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Cardiovascular block > Pathophysiology of atheroma > Flashcards

Pathophysiology of atheroma Flashcards

1
Q

What is the definition of atheroma/atherosclerosis ?

A

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

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2
Q

What are potential outcomes of atheroma ?

A

Ischaemia in coronary arteries - atheromatous plaques narrowing lumen
Angina due to myocardial ischaemia
Complicated thromboembolism

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3
Q

What is the earliest significant lesion of atheroma ?

A

Fatty streak

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4
Q

What makes up the yellow linear elevation of intimal lining of a fatty streak ?

A

Comprises masses of lipid - laden macrophages

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5
Q

What is the clinical significance of fatty streaks ?

A

No clinical significance

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6
Q

Who often gets fatty streaks ?

A

Young children

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7
Q

Who often gets early atheromatous plaques ?

A

Young adults onwards

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8
Q

What is the histological appearance of early atheromatous plaques ?

A

Smooth yellow patches in intima

Lipid-laden macrophages

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9
Q

What can early atheromatous plaques progress to ?

A

Established plaques

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10
Q

What are the features of a fully developed atheromatous plaque ?

A

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

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11
Q

What is responsible for the collagen production in the cap ?

A

Smooth muscle cells

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12
Q

What is the function of the fibrous cap that sits on the central lipid core ?

A

Provides structural strength

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13
Q

What resides in the fibrous cap ?

A

inflammatory cells-

  • Macrophages
  • T-lymphocytes
  • Mast cells
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14
Q

What is contained within the central lipid core ?

A

Cellular lipids/debris derived from macrophages which have died in the plaque
Often a rim of foamy thrombogenic macrophages

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15
Q

Why are some macrophages described as foamy ?

A

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

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16
Q

What marker in angiograms forms in late plaque development ?

A

Dystrophic calcification

17
Q

What is dystrophic calcification ?

A

Dystrophic calcification (DC) is the calcification occurring in degenerated or necrotic tissue

18
Q

What is a complicated atheroma ?

A

Haemorrhage into plaque causing plague rupture and potential thrombosis

19
Q

What is the most important risk factor for atheroma ?

A

Hypercholesterolaemia

20
Q

How does increased LDL cholesterol levels arise ?

A

Lack of cell membrane receptor for LDL

21
Q

What is the epidemiology for the decreased functional receptor mutation ?

A

1/500 Caucasians

22
Q

What are the signs of major hyperlipidaemia ?

A

Familial/ primary vs acquired/secondary (idiopathic?)
Biochemical evidence: LDL, HDL , total cholesterol, Triglycerides
Corneal arcus (premature)
Tendon xanthomata (knuckles, achilleas)
Xanthelasmata
Risk/premature/family history MI/atheroma

23
Q

What are the risk factors for atheroma ?

A 
Smoking 
Hypertension
Diabetes
Male
Elderly 
Accelerate process of plaque formation driven by lipids
24
Q

What are the less strong risk factors for atheroma ?

A 
Obesity 
Sedentary lifestyle
Low socio-economic status 
Low birthweight 
Role of micro-organisms
25
Q

What is arteriosclerosis ?

A

Not atheromatous
Stiffening or hardening or the arterial walls which features smooth muscle hypertrophy, apparent reduplication of internal elastic laminae and intimal fibrosis leading to a decrease in vessel diameter

26
Q

What does arteriosclerosis contribute to ?

A

High frequency of cardiac cerebral, colonic and renal ischaemia in elderly
Clinical effects most apparent when CVS further stressed by haemorrhage, major surgery, infection, shock

27
Q

Who commonly suffers from arteriosclerosis ?

A

The elderly

28
Q

What is the two step development process of atheromatous plaques ?

A
  1. Injury to endothelial lining or artery
  2. Chronic inflammation and healing repsonse of vascular wall to agent causing injury

Chronic/episodic exposure of arterial wall to these processes-> formation of atheromatous plaques

29
Q

What is the steps of the pathogenesis of atherosclerosis ?

