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Year 1-Cardiovascular System > Pathophysiology of Atheroma > Flashcards

Pathophysiology of Atheroma Flashcards

1
Q

What is an atheroma/atherosclerosis?

A

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

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2
Q

What would happen if there was atheroma in coronary arteries?

A

Atheromatous plaques narrow lumen → ischaemia

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3
Q

Give an example of one of the serious consequences of atherosclerosis.

A

Angina due to myocardial ischaemia

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4
Q

What can atheroma be complicated by?

A

Thromboembolism

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5
Q

What is arteriosclerosis?

Read carefully as not referring to atherosclerosis.

A

Age-related change in the muscular arteries

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6
Q

Describe what happens to the smooth muscle in those with arteriosclerosis.

Read carefully :)

A

Smooth muscle hypertrophy
Apparent reduplication of internal elastic laminae
Intimal fibrosis

This causes a decrease in the diameter of arteries.

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7
Q

What can arteriosclerosis increase risks of?

A

Cardiac, cerebral, colonic and renal ischaemia in elderly

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8
Q

When are the clinical signs of arteriosclerosis more apparent?

A

When CVS further stressed by haemorrhage, major surgery, infection, shock

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9
Q

What is the earliest visible lesion of atheroma?

A

Fatty streak

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10
Q

Who might develop a fatty streak?

A

Young children

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11
Q

What is a fatty streak made up of?

A

Masses of lipid-laden macrophages

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12
Q

Discuss what could happen in those with a fatty streak.

A

It could go away
It could go on to form atheromatous plaques

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13
Q

Who may develop an early atheromatus plaque?

A

Young adults and older

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14
Q

What are early atheromatous plaques made of?

A

Lipid-laden macrophages

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15
Q

What may an early atheromatous plaque go on to become?

A

Established plaques

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16
Q

Describe the structure of a fully developed atheromatous plaque.

A

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

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17
Q

What provides a fully developed atheromatous plaque with structural support?

A

Collagen

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18
Q

What can be found in the fibrous cap of fully developed atheromatous plaques?

A

Inflammatory cells- macrophages, T-lymphocytes, mast cells

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19
Q

Where are the inflammatory cells found in the fibrous cap recruited from?

A

Arterial endothelium

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20
Q

Describe the central lipid core of fully developed atheromatous plaques.

A

Rich in cellular lipids/debris derived from macrophages which have died in the plaque
Soft
Highly thrombogenic
Often has a rim of foamy macrophages

->foamy because uptake of oxidised lipoproteins

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21
Q

Where will atheromatous plaques form?

A

At arterial branching points/ bifurcations as there is a turbulent flow

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22
Q

Describe the structure of a complicated atheroma.

A

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

AND

-Haemorrhage into plaque (calcification)
-Plaque rupture/fissuring
-Thrombosis

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23
Q

What is the greatest risk of factor of atheroma?

A

Hypercholesterolaemia

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24
Q

What can hypercholesterolaemia cause to happen?

A

Causes plaque formation and growth in absence of other known risk factors

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25
Q

What would you test biochemically to see if somebody had hypercholesterolaemia?

A

LDL, HDL, total cholesterol, triglycerides

26
Q

What are some clinical signs in those with major hypercholesterolaemia?

A

Premature corneal arcus (pale curve around cornea of eye)
Tendon xanthomata (lipids accumulate in knuckles or Achilles tendon)
Xanthelasmata (collections of foamy macrophages in the skin)

27
Q

List some of the risk factors for atheroma.

A

Smoking
Hypertension
Diabetes mellitus
Male
Elderly
Accelerate process of plaque formation driven by lipids

28
Q

Describe the two step process of the development of atheromatous plaques.

A
  1. injury to endothelial lining of artery
  2. chronic inflammatory and healing response of vascular wall to agent causing injury
29
Q

Discuss the development of atheromatous plaues.

A

Firstly, I know this looks daunting. But just read through it and understand it. They cannot ask you to write it out so just understand the basic principles.

  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 matrix production and T-cell recruitment
  7. Lipid accumulation (extracellular and in foamy macrophages)
30
Q

What are the main two causes of endothelial injury which then lead to atheromatous plaques?

