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esa 2- mechanisms of disease > Atheroma > Flashcards

Atheroma Flashcards

1
Q

What is an atheroma?

A

An accumulation of intracellular and extracellular lipid in the intima and media or large and medium sized arteries

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2
Q

Where do atheromas happen?

A

On the inside of the arteries, and spreads through the wall

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3
Q

Where is the fat deposited in an atheroma?

A

Can be on outside and inside wall

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4
Q

What is atherosclerosis?

A

The thickening and hardening of arterial walls as a consequence of atheoma

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5
Q

What is arteriosclerosis?

A

The thickening of walls of arteries and arterioles, usually as a result of hypertension or diabetes mellitus

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6
Q

What are the three macroscopic stages of an atheroma?

A

The fatty streak
The simple plaque
The complicated plaque

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7
Q

What causes the fatty streak?

A

Lipid deposits in the intima

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8
Q

How does the fatty streak appear macroscopically?

A

Yellow and slightly raised

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9
Q

What is the relationship between the fatty streak and atheroma?

A

Somewhat debatable- generally regarded as the precursor, but some people disagree

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10
Q

Why do some people dispute that the fatty streak is the precursor to atheroma?

A

Fatty streak may be seen in populations that don’t progress to atherosclerosis.
Some discussion about anatomical position of fatty streak compared to atherosclerosis

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11
Q

How does the simple plaque appear macroscopically?

A

Raised yellow/white, with an irregular outline

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12
Q

What happens as simple plaques develop?

A

They enlarge and coalesce, eventually becoming complicated

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13
Q

What occurs when a complicated plaque has formed?

A

Thrombosis

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14
Q

Why do complicated plaques lead to thrombosis?

A

Because the plaque has an irregular surface, which disrupts flow

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15
Q

What can happen to a complicated plaque?

A

It may rupture
Can be haemorrhage into plaque
Calcification
Aneurysm formation

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16
Q

What happens when a complicated plaque ruptures?

A

It releases substances that cause thrombosis

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17
Q

What are the common sites of atheroma?

A 
Aorta, especially abdominal
 Coronary arteries
 Carotid arteries
 Cerebral arteries
 Leg arteries
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18
Q

What do early changes in atheroma include?

A

Proliferation of smooth muscle cells
Accumulation of foam cells and extracellular lipid, either in or between cells
The matrix of the cell may be substantially changed from normal

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19
Q

What do later changes in atheroma include?

A

Fibrosis
Necrosis
May be inflammatory cells
Cholesterol clefts

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20
Q

What are cholesterol clefts?

A

Where cholesterol crystals are laid down, there are needle shaped crystals of cholesterol that are soluble, so when solvents are used they are dissolved, leaving clefts

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21
Q

What is the eventual result of atheroma?

A

Disruption of the internal elastic lamina, with damage that extends into the media.
Ingrowth of blood vessels
Plaque fissuring

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22
Q

Why is there an ingrowth of blood vessels in atheroma?

A

Because whenever there is damage/inflammation, there is always a vascular response

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23
Q

What is plaque fissuring?

A

When the inside can move relative to the outside

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24
Q

What is the problem with plaque fissuring?

A

It allows for the release of materials that cause thrombosis

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25
Q

What are the clinical effects of atheroma?

A

Ischaemic heart disease
Cerebral ischaemia
Mesenteric ischaemia
Peripheral vascular disease

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26
Q

What is ischaemic heart disease?

A

The process of atheroma reducing flow of blood with or without thrombotic occlusion of arteries

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27
Q

What can ischaemic heart disease lead to?

A 
Sudden death
 Myocardial infarction
 Angina pectoris
 Arrhythmias
 Cardiac failure
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28
Q

Why does ischaemic heart disease cause cardiac failure?

A

Causes scarring of the heart so it can’t function properly

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29
Q

What may be seen in cardiac failure caused by ischaemic heart disease?

A

Swollen arteries, scarring

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30
Q

What is cerebral ischaemia a result of?

A

Atherosclerosis in cerebral or carotid vessels

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31
Q

What can cerebral ischaemia lead to?

A 
Transient ischaemic attack
 Cerebral infarction (stroke)
 Multi-infarct dementia
 Can undergo secondary haemorrhages
 Abdominal aortic aneurysm
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32
Q

When may someone undergo secondary cerebral haemorrhages?