A
  1. Endothelial injury and dysfunction
  2. Accumulation of lipoproteins (LDL) in vessel wall
  3. Monocyte adhesion to endothelium-> migration into intima and transformation to foamy macrophages
  4. Platelet adhesion
  5. Factor release from activated platelets, macrophages -> smooth muscle cell recruitment
  6. Smooth muscle cell proliferation, extracellular matric production and T-cell recruitment
    Lipid accumulation (extracellular and in foamy macrophages)
30
Q

What are the possible causes of endothelial injury ?

A

Haemodynamic disturbances (turbulent flow)

Hypercholesterolemia:
- (chronic hypercholesterolaemia can directly impair endothelial cell function by
increasing local production of reactive oxygen species)
- (lipoproteins aggregate in intima and are modified by 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

31
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, lipids-> intimal layer-> plaques

32
Q

How does advanced plaques form ?

A

Large numbers macrophages, T-lymphocytes
Lipid-laden macrophages die through apoptosis-> lipid into lipid core
Response to injury= chronic inflammatory process: 1. inflammatory response 2. process of tissue repair
Growth factors (PDGF) -> proliferation intimal smooth muscle cells, subsequent synthesis in collagen, fibrous, mucopolysaccharide
Fibrous cap encloses lipid rich core
Growth factors secreted by platelets, injured endothelium, macrophages and smooth muscle cells

33
Q

What is the consequence of progressive lumen narrowing due to high grade stenosis ?

A

Stenosis of >50-75% of vessel lumen-> critical reduction of blood flow in distal arterial bed-> reversible tissue ischaemia
E.g. Stenosed atheromatous cornonary artery-> stable angina
Very severe stenosis-> ischamic pain at rest (unstable angina)
E.g. Ileal, femoral, popliteal artery stenosis -> intermittent claudication (peripheral arterial disease)
Longstanding tissue ischemia -> atrophy of affected organ e.g. Atherosclerotic renal artery stenosis-> renal atrophy

34
Q

What is the consequence of acute atherothrombotic occlusion ?

A

Major complications rupture of plaque-> acute event
Rupture exposes highly thrombogenic plaque contents (collagen, lipid, debris) to blood stream-> activation of coagulation cascade and thrombotic occlusion in very short time
Total occlusion -> irreversible ischemia-> necrosis (infarction) of tissues
E.g. Myocardial infarct (coronary artery)
E.g. Stroke (carotid, cerebral artery)
E.g. Lower limb gangrene (ileal, femoral, popliteal artery)

35
Q

What is the consequence of embolization of the distal arterial bed ?

A

Detachment if small thrombus fragments from thrombosed atheromatous arteries-> embolise distal to ruptured plaque
Embolic occlusion of small vessels-> small infarcts in organs
E.g. Heart, dangerous small foci of necrosis-> life-threatening arrhythmias
E.g. Large ulcerating aortic plaques, lipid rich fragments of plaque-> cholestrol emboli in kidney, leg, skin
E.g. Carotid artery atheromatous debris, common cause stroke (cerebral infarct/ TIA)

36
Q

What is the consequence of ruptured atheromatous abdominal aortic anuerysm ?

A

Media beneath atheromatous plauqes gradually weakened (lipid-related inflammatory activity in plaque)
-> gradual dilatation of vessel
Slow but progressive, seen in elderly, often asymptomatic
Sudden rupture-> massive retroperitoneal haemorrhage (high mortality)
Aneurysms >5cm diameter at high risk of rupture
Mural thrombus-> emboli in legs

37
Q

What is the preventative and theraputic approaches to atheroma ?

A 
Stop smoking
Control blood pressure
Weight loss
Regular exercise
Dietary modification
38
Q

What are the secondary prevention measures of atheroma’s ?

A

Cholesterol lowering drugs, aspirin (inhibits platelet aggregation to decrease risk of thrombosis on established atheromatous plaques
Surgical options

Cardiovascular block (28 decks)

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