Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathological Processes * > S6 Atherosclerosis > Flashcards

S6 Atherosclerosis Flashcards

1
Q

What is an 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

What is atherosclerosis?

A

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

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

What is arteriosclerosis?

A

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

Usually occurs in smaller vessels

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

What are the 3 macroscopic features of atherosclerosis?

A
  • fatty streak
  • simple plaque
  • complicated plaque
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the fatty streak? How does it appear?

A

Lipid deposits in the intima

Yellow and slightly raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the simple plaque - how does it appear?

A

It’s raised, yellow/white and irregular

Widely distributed and they enlarge and coalesce (join)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the complicated plaque?

A

Occurs when something else has happened - thrombosis, haemorrhage into the plaque, calcification or aneurysm formation

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

What are 5 common sites of atherosclerosis?

A
  • aorta (abdominal)
  • coronary arteries
  • carotid arteries
  • cerebral arteries
  • leg arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the normal structure of an artery (from lumen outwards)

A
  • endothelium
  • sub-endothelial connective tissue
  • internal elastic lamina
  • muscular media
  • external elastic lamina
  • adventitia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the early stage microscopic features of atherosclerosis?

A
  • proliferation of smooth muscle cells
  • accumulation of foam cells
  • extracellular lipid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the later stage microscopic features of atherosclerosis?

A
  • fibrosis
  • necrosis
  • cholesterol clefts
  • inflammatory cells
  • disruption of internal elastic lamina
  • ingrowth of blood vessels
  • plaque fissuring/splits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the clinical effects of atherosclerosis on the heart?

A

Ischaemic heart disease

  • sudden death
  • MI
  • angina pectoris
  • arrythmias
  • cardiac failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the clinical effects of atherosclerosis on the brain?

A

Cerebral ischaemia

  • transient ischaemic attack
  • cerebral infarction (stroke)
  • multi-infarct dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical effects of atherosclerosis on the lower GI tract?

A

Mesenteric ischaemia

  • ischaemic colitis
  • malabsorption
  • intestinal infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the clinical effects of atherosclerosis on the peripheral vasculature?

A

Peripheral vascular disease

  • intermittent claudication
  • Leriche syndrome (pain in bum on exercise)
  • ischaemic rest pain
  • gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the risk factors for atherosclerosis?

A
  • age (more common the older you are)
  • gender (more common in males)
  • hyperlipidaemia
  • smoking
  • hypertension
  • diabetes mellitus
  • alcohol
  • infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why are women less likely to develop atherosclerosis?

A

There’s a presumed hormonal basis that means women pre-menopause are protected more against atherosclerosis

18
Q

Why is hyperlipidaemia a risk factor for atherosclerosis?

A

Hyperlipidaemia results in high plasma cholesterol e.g. LDL associated with atherosclerosis

19
Q

How are lipids (cholesterol and TAGs) in the blood carried?

A

Carried on lipoproteins which have a hydrophobic lipid core and a hydrophilic outer layer of phospholipid and apolipoproteins (A-E)

20
Q

What is associated with changes in LDL levels? How is this linked to atherosclerosis?

A

Genetic variations in Apo E (6 phenotypes - polymorphisms of the gene can be used as risk markers for atherosclerosis)

21
Q

What is familial hyperlipidaemia? What are the physical signs of it?

A

Genetically determined abnormalities of lipoproteins that lead to early development of atherosclerosis

  • corneal arcus
  • tendon xanthomas
  • xanthelasma
22
Q

What is diabetes mellitus a risk factor for?

A
  • atherosclerosis
  • ischaemic heart disease - doubles the risk
  • cerebrovascular disease
  • peripheral disease
23
Q

What are 3 examples of infections that are risk factors for atherosclerosis?

A
  • Chlamydia pneumoniae
  • Helicobacter pylori
  • Cytomegalovirus
24
Q

What are 5 other risk factors for atherosclerosis?

A
  • lack of exercise
  • obesity
  • soft water
  • oral contraceptives
25
Q

Atherosclerosis has a genetic predisposition, what is this possibly due to?

A
  • variations in apolipoprotein metabolism

* variations in apolipoprotein receptors

26
Q

What are the 4 theories for the pathogenesis of atherosclerosis?

A
  • thrombogenic theory
  • insudation theory
  • monoclonal hypothesis
  • reaction to injury hypothesis
27
Q

What is the thrombogenic theory for atherosclerosis?/

A

That plaques are formed by repeated thrombi, the lipid is derived from the thrombi and there’s an overlying fibrous cap

28
Q

What is the insudation theory for atherosclerosis?

A

Occurs due to endothelial injury which leads to inflammation and increased permeability to lipid from the plasma

29
Q

What is the reaction to injury hypothesis for atherosclerosis?

A
  • plaques form in response to endothelial injury e.g. hypercholesterolaemia leads to endothelial damage (+ oxidised LDL may damage endothelium)
  • the injury increases permeability and allows platelet adhesion
  • monocytes penetrate the endothelium
  • smooth muscle cells proliferate and migrate
  • the injury can be subtle and undetectable visually
30
Q

What is the monoclonal hypothesis for atherosclerosis?

A
  • smooth muscle proliferation
  • each plaque is monoclonal
  • maybe represents abnormal growth control? E.g. could each plaque be a benign tumour?
  • could atherosclerosis have a viral aetiology?
31
Q

What is the process involved in atherosclerosis?

A
  • thrombosis
  • lipid accumulation
  • production of intercellular matrix
  • interactions between cell types
32
Q

What are the cells involved in atherosclerosis?

A
  • endothelial cells
  • platelets
  • smooth muscle cells
  • macrophages
  • lymphocytes
  • neutrophils
33
Q

How are endothelial cells involved in atherosclerosis?

A
  • role in haemostasis
  • result in altered permeability to lipoproteins
  • produce collagen
  • stimulate proliferation and migration of smooth muscle cells
34
Q

How are platelets involved in atherosclerosis?

A
  • role in haemostasis

* stimulate proliferation and migration of smooth muscle cells via platelet derived growth factor

35
Q

How are smooth muscle cells involved in atherosclerosis?

A
  • take up LDL and other lipids to become foam cells

* synthesise collagen and proteoglycans

36
Q

How are macrophages involved in atherosclerosis?

A
  • oxidise LDLs
  • take up lipids to become foam cells
  • secrete proteases which modify the matrix
  • stimulate proliferation and migration of smooth muscle cells
37
Q

How are neutrophils involved in atherosclerosis?

A
  • secrete proteases leading to continues local damage and inflammation
38
Q

What is the current hypothesis for atherosclerosis?

A
  • endothelial injury is due to raised LDL, toxins, hypertension and haemodynamic stress
  • the injury causes platelet adhesion, PDGF release, smooth muscle cell proliferation and macrophages and migration of monocytes into intima
  • stimulated smooth muscle cells produce matrix material
  • foam cells secrete cytokines causing further smooth muscle cell stimulation and recruitment of other inflammatory cells
39
Q

How can you prevent atherosclerosis?

A
  • no smoking
  • reduce fat intake
  • treat hypertension
  • not too much alcohol
  • regular exercise/weight control
40
Q

What are interventions for atherosclerosis?

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

Pathological Processes * (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions