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2. Cardiovascular System > 19. Pathophysiology of Atheroma > Flashcards

19. Pathophysiology of Atheroma Flashcards

1
Q

Define atheroma (atherosclerosis)

A

formation of focal elevated lesions (plaques) in intima of large and medium sized vessels (hardening of arteries)

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2
Q

What are atheromas complicated by particularly?

A

thromboemolism (travelling clot is called embolus which lodges in other lumens)

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3
Q

Define embolus.

A

Blood clot which TRAVELS in the body into passages that it cannot pass and can cause embolism. Often it’s a blood clot that breaks off (thromboembolus)

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4
Q

Define thrombus.

A

When a blood clot forms in the VESSEL and impedes blood flow

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5
Q

What do atheromatous plaques cause eventually?

A
  • plaques narrow lumen

- lead to ischaemia (in serious consequences angina can be as a result of myocardial ischaemia)

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6
Q

Define ischaemia.

A

inadequate blood supply to tissues or organs/ part of body

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7
Q

Define atherosclerosis.

A
  • build up of fatty materials inside vessels (atheromatous plaques)
  • biggest causes of MIs and strokes
  • proliferation of intimal smooth-muscle cells creating atheromatous plaques
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8
Q

Define arteriosclerosis.

A
  • thickening and hardening of artery walls usually due to age
  • age-related change in muscular arteries
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9
Q

What pathological process occur in arteriosclerosis? (3)

A
  • smooth muscle hypertrophy
  • apparent reduplication of internal elastic laminae
  • internal fibrosis which decreases vessel diameter
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10
Q

What occurs to vessel diameter in arteriosclerosis and atherosclerosis?

A

it decreases (gets smaller)

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11
Q

What does arteriosclerosis mainly contribute to in elderly people? (4)

A

High frequency of…

  • cardiac ischaemia
  • cerebral ischaemia
  • colonic ischaemia
  • renal ischaemia
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12
Q

When are clinical effects more apparent in arteriosclerosis? (4)

A

When CV system is further stressed by :

  1. haemorrhage
  2. major surgery
  3. infection
  4. shock
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13
Q

What are 3 layers which make up the artery wall?(from top to bottom)

A
  1. tunica adventitia/externa
  2. tunica media
  3. tunica intima
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14
Q

What is the earliest stage of atheroma formation?

A

fatty streak (earliest significant lesion)

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15
Q

When does fatty streak in arteries usually appear? (earliest stage of atheroma)

A

in young children

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16
Q

Describe the fatty streak. What is it? (2)

A
  • yellow linear elevation of intimal lining

- comprises masses of lipid-laden macrophages

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17
Q

What is the clinical significance of a fatty streak? (2)

A
  • no clinical significance

- may disappear with time

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18
Q

What are patients with a fatty streak at risk of?

A

at risk of atheromatous plaques

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19
Q

What are the 3 stages of atheroma development?

A
  1. fatty streak
  2. early atheromatous plaque
  3. fully developed atheromatous plaque
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20
Q

What is the 2nd stage of atheroma formation?

A

early atheromatous plaque

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21
Q

When does early atheromatous plaque develop?

A

in young adults onwards

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22
Q

Describe the early atheromatous plaque. What is it? (3)

A
  • smooth yellow patches in intima
  • lipid-laden macrophages
  • progresses to establish plaques
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23
Q

What is the 3rd stage of atheroma formation?

A

fully developed atheromatous plaque

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24
Q

Describe the appearance of a fully developed atheromatous plaque.

A

Central lipid core with fibrous tissue cap covered by arterial endothelium

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25
Q

What are fibres found in fibrous tissue cap of atheroma?

A

collagens (produced by smooth muscle cells) in cap provide structural strength

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26
Q

What cells are found in fibrous tissue cap of atheroma?

A

inflammatory cells (macrophages, t-lymphocytes,mast cells) reside in fibrous cap which release debris and waste

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27
Q

Where are inflammatory cells in fibrous tissue cap produced from?

A

recruited from arterial endothelium

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28
Q

Where are collagens in fibrous tissue cap produced from?

A

produced by smooth muscle cells

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29
Q

What appearance does atheroma give histologically?Why is this?

A

gives a foamy-like appearance due to presence of collagens and inflammatory cells in the fibrous tissue cap

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30
Q

What is central lipid core in atheroma rich in/ full of?

A

rich in cellular lipids and debris which are derived from macrophages (died in plaque)

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31
Q

What is the main property of atheromas which contributes to CV disease?

A

they are thrombogenic; often rim of foamy macrophages (cause thrombus; blood clots in situ of vessels)

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32
Q

Why are macrophaes regarded as “foamy”?

A

foamy due to uptake of oxidised lipoproteins via specialised membrane bound scavenger receptor

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33
Q

What other substances are often found deposited on atheromas except from fatty material?

A
  • cholesterol crystals

- calcified material

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34
Q

What occurs LATE in plaque development?

A

dystrophic calcification is extensive in late stage

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35
Q

How can extensive dystrophic calcification be used diagnostically?

