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Semester 2 - PathPro > 10. Atherosclerosis > Flashcards

10. Atherosclerosis Flashcards

1
Q

Which type of blood vessels does atherosclerosis affect?

A

Arteries, does not affect veins or capillaries

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2
Q

At what percentage lumen reduction is blood flow significantly affected?

A

70-80%

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3
Q

What is the key event in atherscleosis?

A

Focal accumulation of lipid and cells beneath the endothelium which forms a raised flat plaque. The plaque is usually about 1-2mm thick

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4
Q

Which part of arteries does atherscleosis occur?

A

in patches of the intima often where flow is disturbed, e.g., around the opening of a branch

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5
Q

In which arteries do plaques usually form?

A

In elastic arteries (such as aorta, carotid and iliac arteries) and large and medium sized muscular arteries (such as coronary and popliteal arteries). It is commoner in the abdominal rather than the thoracic aorta9405

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6
Q

Define arteriosclerosis.

A

hardening of the arteries

- walls are thickened and lose their elasticity

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7
Q

What 3 diseases does arteriosclerosis encompass?

A
  • atherosclerosis
  • arteriolosclerosis
  • Monkeberg’s disease
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8
Q

Define atherosclerosis.

A

A disease of large and medium sized arteries
that begins in the intima. Plaques are formed in the arterial wall and these are filled with atheroma (a necrotic gruel-like material). The plaques often calcify.

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9
Q

Define arteriolosclerosis.

A

Hardening of the arterioles. This disease affects arterioles throughout the body but especially those of the kidney. It has little or no connection with atherosclerosis and usually occurs secondary to severe hypertension or in diabetes mellitus.

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10
Q

What is Monkeberg’s disease?

A

An uncommon disease where there is calcification of the media of large arteries

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11
Q

What is atheroma and what does it consist of?

A

Necrotic core of the atherosclerotic plaque. It consists of dead cells, debris and cholesterol crystals

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12
Q

What is the atherosclerotic plaque?

A

The basic lesion of atherosclerosis

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13
Q

What are the 3 basic components of the atheroscleotic plaque?

A
  • Cells: macrophages, leucocytes, smooth muscle cells
  • Intra and extracellular lipid,
  • Extracellular matrix: collagen, elastin, proteoglycans.
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14
Q

Describe plaque formation.

A
  1. Chronic endothelial insult result in endothelial dysfunction
  2. Lipid droplets, mainly from LDLs, and monocytes cross the endothelium and accumulate in the intima. The lipids become oxidised and the macrophages ingest the lipid.
  3. lots foam cells cause the endothelium to bulge. Smooth muscle cells migrate into the lesion from the media and start to proliferate. The lesion at this stage is called a fatty streak
  4. plaque grows as the number of foam cells and smooth muscle cells increases. Some smooth muscle cells will also take up lipid and appear foamy.
  5. Fibrous cap forms. As the endothelium stretches over the plaque, gaps appear between the endothelial cells. Platelets adhere to the gaps.
  6. Cells in the centre of the plaque die and necrosis develops. The dead cells release cholesterol and cholesterol crystals appear in the plaque. Small blood vessels grow into the plaque from the adventitia and the plaque may undergo calcification
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15
Q

What may cause chronic endothelial insult?

A

Conditions such as hyperlipidaemia, hypertension, smoking or from haemodynamic factors

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16
Q

What is and forms the fibrous cap?

A

Layer of fibrous connective tissue that covers a plaque

Some smooth muscle cells will lie over the plaque but beneath the endothelium forming a ‘roof’. This roof is reinforced by collagen, elastin and other matrix proteins and the result is a fibrous cap

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17
Q

What are macrophages that ingest lipids called?

A

Foam cells

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18
Q

What are cholesterol clefts?

A

when cells in the centre of the plaque dies and release cholesterol, cholesterol crystals appear. These are removed during tissue processing for microscopy leaving behind linear holes in the tissue section = cholesterol clefts

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19
Q

What contribute to fatty streaks and what effects do they have on blood flow?

A

Consist of intimal foam cells, some smooth muscle cells and some extracellular lipid
- are flat and cause no disturbance to blood flow

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20
Q

What forms as fatty streaks grow?

A

Plaques

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21
Q

What contributes to plaques?

A

Fibrosis, necrosis, cholesterol clefts, disruption of the internal elastic lamina, extension into the media and ingrowth of small vessels from the adventitia

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22
Q

Describe the appearance of simple and complicated plaques.

A 
The Simple Plaque:
● Raised yellow/white
● Irregular outline
● Widely distributed
● Enlarge and coalesce
The Complicated Plaque
● Thrombosis
● Haemorrhage into plaque
● Calcification
● Aneurysm formation
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23
Q

What are some plaque complication?

A
  1. Ulceration
  2. Thrombosis on the plaque
  3. Spasm at the site of the plaque
  4. Embolisation
  5. Calcification
  6. Haemorrhage
  7. Aneurysm formation
  8. Rupture of the atherosclerotic artery
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24
Q

What is plaque ucleration?

