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Sem 2 - Pathological Processes > Athlerosclerosis > Flashcards

Athlerosclerosis Flashcards

1
Q

Define atherosclerosis

A

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

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

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2
Q

Define arteriosclerosis

A

The thickening of the walls of arteries and arterioles usually as a result of hypertension or diabetes mellitus

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3
Q

What are the macroscopic features of atherosclerosis?

A

Fatty streak

Simple plaque

Complicated plaque

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4
Q

What is a fatty streak?

A

Lipid deposits in intima

Yellow, slightly raised

Relationship to atherosclerosis somewhat debatable but, seen as precursors for it.

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5
Q

What is a simple plaque?

A

raised yellow / white

Irregular outline

Widely distribute

Enlarge and coalesce

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6
Q

What is a complicated plaque?

A

Thrombosis

Haemorrhage into plaque

Calcification - Can see on x-rays

Aneurysm formation - expansion of artery

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7
Q

What are some common sites of atherosclerosis?

A
  • Aorta - particularly abdominal (renal and could go into iliac)
  • Coronary arteries
  • Carotid arteries
  • Cerebral arteries
  • Leg arteries
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8
Q

What is normal arterial structure?

A
  • Endothelium
  • Sub-endothelial CT
  • Internal elastic lamina (closer to heart, more elastic and muscle)
  • Muscular media
  • External elastic lamina
  • Adventitia
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9
Q

Microscopic features of atherosclerosis (early changes)

A

Early changes:

  • Proliferation of smooth muscle cells
  • Accumulation of foam cells
  • Extracellular lipid
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10
Q

Microscopic features of atherosclerosis (later changes)

A

Later changes:

  • Fibrosis
  • Necrosis
  • Cholesterol clefts - where cholesterol was
  • +/- inflammatory cells
  • Disruption of internal elastic lamina
  • Damage extends into media
  • Ingrowth of blood vessels - leaky, can lead to haemorrhage
  • Plaque fissuring
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11
Q

What are the clinical effects of atherosclerosis?

A
  • Ischaemic heart disease
  • Sudden death
  • Myocardial infarction
  • Angina pectoris (chest pain on exertion - goes away when rested)
  • Arrhythmias
  • Cardiac failure - due to fibrosis.
  • Manifest as shortness of breath and pulmonary oedema.
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12
Q

What are the clinical effects of athlerosclerosis in the brain?

A

Cerebral ischaemia

  • Transient ischaemic attach (TIA - mini stroke as resolve in 24hrs)
  • Cerebral infarction (stroke) - thrombus in cerebral artery or thromboembolus
  • Multi-infarct dementia
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13
Q

Clinical effects of atherosclerosis of the bowel

A

Mesenteric ischaemia

  • Ischaemic colitis
  • Malabsorption
  • Intestinal infarction
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14
Q

What are the clinical effects of peripheral vascular disease?

A
  • Arms are rare so usually legs
  • Intermittent claudication - distance can walk before pain in calf.
  • Leriche syndrome (blockage of abdominal aorta as it goes to common iliac arteries.)
  • Ischaemic rest pain - when worse
  • Gangrene - once tissue has infarcted.
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15
Q

Why do people get athleroscleosis?

A
  • Age - slowly progressive throughout adult life. Risk factors operate over years
  • Gender - males more affected than females as women are protected relatively before menopause. There is a presumed hormonal basis
  • Hyperlipidaemia
  • Cigarette smoking
  • Hypertension
  • Diabetes mellitus
  • Alcohol
  • Infection
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16
Q

Why does hyperlipidaemia cause athlerosclerosis?

A
  • High plasma cholesterol associated with athlerosclerosis
  • LDL most significant
  • HDL protective
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17
Q

Lipid metabolism

A
  • Lipid in the blood is carried on lipoproteins
  • Lipoproteins carry cholestrol and triglycerides (TG)
  • Hydrophobic lipid core
  • Hydrophilic outer later of phospholipid and apolipoprotein (A-E)
  • Chylomicrons - Transport lipid from intestine to liver
  • LDL - Rich in cholestrol and carries to choletrol to non-liver cells.
  • VLDL - Carry cholestrol and TG to liver. TG removed leaving LDL.
  • HDL - Carry cholestrol from periphery back to liver
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18
Q

Apolipoprotein E

A
  • Genetic variations in Apo E are associated with changes in LDL levels
  • Polymorphisms of the genes involved lead to at least 6 Apo E phenotypes.
  • Polymorphisms can be used as risk markers for atherosclerosis
19
Q

Familial Hyperlipidaemia

A

Genetically determined abnormalities of lipoproteins

Lead to early development of atherosclerosis

Associated physical signs:

  • Arcus (A thin, whitish circle around the iris; normal finding in old people.)
  • Tendon xanthoma (deposits of cholestrol)
  • xanthelasma (depositions of cholestrol)
20
Q

How does cigarette smoking cause atherosclerosis?

