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2C week 1 - acute coronary syndrome > atherogenesis > Flashcards

atherogenesis Flashcards

1
Q

what is arteriosclerosis

A

hardening of the arteries - a generic term reflecting arterial wall thickening and loss of elasticity

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2
Q

what are the 3 patterns of arteriosclerosis

A

arteriolosclerosis; Monckeberg medial sclerosis; atherosclerosis

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3
Q

what is arteriolosclerosis and what can it cause

A

the hardening of small arteries and arterioles; it can be hyaline (thickening of the vessel wall) or hyperplastic (onion skin thickening of vessel wall); it can cause downstream ischaemic injury

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4
Q

what is monckeberg medial sclerosis

A

calcific deposits in muscular arteries; may undergo metaplastic change into bone; does not affect the vessel lumen

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5
Q

what is atherosclerosis characterised by?

A

characterised by intimal lesions (atheromas/atherosclerotic plaques) that protrude into the vessel lumens; plaques made of a rasied lesion with a soft, yellow lipid core covered by a fibrous cap

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6
Q

what can atherosclerosis cause?

A

plaque can obstruct blood flow; rupture can lead to vessel thrombosis; underlying media is weakened thus increasing risk of aneurysm

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7
Q

major targets of atherosclerosis

A

large elastic arteries (aorta, carotid); medium sized muscular arteries (coronary, popliteal)

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8
Q

what areas does atherosclerosis most affect

A

arteries supplying the brain, heart, kidneys, lower extremities

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9
Q

4 major consequences of atherosclerosis

A

MI; cerebral infarction (stroke); aortic aneurysm; PVD

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10
Q

non modifiable risk factors for atherosclerosis (4)

A

increasing age; being male; genetic abnormalities; family history

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11
Q

modifiable risk factors for atherosclerosis (5)

A

hyperlipidemia; hypertension; smoking; T2DM; high CRP levels

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12
Q

what is the contemporary view of artherogenesis

A

the response to injury hypothesis - endothelial injury leads to chronic inflammatory response, lesions progress due to the interaction of modified lipoproteins, monocyte derived macrophages, and t-lymphocytes with the normal cellular components of the arterial wall

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13
Q

atherosclerosis pathway (7)

A
  1. endothelial injury (increased vascular permeability, upreg of adhesion proteins resulting in enhances leukocyte adhesion, thrombosis)
  2. accumulation of lipoproteins (LDLs + oxidised LDLs are deposited in vessel wall)
  3. monocyte adhesion to endothelium (migration into the intima, transformation into foam cells)
  4. platelet adhesion
  5. factor release (from activated platelets/vessel wall cells, induce smooth muscle recruitment from media or circulating precursors, uptake of modified lipids)
  6. smooth muscle proliferation (and extra cellular matrix production)
  7. lipid accumulation (extracellularly and intracellularly, forms a well developed plaque)
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14
Q

examples of chronic endothelial injury (8)

A

hyperlipidemia; hypertension; smoking; homocysteine; haemodynamic factors; toxins; viruses; immune reactions

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15
Q

why are bifurcations more at risk of atherosclerosis

A

due to turbulent blood flow (disturbed shear) leading to increased endothelial injury (high EC turnover, poor alignment of EC, inflammatory genes, high permeability, oxidative stress)

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16
Q

what is turbulent blood flow known as

A

oscillatory flow - flow is slow and can be reversed during the cardiac cycle

17
Q

properties of endothelial cells in areas of high lamina shear (5)

A

quisecent, anti-inflammatory phenotype; characterised by alignment and direction of flow; expression of anti-inflammatory genes; low levels of oxidative stress/turnover; protected from atherosclerosis

18
Q

properties of endothelial cells in areas of disturbed lamina shear (5)

A

activated, pro-inflammatory phenotype; characterised by poor alignment; expression of inflammatory genes; high levels of oxidative stress/turnover; susceptible to atherosclerosis

19
Q

what is a fatty streak

A

the earliest lesion in atherosclerosis; comprised of lipid filled macrophages; not significantly raised and so do not cause any flow disturbances

20
Q

what is the relationship between fatty streaks and atherosclerosis

A

they may develop into precursors of plaques;

21
Q

what is plaque ulceration

A

indentation, fissure, or erosion on the luminal surface of a plaque, exposing a portion of the inner plaque to direct contact with the circulating blood; often occur preceding ischaemic events

22
Q

character of atherosclerotic lesions

A

patchy (only on a part of the wall); eccentric (rarely circular); focal and sparsely distributed at first

23
Q

why are lesion focal?

A

due to the vagaries (unexpected changes) of vessel haemodynamic

24
Q

arteries most commonly involved in atherosclerosis (descending order - 5)

A

lower abdominal aorta; coronary; popliteal; internal carotid; circle of willis

25
Q

3 principle components of atherosclerotic plaques

A
  1. cells - smooth muscle, T lymphocytes, macrophages
  2. extra cellular matrix - collagen, elastic fibres, proteoglycans
  3. intracellular and extracellular lipids
26
Q

components of a typical atherosclerotic lesion (4)

A
  1. superficial fibrous cap (smooth muscle cells, dense collagen)
  2. cellular area beneath and to side of cap (macrophages, T cells, smooth muscle cells)
  3. necrotic core (lipid, debris from dead cells, foam cells, fibrin, organised thrombus)
  4. neovascularisation
27
Q

what often causes plaques to enlarge

A

cell death/degeneration, synthesis and degradation of ECM, thrombus organisation (calcification can also happen to atheroma - complication)

28
Q

what does calcification make difficult?

A

angioplasty

29
Q

what changes are atherosclerotic plaques susceptible to?

A

rupture, ulceration, erosion - leading to thrombosis; haemorrhage; atheroembolism; aneurysm formation

30
Q

stable vs unstable plaque

A

stable - dense fibrous cap, minimal lipid accumulation, little inflammation
unstable - thin caps, large lipid cores, dense inflammatory filtrate

31
Q

morphologic changes in an MI (3)

A
  1. ischaemic coagulative necrosis
  2. inflammation
  3. repair
32
Q

progression of an MI pathology

A

<12hrs - recognition may be difficult -> 12-24hrs - red-blue area of trapped, stagnant blood -> more sharply defined, yellow-tan colour -> 10+ days infarct rimmed by zone of hyperaemic vascular granulation zone -> infarct replaced by fibrous scar

33
Q

progression of an MI histology

A

changes of coagulative necrosis -> acute inflammation elicited by necrotic muscle fibres -> macrophages remove the necrotic muscle fibres -> damaged zone replaced by ingrowth of vascularised granulation tissue -> well developed scar tissue

2C week 1 - acute coronary syndrome (7 decks)

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