atherosclerosis Flashcards

1
Q

define atheroma

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define atherosclerosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

define arteriosclerosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the macroscopic features of aatherosclerosis

A

fatty streak -represents earliest stage of atherosclerosis. lipid deposits in intimate of artery. yellow and slightly raised
the simple plaque - raised yellow/white. irregular outline. enlarge and coalesce
the complicated plaque- thrombosis, haemorrhage into plaque, calcification and aneurysm formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the common sites of atherosclerosis

A
aorta 
coronary arteries 
carotid arteries
cerebral arteries 
leg arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe normal arterial structure

A
endothelium 
internal elastic lamina
muscular media 
external elastic lamina
adventitia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the early microscopic features of atherosclerosis

A

proliferation of smooth muscle cells
accumulations of foam cells
extracellular lipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the late microscopic features of atherosclerosis

A

fibrosis
necrosis
cholesterol clefts
increase/ decrease in inflammatory cells
disruption of internal elastic lamina and then damage extending to media
ingrowth of blood vessels
plaque fissuring (surface of plaque ruptures)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do cholesterol clefts appear in microscopy

A

needle shaped holes in tissue as cholesterol gets dissolved out when we prepare cell for microscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the clinical affects of ischaemic heart disease

A
sudden death 
myocardial infarction 
angina pectoris -chest pain on exertion due to poor blood supply 
arrhythmias
cardiac failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

clinical effects of cerebral ischaemia

A

transient ischaemic attack (mini stroke)
cerebral infarction (stroke)
multi-infarct dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

clinical effects of mesenteric ischaemia

A
ischaemic colitis - characterised by bleeding in rectum 
malabsorption (chronic form)
intestinal infarction (acute form)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

clinical affects of peripheral vascular disease

A

intermittent claudication- pain in calves on exercise
leriche syndrome -buttock pain & impotence
ischaemic rest pain
gangrene- blood flow to large areas of tissue is cut off. skin becomes greenish-black colour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

risk factors of atherosclerosis

A
age 
gender- women protected before menopause due to hormones 
hyperlipidaemia 
cigarette smoking
hypertension 
diabetes mellitus 
alcohol 
infection
obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does smoking cause atherosclerosis

A

reduced PG12

Increased platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the theories behind atherosclerosis

A

thrombogenic theory-plaques formed by repeated thrombi, lipid derived from thrombi, overlying fibrous cap
insudation theory- endothelial injury, inflammation, increased permeability to lipid from plasma
reaction to injury hypothesis-plaques form in response to endothelial injury, hypercholestrolaemia leads to endothelial damage, injury increases permeability and allows platelet adhesion, monocytes penetrate endothelium , smooth muscle cells proliferate and migrate.
the monoclonal hypothesis- each plaque is monoclonal, might represent abnormal growth control, each plaque might be a benign tumour , viral cause ?

17
Q

what processes are involved in atherosclerosis

A

thrombosis
lipid accumulation
production of intercellular matrix
interactions between cell types

18
Q

what cells are involved in atherosclerosis

A
endothelial cells 
platelets 
smooth muscles 
macrophages 
lymphocytes 
neutrophils
19
Q

how are endothelial cells involved in atherosclerosis

A

key role in Haemostasis
altered permeability to lipoproteins
production of collagen
stimulation of proliferation and migration of smooth muscle cells

20
Q

how are platelets involved in atherosclerosis

A

key role in Haemostasis

stimulate proliferation and migration of smooth muscle cells (PDGF)

21
Q

how are smooth muscle cells involved in atherosclerosis

A

take up LDL and other lipid to become foam cells

synthesise collagen and proteoglycans

22
Q

how are macrophages involved in atherosclerosis

A

oxidise LDL (they are more damaging in oxidising form)
take up lipids to become foam cells
secrete proteases which modify matrix
stimulate proliferation and migration of smooth muscle cells

23
Q

how are lymphocytes involved in atherosclerosis

A

TNF (tumour necrosi factor) may affect lipoprotein metabolism
stimulate proliferation and migration of smooth muscle cells

24
Q

how are neutrophils involved in atherosclerosis

A

secrete proteases leading to continued local damage and inflammation

25
Q

what causes endothelial injury

A

raised LDL
toxins - cigarette smoke
hypertension
haemodynamic stress

26
Q

what does endothelial injury cause

A

platelet adhesion , PDGF release, SMC proliferation and migration
insulation of lipid , LDL oxidation, uptake of lipid by SMC and macrophages
migration of monocytes into intima

27
Q

foam cells produce cytokines what does this cause

A

further SMC stimulation

recruitment of other inflammatory cells

28
Q

how can atherosclerosis be prevented

A
no smoking 
reduced fat intake 
treat hypertension
decrease alcohol intake 
regular exercise
29
Q

atherosclerosis intervention

A
stop smoking 
modify diet 
treat hypertension 
treat diabetes 
lipid lowering drugs