A
  • Don’t know - effect coagulation system, reduced Prostaglanin I2, Incresed platelet aggregation.
  • Powerful risk factor for IHD
  • Risk falls after giving up.
21
Q

Hypertension and atherosclerosis

A
  • Strong link between IHD and high systolic / diastolic BP
  • Mechanism uncertain
  • Maybe endothelial damage caused by raised pressure.
22
Q

Atherosclerosis and diabetes Mellitus

A
  • DM doubles IHD risk.
  • Protective effect in premenopausal women lost
  • DM also associated with high risk of carebrovascular and peripheral vascular disease
  • It is maybe related to hylerlipidaemia?
23
Q

Atherosclerosis - Alcohol Consumption

A

Over 5 units per day is associated with increased risk of IHD

Alcohol consumption after associated with other risk factors e.g. smoking and high BP but still an independent risk factor.

Smaller amounts of alcohol may be protective.

24
Q

Atherosclerosis-Infection

A
  • Chlamydia pneumoniae
  • Helicobacter pylori
  • Cyromegalovirus

All look at but no hard evidence.

25
Q

Atherosclerosis - Other Risk Factors

A
  • Lack of exercise
  • Obesity
  • Soft water
  • Oral contraceptives
  • Stress and personality type?
26
Q

Atherosclerosis - Genetic Predisposition

A

Familial predisposition well known

Possibly due to:

  • variations in apolipoprotein metabolism
  • variations in apolipoprotein receptors
27
Q

What are the theories as to how atherosclerosis develops?

A
  • Thrombogenic theory
  • Isudation theory - Movement from lumen into the wall
  • Monoclonal hypothesis
  • Reaction to injury hypothesis
28
Q

The thrombogenic theory of atherosclerosis

A

Though that plagues formed by repeated thrombi.

Lipids derived from thrombi

Overlying fibrous cap.

29
Q

Insudation theory of atherosclerosis

A

Endothelial injury causes inflammation.

This makes the vessel leaky and allows lipid from the plasma into wall and develop.

30
Q

Reaction to injury hypothesis

A

Plaques form in response to endothelial injury

Hypercholestrolaemia leads to endothelial damage in experimental animals

Injury increases permeability and allows platelet adhesion.

Monocytes penetrate endothelium

Smooth muscle cells proliferate and migrate.

Endothelial injury may be very subtle and be undetectable visually.

LDL, especially oxidised, may damage endothelium.

31
Q

The monoclonal hypothesis

A

Aside, not widely accepted

Crucial role for smooth muscle proliferation

Each plaque is monoclonal

Might represent abnormal growth control

32
Q

What are the stages of atherosclerosis?

A

Thrombosis

Lipid accumulation

Production of intercellular matrix

Interactions between cell types

33
Q

What cells are involved in atherosclerosis?

A

Endothelial cells

Platelets

Smooth muscle cells (become foam cells)

Macrophages

Lymphocytes

Neutrophils

34
Q

Endothelial cells in Atherosclerosis

A

Key role in haemostasis

Altered permeability to lipoproteins

Production of collagen

Stimulation of proliferation and migration of smooth muscle cells.

35
Q

Platelets in atherosclerosis

A

Key role in haemostasis

Stimulate proliferation and migration of smooth muscle cells (PDGF - platelet derived growth factor)

36
Q

Smooth muscle cells in atherosclerosis

A

Take up LDL and other lipid to become foam cells

Synthesise collagen and proteoglycans

37
Q

Macrophages in atherosclerosis

A

Oxidise LDL

Take up lipids to become foam cells

Secrete proteases which modify matrix

Stimulate proliferation and migration of smooth muscle cells.

38
Q

Lymphocytes in atherosclerosis

A

TNF May affect lipoprotein metabolism. Stimulate proliferation and migration of smooth muscle cells.

39
Q

Neutrophils in atherosclerosis

A

Secrete proteases leading to continued local damage and inflammation

40
Q

What causes endothelial injury?

A

Endothelial injury due to:

Raised LDL

‘Toxins; e.g. cigarette smoke.

Hypertension

Haemodynamic stress

41
Q

What are the consequences of endothelial injury?

A

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

42
Q

What are final things cause atherosclerosis?

A

Stimulated SMC (smooth muscle cells) produce matrix material

Foam cells secrete cytokines causing:

  • Further SMC stimulation
  • Recruitment of other inflammatory cells
43
Q

How do you prevent atherosclerosis?

A

No smoking

Reduce fat intake (ish.. not matter too much if good fat metabolism)

Treat hypertension

Not too much alcohol

Regular exercise / weight control

BUT, some people will still develop atherosclerosis!

44
Q

What interventions can reduce the risk of atherosclerosis?

A
  • Stop smoking
  • Modify diet
  • Treat hypertension
  • Treat diabetes
  • Lipid lowering drugs

Sem 2 - Pathological Processes (13 decks)

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