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CVS > 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 arteriosclerosis?

A

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.

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4
Q

When is the difference between arteriosclerosis and atherosclerosis?

A

Atherosclerosis is a type of arteriosclerosis

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5
Q

When are the effects of arteriosclerosis most apparent?

A

When the CVS is further stressed by haemorrhage, major surgery , infection or shock

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6
Q

Who commonly suffers from arteriosclerosis?

A

Elderly

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7
Q

What is the earliest significant lesion of atheroma?

A

Fatty streak

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8
Q

What makes up the yellow linear elevation of intimal lining?

A

Comprises masses of lipid - laden macrophages

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9
Q

Who often gets early atheromatous plaques?

A

Young adults onwards - fatty streaks are present in children although they may disappear

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10
Q

What does early atheromatous plaque progress to?

A

Established plaques

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11
Q

What are the structural features of a fully developed atheromatous plaque?

A

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

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12
Q

What is responsible for the collagen production in the cap?

A

Smooth muscle cells

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13
Q

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

A

Provides structural strength

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14
Q

What resides in the fibrous cap?

A

Inflammatory cells - macrophages, T lymphocytes and mast cells - recruited from the arterial endothelium

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15
Q

What is contained within the central lipid core?

A

Cellular lipids/debris derived from macrophageswhich have died in the plaque

Often a rim of foamy thrombogenic macrophages

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16
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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17
Q

What marker in angiograms forms in late plaque development?

A

Dystrophic calcification

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18
Q

What is dystrophic calcification?

A

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

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19
Q

Where does atheroma normally occur?

A

•Form at arterial branching points/bifurcations (turbulent flow)

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20
Q

What is meant by a complicated atheroma?

A

Haemorrage into plaque causing plague rupture and potential thrombosis

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21
Q

Define haemorrhage

A

an escape of blood from a ruptured blood vessel.

22
Q

What is the most important risk factor for atheroma?

A

Hypercholesterolaemia

23
Q

How may increased LDL cholesterol levels arise?

A

•lack of cell membrane receptors for LDL

24
Q

What are signs of major lipidaemia?

A

Familial

Biochemical evidence (•LDL, HDL, total cholesterol, triglycerides)

  • Corneal arcus (premature)
  • Tendon xanthomata (knuckles, Achilles)
  • Xanthelasmata – fatty lumps on the eyelid
25
Q

What are the risk factors for atheroma?

A
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Male
  • Elderly
  • Accelerate process of plaque formation driven by lipids
26
Q

What are the less strong risk factors?

A
  • Obesity
  • Sedentary lifestyle
  • Low socio-economic status
  • Low birthweight
  • ?role of micro-organisms
27
Q

What is the two step development process of athermoatous plaques?

A
    1. injury to endothelial lining of artery
    1. chronic inflammatory and healing response of vascular wall to agent causing injury
  • Chronic/episodic exposure of arterial wall to these processes → formation of atheromatous plaques
28
Q

What is the step by step process of development of atheromatous plaques?

A

Endothelial injury

LDL accumulation in vessel wall

Monocyte adhesion to endothelium

Migration of monocytes to intima and transformation into foamy macrophages

Platelet adhesion

Activated platelets release factors causing macrophage recruitment to smooth muscle cell

Smooth muscle cell proliferation - extracellular matrix production and T-cell recruitment

Lipid accumulation (extracellular and in foamy macrophages)

29
Q

What are the possible causes of atheromatous plaques?

A

•haemodynamic disturbances (turbulent flow)

•hypercholesterolaemia

(chronic hypercholesterolaemia increases production of reactive oxygen species)

(lipoproteins aggregate in intima and are modified by free radicals produced by inflammatory cells → modified LDL is gathered by macrophages but not completely degraded forming foamy macrophages → partly broken down LDL is toxic to endothelial cells plus release of growth factors, cytokines

30
Q

How are injured endothelial cells functionally altered?

A

Enhanced expression of cell adhesion molecules •(ICAM-1, E-selectin)

•High permeability for LDL – normally LDL wouldn’t be able to cross the barrier

Increased thrombogenicity

31
Q

How do lipid laden macrophages die?

A

Through apoptosis - lipid into lipid core

32
Q

What is the effect of PDGF? (Platelet derived growth factor)

A

Results in proliferation of intimal smooth muscle cells and subsequent synthesis of collagen, elastin and mucopolysaccharide

33
Q

Where are growth factors secreted?

A

Platelets, injured endothelium, macrophages and smooth muscle cells

34
Q

Where do microthrombi form?

A

Denuded area of the plaque surface

35
Q

How are microthrombi organised?

A

•By same repair process (smooth muscle cell invasion and collagen deposition) - repeated cycles eventually increase plaque volume

36
Q

What is normally the level of occlusion resulting in •reversible tissue ischaemia

A

Stenosis of > 50-75% of vessel lumen → critical reduction of blood flow in distal arterial bed

37
Q

What causes stable angina?

A

stenosed atheromatous coronary artery

38
Q

What causes ischaemic pain at rest?

A

Very severe stenosis - unstable angina

39
Q

What causes intermittant claudication?

A

ileal, femoral, popliteal artery stenosis

40
Q

What is the effect of Longstanding tissue ischaemia?

A

•atrophy of affected organ e.g. atherosclerotic renal artery stenosis → renal atrophy

41
Q

What are the immediate events following the rupture of a plaque?

A

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

42
Q

What is the effect of total occlusion?

A

Irreversible ischaemia - 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)
43
Q

Where do detatchments of small thrombus fragments from thrombosed atheromatous arteries embolise?

A

Distal to the ruptured plaque

44
Q

What is the result of emolic occlusion of small vessels?

A
  • 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 → cholesterol emboli in kidney, leg, skin
  • E.g. carotid artery atheromatous debris, common cause stroke (cerebral infarct/TIA)
45
Q

What causes an atheromatous abdominal aortic aneurysm?

A

Weakened media beneath atheromatous plaques - causing the gradual dilation of the vessel

46
Q

What is the result of a ruptured abdominal aortic annyeurism?

A
  • massive retroperitoneal haemorrhage (high mortality)
  • Aneurysms > 5cm diameter at high risk of rupture
  • Mural thrombus → emboli to legs
47
Q

Define mural thrombus

A

A thrombus in a large blood vessel that decreases blood flow through that vessel

48
Q

What plaques have a high risk of developing thrombitic complications?

A

•Typically thin fibrous cap, large lipid core, prominent inflammation

49
Q

What is the effect of pronounced inflammatory activity?

A

Degradation and weakening of plaque

Increased risk of rupture

50
Q

What do inflammatory cells release that increase the risk of rupture and cause degradation?

A

Secretion of proteolytic enzymes, cytokines and reactive oxygen species

51
Q

Which plaques are less likely to rupture?

A

Highly stenotic plaques with large fibrocalcific component, little inflammation

52
Q

What are the preventative and therapeutic options?

A
  • Stop smoking
  • Control blood pressure
  • Weight-loss
  • Regular exercise
  • Dietary modifications
  • Secondary prevention:
  • Cholesterol lowering drugs, aspirin (inhibits platelet aggregation to decrease risk of thrombosis on established atheromatous plaques)

•

•Surgical options

CVS (21 decks)

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