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Stage 2: Supporting Life > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

What % of patients with new incidence angina die or have an MI in the next year?

A

10%

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2
Q

What is atherosclerosis?

A
  • The build up of cholesterol rich plaques
  • A progressive disease affecting the intima of elastic and muscular arteries characterised by focal atheroma (fibrofatty plaques) consisting of a lipid core covered by a fibrous cap
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3
Q

What does atherosclerosis cause?

A

Stenosis (narrowing) of coronary arteries

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4
Q

What does the fibrous cap of plaque contain?

A

Smooth muscle cells and CT

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5
Q

What is the atheroma?

A

A soft pool of extracellular lipid, cell debris and activated immune cells → progressively calcifies over time

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6
Q

Where do plaques generally form?

A

In the proximal region of the coronary arteries, within 6cm of the aorta

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7
Q

How many directions can plaque develop in?

A

2

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8
Q

What can one direction of plaque development lead to?

A

Acute coronary syndrome which causes a big blood clot to form

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9
Q

Describe the fibrous cap

A

Thin and vulnerable to rupture

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10
Q

How does (stable) plaque cause ischaemia?

A

Patient cannot get enough blood to region of the heart

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11
Q

What is arteriosclerosis?

A

A group of disorders that have in common thickening and loss of elasticity of material walls = hardening of arteries

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12
Q

What are the 3 types of arteriosclerosis?

A

1) Atherosclerosis
2) Monckeberg’s medial sclerosis
3) Arteriolosclerosis

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13
Q

What is Monckeberg’s medial sclerosis?

A

Disease characterised by calcification fo the media of muscular arteries

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14
Q

What is arteriolosclerosis?

A

Disease characterised by the proliferative or hyaline thickening of the walls of small arteries and arterioles

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15
Q

What might the layers of a blood vessel with arteriosclerosis look like?

A

Fragmented

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16
Q

Describe atherosclerosis in the aorta

A
  • Area of bifurcation is an area of turbulence so would look here for fatty streaks and plaque
  • Can become extremely calcified
17
Q

What do the edges of atheromatous plaques look like?

A

They are calcified

18
Q

What are major predisposing factors for atherosclerosis?

A

1) Diet and hyperlipidaemias
2) Hypertension (systolic and diastolic)
3) Cigarette smoking esp. women
4) Diabetes

19
Q

What are minor predisposing factors for atherosclerosis?

A

Obesity, physical inactivity, male gender, increasing age, family history, stress, oral contraceptives (?), high carb intake (?)

20
Q

What happens to atheroma in small arteries?

A

In small arteries, atheroma are occlusive, compromising blood flow to distal tissues and causing ischaemic injury

21
Q

What sits between the media and intima in an atherosclerotic vessel?

A

Macrophages containing lipid which occlude the vessel

22
Q

What does endothelial injury lead to?

A

Thrombus

23
Q

What is acute coronary syndrome?

A

Transient occlusion of the coronary artery precipitated by a sudden decrease in coronary flow → chest pain that comes and goes, doesn’t occur with exertion

24
Q

What are the 4 stages in the development of an atheromatous plaque/lesion?

A

1) Lipid is present in macrophages in the intima of the blood vessels
2) Lipid is present in both macrophages and (proliferating) smooth muscle cells
3) Fibrous plaque
4) Complex plaque (fibrous cap overlying a lipid core) incl. cholesterol clefts

25
Q

In response to what are the lesions of atherosclerosis initiated?

A

To some form of injury to arterial endothelium

26
Q

What mechanisms of pathogenesis lead to atherosclerosis?

A

1) Endothelial injury
2) Macrophages and other inflammatory and immunological mechanisms
3) Smooth muscle cell proliferation
4) Hyperlipidaemia
5) Thrombosis

27
Q

How does endothelial injury lead to atherosclerosis?

A
  • Endothelial damage is a major risk factor in atherogenesis but early lesions develop at sites of intact endothelium
  • Endothelial dysfunction (increased permeability, increase blood monocyte adhesion and increased EC replication) starts the process
  • Risk factors e.g. HTN and smoking increase endothelial permeability
  • Increased expression of the vascular cell adhesion molecules ICAM-1 and VCAM-1 increase monocyte adhesion
28
Q

How do macrophages and other inflammatory immunological mechanisms lead to atherosclerosis?

A
  • Monocytes migrate into the intima and then accumulate LDL to produce foam cells
  • Monocytes/macrophages express the LDL receptor and a specific receptor (scavenger) for oxidised LDL (oxidised by EC< platelet or WBC enzymes)
  • T cells are found in plaques (uncertain role)
29
Q

How does smooth muscle cell proliferation lead to atherosclerosis?

A

With lipid accumulation, smooth muscle cell proliferation and ECM deposition in the intima are the major processes for the progressive growth of plaques

30
Q

How does hyperlipidaemia lead to atherosclerosis?

A
  • Hyperlipoproteinaemia is the abnormality common to most syndromes of premature atherosclerosis
  • Can be primary (genetic) or secondary to e.g. nephrotic syndrome, alcoholism, hypothyroidism, diabetes
  • Increases in the plasma level of LDL may increase the level of lipid penetration in the arterial wall
  • Hyperlipoproteinaemia may also directly alter EC function
31
Q

What is the effect of atherosclerosis on the legs?

A

1) Slow, insidious narrowing of the vascular lumina results in ischaemia of the tissues perfused by the involved vessels
2) This is seen as intermittent claudication in the legs → atherosclerosis of iliac trunk and femoral arteries leading to angina of legs
3) V narrow iliac and femoral arteries lead to ischaemia in legs, causing leg pain

32
Q

How does atherosclerosis lead to infarct?

A

Sudden occlusion of the lumen by super-imposed thrombosis or haemorrhage into an atheroma produces ischaemia and if severe and prolonger, infarction of the tissues in the perfusion zone

33
Q

How does atherosclerosis lead to embolism?

A

Provides a site for thrombosis → embolism

34
Q

How can atherosclerosis cause aneurysm even in the heart and what can this lead to?

A
  • Weakening the wall of a vessel can cause aneurysm or rupture
  • This can happen in the heart itself → ventricles burst or blood is released between the heart and pericardium → tamponade (no room for heart to beat)
  • This can happen 10-15 days after infarct → death
35
Q

What is thrombosis?

A

A complication of late-stage atherosclerosis

36
Q

What may organisation of thrombi contribute to?

A

Plaque formation and luminal encroachment

37
Q

What substance can be detected (immunohistologically) in up to 40% of plaques in an individual person at any given time?

A

Fibrin

38
Q

When is there a significant risk of sudden death and occlusion with plaque?

A

Once an atheromatous plaque occludes 70% of the cross sectional area of the coronary artery

39
Q

Describe a rupture abdominal aortic aneurysm

A
  • In distal aspect of abdominal aorta before bifurcation
  • Catastrophic → can’t be saved
  • Even leaking aneurysm v difficult to solve

Stage 2: Supporting Life (30 decks)

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