A

it can be used as a marker for atherosclerosis in angiograms and CT scans

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36
Q

At which locations in the body are atheromas likely to form at? Why?

A
  • form at arterial branching points/ bifurcations

- because it’s a site of turbulent blood flow

37
Q

What do late stage plaques look like? (2)

A
  • confluent (merge together)

- cover large areas

38
Q

What are features of a complicated atheroma which cause clinical problems? (3)

A

Features of established atheromatous plaque (lipid-rich core and fibrous cap) PLUS

  1. haemorrhage into plaque (calcification)
  2. plaque rupture/ fissuring
  3. thrombosis (detaching of blood clot)
39
Q

What is the most important risk factor for an atheroma?

A

hypercholesterolaemia

40
Q

Why is hypercholesterolaemia so dangerous for atheroma formation?

A

causes plaque formation and growth in absensce of other known risk factors

41
Q

What type of cholesterol is important in hypercholesterolaemia patients?

A

LDL choleserol (low density lipoprotein cholesterol

42
Q

Why is it a problem if there aren’t enough functional receptors on cell surfaces for LDL?

A
  • some people have genetically determined lack of cell membrane receptors for LDL
  • less functional receptors for LDL, means elevated plasma LDL cholesterol levels
43
Q

What type of mutation is hypercholesterolaemia in most patients with the gene?

A

Caucasians heterozygous for this mutation type (1/500 Caucasians)

44
Q

What type of mutation is hypercholesterolaemia in rare patient cases?

A
  • can be homozygous (1/million) but very rare

- causes VERY high cholesterol levels

45
Q

What do patients with a rare homzygotic type hypercholesterolaemia often die from?

A

they die from coronary artery atheroma in infancy/teens

46
Q

What are common signs for hyperlipidaemia? (6)

A
  1. familial/ primary vs acquired/ secondary (can be idiopathic)
  2. biochemical evidence
  3. corneal arcus (premature)
  4. tendon xanthomata (knuckles, Achilles)
  5. Xanthelasmata
  6. Risk/ premature/ family history MI/ atheroma
47
Q

What biochemical evidence can suggest hyperlipidaemia? (what needs to be increased) (4)

A

Increase in:

  1. LDL
  2. HDL
  3. total cholesterol
  4. triglycerides
48
Q

What is a corneal arcus (premature)?

A

white, grey or blue opaque ring in the corneal margin (peripheral corneal opacity) or white ring in front of the periphery of the iris

49
Q

What is tendon xanthomata?

A
  • fatty lumps in tendons
  • accumulation of fat in macrophages in skin and more rarely adipose tissue in skin (yellow fatty lumps)
  • lipids accumulate in foam cells (fat laden macrophages) in skin
50
Q

Except from hypercholesterolaemia, what are other possible risk factors for atheroma? (5)

A
  1. smoking
  2. hypertension
  3. diabetes mellitus
  4. male
    5.elderly
    (accelerate process of plaque formation_
51
Q

What are less strong risk factors for atheroma formation? (5)

A
  1. obesity
  2. sedentary lifestyle
  3. low socio-economic status
  4. low birthweight
  5. role of micro-organisms potentially
52
Q

What is the 2 step process for development of atheromatous plaques?

A
  1. injury to endothelial lining of the artery

2. CHRONIC inflammatory and healing response of vascular wall to agent causing injury

53
Q

When do atheromatous plaques form taking into account the 2 main processes?

A

when chronic/episodic exposure of arterial wall to the 2 processes (injury to endothelial lining and chronic inflammatory healing); injury and repair processes continue until atheroma forms

54
Q

Describe steps for advanced plaque formation. (5)

A
  1. Large number of macrophages, t lymphocytes and lipid-laden macrophages (foam cells) die through apoptosis forming the LIPID CORE
  2. This induces response to injury= chronic inflammatory process
  3. This process is: inflammatory reaction AND process of tissue repair (injury and repair)
  4. Growth factors (PDGF) induce proliferation of intimal smooth muscle cells, subsequent synthesis collagen, elastin and mucopolysaccharide
  5. Fibrous cap encloses lipid rich core
55
Q

What are growth factors secreted by? (4)

A
  1. platelets
  2. injured endothelium
  3. macrophages
  4. smooth muscle cells
56
Q

What growth factor is released in atheromatous development?

A

PDGF growth factor

57
Q

What forms the lipid core in atheroma?

A

increased numbers of macrophages, t-lymphocytes, lipid-laden macrophages with debris undergoing to apoptosis

58
Q

What are established plaques?

A

Plaques which have already fully formed not the ones which are still forming

59
Q

Except from loss and repair, what else initiates plaque growth?

A

initiated by small areas of endothelial loss

60
Q

Where are microthrombi formed?

A

Formed at stripped/ denuded areas of plaque surfaces (organised by same repair process)

61
Q

What is the repair process made of? 92)

A
  1. smooth muscle cell invasion 2. collagen deposition

repeated cycles gradually increase plaque volume

62
Q

What is the range of plaques as a clinical disease?

