L11 - atherosclerosis

Question 1

Define ‘atherosclerosis’

Answer 1

The accumulation of lipid in the intima and media of medium and larger arteries

Question 2

Define ‘arteriosclerosis’

Answer 2

The hardening of artery walls as a consequence of atherosclerosis’

Question 3

What are the macroscopic features of atherosclerosis?

Answer 3

Presence of fatty streaks and plaques

Question 4

What are ‘fatty streaks’?

Answer 4

Accumulation of foam cells in the artery walls

Question 5

What are the three major components of an atherosclerotic plaque?

Answer 5

Cells (macrophages, SMC’s, leukocytes)/lipid/ECM

Question 6

Give two common sites where atherosclerosis takes place

Answer 6

Aorta/coronary arteries/carotid arteries/cerebral arteries/leg arteries

Question 7

Give the early microscopic features of atherosclerosis

Answer 7

Proliferation of SMC’s/accumulation of foam cells/ EC lipid deposition

Question 8

Give some late microscopic features of atherosclerosis

Answer 8

Fibrosis/plaque necrosis/cholesterol clefts/inflammatory cells/plaque fissures/ingrowth of blood vessels

Question 9

Describe the cellular events leading to the formation of atherosclerotic lesions

Answer 9

1) Chronic endothelial injury
2) Lipid accumulation by LDL’s in the wall and formation of foam cells
3) Endothelium bulges due to accumulation of foam cells -> this is a fatty streak
4) SMC’s proliferation and formation of a fibrous plaque and a fibrous cap
5) Central necrosis of the plaque, small blood vessels grow into the plaque
6) Plaque injury resulting in thrombosis or haemorrhage

Question 10

Distinguish between thrombosis and atherosclerosis

Answer 10

Atherosclerosis is the deposition of lipids in arterial walls
Thrombosis is a local solid blood clot in the circulatory system

Question 11

What can make a plaque ‘complicated’?

Answer 11

Ulceration (exposure of the central plaque which is highly thrombogenic)/haemorrhage/thrombosis

Question 12

How are foam cells formed?

Answer 12

Lipid accumulates in the intima, LDL’s are oxidised and ingested by macrophages -> formation of foam cells

Question 13

What is the main difference between an early and late atheromatous plaque?

Answer 13

Inovlement of the tunic media

Question 14

What are some local complications of atheroma?

Answer 14

Calcification/ulceration/rupture/thrombosis/aneurysm formation/downstream ischaemia/emobolism

Question 15

Give the effects of severe atherosclerosis at the following sites:

• Iscahemic heart disease
• cerebral ischaemia
• mesenteric ischaemia
• peripheral vascular disease
• abdominal aortic -aenurysm

Answer 15

IHD - death/MI/angina/arrythmias/heart failure

Cerebral ischaemia - Stroke/multi-infarct dementia/TIA (transient ischaemic attack, brief episode of loss of neurological function)

Mesenteric ischaemia - malabsorption/intestinal infacrtion/ischaemic colitis

Peripheral vascular disease - intermittent claudication/Leriche syndrome (claudication in the buttocks due ot ischaemia)/gangrene/ischaemic rest pain

Abdominal aortic aneurysm - Exsanguination (bleeding out)/embolism

Question 16

Give four major risk factors for atherosclerosis

Answer 16

Cigarette smoking/diabetes mellitus/alcohol/infection/hypertension/hyperlipidaemia/age/apoE genotype

Question 17

Polymorphisms of which apolipoprotein are assoiated with high LDL levels?

Answer 17

ApoE

Question 18

Familial hyperlipidaemia (main one is famililal hypercholesterolemia) is a genetic disorder characterised by naturally very high levels of LDL -> longer half life -> increased risk of fatty streak formation. What are some associated physical signs of this condition?

Answer 18

Corneal arcus/tendon xanthomas (tendon nodules)/xanthelasma (yellowed eyelids)

Question 19

There is a protective effect against atherosclerosis in _______ women.

Answer 19

Menopausal

Question 20

WHat infection causing bacteria are most atherosclerotic?

Answer 20

Chlamydia pneumoniae/Helicobacter pylori/Cytomegalovirus

Question 21

Briefly describe the insudation theory of atherogenesis

NOTE you only need to understand the hypotheses not be able to quote them

Answer 21

endothelial injury -> inflammation -> increased permeabilty for lipids to enter the wall from the plasma

Question 22

Briefly describe the reaction to injury hypothesis

Answer 22

plaques form in response to endothelial injury -> injury increases permeability -> ->SMC’s migrate in an proliferate

Question 23

What is the monoclonal hypothesis?

Answer 23

Idea that each plaque is monoclonal and is an abnormal growth that might act like a benign tumour

Question 24

Briefly explain the unifying hypothesis

Answer 24

Atherosclerosis is a result of endothelial injury due to rasied LDL, toxins, hypertension and haemodynamic stress

Question 25

Describe some preventative measures for atherosclerosis

Answer 25

Stop smoking/decrease fat intake/treat hypertension/reduce alcohol intake/control and treat diabetes/lipid lowering drugs when needed/regular exercise/aspirin

Question 26

What kind of aneurysms commonly form in the cerebral arteries?

Answer 26

Berry aneurysms (form of sacular aneurysm)

Question 27

Fusiform aneuryms are shaped like a spindle and invovle the full circumference of the cell wall. T/f

Answer 27

T

Question 28

What is a carotid bruit?

Answer 28

A heart murmur indicting carotid artery disease