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EMS - MoD > 13. Atheroma and thrombosis > Flashcards

13. Atheroma and thrombosis Flashcards

1
Q

Define atherosclerosis

A

Degeneration of arterial walls characterised by fibrosis, lipid deposition, and inflammation, which limits blood circulation and predisposes to thrombosis

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2
Q

Where in the vessels is endothelial injury/atherosclerosis most likely to occur?

A

Where the vessels bifurcate, as this is where the blood flow is most turbulent

Less likely where the blood flow is more laminar

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3
Q

Why does atherosclerosis occur?

A

Due to chronic injury and repair of the endothelium (first step = endothelial injury)

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4
Q

Why is hyperlipidaemia a risk factor for atherosclerosis?

A

In hyperlipidaemia, lipid will accumulate in the innermost part of the vessel wall (the intima)

Monocytes (or macrophages when they are in the tissue ) will migrate into the intima due to lipid endothelial injury and ingest the lipid becoming foam cells

= FATTY STREAK

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5
Q

In which layer of the vessel wall does lipid accumulate at the begging of atherosclerosis?

A

In the intima (innermost layer)

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6
Q

Which type of cell ingests deposited lipid?

A

Monocytes (called macrophages when they are in the tissue)

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7
Q

After macrophages have ingested lipid, what do they become?

A

Foam cells

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8
Q

What is a fatty streak?

A

Early stage of atherosclerosis (first grossly visible lesion)

It is when the macrophages are ingesting lipid deposits and becoming foam cells

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9
Q

What do foam cells do?

A

They secrete chemokines, attracting more monocytes/macrophages, lymphocytes and smooth muscle cells

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10
Q

Foam cells secrete chemokines which attract smooth muscle cells as well as other cells. What do smooth cells do?

A

Proliferate and secrete connective tissue

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11
Q

What does an atherosclerotic plaque consist of?

A

Fat, extracellular material and leukocytes and smooth muscle

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12
Q

What is another name for a white blood cell?

A

A leukocyte

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13
Q

An atherosclerotic plaque has a specific structure. What does it consist of?

A
  • dead central CORE
  • SHOULDER region which might contain some new blood vessels
  • thin CAP which might be unstable and rupture
  • fibrous CAP which consists of collagen and smooth muscle
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14
Q

What is the sequelae of atherosclerosis?

A
  • occlusion
  • block a blood vessel
  • tissue dies
  • could lead to gangrene
  • weakening of vessel wall
  • aneurysm formation
  • haemorrhage
  • erosion (due to turbulence of blood e.g.)
  • possible thrombus formation on top of atherosclerotic plaque
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15
Q

What is an embolus?

A

A mass of material in the vascular system able to lodge in a vessel and block it

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16
Q

What is the most common embolus?

A

A thrombus (a thromboembolus)

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17
Q

What is thrombosis?

A

Solidification of blood contents formed in the vessel during life

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18
Q

How is thrombosis different to a blood clot?

A

Different in pathogenesis and morphology

Thrombosis = within body during life, dependent on platelets, firm

Clot = stagnant blood, enzymatic process, elastic, adopts shape of vessel

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19
Q

Do platelets have a nucleus?

A

No

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20
Q

`What are platelets activated by?

A

Collagen exposed by endothelial damage

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21
Q

What two types of secretory granules do platelets contain?

A
  • alpha granules

- dense granules

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22
Q

What do platelet alpha granules secrete?

A
  • fibrinogen
  • fibronectin
  • PDGF
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23
Q

What do platelet dense granules secrete?

A
  • chemotactic chemicals
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24
Q

Where are megakaryocytes located and what are they responsible for?

A

In the bone marrow

Responsible for the production of platelets

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25
Q

Where are platelets?

A

They circulate in the blood stream

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26
Q

What is subsequent to platelet adhesion?

A

Thrombus formation

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27
Q

What are the 3 aspects of Virchow’s triad?

A
  • endothelial injury
  • stasis
  • hypercoagulabilty
28
Q

What does Virchow’s triad describe?

A

The three broad categories of factors that are thought to contribute to thrombosis

29
Q

Change in blood constituents is part of Virchow’s triad. Give an example of this

A

Hyperlipidaemia

30
Q

How would a plaque rupture increase chance of thrombosis?

A
  • creates turbulent flow
  • intimal change

(Virchow’s triad)

31
Q

What do lines of Zahn show?