A

Where dying tissues start to degenerate

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33
Q

How does mesenteric ischaemia often present?

A

Rectal bleeding

Maybe abdominal pain

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34
Q

What can mesenteric ischaemia lead to?

A

Ischaemic colitis
Malabsorption
Intestinal infarction

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35
Q

What is an acute intestinal infarction more likely to be caused by?

A

Thrombus or embolus

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36
Q

Where are intenstinal infarctions most common?

A

In superior mesenteric artery

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37
Q

What is peripheral vascular disease?

A

Atherosclerosis affecting vessels supplying the legs

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38
Q

What can peripheral vascular disease lead to?

A

Intermittent claudication
Leriche syndrome
Ischaemic rest pain
Gangrene

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39
Q

What is intermittent claudication?

A

Pain in legs because of reduced blood supply

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40
Q

What happens to claudication distance as time goes on?

A

It gets shorter

41
Q

What is meant by claudication distance?

A

How long can walk for before gets too painful

42
Q

What is Leriche syndrome?

A

Buttock claudication

43
Q

What is Leriche syndrome often associated with?

A

Impotence

44
Q

What is ischaemic rest pain?

A

When muscles hurt even when not exercising

45
Q

What causes gangrene?

A

No oxygen supply to tissue

46
Q

Why is gangrene problematic when amputating?

A

Needs to heal, but that increases oxygen demand, causing further gangrene, so need amputation stump in good, healthy tissue

47
Q

How can the clinical affect of peripheral vascular disease be delayed?

A

The development of a collateral channel

48
Q

What are the risk factors for atheroma?

A 
Age
 Gender
 Hyperlipidaemia
 Cigarette smoking
 Hypertension
 Diabetes mellitus
 Alcohol
 Infection
 Lack of exercise
 Obesity
 Soft water
 Oral contraceptive
 Stress and personality type
49
Q

How does age affect the risk of atheroma?

A

The older you are, the more likely you are to have it, until you get to right at the top of the age range (because people living that long are likely not to have atheroma, or they wouldn’t have lived that long)

50
Q

Why does risk of atheroma increase with age?

A

Because risk factors operative over years, building up

51
Q

How does gender affect the risk of atheroma?

A

Men are at a high risk than women, until the menopause where women catch up

52
Q

How is hyperlipidaemia associated with atheroma?

A

High plasma cholesterol associated with atheroma

53
Q

How do the different types of cholesterol impact on the risk of atheroma?

A

LDL most significant risk of the types

HDL protecting

54
Q

What happens to the risk of atheroma after giving up smoking?

A

It falls

55
Q

Why does cigarette smoking increase the risk of atheroma?

A

Mode of action uncertain, but possible causes are-
Changes to coagulation system
Reduced PGI2
Increased platelet aggregation

56
Q

What is strongly linked to high systolic/diastolic BP?

A

IHD

57
Q

Why does hypertension cause IHD?

A

Mechanism uncertain, but could be due to endothelial damage caused by raised pressure

58
Q

By how much does diabetes mellitus increase the risk of atheroma?

A

Doubles it

59
Q

Why does diabetes mellitus increase the risk of atheroma?

A

Protective effect in premenopausal women lost

Could be related to hyperlipidaemia and hypertension

60
Q

What else is diabetes mellitus associated with high risk of?

A

Cerebrovascular and peripheral vascular disease

61
Q

How much alcohol is associated with high risk of atheroma?

A

> 5 units a day

62
Q

What other risk factors is alcohol associated with?

A

Smoking

High BP

63
Q

What effect can small amount of alcohol have on risk of atheroma?

A

Can be protecting

64
Q

How is lipid carried in the blood?

A

On lipoproteins

65
Q

What do lipoproteins carry?

A

Cholesterol and triglycerides

66
Q

What do lipoproteins consist of?

A

Hydrophobic lipid core

Hydrophilic outer layer of phospholipid and apolipoprotein (A-E)

67
Q

What do chylomicrons do?

A

Transport lipid from intestine to liver

68
Q

What do VLDL do?

A

Carry cholesterol and TG from liver, and TG is removed leaving LDL

69
Q

What is LDL rich in?

A

Cholesterol

70
Q

What do LDLs do?

A

Carry cholesterol to non-liver cells

71
Q

What do HDLs do?

A

Carry cholesterol from periphery back to liver

72
Q

What are genetic variations in ApoE associated with?

