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Cardiovascular System > Pathophysiology of Atheroma > Flashcards

Pathophysiology of Atheroma Flashcards

1
Q

What is atherosclerosis?

A

Formation of focal elevated lesions (plaques) in the intima of large and medium sized arteries

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2
Q

What does atheroma in the coronary arteries result in?

A

Narrowing of the lumen due to atheromatous plaques, this in turn causes ischaemia and angina and can be complicated by thromboembolism

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3
Q

What is arteriosclerosis?

A

Age-related change in the muscular arteries

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4
Q

What does arteriosclerosis result in?

A

Smooth muscle hypertrophy
Apparent reduplication of internal elastic laminae
Intimal fibrosis leading to decreased vessel diameter

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5
Q

What does arteriosclerosis contribute to in the elderly?

A

High frequency of cardiac, cerebral, colonic and renal ischaemia

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6
Q

When are the clinical effects of arteriosclerosis most apparent?

A

When CVS is further stressed by haemorrhage, major surgery, shock, infection etc.

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7
Q

What is atheroma?

A

Fatty streak
The earliest significant lesion in atherosclerosis
Yellow linear elevation of the intimal lining

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8
Q

What is an atheroma lesion comprised of?

A

Masses of lipid-laden macrophages

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9
Q

In what way is atheroma relevant?

A

No clinical significance, only relevant in patients at risk as it may develop into an atheromatous plaque

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10
Q

When are early atheromatous plaques seen?

A

Young adults onwards

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11
Q

What are the features of early atheromatous plaques?

A

Smooth yellow patches in the intima
Lipid-laden macrophages
Can progress to established plaques

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12
Q

What are the features of a fully developed plaque?

A

Central lipid core with fibrous tissue cap
Covered by arterial endothelium
Collagens in the cap provide structural strength
Inflammatory cells reside in the fibrous cap
Central lipid core is rich in cellular lipids and debris derived from the macrophages
Soft, highly thrombogenic ring of foamy macrophages
Extensive dystrophic calcification
Late stage plaques are confluent and cover large areas

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13
Q

What do macrophages in fully developed plaques have a foamy appearance?

A

Due to uptake of oxidised lipoproteins via specialised membrane bound scavenger receptors

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14
Q

What might provide a marker for atherosclerosis in angiograms and CT scans?

A

Dystrophic calcification

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15
Q

Where do calcifications form?

A

At arterial branching points and bifurcations due to turbulent flow

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16
Q

What are the features of a complicated atheroma?

A

Features of established atheromatous plaque plus;
Haemorrhage into the plaque, calcification
Plaque rupture/fissuring
Thrombosis
Clinical consequences

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17
Q

What are the two steps involved in the development of atheromatous plaques? How do these steps result in formation of atheromatous plaques?

A

Injury to the endothelial lining of the artery
Chronic inflammatory and healing response of the vascular wall to the agent causing the injury

Chronic and episodic exposure of arterial wall to these processes is what results in the formation of atheromatous plaques

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18
Q

What is the order of events in atherosclerosis development?

A

Endothelial injury and dysfunction
Accumulation of lipoproteins in the vessel wall
Monocyte adhesion to the endothelium, migration into the intima and transformation to foamy macrophages
Platelet adhesion
Factor release from activated platelets and macrophages causing smooth muscle cell recruitment
Smooth muscle cell proliferation, ECM production and T-cell recruitment
Lipid accumulation

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19
Q

What are the most important causes of endothelial injury?

A

Haemodynamic disturbances e.g. turbulent flow, hypercholesterolaemia

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20
Q

How can chronic hypercholesterolaemia directly impair endothelial cell function?

A

By increasing local production of reactive oxygen species;

Lipoproteins aggregate in the intima and are modified by free radicals produced by inflammatory cells
Modified LDL accumulated by macrophages but not completely degraded
Foamy macrophages accumulate
These are toxic to endothelial cells plus release growth factor and cytokines

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21
Q

How are injured endothelial cells functionally altered?

A

Enhanced expression of cell adhesion molecules (ICAM-1, E-selectin)
High permeability for LDL
Increased thrombogenicity
Inflammatory cells and lipids accumulate in intimal layer and form plaques

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22
Q

In advanced plaque formation there are large number of what cells?

A

Macrophages and T-lymphocytes

23
Q

What does response to endothelial injury involve?

A

The chronic inflammatory process

24
Q

What do growth factors cause in the intimal smooth muscle cells?

A

Proliferation of the intimal smooth muscle cells and subsequent synthesis of collagen, elastin and mucopolysaccharides

25
Q

What are growth factors secreted by?

A

Platelets
Injured endothelium
Macrophages
Smooth muscle cells

26
Q

In established plaques, what is plaque growth initiated by (besides growth factors)?

