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Systems: Cardiovascualar AB > Pathophysiology of Atheroma > Flashcards

Pathophysiology of Atheroma Flashcards

1
Q

Atheroma/ atherosclerosis

A

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

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2
Q

How is ischaemia caused in the coronary arteries?

A

Atheromatous plaques narrow lumen meaning that not enough oxygenated blood gets through

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3
Q

What is a serious consequence of myocardial ischaemia?

A

Angina

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4
Q

What can complicate atheroma?

A

Thromboembolism

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5
Q

Arteriosclerosis

A

Age-related change in muscular arteries

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6
Q

What is arteriosclerosis characterised by?

A
  • Smooth muscle hypertrophy
  • Apparent reduplication of internal elastic laminae
  • Intimal fibrosis which leads to a decrease in vessel diameter
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7
Q

What doe arteriosclerosis contribute to?

A

High frequency of cardiac, cerebral, colonic and renal ischaemia in the elderly

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8
Q

When are the clinical effects of arteriosclerosis most apparent?

A

When the CVS is stressed:

  • Haemorrhage
  • Major surgery
  • Infection
  • Shock
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9
Q

What is the earliest significant lesion?

A

Fatty streak

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10
Q

How does the fatty streak appear?

A

Yellow linear elevation of intimal lining

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11
Q

What is the fatty streak comprised of?

A

Comprises masses of lipid-laden macrophages

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12
Q

What is the clinical significance of fatty streaks?

A

No clinical significance

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13
Q

What is the fate of fatty streaks?

A
  • May disappear

- May form artheromatous plaques in patients at risk

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14
Q

Who do fatty streaks form in?

A

Young children

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15
Q

When do early artheromatous plaques form?

A

Young adults onwards

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16
Q

How do early artheromatous plaques appear?

A

Smooth yellow patches in intima

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17
Q

What are early artheromatous plaques compose of?

A

Lipid-laden macrophages

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18
Q

What is the fate of early atheromatous plaques?

A

Progress to established plaques

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19
Q

What is the composition of a fully developed atheromatous plaque?

A

Central lipid core, rich in cellular lipids/ debris derived from macrophages with fibrous tissue cap, covered by arterial enothelium

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20
Q

What produces collagen?

A

Smooth muscle cells

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21
Q

What does the collagens in the cap provide?

A

Structural strength

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22
Q

What resides in the fibrous cap?

A

Inflammatory cells including:

  • Macrophages
  • T lymphocytes
  • Mast cells
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23
Q

Where are the inflammatory cells recruited from?

A

Arterial endothelium

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24
Q

How doe fully developed atheromatous plaques appear?

A

Soft, highly thrombogenic, often rim of foamy macrophages

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25
Q

Why do fully developed atheromatous plaques appear foamy?

A

Due to the uptake of oxidised lipoproteins via specialised membrane bound scavenger receptor

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26
Q

What occurs later in the development of fully developed atheromatous plaques?

A

Dystrophic calcification extensive

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27
Q

Where does calcification occur in plaques?

A

Form at arterial branching points/bifurcations (turbulent flow)

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28
Q

How can late stage plaques be described?

A

Confluent, cover large areas

29
Q

What makes a complicated atheroma?

A

Features of established atheromatous plaque +

  • Haemorrhage into plaque(calcification)
  • Plaque rupture/ fissuring
  • Thromobsis
30
Q

What is the most important risk factor in the aetiology of atheroma?

A

Hypercholesterolemia

31
Q

What does hypercholesterolemia cause?

A

Plaque formation and growth in the absence of other known risk factors

32
Q

What usually happens to people who are homozygous for hypercholesterolemia?

A

Much higher cholesterol levels which leads to death from coronary artery atheroma in infancy/teens

33
Q

What is the mutation which causes hypercholesterolemia?

A

Decreased functional receptors on cell surfaces which leads to elevated plasma LDL cholesterol levels

34
Q

What are the different types of causes of hyperlipidaemia?

A
  • Familial/primary

- Acquired/secondary

35
Q

What is the biochemical evidence of hyperlipidaemia?

A

-LDL
-HDL
-Total cholesterol
Triglycerides

36
Q

What are the signs of major hyperlipidaemia?

A
  • Corneal arcus
  • Tendon xanthomata
  • Xanthelasmata
37
Q

What other risk factors are there for atheroma?

A
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Male
  • Elderly
  • Accelerate process of plaque formation driven by lipids
38
Q

What less strong risk factors are there for atheroma?

A
  • Obesity
  • Sedentary lifestyle
  • Low socio-economic status
  • Low birthweight
  • Role of micro-organisms
39
Q

What are the 2 steps in the development of atheromatous plaques?

A
  • Injury to endothelial lining of artery
  • Chronic inflammatory and healing response of vascular wall to agent causing injury
  • It is chronic/ episodic exposure of arterial wall to these process which leads to the formation of atheromatous plaques
40
Q

What is the pathogenesis of atherosclerosis?

