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Y2 MECHANISMS OF DISEASE > Atheroma, Thrombosis & Embolism > Flashcards

Atheroma, Thrombosis & Embolism Flashcards

1
Q

What is the definition of an atheroma?

A

an intimal lesion that protrudes into a vessel wall

it consists of a raised lesion with a soft core of lipid and is covered by a fibrous cap

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2
Q

What is meant by an “intimal lesion”?

A

intimal means that the atheroma is present in the innermost layer of the blood vessel wall

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3
Q

What does the lipid core of an atheroma mostly consist of?

A

cholesterol and cholesterol esters

cell debris

foam cells

calcium

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4
Q

How does the fibrous cap of an atheroma occur?

A

Macrophages and smooth muscle cells produce collagen and elastin

These are extracellular matrix proteins that will form over the top of the lesion

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5
Q

What cells are present within an atherosclerotic plaque?

A

smooth muscle cells

macrophages

foam cells

lymphocytes

collagen

elastin

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6
Q

On which layer of the blood vessel does an atheroma occur?

A

The intima (innermost layer)

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7
Q

What are foam cells?

A

macrophages or smooth muscle cells that migrate from the media and have engulfed lipid

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8
Q

What makes vessels more prone to developing an atheroma?

A

If they are sites of turbulent flow

This is typically where there is a bifurcation of an artery

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9
Q

What are examples of vessels that are commonly affected by atheroma?

A
  1. abdominal aorta
  2. coronary arteries
  3. popliteal arteries
  4. carotid vessels
  5. circle of willis in the brain
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10
Q

What are the 2 categories of risk factors for atheroma?

A

non modifiable and modifiable

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11
Q

What are examples of non-modifiable risk factors for atheroma?

A
  1. increasing age
  2. male gender
  3. family history
  4. genetic abnormalities
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12
Q

What are examples of modifiable risk factors for atheroma?

A
  1. hyperlipidaemia (LDL:HDL)
  2. cigarette smoking
  3. diabetes
  4. c-reactive protein
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13
Q

What is the difference in function of HDL and LDL?

A

HDL removes cholesterol from lesions

LDL brings cholesterol into the atherosclerotic lesions

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14
Q

What starts the process of atherosclerosis?

A

Damage or injury to the endothelium of an artery

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15
Q

What 4 categories tend to cause endothelial damage that leads to atherosclerosis?

A
  1. high blood pressure
  2. high cholesterol
  3. an irritant, such as nicotine
  4. certain diseases, such as diabetes
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16
Q

Why is C-reactive protein a risk factor for atherosclerosis?

A

It is a sign of inflammation

Atherosclerosis develops as a chronic inflammatory response of the arterial wall to endothelial injury

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17
Q

What causes an atherosclerotic lesion to progress after it has initially developed?

A

it progresses through interactions of modified lipoproteins, macrophages, T-cells and the normal cellular constituent of the arterial wall

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18
Q

What are the first 3 stages in the development of atherosclerosis?

A
  1. endothelial injury leads to increased permeability
  2. leukocytes adhere to the endothelium and emigrate through to the intima
  3. cytokines and chemokines cause smooth muscles cells to emigrate to the intima from the media
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19
Q

What are the stages involved in the development of atherosclerosis, leading up to fibrous plaque formation?

A
  1. chemokines and cytokines activate macrophages
  2. macrophages and smooth muscle cells engulf the lipid
  3. smooth muscle cells proliferate and produce ECM proteins that form the fibrous plaque
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20
Q

What are the stages involved in development of atherosclerosis after fibrous plaque formation?

A
  1. cells start to die and a necrotic core forms in this region
  2. neovascularisation occurs - small vessels form at the edges of the lesions
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21
Q

What is the earliest lesion in atherosclerosis?

When does it develop?

A

a fatty streak

they begin to form in adolescence

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22
Q

What do fatty streaks look like when they first develop?