A

Small areas of endothelial loss
Microthrombi formed at denuded areas of the plaque surface are organised by the same rear process
Repeated cycles gradually increase the plaque volume

27
Q

What are the main components of an atheromatous plaque?

A 
Central lipid core
Fibrous tissue cap 
Arterial endothelial lining 
Collagen in fibrous cap 
Inflammatory cells in fibrous cap
Rim of foamy macrophages
28
Q

What is the most important risk factor for atheroma? Why?

A

Hypercholesterolaemia

It causes plaque formation and growth in the absence of other known risk factors

29
Q

What proportion of Caucasians are heterozygous for a mutation resulting in genetically determined lack of cell membrane receptors for LDL?

A

1/500

30
Q

What is the prognosis of patients who are homozygous for the mutation resulting in a genetically determined lack of cell membrane receptors for LDL?

A

Much higher cholesterol levels, these patients usually die from coronary artery atheroma in infancy or teens
1 in 1 million people - rare

31
Q

Other than hypercholesterolaemia, what are some risk factors for atheroma?

A 
Smoking 
Hypertension 
Diabetes mellitus
Male 
Elderly 
Less strong risk factors;
Obesity 
Sedentary lifestyle
Low socio-economic status
Low birthweight
Possible role of micro-organisms
32
Q

What biochemical levels are needed in investigation of atheroma?

A

LDL
HDL
Total cholesterol
Triglycerides

Results in the above which are higher than expected are indicative of hyperlipidaemia

33
Q

What features of a physical examination are indicative of atheroma?

A

Corneal arcus
Tendon xanthoma (knuckles, Achilles tendon)
Xanthelasmata

34
Q

What changes in plaques have serious complications?

A

Acute changes

35
Q

What will stenosis of 50-75% of the vessel lumen result in?

A

Critical reduction of blood flow in the distal arterial bed, resulting in reversible tissue ischaemia

36
Q

What will a stenosed atheromatous coronary artery cause?

A

Stable angina and ischaemic pain when exercising

37
Q

What does severe stenosis of a coronary artery result in?

A

Unstable angine - ischaemic pain at rest

38
Q

What does iliac, femoral or popliteal artery stenosis result in?

A

Intermittent claudication (peripheral arterial disease)

39
Q

What will longstanding tissue ischaemia result in?

A

Atrophy of the affected organ

40
Q

What does rupture of an atheromatous plaque cause?

A

Exposure of the highly thrombogenic plaque contents to the blood stream, causing activation of the coagulation cascade and thrombotic occlusion in a very short time (thrombus formation)

41
Q

What will total vessel occlusion result in?

A

Irreversible ischaemia resulting in necrosis or infarction of the affected tissues
e.g. MI in coronary artery
stroke in cerebral or carotid artery
lower limb gangrene in iliac, femoral or popliteal artery

42
Q

What causes embolisation of the distal arterial bed?

A

Detachment of small thrombus fragments from thromboses atheromatous arteries which emolise distal to the ruptured plaque

43
Q

What does embolic occlusion of small vessels cause?

A

Small infarcts in the affected organs

44
Q

What can embolic occlusion of small vessels in the heart cause?

A

Dangerous small foci of necrosis leading to life-threatening arrythmias

45
Q

What can lipid-rich fragments of large ulcerating aortic plaques cause?

A

Cholesterol emboli in the kidneys, legs and skin

46
Q

What is atheromatous debris a common cause of in the carotid arteries?

A

Cerebral infarct or TIA

47
Q

Why does the media beneath the atheromatous plaques gradually weaken?

A

Due to lipid related inflammatory activity in the plaque causing gradual dilatation of the vessel

48
Q

What does sudden rupture of an atheromatous abdominal aortic aneurysm result in?

A

Massive retroperitoneal haemorrhage with a high mortality

49
Q

When are abdominal aortic aneurysms at risk of rupture?

A

when > 5cm

50
Q

What are the features typical of atheromatous plaques which are vulnerable to rupture?

A

Thin fibrous cap
Large lipid core
Prominent inflammation
Secretion of proteolytic enzymes, cytokines and reactive oxygen species by plaque inflammatory cells

51
Q

What does pronounced inflammatory activity lead to?

A

Degradation and weakening of the plaque resulting in increased risk of plaque rupture

52
Q

What is a typical feature of highly stenotic plaques?

A

Often have a large fibrocalcific component with little inflammation

53
Q

What are some primary preventative measures that can be taken against atheromatous plaque development?

A 
Smoking cessation 
BP control
Weight loss
Regular exercise 
Dietary modification
54
Q

What are the options for secondary prevention of atheromatous plaques?

A

Cholesterol lowering drugs
Aspirin
Surgical options

Cardiovascular System (40 decks)

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