A

Fibrous cap is eroded from underneath and the

core of the plaque is exposed to the blood. This core is highly thrombogenic

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25
Q

When might plaque thrombus form and what is the implication of this?

A

often on an ulcerated plaque, however it can sometimes occur on a plaque with intact endothelium

Occludes vessel lumen

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26
Q

How do spasms at sites of plaque occur?

A

Caused by vasoconstrictors released from thrombi.

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27
Q

What can embolise from plaque?

A

Pieces of exposed atheroma or overlying thrombus

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28
Q

Where does calcification of plaque occur and what does this result in?

A

in and around the plaque making the artery even stiffer

29
Q

Where does plaque haemorrhage occur and what does this result in?

A

of one of the new vessels within the plaque.

This suddenly expands the plaque which can result in vessel occlusion or the pressure from the haemorrhage may break the plaque open

30
Q

Why might plaque lead to aneurysm?

A

Local dilatation may result when elastic tissue within the arterial wall is destroyed by the plaque. This weakens the wall and may result in rupture of the vessel

31
Q

Why might plaque lead to rupture of the atherosclerotic artery?

A

This occurs as a result of a weakened media.

– with resulting bleeding

32
Q

Where is rupture of an atherosclerotic artery usually seen?

A

Cerebral arteries when the patient has hypertension in addition to atherosclerosis

33
Q

What are aneurysms?

A

Aneurysms are local dilutions of an artery due to weakening of the arterial wall.

The vessel wall is stretched during systole, however it’s lost its ability to recoil back to its original shape and size so it remains dilated.

In large arteries they are almost always secondary to atherosclerosis. Like atherosclerosis, they are a disease of arteries.

34
Q

What are dilated veins called?

A

Varices

35
Q

What are saccular and fusiform aneurysms shaped like?

A

Saccular: shaped like a sac
Fusiform: shaped like a spindle

36
Q

Where do saccular aneuryms usually occur?

A

Abdominal aorta

37
Q

What are saccular aneurysms line/filled with and why is this important?

A

lined and/or filled by thrombus, which may be adventitious as it can protect the aneurysm from bursting

38
Q

What are the 2 major complications of aortic aneurysms?

A

If large they may rupture and thrombus or plaque material within them may embolise

39
Q

Where do dissecting aneurysms occur?

A

Occur virtually only in the aorta and its major branches

40
Q

What are dissecting aneurysms?

A

Aneurysm in which the inner wall of the artery tears open

41
Q

What happens in a dissecting aneurysm?

A

Blood enters the tear and separates the media into two layers. As the tear fills with blood the lumen of the artery can be occluded. Occasionally blood can push its way back into the lumen by means of a second tear.

42
Q

Where do symptoms of atherosclerosis usually occur?

A
  • Heart
  • Brain
  • Kidneys
  • Legs
  • Bowel

conditions are either due to narrowing/blockage of vessels or embolism of plaque material or thrombus that has formed on a plaque

43
Q

What effects does atheorsclerosis have on the heart?

A

Myocardial infarction, chronic ischaemic heart disease, arrhythmias, cardiac failure and sudden cardiac death.

These conditions are caused by reduced blood flow to cardiac tissue due to atherosclerotic plaques in the coronary arteries.

44
Q

What effects does atherosclerosis have on the brain?

A

In the brain you can develop cerebral Ischaemia.
This is caused by a sudden decrease in blood supply to the brain.
This can be due to a carotid or cerebral artery atherosclerosis, thromboembolism, haemorrhage or cardiac arrest.
This causes:
Transient ischaemic attacks (TIAs), cerebral infarction,
multi-infarct dementia

45
Q

What effects does atherosclerosis have on the kidneys?

A
  1. Hypertension:
    Renal artery stenosis causes a reduction renal perfusion resulting in an increase in systemic blood pressure through activation of RAAS.
  2. Renal failure:
    Renal artery stenosis can cause chronic kidney disease and end stage kidney failure
46
Q

What effects does atherosclerosis have on the legs?

A

In the legs you can develop a group of conditions know as peripheral vascular disease.
These present as:
1. Intermittent claudication -
Cramping pain in the legs induced by exercise and relieved by rest caused by stenosis of the arteries to the legs.
2. Leriche syndrome -
Stenosis of the iliac arteries, causes cramping pain in the buttocks and legs, and impotence.
3. Ischaemic rest pain - continuous pain in the lower limb caused by ischaemia.
4. Gangrene - loss of blood supply resulting in tissue death.

47
Q

What effects does atherosclerosis have on the bowel?

A

Mesenteric ischaemia is ischaemia caused by a reduction in blood supply to the bowel.
It can cause:

  1. Ischaemic colitis -
    Inflammation and injury to the large bowel due to inadequate blood supply, it can result in acute ulceration and haemorrhage.
  2. Malabsorption
    Resulting from chronic mesenteric ischaemia.
  3. Bowel infarction
    Occlusion of an artery supplying the intestines resulting in infarction.
48
Q

What are the 3 different hypotheses of atherogenesis?