A

they begin as multiple small flat yellow spots

these eventually coalesce into streaks that are >/= 1 cm

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23
Q

How do fatty streaks affect blood flow?

A

The initial lesions are not significantly raised

They do not cause flow disturbance

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24
Q

Do all fatty streaks develop into atherosclerotic plaques?

A

Not all fatty streaks are destined to progress to an atheromatous plaque

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25
Q

What colour does an atherosclerotic plaque appear?

A

It appears white yellow

The superimposed thrombus on the plaque appears red

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26
Q

What does an initial atherosclerotic plaque consist of?

A

intimal thickening and lipid accumulation

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27
Q

What are ostia and how do they relate to fatty streak formation?

A

They are holes where branching arteries come off of the aorta

Fatty streaks form around the ostia

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28
Q

What are the 6 stages in atherosclerotic lesion development?

A
  1. initial lesion
  2. fatty streak
  3. intermediate lesion
  4. atheroma
  5. fibroatheroma
  6. complicated lesion
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29
Q

What are the 4 sequelae of atherosclerosis?

A
  1. rupture, ulceration or erosion
  2. haemorrhage into plaque
  3. atheroembolism
  4. aneurysm formation
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30
Q

What happens during the rupture, ulceration and erosion of an atherosclerotic plaque?

A

rupture, ulceration and erosion of the intimal surface exposes the blood to highly thrombogenic substances

this induces thrombosis which leads to lumen occlusion

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31
Q

What can thrombus generation and lumen occlusion lead to?

A

the blood can no longer flow to downstream tissues

this leads to ischemia and possible infarction

32
Q

Why may haemorrhage into an atherosclerotic plaque occur?

A

New vessels may form at the edge of the lesion and bleed into it

This causes the lesion to enlarge and lead to haemorrhage

33
Q

What is the definition of a thrombus?

A

a solid mass of blood constituents formed within the vascular system in vivo

34
Q

What are the 2 types of thrombus?

A

Arterial thrombosis

Venous thrombosis

35
Q

What are arterial and venous thrombosis most commonly due to?

A

Arterial thrombosis is most commonly superimposed on atheroma

Venous thrombosis is most commonly due to stasis

36
Q

What are the 3 components of Virchow’s Triad?

A
  1. endothelial injury
  2. abnormal blood flow
  3. hypercoagulability
37
Q

What is the mechanism for arterial thrombosis?

A

typically from rupture of an atherosclerotic plaque

38
Q

What is the mechanism for venous thrombosis?

A

typically from a combination of factors from Virchows triad

39
Q

What locations are mostly affected by arterial thrombosis?

A

Left heart chambers and arteries

Often occurs in atrial fibrillation when there is pooling and stasis of the blood

40
Q

What locations are mostly affected by venous thrombosis?

A

Venous sinusoids of muscle and valves of veins

It tends to affect more dilated wide veins

41
Q

What diseases can result from arterial thrombosis?

A
  1. acute coronary syndrome
  2. ischaemic stroke
  3. claudication in peripheral vascular disease
42
Q

What diseases can result from venous thrombosis?

A
  1. deep vein thrombosis

2. pulmonary embolism

43
Q

What are the compositions of arterial and venous thromboses like?

A

Arterial is mainly platelets

Venous is mainly fibrin

44
Q

What are the treatments for arterial and venous thromboses?

A

Arterial - anti-platelet agents

Venous - anticoagulants

45
Q

What are examples of anti-platelet agents?

A

clopidogrel

46
Q

What are examples of anticoagulants?

A

heparin, warfarin

47
Q

Why does peripheral vascular disease cause pain on walking?

A

the arterial supply to the legs is reduced due to thrombosis

48
Q

What kind of things cause endothelial damage?

A

smoking and hypertension cause endothelial dysfunction

surgery, trauma and catheterisation cause endothelial damage

49
Q

What are the 2 categories of ‘hypercoaguability’?

A

hereditary and acquired

50
Q

What are examples of hereditary hypercoagulability conditions?