A

They are lines of alternating pale pink bands of platelets and fibrin and red bands of RBCs

They are characteristic of thrombi

32
Q

In lines of Zahn, what do the pale pink bands contain?

A

Platelets mixed with fibrin

33
Q

Lines of Zahn are characteristic of thrombi, particular when formed where?

A

In the heart or aorta

34
Q

In lines of Zahn, what do the darker pink/red layers contain?

A

Red blood cells

35
Q

What are the characteristics of venous thrombosis?

A
  • intimal change = valves
  • change in blood flow = immobile
  • change in blood constituents = prothrombotic effect of inflammatory mediators (infection malignancy)
36
Q

What is the most common inherited disorder of blood clotting?

A

Factor V Leiden thrombophilia

37
Q

What type of clot are you more at risk of if you have Factor V Leiden?

A

Deep vein thrombosis (DVT)

38
Q

What are thrombi in the heart known as?

A

A mural thrombi

39
Q

Where do mural thrombi (cardiac thrombi) occur?

A

Over areas of endomyocardial injury

  • MI
  • myocarditis

Can also occur with arrhythmias and cardiomyopathy

40
Q

What is the sequelae of thrombosis?

A
  • occlusion of vessel
  • resolution
  • incorporation into vessel wall
  • recanalisation
  • EMBOLISATION!
41
Q

How can a thrombus turn into an embolus?

A

Thrombus might detach and embolise

42
Q

What is a paradoxical embolism?

A

A kind of arterial thrombosis caused by embolism of a thrombus (blood clot) of venous origin through a lateral opening in the heart, such as a patent foramen ovale (RARE)

43
Q

What is a saddle embolus?

A

Saddle pulmonary embolism (PE) is a form of large pulmonary thrombo-embolism that straddles the main pulmonary arterial trunk at its bifurcation. Its incidence among patients diagnosed with PE was found to be approximately 2.6%.

44
Q

What are the clinical effects of a small pulmonary embolism?

A

Initially asymptomatic, if multiple it may result in pulmonary hypertension

45
Q

What are the clinical effects of a medium-sized pulmonary embolism?

A

Cause acute respiratory and cardiac failure (V/Q mismatch, RV strain)

46
Q

What are the clinical effects of a large pulmonary embolism?

A

Death

saddle emboli

47
Q

Where do systemic emboli go?

A

Anywhere in circulation

48
Q

Where do systemic emboli normally arise?

A
  • within the heart (MI or AF)

- or within arterial circulation (atheroma)

49
Q

Where do infective emboli arise?

A

Usually from the vegetations on infected heart valves

50
Q

What may infective embolism lead to?

A

Mycotic aneurysm formation

the effects are compounded by the infective nature

51
Q

Who is infective embolism common in?

A

People with prosthetic valves

Intravenous drug users

52
Q

What is a tumour embolism?

A

When bits break off a tumour as they penetrate vessels

Do not usually cause intermediate physical problems

53
Q

What is a major route of dissemination (spread) of tumours?

A

Tumour embolism

54
Q

What are the 2 types of gas embolism?

A
  • air

- nitrogen

55
Q

How is air embolism caused?

A

When vessels are opened into the air during obstetric procedures/chest wall injury

56
Q

How much air is needed to enter in an air embolism to cause clinical effects?

A

> 100ml

57
Q

What is nitrogen embolism commonly known as?

A

Decompression sickness (“the bends”)

58
Q

Who is affected by decompression sickness/ nitrogen embolism?

A

Divers

Tunnel workers

59
Q

What happens in nitrogen embolism?

A

Increased pressure at depth - blood absorbs more nitrogen - come back up and the nitrogen is forced out of the blood

Nitrogen bubbles enter bones, joints and the lungs

60
Q

How does amniotic fluid embolism occur?

A

Increased uterine pressure during labour forces amniotic fluid into maternal uterine veins

61
Q

How common is amniotic fluid embolism?

A

1 in 50,000 deliveries

62
Q

Why is amniotic fluid embolism a medial emergency?

A

Can lodge in the lungs and cause respiratory distress

63
Q

What can you see histologically in an amniotic fluid embolism?

A

Shed skin cells

64
Q

What is fat embolism caused by?

A

Trauma

Mainly fractures but also seen in severe burns

65
Q

What does fat embolism cause?

A

Sudden onset of respiratory distress

66
Q

How is foreign body embolism caused?

A

Particles injected intravenously

Eg, talc in intravenous drug users

67
Q

What does foreign body embolism lead to?

A

A granulomatous reaction

EMS - MoD (17 decks)

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