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Pathological Processes > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

Define atheroma

A

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

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2
Q

Define atherosclerosis

A

The thickening and hardening of arterial

walls as a consequence of atheroma

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3
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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4
Q

What are the macroscopic features of atherosclerosis

A

 Fatty streak
 Simple plaque
 Complicated plaque

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5
Q

What is the fatty streak?

A

 Lipid deposits in intima
 Yellow, slightly raised
 Relationship to atherosclerosis somewhat debatable - positions dont exactly match - but consider the fatty streak an early stage of atherosclerosis

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6
Q

What is the simple plaque

A

 Raised yellow/white
 Irregular outline
 Widely distributed
 Enlarge and coalesce

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7
Q

What is the complicated plaque?

A

 Thrombosis
 Haemorrhage into plaque
 Calcification
 Aneurysm formation
Abnormality of vessel wall causing abnormal flow (2 components of Virchow triad)
sheer force may lead to bleeding, rapid expansion
rupture can release thrombogenic substances
atheromatic arteries tend to lose elastic recoil - gradual expansion of artery

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8
Q

What are the common sites of atherosclerosis?

A 
 Aorta - especially abdominal
 Coronary arteries
 Carotid arteries
 Cerebral arteries
 Leg arteries
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9
Q

Describe the normal arterial structure

A 
 Endothelium
 Sub-endothelial c.t.
 Internal elastic lamina
 Muscular media
 External elastic lamina
 Adventitia
More elastic tissue closer to the heart
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10
Q

What are the early microscopic features of atherosclerosis?

A

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

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11
Q

What are the late microscopic features of atherosclerosis?

A 
Later changes
 fibrosis
 necrosis
 cholesterol clefts - needle shape
 +/- inflammatory cells
 disruption of internal elastic lamina
 damage extends into media
 ingrowth of blood vessels - leaky and can lead to hemorhage 
 plaque fissuring

Variation between individuals despite having the same symptoms and variation between one individual at different times

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12
Q

What are the clinical effects of atherosclerosis

A 
Ischaemic heart disease
 sudden death
 myocardial infarction
 angina pectoris
 arrhythmias
 cardiac failure

Cerebral ischaemia
 transient ischaemic attack - stroke symptoms but resolve within 24 hours
 cerebral infarction (stroke) - thrombus in cerebral vessel or thromboembolism in carotid artery
 multi-infarct dementia

Mesenteric ischaemia
 ischaemic colitis
 malabsorption
 intestinal infarction

Peripheral vascular disease (usually leg arteries - arms unaffected)
 intermittent claudication - limping - pain after short amount of walking, take a break, then pain again after a shorter time
 Leriche syndrome
 ischaemic rest pain
 gangrene

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13
Q

What are risk factors of atherosclerosis

A 
 Age - slowly oregressive throughout adult life, risk factors operate over years 
 Gender - males more affected than females up to menopause due to hormonal effects 
 Hyperlipidaemia
 Cigarette smoking
 Hypertension
 Diabetes mellitus
 Alcohol
 Infection
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14
Q

What is hyoerlipidaemia

A

 Hyperlipidaemia
 high plasma cholesterol associated with atherosclerosis
 LDL most significant
 HDL protective

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15
Q

What are chylomicrons, LDLs, VLDLs and HDLs?

A

 Chylomicrons - transport lipid from intestine to liver
 VLDL - carry cholesterol and
TG from liver - TG removed leaving LDL
 LDL - rich in cholesterol, carry cholesterol to
non-liver cells
 HDL - carry cholesterol from periphery back to liver

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16
Q

Describe th relationship between atherosclerosis and 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

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17
Q

What is familial hyperlipidaemia?

A

 Genetically determined abnormalities of lipoproteins
 Lead to early development of atherosclerosis

Associated physical signs
 arcus
 tendon xanthomas
 xanthelasma

18
Q

How is cigarette smoking related to atherosclerosis?

A

 Powerful risk factor for IHD
 Risk falls after giving up

Mode of action uncertain

  • coagulation system
  • reduced PGI2
  • increased platelet aggregation
19
Q

What is the link between atherosclerosis and hypertension?

A

 Strong link between IHD and high systolic/diastolic blood pressure
 Mechanism uncertain
 ? endothelial damage caused by raised pressure

20
Q

What is the relationship between atherosclerosis and diabetics mellitus?

