

A

accelerated smooth muscle and collagen increase

50
Q

What is type VI lesion’s main growth mechanism?

A

Thrombosis, hematoma

51
Q

Which types of lesions occur from first decade?

A

Type I and type II

52
Q

Which types of lesions occur from third decade?

A

Type III and type Iv

53
Q

What types of lesions occur from the fourth decade?

A

Type V and type VI

54
Q

What does the fibrous cap of an atheroma lesion consist of?

A

Smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularisation

55
Q

What does the necrotic centre of an atheroma lesion contain?

A

Cell debridement cholesterol crystal sum foam cell am calcium

56
Q

What are the consequences of atherosclerosis?

A

Atheroma often silent due to pre-clinical phase until sudden onset of symptoms (due to rupture haemorrhage or thrombosis)

Common clinical consequences of atherosclerosis:
Myocardial infarction, peripheral vascular disease, and cerebrovascular disease

NancyMEDSCI203 (12 decks)

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