A
  1. factor v leiden
  2. prothrombin G20210A
  3. protein c and s deficiency
51
Q

What are examples of acquired hypercoaguability conditions?

A
  1. cancer
  2. chemotherapy
  3. oral contraceptives, hormone replacement therapy
  4. pregnancy
  5. obesity
  6. HIT
52
Q

What are examples of things that cause stasis?

A
  1. immobility
  2. polycythemia

These can cause endothelial injury

53
Q

What is the role of Factor V?

How does Factor V Leiden affect this?

A

Factor V is a component of the coagulation cascade

It is inactivated by protein C and S acting together

Mutation of factor V leads to an increased risk of thrombosis as Factor V is resistant to inactivation by protein C and S

54
Q

What is the prothrombin G20210A mutation?

A

a mutation in the prothrombin gene that leads to increased thrombosis as there is more activated prothrombin

55
Q

What tends to be a sign that there may be a hereditary hypercoagulability condition?

A

if a patient tends to develop multiple DVTs and develops DVTs at a young age with no other predisposing risk factors

56
Q

How does stasis affect the flow of platelets in a blood vessel?

A

Platelets usually flow in the centre of the blood vessel

In stasis, the platelets move to the side of the vessel where they are in contact with the endothelium

57
Q

In what other way can stasis lead to thrombosis?

A

stagnant blood flow means there is no removal of pro-thrombotic factors

58
Q

What is polycythemia?

A

having more red blood cells in the blood than normal

59
Q

What is the difference between a clot and a thrombus when it comes to platelets?

A

Platelets are not involved in a clot

Platelets and fibrin are involved in a thrombus and form lines of Zahn

60
Q

What is the difference in appearance between a clot and a thrombus?

A

a clot is red and gelatinous

a thrombus is firm
a venous thrombosis is red
an arterial thrombus is pale

61
Q

How do clots and thromboses attach to the vessel wall?

A

Clots do not attach to the vessel wall

a thrombus is attached to the vessel wall

62
Q

Do clots and thromboses form inside or outside of blood vessels?

A

a clot can occur inside or outside a vessel

a thrombus only occurs inside the vessel

63
Q

What are the 5 sequelae of thrombosis?

A
  1. occlusion of vessel
  2. dissolution
  3. incorporation into vessel wall
  4. recanalisation
  5. embolisation
64
Q

What happens in occlusion of a vessel due to thrombosis?

A

there will be no blood flow to downstream tissues

this leads to ischemia and infarction

65
Q

What is dissolution of a thrombus?

A

the thrombus is broken down and dissolved

66
Q

What is recanalisation of a thrombus?

A

macrophages/smooth cells grow into a thrombus, leading to new blood vessel formation

small capillaries grow into the thrombus, which join up and form channels

67
Q

What is embolisation?

A

part of the thrombus breaks off and travels somewhere else in the body

68
Q

What is the definition of an embolus?

A

a mass of material in the vascular system able to become lodged in a vessel and block its lumen

69
Q

What is the most common embolus?

A

pulmonary embolus derived from a deep vein thrombosis

70
Q

What are most emboli derived from?

A

thrombi

71
Q

What are the different types of emboli?

A
  1. atheromatous plaque materia
  2. vegetation on heart valves
  3. fragments of tumour
  4. amniotic fluid
  5. gas
  6. fat
72
Q

Why does the size of the embolus affect the effects it has?

A

the pulmonary arteries branch and become smaller and smaller

the size of the embolus determines where it lodges in the arteries

73
Q

What is a saddle embolus?

A

a large embolus that blocks all of the blood going from the heart into the lungs

blockage of the circulation leads to acute respiratory and cardiac problems and sudden death

74
Q

Where do systemic emboli tend to originate from?

A

the heart or an atheromatous plaque

75
Q

What can a systemic emboli cause?

A
  1. cerebrovascular accident
  2. transient ischaemic attack
  3. gangrene
  4. bowel necrosis

Y2 MECHANISMS OF DISEASE (36 decks)

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