A

 DM doubles IHD risk
 Protective effect in premenopausal women lost
 DM also associated with high risk of
cerebrovascular and peripheral vascular disease
 ?related to hyperlipidaemia and hypertension

21
Q

What is the relationship between atherosclerosis and alcohol consumption?

A

 >5 units /day associated with increased risk of IHD
 Alcohol consumption often associated with other risk factors eg smoking and high BP but still an independent risk factor
 Smaller amounts of alcohol may be protective

22
Q

What is the relationship between atherosclerosis and infection?

A

 Chlamydia pneumoniae
 Helicobacter pylori
 Cytomegalovirus
Not much of a link

23
Q

What are other risk factors o atherosclerosis

A 
 Lack of exercise
 Obesity
 Soft water
 Oral contraceptives
 Stress and personality type?
24
Q

Describe atherosclerosis and genetic predisposition

A

 Familial predisposition well known
 Possibly due to
- variations in apolipoprotein metabolism
- variations in apolipoprotein receptors

25
Q

What are the pathogenesis theories for atherosclerosis?

A

 Thrombogenic theory
 Insudation theory - Sometime coming from lumen into the arterial wall
 Monoclonal hypothesis
 Reaction to injury hypothesis

26
Q

What is teh thrombogenic theory?

A

 1852 Karl Rokitansky
 plaques formed by repeated thrombi
 lipid derived from thrombi
 overlying fibrous cap

27
Q

What is the insulation theory?

A

 1856 Rudolf Virchow
 endothelial injury
 inflammation
 increased permeability to lipid from plasma

28
Q

What is the reaction to injury hypothesis?

A

 1972 Ross and Glomset
 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
 smooth muscle cells proliferate and migrate

 1986 Ross
 endothelial injury may be very subtle and be
undetectable visually
 LDL, especially oxidised, may damage
endothelium
29
Q

What is the monoclonal hypothesis

A

 Benditt and Benditt
 crucial role for smooth muscle proliferation
 each plaque is monoclonal
 might represent abnormal growth control
 is each plaque a benign tumour?
 could atherosclerosis have a viral aetiology?

30
Q

What are the processes involved in atherosclerosis

A

 Thrombosis
 Lipid accumulation - fat between the cells of the lumen that shouldnt normally be there
 Production of intercellular matrix
 Interactions between cell types

31
Q

What are the cels involved in atherosclerosis

A

 Endothelial cells - increased permeability so lipids and lipoprotein get through - abnormal collagen production
 Platelets
 Smooth muscle cells - stimulation, migration and proliferation
 Macrophages
 Lymphocytes
 Neutrophils

32
Q

What is the role of 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

33
Q

What is the role of platelets in atherosclerosis

A

 Key role in haemostasis

 Stimulate proliferation and migration of smooth muscle cells (PDGF)

34
Q

What do smooth muscle cells do in atherosclerosis

A

 Take up LDL and other lipid to become
foam cells
 Synthesise collagen and proteoglycans

35
Q

What do macrophages do 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
36
Q

What do lymphocytes do in atherosclerosis

A

 TNF may affect lipoprotein metabolism
 Stimulate proliferation and migration of
smooth muscle cells
Multi factorial effect particularly on smooth muscle cell

37
Q

What do eutrophic do in atherosclerosis

A

Secrete proteases leading to continued

local damage and inflammation

38
Q

Describe 3 unifying hypothesis of atherosclerosis?

A

Endothelial injury due to
 raised LDL - particularly oxidised
 ‘toxins’ eg cigarette smoke - some cause endotheliall damage
 hypertension - subtle endothelial damage
 haemodynamic stress - certain sites in arterial system where atherosclerosis is common

Endothelial injury causes
 platelet adhesion, PDGF release, SMC proliferation and migration
 insudation of lipid, LDL oxidation, uptake of lipid by SMC and macrophages - lipid gets into vessel walls
 migration of monocytes into intima
Endothelium not fucntioning i contribute to the development of atherosclerosis

Stimulated SMC produce matrix material
Foam cells secrete cytokines causing
 further SMC stimulation
 recruitment of other inflammatory cells

39
Q

How can atherosclerosis be prevented?

A 
 No smoking - main thing
 Reduce fat intake
 Treat hypertension
 Not too much alcohol
 Regular exercise/weight control
 BUT some people will still develop atherosclerosis!
40
Q

Describe methods of atherosclerosis intervention

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

Pathological Processes (12 decks)

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