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Systems 2: Cardiovascular > Pathophysiology of Atheroma > Flashcards

Pathophysiology of Atheroma Flashcards

1
Q

What is the definition of atherosclerosis?

A

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

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2
Q

What is narrowing of coronary artery lumen known as?

A

Ischaemia

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3
Q

What does myocardial ischaemia lead to?

A

Angina

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4
Q

What is a thromboembolism?

A

An embolism broken off from a thrombus

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5
Q

What is the pathology of atherosclerosis?

A
  • Not atheromatous
  • Age related change in muscular arteries
  • Smooth muscle hypertrophy
  • Reduplication of internal elastic laminae
  • Intimal fibrosis
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6
Q

When are the clinical affects of atherosclerosis most apparent?

A
  • Haemorrhage
  • Major surgery
  • Infection
  • Shock
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7
Q

What is an atheroma?

A
  • Fatty streak
  • Seen in young children
  • Yellow linear elevation of intimal lining
  • Contains lipid laden macrophages
  • May disappear
  • Can progress to early atheromatous plaque
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8
Q

What is an early atheromatous plaque?

A
  • Young adults onwards
  • Smooth yellow patches in intima
  • Lipid laden macrophages
  • Progresses to established plaques
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9
Q

What is a fully developed atheromatous plaque?

A
  • Central lipid core with fibrous cap

- Covered by arterial epithelium

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10
Q

What does the fibrous cap of a fully developed atheromatous plaque provide?

A
  • Made from collagens

- Provides structural strength

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11
Q

What cells reside in the fibrous cap?

A
  • Macrophages
  • T lymphocytes
  • Mast cells
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12
Q

What is commonly present to do with the immune system in a fully established plaque?

A
  • Thrombogenic soft ring of “foamy” macrophages
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13
Q

What occurs late in plaque development that will show on an angiogram?

A

Dystrophic calcification

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14
Q

What can be detected if the calcification occurs at branching points or bifurcations?

A

Turbulent flow

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15
Q

What is a complicated atheroma?

A
  • A fully established atheroma but
  • Haemorrhage into the plaque leading to calcification
  • Plaque rupture can occur
  • Thrombosis
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16
Q

What is the most important risk factor for atheromatous plaque?

A
  • Hypercholesteraemia
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17
Q

What ways can hypercholesteraemia lead to plaque?

A
  • Causes plaque formation + growth

- LDL cholesterol (lack of cell LDL receptors causes LDL to be deposited

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18
Q

What ratio of caucasians are heterozygous for hypercholesteraemia?

A

1/500

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19
Q

What ratio of caucasians are homozygous for the condition?

A

1/million

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20
Q

What will the hetorozygous mutation lead to?

A
  • Loss of function cell LDL receptors

- Elevated plasma LDL

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21
Q

What will the homozygous mutation lead to?

A
  • Much higher cholesterol level

- Patients usually die from a coronary heart atheroma in infancy

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22
Q

What are the two types of major hyperlipidaemia?

A
  • Familial/primary

- Acquired/secondary

23
Q

What are the evidence on bloods of hyperlipidaemia?

A
  • High LDL
  • Low HDL
  • High total cholesterol
  • Triglycerides
24
Q

What are the clinical signs of hyperlipidaemia?

A
  • Corneal arcus
  • Tendon xanthomota (knuckles/achilles)
  • Xanthelasmata
25
Q

What other risk factors to atheroma are there?

A
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Male
  • Elderly
26
Q

What are the weaker risk factors?

A
  • Obesity
  • Sedentary lifestyle
  • Low socio-economic status
  • Low birthweight
27
Q

What is the overall two step process of atheromatous plaque formation?

A
  • Injury to endothelial lining

- Chronic inflammatory and healing response to vascular wall

28
Q

What do injured endothelial cells usually do?

A
  • Express more cell adhesion molecules (ICAM-1, E-selectin)
  • High permeability for LDL
  • Increased thrombogenicity
29
Q

What role do growth factors play in the development of plaques?

A
  • PDGF
  • Proliferation of intimal smooth muscle
  • Synthesis of collagen, elastin and mucopolysaccharide
30
Q

What are growth factors secreted by?

A
  • Platelets
  • Endothelium (injured)
  • Macrophages
  • Smooth muscle
31
Q

Where do microthrombi form?

A

Areas of a “strip” of plaque surface

32
Q

What happens to microthrombi?

A
  • Usually healed by the healing process
33
Q

What does the repetition of formation of microthrombi and healing lead to?

A

Increased size of atheromatous plaque

34
Q

What are the clinical consequences of advanced atheroma?

A
  • Stenosis of > 50-75% will critically reduce the blood flow in distal arterial beds
35
Q

What occurs from stenosed coronary arteries?

A
  • Unstable angina

- Very severe angina at rest

36
Q

What occurs from stenosed peripheral arteries of the legs?

A
  • Intermittent claudication

- Longstanding tissue ischaemia

37
Q

What occurs from acute atherothrombotic occlusion?

A
  • Rupture of plaque
  • Highly thrombogenic plaque contents released into blood stream triggering coagulation cascade and occluded vessel very quickly
  • Total occlusion = irreversible iscaemia
38
Q

What does irreversible ischaemia lead to?

A
  • Necrosis of tissues
39
Q

What can a total occlusion lead to?

A
  • Myocardial infarct
  • Stroke
  • Lower limb gangrene
40
Q

What is embolisation of the distal arterial bed?

A
  • Small thrombus fragments from thrombosed atheromatous arteries
  • Embolise distal plaque
41
Q

What can embolisation of the distal arterial bed cause?

A
  • Small infarcts in organs
42
Q

What can a small infarct in the heart lead to?

A
  • Necrosis

- Arrhythmias

43
Q

What can embolytic plaques of the aorta lead to?

A
  • Cholesterol emboli in kidney, leg, skin
44
Q

What can carotid artery atheromatous plaques lead to?

A

Stroke, TIAs

45
Q

What is the pathology of a ruptured atheromatous abdominal aortic aneurysm?

A
  • Media beneath atheromatous plaques gradually weakened (lipid related inflammation)
  • Gradual dilation of vessel
46
Q

In whom are abdominal aortic aneurysms common?

A
  • Elderly

- Often asymptomatic

47
Q

What occurs when an aortic aneurysm ruptures?

A
  • Massive retroperitoneal haemorrhage (high mortality)
48
Q

What size aneurysms have a high rupture chance?

A

> 5cm

49
Q

What is a mural thrombus?

A

A stationary thrombus across the lumen of a vessel

50
Q

What will arise from a mural thrombus of the aorta?

A
  • Emboli into the legs

- Increase MAP

51
Q

What features of an atheromatous plaque tend to mean it is close to rupture?

A
  • Thin fibrous cap
  • Large lipid core
  • Prominent inflammation
  • Pronounced inflammatory activity
52
Q

What is secreted by plaques close to rupture?

A
  • Proteolytic enzymes
  • Cytokines
  • ROS’s
53
Q

What personal prevention methods are there for atheroma?

A
  • Smoking cessation
  • Control BP
  • Weight loss
  • Regular exercise (starting off SLOW)
  • Dietary changes
54
Q

What secondary prevention methods exist for atheroma?

A
  • Cholesterol lowering drugs
  • Aspirin
  • Surgical options

Systems 2: Cardiovascular (19 decks)

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