A

Changes in LDL levels

73
Q

What do polymorphisms of genes involved in lipid metabolism lead to?

A

At least 6 ApoE phenotypes

74
Q

How can polymorphisms of genes involved in lipid metabolisms be used?

A

As risk markers for atheromas

75
Q

What is familial hyperlipidaemia?

A

Genetically determined abnormalities of lipoproteins

76
Q

What does familial hyperlipidaemia lead to?

A

Early development of atheroma

77
Q

What are the associated physical signs of familial hyperlipidaemia?

A

Arcus
Tendon xanthomas
Xanthelasma

78
Q

What is a corneal arcus?

A

A ring around the iris due to lipid

79
Q

What is an xanthalasma?

A

A small accumulate of fat in skin and subcutaneous tissue

80
Q

What could genetic predisposition to atheroma be due to?

A

Variations in apolipoprotein metabolism

Variations in apolipoprotein receptors

81
Q

What are the theories of pathogenesis of atheroma?

A

Thrombogenic theroy
Insudation theory
Reaction to injury hypothesis
Monoclonal hypothesis

82
Q

What is thrombogenic theory?

A

Plaques formed by repeated thrombi. Lipid derived from

thrombi. Overlying fibrous cap.

83
Q

What is insudation theory?

A

Endothelial injury. Inflammation. Increased

permeability to lipid from plasma

84
Q

What is the reaction to injury hypothesis?

A

Plaques form in response to endothelial injury.
Hypercholesterolemia leads to endothelial damage in experimental animals.
Injury increases permeability and allows platelet adhesion. Monocytes penetrate
endothelium. Smooth muscle cells proliferate and migrate.

Amended to say that endothelial injury may be very
subtle and undetectable visually and that LDL, especially oxidised, may damage
endothelium

85
Q

What is the monoclonal hypothesis?

A

Crucial role for smooth muscle proliferation. Each
plaque is monoclonal. Might represent abnormal growth control. Each plaque
could be benign tumour, or atheroma could have viral aetiology.

86
Q

What processes are involved in atheroma?

A

Thrombosis
Lipid accumulation
Production of intercellular matrix
Interactions between cell types

87
Q

What cells are involved in atheroma?

A 
Endothelial cells
 Platelets
 Smooth muscle cells
 Macrophages
 Lymphocytes
 Neutrophils
88
Q

What is the role of endothelial cells in atheroma?

A

Key role in haemostasis
Alter their permeability to lipoproteins
Produce collagen
Stimulate proliferation and migration of smooth muscle cells

89
Q

What is the role of platelets in atheroma?

A

Key role in haemostasis

Stimulate proliferation and migration of smooth muscle cells

90
Q

How do platelets stimulate the proliferation and migration of smooth muscle cells?

A

Using PDGF

91
Q

What is the role of smooth muscle cells in atheroma?

A

Take up LDL and other lipids to become foam cells

Synthesis collagen and other proteoglycans

92
Q

What is the role of macrophages in atheroma?

A

Oxidise LDL
Secrete proteases
Stimulate proliferation and migration of smooth muscle cells

93
Q

What do the proteases secreted by macrophages do?

A

Modify the matrix

94
Q

What is the role of lymphocytes in atheroma?

A

TNF may affect lipoprotein metabolism

Stimulate proliferation and migration of smooth muscle cells

95
Q

What is the role of neutrophils in atheroma?

A

Secrete proteases leading to continued local damage and inflammation

96
Q

What is the unified atheroma hypothesis?

A 
Endothelial injury occurs due to- 
Raised LDL
Toxins, e.g. cigarette smoke 
Hypertension 
Haemodynamic stress
Endothelial injury causes- 
Platelet adhesion
PDGF release
Smooth muscle proliferation and migration
Insudation of lipid
LDL oxidation
Uptake of lipid by smooth muscle cells and macrophages
Migration of monocytes into intima

Stimulated smooth muscle cells produce matrix material, and foam cells secrete cytokines, causing further smooth muscle stimulation and recruitment of inflammatory cells

97
Q

How can atheroma be prevented?

A 
No smoking
 Reduce fat intake
 Treat hypertension
 Reduce alcohol intake
 Regular exercise
 Weight control
98
Q

What interventions can be made to help with atheroma?

A 
Stop smoking
 Modify diet
 Treat hypertension
 Treat diabetes
 Lipid lowering drugs

esa 2- mechanisms of disease (11 decks)

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