A

-Haemodynamic disturbances (turbulent flow)
-Hypercholesterolaemia

31
Q

How can chronic hypercholesterolaemia impair endothelial function?

A

Increases the local production of reactive oxygen species.

32
Q

What happens when the injured endothelial cells are functionally altered?

A

Enhanced expression of cell adhesion molecules (ICAM-1, E-selectin)
High permeability for LDL so can cross the membrane, increasing thrombogenicity

33
Q

Briefly discuss formation of plaques.

A

Inflammatory cells, lipids → intimal layer → plaques

34
Q

In advanced plaque formation, how do the lipid-laden macrophages die?

A

Through apoptosis

35
Q

What happens after the lipid-laden macrophages die?

A

They release lipid into the lipid core

36
Q

In response to injury, what happens in the chronic inflammatory process?

A
  1. Inflammatory reaction
  2. Tissue repair process
37
Q

What do growth factors, like PDGF, do?

A

Cause proliferation of intimal smooth muscles and any subsequent synthesis of collagen, elastin and mucopolysaccharide.
This forms fibres which enclose the lipid rich core .

38
Q

Where are growth factors released from?

A

Secreted by platelets, injured endothelium, macrophages and smooth muscle cells

39
Q

In established plaques, how is plaque growth initiated?

A

Small areas of endothelial loss

40
Q

How does plaque volume increase?

A

Repeated cycles of smooth muscle invasion and collagen deposition.

41
Q

Discuss the clinical significance of plaques.

A

Can have many plaques over a lifetime which go clinically unnoticed.
Can be benign or life-threatening.
Acute changes in plaques have have large consequences.

42
Q

What causes progressive lumen narrowing in atheroma?

A

High grade plaque stenosis

43
Q

What is high grade plaque stenosis?

A

Stenosis of 50-75% of the vessel which greatly affects blood flow

44
Q

What can high grade plaque stenosis lead to?

A

Reversible tissue ischaemia

45
Q

Given an example of reversible tissue ischaemia due to high grade plaque stenosis.

A

Stenosed atheromatous coronary artery may lead to stable angina

46
Q

However, what can severe stenosis cause?

A

Irreversible tissue ischaemia- ischaemic pain at rest, unstable angina

47
Q

Stenosis of which arteries can cause claudication (pain in legs/arms while walking)?

A

Ileal, femoral, popliteal artery stenosis

48
Q

What can longstanding tissue ischaemia lead to?

A

Atrophy of affected organ due to lack of blood supply

btw atrophy= decrease in size

49
Q

What could cause a major complication in acute atherothrombotic occlusion?

A

Rupturing of a plaque

50
Q

What can rupturing of a plaque do?

A

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

51
Q

What is total atheroma occlusion?

A

Irreversible ischaemia which can lead to necrosis of some tissues

52
Q

What causes embolism of the distal arterial bed?

A

Detachment of small thrombus fragments from thrombosed atheromatous arteries and then travel in the blood and embolise distal to ruptured plaque

53
Q

What does embolic occlusion of small vessels lead to?

A

Small infarcts in organs

54
Q

What happens if there is a embolic occlusion of small vessels in the heart?

A

Dangerous small foci of necrosis → life-threatening arrhythmias

55
Q

Why may there be a ruptured atheromatous abdominal aortic aneurysm?

A

Media beneath atheromatous plaques gradually weakened

56
Q

What does the weakening of the media beneath atheromatous plaques cause?

A

Gradual dilation of vessel, slow byt progressive

57
Q

Who will usually get a ruptured atheromatous abdominal aortic aneurysm?

A

Elderly

58
Q

Aneurysms of what size are said to be at high risk of rupturing?

A

> 5cm diameter

59
Q

What features might a vulnerable atheromatous plaque have?

A

Typically thin fibrous cap, large lipid core, prominent inflammation

60
Q

What does pronounced inflammatory activity cause?

A

Weakening of the plaque, increasing risks of a rupture

61
Q

List some of the preventative measures for atheroma.

A

Stop smoking
Control blood pressure
Weight loss
Regular exercise
Dietary modifications

Year 1-Cardiovascular System (41 decks)

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