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8. MoD > 6. Atheroma > Flashcards

6. Atheroma Flashcards

1
Q

What are atheromas?

A

The accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries.

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2
Q

What is atherosclerosis?

A

The thickening and hardening of arterial walls as a consequence of atheroma.

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3
Q

What is arteriosclerosis?

A

The thickening and hardening of arteries and arterioles usually as a result of hypertension of diabetes mellitus.

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4
Q

What are the macroscopic features of atheromas?

A

Fatty streak, simple plaque or complicated plaque.

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5
Q

What is the fatty streak in atheromas?

A

Lipid deposits in the intima. Yellow and slightly raised.

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6
Q

What is the appearance of atheroma simple plaques?

A

Raised yellow/white, irregular outline, widely distributed, enlarge and coalesce.

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7
Q

What is the appearance of atheroma complicated plaques?

A

Thrombosis, haemorrhage into plaque, calcification, aneurysm formation.

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8
Q

What are the common sites of atheroma?

A

Aorta, coronary arteries, carotid arteries, cerebral arteries, and leg arteries.

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9
Q

What is the normal structure of arteries?

A

Endothelium, sub-endothelium, internal elastic lamina, muscular media, external elastic lamina, adventitia.

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10
Q

What are the early changes seen microscopically with atheromas?

A

Proliferation fo smooth muscle cells, accumulation of foam cells, extracellular lipid.

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11
Q

What are the later changes seen microscopically with atheromas?

A

Fibrosis, necrosis, cholesterol clefts (needle shaped crystals of cholesterol), and more or less inflammatory cells.
Also disruption of internal elastic lamina, damage can extend into media, ingrowth of blood vessels and plaque fissuring.

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12
Q

What are the possible clinical effects of atheromas?

A

Ischaemic heart disease, cerebral ischaemia, mesenteric ischaemia, peripheral vascular disease.

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13
Q

What are the risks of ischaemic heart disease?

A

Sudden death, myocardial infarction, angina pectoris, arrhythmias, and cardiac failure.

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14
Q

What are the risks of cerebral ischaemia?

A

Transient ischaemic attacks, cerebral infarction/stroke, multi-infarct dementia.

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15
Q

What are the risks of mesenteric ischaemia?

A

Ischaemic colitis, malabsorption, intestinal infarction.

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16
Q

What are the risks of peripheral vascular disease?

A

Intermittent claudication, Leriche syndrome, ischaemic rest pain, gangrene (if untreated).

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17
Q

What are the risk factors of developing atheromas?

A

Age, gender, hyperlipidaemia, cigarette smoking, hypertension, diabetes mellitus, alcohol, infection.

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18
Q

How does age affect atheroma development?

A

Risk increases throughout adult life.

19
Q

How does gender affect atheroma development?

A

Women are protected before menopause so lower risk, thought to be hormonally linked.

20
Q

How does hyperlipidaemia affect atheroma formation?

A

High plasma cholesterol is associated with atheroma, LDL more importantly as HDL is protective.

21
Q

What are the roles of the following lipids?

a. Chylomicrons
b. LDL
c. VLDL
d. HDL

A

a. transport lipid from intestine to liver.
b. rich in cholesterol, carry cholesterol to non-liver cells.
c. carry cholesterol and TG from liver, TG removed leaving LDL.
d. carry cholesterol from periphery back to liver.

22
Q

What is familial hyperlipidaemia?

A

Genetically determined abnormalities of lipoproteins that lead to early development of atheroma.

23
Q

What are the physical signs associated with familial hyperlipidaemia?

A

Corneal arcus, tendon xanthomas, xanthelasma.

24
Q

How does cigarette smoking affect atheroma formation?

A

Powerful risk factor, risks fall after giving up smoking. Could be due to cigarette affect on coagulation system, reduced PIP2, or increased platelet aggregation.

25
Q

What is the possible link between hypertension and atheroma formation?

A

Could be because of more endothelial damage with raised pressure.

26
Q

How does diabetes mellitus affect atheroma formation?

A

It doubles the risk of ischaemic heart disease and loses the protective effect in premenopausal women. Could be linked to hyperlipidaemia and hypertension.

27
Q

How does alcohol consumption affect atheroma formation?

A

> 5 units a day are associated with increased risk of ischaemic heart disease. Small amounts of alcohol could be protective though.

28
Q

What infections could raise risk of atheroma?

A

Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus.

29
Q

Why could genetic predisposition raise risk of atheroma formation?

A

Because of variations in apolipoprotein metabolism and apolipoprotein receptors.

30
Q

What is Rokitansky’s thrombogenic theory?

A

Plaques formed by repeated thrombi and lipid is derived from thrombi. There is an overlying fibrous cap.

31
Q

What is Virchow’s insudation theory?

A

Endothelial injury causes inflammation and increased permeability to lipid from plasma.

32
Q

What is Ross and Glomset’s reaction to injury hypothesis?

A

Plaques form in response to endothelial injury. Hypercholesterolaemia leads to endothelial damage in experimental animals. Injury increases permeability and allows platelet adhesion, monocytes penetrate endothelium and smooth muscle cells proliferate and migrate.

33
Q

What is Benditt and Benditt’s monoclonal hypothesis?

A

Crucial role for smooth muscle proliferation, each plaque is monoclonal, could represent abnormal growth control. So each plaque could be a benign tumour or have a viral artiology.

34
Q

What are the four main process involved in atheromas?

A

Thrombosis, lipid accumulation, production of intercellular matrix and interactions between cell types.

35
Q

What are the cells involved in atheroma?

A

Endothelial cells, platelets, smooth muscle cells, macrophages, lymphocytes, and neutrophils.

36
Q

What is the role of endothelial cells in atheroma?

A

In haemostasis: altered permeability to lipoproteins, production of colalgen and stimulation of proliferation and migration of smooth muscle cells.

37
Q

What is the role of platelets in atheroma?

A

In haemostasis: stimulate proliferation and migration of smooth muscle cells (PDGF).

38
Q

What is the role of smooth muscle cells in atheroma?

A

Take up LDL and other lipid to become foam cells and synthesise collagen and proteoglycans.

39
Q

What is the role of macrophages in atheroma?

A

Oxidise LDL, take up lipids to becomes foams cells, secrete proteases which modify matrix, and stimulate proliferation and migration of smooth muscle cells.

40
Q

What is the role of lymphocytes in atheroma?

A

TNF may affect lipoprotein metabolism, stimulate proliferation and migration of smooth muscle cells.

41
Q

What is the role of neutrophils in atheroma?

A

Secrete proteases leading to continues local damage and inflammation.

42
Q

What is the unifying hypothesis of atheroma?

A

Endothelial injury due to: raised LDL, toxins, hypertension, and haemodynamic stress.
Endothelial injury causes: platelet adhesion, PDGF release, SMC proliferation and migration, insudation of lipid, LDL oxidation, uptake of lipid by SMC and macrophages, migration of monocytes into intima.
Stimulated SMC produce matrix material.
Foam cells secrete cytokines causing further SMC stimulation and recruitment of other inflammatory cells.

43
Q

How can atheromas be prevented?

A

No smoking, reduce fat intake, treat hypertension, not too much alcohol, regular exercise and weight control.

8. MoD (11 decks)

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