A
  • Endothelial injury and dysfunction
  • Accumulation of lipoproteins (LDL) in vessel wall
  • Monocyte adhesion to endothelium leads to the migration into intima and transformation to foamy macrophages
  • Platelet adhesion
  • Factor release from activated platelets, macrophages which leads to smooth muscle recruitment
  • Smooth muscle cell proliferation, extracellular matrix production an T cell recruitment
  • Lipid accumulation (extracellular an in foamy macrophages)
41
Q

What is the most important cause of endothelial injury?

A

Haemodynamic disturbances (turbulent flow)

42
Q

How can hypercholesterolemia directly impair endothelial cell function?

A
  • By increasing local production of reactive oxygen species
  • Lipoproteins aggregate in intima and are modified y free radicals produced by inflammatory cells
  • Modified LDL accumulated by macrophages but not completely degraded
  • Foamy macrophages
  • Toxic to endothelial cells plus release of growth factors, cytokines
43
Q

How are injured endothelial cells functionally altered?

A
  • Enhance expression of cell adhesion molecules (ICAM-1, E-selectin)
  • High permeability for LDL
  • Increased thrombogenicity
44
Q

What response to injury of the endothelial surface is there?

A

Chronic inflammatory process

  • Inflammatory reaction
  • Process of tissue repair
45
Q

What doe growth factors stimulate?

A

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

46
Q

What does the fibrous cap enclose?

A

Lipid rich core

47
Q

What are growth factors secreted by?

A
  • Platelets
  • Injured endothelium
  • Macrophages
  • Smooth muscle cells
48
Q

Where are microthrombi formed?

A

At denuded areas of plaque surface

49
Q

What are the consequence of the clinical manifestations of atheroma?

A
  • Progressive lumen narrowing due to high grade plaque stenosis
  • Acute atherthrombotic occlusion
  • Embolisation of the distal arterial bed
  • Ruptured atheromatous abdominal aortic aneurysm
50
Q

What does stenosis of >50-75% of the vessel lumen lead to?

A

Critical reduction of blood flow in distal arterial bed leading to reversible tissue ischaemia (stenosed atheromatous coronary artery leads to stable angina)

51
Q

What will very severe stenosis lead to?

A

Ischaemic pair at rest ( unstable angina)

52
Q

What can ileal, femoral or popliteal artery stenosis lead to?

A

Intermittent claudication (peripheral artery disease)

53
Q

What can longstanding tissue ischaemia lead to

A

Atrophy of affected organ ( e.g. atherosclerotic renal artery stenosis leading to renal atrophy)

54
Q

What are the major complications of acute atherothrombotic occlusion?

A

Rupture of plaques leading to acute event

55
Q

What does rupture of plaque lead to?

A

Rupture exposes highly thrombogenic plaque contents (collagen, lipid, debris) to blood stream which leads to the activation of coagulation cascade and thrombotic occlusion in very short time

56
Q

What does total occlusion lead to?

A

Irreversible ischaemia which leads to necrosis (infarction) of tissues

57
Q

What are examples of necrosis due to irreversible ischaemia?

A
  • Myocardial infarct caused by coronary artery
  • Stroke caused by carotid/ cerebral artery
  • Lower limb gangrene caused by ileal/femoral/popiteal artery
58
Q

What leads to the embolization of the distal arterial bed?

A
  • Detachment of small thrombus fragments from thrombosed atheromatous arteries leads to embolus distal to ruptured plaque
  • Embolic occlusion of small vessels leads to small infarcts in organs
59
Q

What are examples of consequences of embolic occlusion of small vessels?

A
  • Heart, dangerous small foci of necrosis- life threatening arrhythmias
  • Large ulcerating aortic plaques, lipid rich fragments of plaque leads to cholesterol emboli in kidney, leg and skin
  • Carotid artery atheromatous debris, common cause of stroke
60
Q

What causes an atheromatous abdominal aortic aneurysm to rupture?

A
  • Media beneath atheromatous plaques gradually weakened leads to gradual dilatation of the vessel
  • Sudden rupture leads to massive retroperitoneal haemorrhage
61
Q

Which AAA are at risk of rupture?

A

> 5cm

62
Q

Where do mural thrombus emboli to

A

Legs

63
Q

What atheromatous plaques are vulnerable and at high risk of developing thrombotic complications?

A

Typically thin fibrous cap, large lipid core with prominent inflammation

64
Q

What does pronounced inflammatory activity in vulnerable plaques lead to?

A

Degradation and weakening of plaque which increases the risk of plaque rupture

65
Q

How do highly stenotic plaques usually appear/

A

Large firbrocalcific component with little inflammation

66
Q

What do plaque inflammatory cells secrete?

A
  • Proteolytic enzymes
  • Cytokines
  • Reactive oxygen species
67
Q

What preventative and therapeutic measures are there?

A
  • Stop smoking
  • Control blood pressure
  • Weight-loss
  • Regular exercise
  • Dietary modifications
68
Q

What secondary prevention is there?

A
  • Cholesterol lowering drugs

- Aspirin (inhibits platelet aggregation to decrease risk of thrombosis on established atheromatous plaques)

Systems: Cardiovascualar AB (42 decks)

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