A

can be relatively benign OR can be life-threatening/ fatal (big range of symptoms and severities)

63
Q

What effect do acute changes in plaques have on complicated atheromas?

A

can have serious consequences

64
Q

What effect on lumen does high grade plaque stenosis have?

A

progressive lumen narrowing

65
Q

What does stenosis of >50-75% of vessel lumen cause?

A
  • critical reduction of blood flow in distal arterial bed
  • REVERSIBLE tissue ischaemia caused
  • for example stenosed atheromatous coronary artery can lead to STABLE angina (can be reversed)
66
Q

What does severe stenosis cause?

A
  • ischaemic pain at rest (UNSTABLE angina)
  • for example ileal, femoral, popliteal artery stenosis can lead to intermittent claudication (peripheral arterial disease)
67
Q

What can longstanding ischaemia lead to?

A
  • atrophy (wastage) of affected organ

- eg. atherosclerotic renal artery stenosis can lead to renal atrophy

68
Q

What is acute atherothrombotic occlusion caused by?

A

rupture of plaque (acute event); exposes highly thrombogenic plaque contants (e.g. collagen, lipid, debris) to bloodstream which activates coagulation cascade and thrombotic occlusion in short time

69
Q

What does total occlusion lead to?

A
  • irreversible ischaemia

- necrosis (infarction) of tissues

70
Q

What are common infarcts and which arteries are involved which have acute atherothrombotic occlusion?

A
  1. myocardial infarct; coronary artery
  2. stroke; carotid or cerebral artery
  3. lower limb gangrene; ileal, femoral or popliteal artery
71
Q

What does embolisation of the distal arterial bed cause? (2)

A
  • detachement of small thrombus fragments from thrombosed atheromatous arteries which embolise distal to ruptured plaque
  • embolic occlusion of small vessels which cause a small infarct in organs
72
Q

What can embolisation of distal arterial bed in the heart cause?

A
  • dangerous small foci of necrosis

- life-threatening arrhythmias

73
Q

What can embolisation of distal arterial bed in the large ulcerating aortic plaques cause?

A
  • lipid- rich fragments of plaque cause cholesterol emboli in kidneys, legs and skin
74
Q

What can embolisation of distal arterial bed in carotid artery cause?

A
  • atheromatous debris in coronary arteries commonly cause strokes (cerebral infarcts/ TIA; transient ischaemic attack)
75
Q

Define aneurysm.

A

Localised blood-filled balloon-like bulge in the wall of a blood vessel. The bulge in blood vessel is caused by the weakness in the blood vessel wall usually where it branches

76
Q

Describe how a ruptured atheromatous abdominal aortic aneurysm is formed.

A
  • media beneath atheromatous plaques gradually weakened (lipid-related inflammatory activity in plaque)
  • gradual dilation of the vessel
77
Q

Are ruptured atheromatous abdominal aortic aneurysms symptomatic?

A

Can be, but are often asymptomatic; they are slow and progressive

78
Q

If there is a rupture of atheromatous abdominal aortic aneurysm, what are the mortality outcomes like?

A

high mortality since sudden rupture leads to a massive retroperitoneal haemorrhage

79
Q

How big do aneurysms have to be to be considered at high risk of rupture?

A

> 5cm

80
Q

What is a mural thrombus?

A

thrombus in contact with endocardial lining of the cardiac chamber or with a wall of a large blood vessel

81
Q

Where do mural thrombi usually spread to? (from ruptured atheromatous abdominal aortic aneurysms)

A

emboli move to legs

82
Q

What are the 4 main consequences of atheroma clinical manifestations?

A
  1. progressive lumen narrowing due to high grade plaque stenosis
  2. acute atherothrombotic occlusion
  3. embolisation of the distal arterial bed
  4. ruptured atheromatous abdominal aortic aneurysm
83
Q

What are vulnerable atheromatous plaques?

A
  • have high risk of developing thrombotic complications

- atheromatous plaques that rupture with subsequent thrombosis

84
Q

What are the main features of vulnerable atheromatous plaques? (3)

A
  1. thin fibrous cap
  2. large lipid core
  3. prominent inflammation
85
Q

How do atheromatous plaques become at risk of rupture?

A
  • pronounced inflammatory activity leads to degradation
  • this weakens plaque
  • increases risk of rupture
86
Q

What do plaque inflammatory cells release that create vulnerable atheromatous plaques?

A

secretion of…

  1. proteolytic enzymes
  2. cytokines
  3. reactive oxygen species
87
Q

What are the features of highly stenotic plaques? (2)

A
  • often have large fibrocalcific component

- little inflammation

88
Q

What are primary preventive and therapeutic approaches to atherosclerosis? (5)

A
  1. stop smoking
  2. control of BP
  3. weight- loss
  4. regular exercise
  5. dietary modifications
89
Q

What are the secondary prevention measure for atherosclerosis? (2)

A
  1. Cholesterol lowering drugs; e.g. aspirin which inhibits platelet aggregation to decrease risk of thrombosis on established atheromatous plaques
  2. surgical options

2. Cardiovascular System (42 decks)

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