A
  • The response to injury hypothesis
  • The encrustation hypothesis / thrombogenic theory
  • The monoclonal hypothesis
49
Q

What is the response to injury hypothesis for atherogenesis?

A

Postulates that atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to the endothelium. Lesion progression is sustained by interaction between modified lipoproteins, macrophages, T lymphocytes and cells of the arterial wall

50
Q

What is the encrustation hypothesis for atherogenesis?

A

In this model plaques are formed by repeated thrombi overlying thrombi. The lipid core is derived from the thrombi

51
Q

What is the monoclonal hypothesis for atherogenesis and why hasn’t this theory gained popularity?

A

This hypothesis arose following the finding that some plaques are monoclonal or oligoclonal.
This raised the question of whether plaques are benign neoplastic growths, perhaps induced by cholesterol or a virus.

However as some areas of normal arteries are clonal this theory hasn’t gained widespread popularity.

52
Q

List the common sites for atherosclerosis

A
  1. Aorta (particularly abdominal)
  2. Coronary arteries
  3. Carotid arteries
  4. Cerebral arteries
  5. Leg arteries
53
Q

What are the early and later changes due to atherosclerosis?

A

Early changes
● proliferation of smooth muscle cells
● accumulation of foam cells
● extracellular lipid

Later changes
● fibrosis
● necrosis
● cholesterol clefts
● +/- inflammatory cells
● disruption of internal elastic lamina
● damage extends into media
● ingrowth of blood vessels
● plaque fissuring
54
Q

What are the non-modifiable risk factors for atherosclerosis?

A
  • age
  • gender
  • genetic predisposition
55
Q

Which gender does atherosclerosis affect more?

A

Men

56
Q

Which women are affected more by atherosclerosis and why?

A

After menopause, becuase oestrogen is protective.

57
Q

What are some genetic predispositions to atherosclerosis?

A

Some people are genetically predisposed to conditions such as hypertension, hyperlipidaema, diabetes mellitus.
It can also be due to derangements in lipoprotein metabolism resulting in high lipid levels, e.g.
homozygous familial hypercholesterolaemia.

A further genetic risk factor is a person’s apolipoprotein E genotype. Some of the genotypes are associated with high LDL levels and therefore a predisposition to atherosclerosis.

58
Q

Why is diabetes mellitus associated with atherosclerosis?

A

It causes hypercholesterolaemia

59
Q

What are the modifiable risk factors for atherosclerosis?

A
  • Hyperlipidaemia
  • Hypertension (damages blood vessels)
  • Cigarette smoking
  • Geography
  • Obesity
  • Infection
60
Q

Explain what homozygous familial hypercholesterolaemia is

A

People with this condition have defects in the LDL receptor which result in decreased hepatic uptake of LDL and therefore increased circulating LDL.

Such people tend to have myocardial infarctions before the age of 20 years.

61
Q

How is hyperlipidaemia a risk for atherosclerosis?

A

Any increase in LDL cholesterol (which delivers cholesterol to the peripheral tissues) is associated with an increased incidence of atherosclerosis. HDL removes cholesterol from atheromatous plaques and delivers it to the liver for excretion in bile. HDL is therefore protective.

62
Q

What can increase or decrease HDL levels?

A

Increase: exercise, moderate alcohol
Decrease: obesity, smoking

63
Q

How does smoking increase risk of atherosclerosis?

A

Number of mechanisms including:

  • inflammation in and damage to the blood vessel wall
  • increased predisposition to thrombosis
  • and oxidation of lipids
  • decrease HDL
64
Q

How does obesity increase risk of atherosclerosis?

A

Produces hypertension, diabetes mellitus, hypertriglyceridaemia and reduced HDL,

65
Q

How does hypertension increase risk of atherosclerosis?

A

as the increased pressure damages blood vessel walls which predisposes to plaque formation

66
Q

Infections with what bacteria have shown to be associated with increase risk of atherosclerosis?

A

Chlamydia pneumoniae or cytomegalovirus (CMV)

67
Q

How is excess alcohol associated with atherosclerosis?

A

Excess alcohol produces secondary hyperlipidaemia

68
Q

What are the prevention strategies for atherosclerosis?

A
  • Decreasing total and LDL cholesterol and increasing HDL. Dietary measures include a low fat and high fibre diet. Food high in soluble fibre reduces circulating lipid,
  • Stopping smoking,
  • Controlling hypertension,
  • Controlling weight and regular exercise,
  • Sensible alcohol intake
  • Treating diabetes mellitus,
  • Anti-oxidants, such as vitamin E, may be protective.
69
Q

What are intervention strategies for atherosclerosis?

A
  • Lipid-lowering drugs, e.g., statins, and aspirin prophylaxis,
  • Thrombolysis, angioplasty, stents, and coronary artery bypass grafts (CABG).

Semester 2 - PathPro (16 decks)

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