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Cardiovascular System > Pathophysiology of Atheroma > Flashcards

Pathophysiology of Atheroma Flashcards

1
Q

What is atherosclerosis?

A

The formation of focal elevated lesions (plaques) in the intimate of large ad medium-sized arteries

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2
Q

What happens when atheomas form in places like coronary arteries?

A

Atheromatous plaques narrow lumen which leads to ischaemia and can cause angina

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3
Q

What is ARTERIOsclerosis?

A

Thickening of the artery walls due to smooth muscle hypertrophy, thickening of elastic laminae and intimal fibrosis which narrows the lumen

Not atheromatous (no plaque build up)
Age-related change in muscular arteries
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4
Q

Describe the initial fatty streak

A

Can occur in young children
Yellow linear elevation of intimal lining
Contains lipid-laden macrophages
No clinical significance
May disappear
Patients at risk of developing atheromatous plaques

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5
Q

Describe the early atheromatous plaque

A

Occurs in young adults onwards
Smooth yellow patches in initial
Lipid-laden macrophages
Progress to established plaques

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6
Q

Describe the fully developed atheromatous plaque

A

Central lipid core with fibrous tissue cap, covered by arterial endothelium

Collagen (produced by smooth muscle cells) are stored in the cap and provide structural strength

Inflammatory cells (macrophages, T-lymphocytes, mast cells) reside in fibrous cap - have been recruited by endothelium

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7
Q

Where are common places for atheroma to develop?

A

At arterial branching points - bifurcation - due to turbulent flow

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8
Q

What does the core of an atheroma contain?

A

Central lipid core rich in cellular lipids/debris derived from macrophages (dies in plaque)

Soft, highly thrombogenic rim of ‘foamy’ macrophages

‘foamy’ due to uptake of oxidised lipoproteins

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9
Q

What occurs at age stage of plaque development?

A

Dystrophic calcification (calcification occurring in degenerated or necrotic tissue)

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10
Q

What are features of complicated atheroma?

A

Normal lipid-rich core and fibrous cap, plus:
Haemorrhage into plaque (calcification)
Plaque rupture/fissuring
Thombosis

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11
Q

Aetiology of atheroma

A

Hypercholesterolaemia - causes plaque formation and growth without other risk factors

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12
Q

Signs of severe hyperlipidaemia

A

Biochemistry: LDL, HDL, total cholesterol, triglycerides
Corneal Marcus
Tendon xanthomata
Xanthelasmata

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13
Q

Risk factors for atheroma

A 
Hypercholesterolaemia 
Smoking 
Hypertension
Diabetes mellitus 
Male
Elderly
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14
Q

What is the basic formation of the atheromatous plaque - two step process

A
  1. Injury to endothelial lining of artery
  2. Chronic inflammatory and healing response of vascular wall to agent causing injury

Chronic/episodic exposure of endothelium to these process lead to formation of atheromatous plaques

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15
Q

Outline the development of atheromatous plaques

A
  1. Endothelium injury
  2. Lipoprotein (LDL) accumulation in wall
  3. Monocyte adhesion -> into intimal and becomes foamy macrophages
  4. Platelet adhesion
  5. Activated platelets and macrophages release factor -> smooth muscle cell recruitment
  6. Smooth muscle cell proliferation forming fibrous plaque
  7. Lipid accumulation (extracellular and in foamy macrophages)
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16
Q

What causes endothelial damage?

A 
Haemodynamic disturbances (turbulent flow)
Hypercholesterolaemia
17
Q

How does hypercholesterolaemia damage the endothelium?

A

Increasing local production of reactive oxygen species

When the endothelium is injured, lipoprotein molecules can gain entry where they are then modified by oxidation via free radicals. This modified LDL is inflammatory and able to be ingested by macrophages, creating “foam cells” and causing a “fatty streak” in the arterial wall.

Inflammatory cells and lipids -> intimal -> plaques

18
Q

What changed occur in endothelial cells after injury?

A

Increased expression of cell adhesion molecules (ICAM-1, E-selectin)
High permeability for LDL
Increased thrombogenicity

19
Q

Outline the advanced plaque formation

A
  1. Foamy macrophages die through apoptosis -> lipid released into lipid core
  2. Response to injury - chronic inflammatory process: Inflammation and process of tissue repair
  3. Injured epithelium and platelets release growth factors (PDGF) -> proliferation of intimal smooth muscle cells, then subsequent synthesis collagen, elastin and mucopolysaccharide
  4. Enclosed by fibrous cap
20
Q

Why does endothelial loss initiate plaque growth?

A

Microthrombi formed at denuded areas of plaque surface -> organised by same repair process (smooth muscle cell invasion and collagen deposit)

21
Q

How can atheromas cause ischaemia?

A

Progressive narrowing of lumen due to high grade plaque stenosis

Stenosis of > 50% of lumen -> critical reduced blood flow -> reversible ischaemia

22
Q

What can lower limb artery stenosis cause?

A

Intermittent claudication

23
Q

What can prolonged artery stenosis cause?

A

Long standing tissue ischaemi -> atrophy of affected organ

24
Q

What is a major consequence of atheroma?

A

Acute atherothrombotic occlusion

25
Q

How can an atheroma cause an occlusion of an artery?

A

Rupture of plaque exposes highly thrombogenic plaque contents (collagen, lipid, debris) to blood stream

This activates a coagulation cascade and thrombotic occlusion

26
Q

What does total occlusion lead to?

A

Total occlusion -> irreversible ischaemia -> necrosis (infarction) of tissue

27
Q

Types of infarctions

A

Myocardial (coronary artery)
Stroke (carotid, cerebral artery)
Lower limb gangrene (lower limb arteries)

28
Q

How do atheroma cause embolisation?

A

Detachement of small thrombus fragments -> embolism distal to ruptured plaque

Embolic occlusion of small vessels -> small infarcts (i.e. cause arrhythmia, TIA)

29
Q

How do atheromas cause abdominal aortic aneurysms?

A

Media beneath plaque gradually weakened -> gradual dilation of vessel

30
Q

Complication of AAA

A

Aneurysms > 5cm risk of rupture

Sudden rupture -> massive retoperitoneal haemorrhage

31
Q

Describe a vulnerable atheromatous plaque

A

Thin fibrous cap, large lipid core and prominent inflammation (weakens plaque, increasing risk of rupture)

High stenotic plaques, large fibrocalcific component, little inflammation

32
Q

Primary prevention/therapy

A 
Smoking cessation 
Control bp 
Weight loss 
Exercise 
Dietary modification
33
Q

Secondary prevention/therapy

A

Cholesterol lowering drugs
Aspiring (inhibits platelet aggregation to decrease risk of thrombosis on established plaques)

Then consider surgery

Cardiovascular System (37 decks)

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