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Path Processes > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

Define Atherosclerosis

A

The thickening and hardening of the arteries due to conditions that cause a loss of elasticity

plaques begin in the intima of arterial walls

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2
Q

What is Arteriolosclerosis?

A

The hardening of ARTERIOLES

  • affects arterioles throughout the body but mainly those in the kidney
  • usually occurs secondary to hypertension or in diabetes mellitus
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3
Q

What is Monkeberg’s disease?

A

Calcification of the media of large arteries (uncommon disease)

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4
Q

What is an atheroma?

A

The necrotic core of an atherosclerotic plaque

Consists of:

  • dead cells
  • debris
  • cholesterol crystals
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5
Q

What are the 3 basic components of an atherosclerotic plaques?

A

1) Cells - macrophages, leucocytes, smooth muscle cells
2) Intra- an extracellular lipid
3) Extracellular matrix- collagen, elastin, proteoglycans

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6
Q

There are 5 steps in atherosclerotic plaque formation- briefly describe them

A

1) Chronic endothelial insult
2) accumulation of lipid droplets (LDLs) in the endothelium accumulate in the intima. Lipids become oxidised and englufed by macrophages forming foam cells
3) Foam cells cause endothelium to bulge, smooth muscles migrate to the lesion and proliferate forming a FATTY STREAK
4) Plaque continues to grow. smooth muscle cells over the plaque but underneath epithelium form a roof, reinforced by collagen, elastin and matrix proteins to form a FIBROUS CAP.
5) Cells in the plaque undergo necrosis and release cholesterol. Small blood vessels grow into the plaque and plaque may undergo calcification

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7
Q

Describe some of the chronic insults that can damage endothelia

A
  • hyperlipidaemia
  • hypertension
  • smoking
  • haemodynamic factors
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8
Q

Describe the macroscopic features seen in atherosclerosis

A
  • Fatty Streak earliest lesion seen
  • Fatty streaks develop into simple plaques which start to impinge on the lumen
  • Simple plaques develop into complicated plaques which may rupture causing haemorrhage
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9
Q

What are fatty streaks made of?

A

Lipid deposits in intima, some smooth muscle cells and some foam cells - don’t disrupt blood flow

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10
Q

Give 5 common sites of atherosclerosis

A
  • Aorta (especially abdominal)
  • Coronary arteries
  • Carotid arteries
  • Cerebral arteries
  • Leg arteries
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11
Q

Give 8 complications of atherosclerotic plaques

A

1) Ulceration
2) Thrombosis
3) Spasm
4) Embolism
5) Calcification
6) Haemorrhage
7) Aneurysm
8) Rupture of atherosclerotic artery

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12
Q

How do ulcers form from atherosclerotic plaques?

A

When the fibrous cap erodes, exposing the core to the blood

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13
Q

Which type of plaques typically undergo thrombosis?

A

Often ulcerated plaques, but occasionally can occur with intact epithelium

The the thrombus can occlude the lumen

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14
Q

Why can spasms occur at the site of atherosclerosis?

A

Thrombi release vasoconstrictors which reduce 02 supply

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15
Q

What is an aneurysm?

A

A local dilatation of an artery due to weakening of the arterial wall

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16
Q

What are varices?

A

Dilations in veins

17
Q

What is a saccular aneurysm?

A

Aneurysm that is shaped like a sac, commonly seen in:

abdominal aorta - generally lined or filled by thrombus

18
Q

What is a fusiform aneurysm?

A

Aneurysm shaped like a spindle

19
Q

What are the 2 main complications of aortic aneurysms?

A

1) May rupture
2) Thrombus or plaque material may embolise

20
Q

What complications can atherosclerosis lead to in the heart?

A
  • MI
  • chronic ischemic heart disease
  • arrhythmia
  • cardiac failure
  • sudden cardiac death
21
Q

What complications can atherosclerosis lead to in the brain?

A
  • TIA
  • cerebral infarction
  • multi-infarct dementia
22
Q

What complications can atherosclerosis lead to in the kidney?

A

HYPERTENSION

(reduced perfusion affects RAAS)= more water →renal failure

23
Q

What complications can atherosclerosis lead to in the legs?

A
  • peripheral vascular disease
  • gangrene
24
Q

What complications can atherosclerosis lead to in the bowel?

A
  • ischemic colitis
  • malabsorption
  • bowel infarction
25
Q

There are 3 models that have been proposed to why atherogenesis occurs, describe them

A

1) Response to injury hypothesis- chronic inflammatory response from injury to endothelium
2) Encrustation hypothesis- plaques form from repeated thrombi overlying thrombi
3) Monoclonal hypothesis-plaques may be benign neoplastic growths induced by cholesterol or a virus (not well supported)

26
Q

What are some of the symptoms of peripheral vascular disease?

A
  • intermittent claudication
  • Leriche syndrome (iliac vessels occluded gives pain in buttock)
  • ischaemic pain at rest
  • gangrene - 02 supply not sufficient to maintain tissue viability
27
Q

Give some non-modifiable risk factors for atherosclerosis

A
  • Age
  • Gender (Men>Women)
  • Genetic predisposition
28
Q

Give some modifiable risk factors for atherosclerosis

A
  • Hyperlipidaemia (increases LDL cholesterol)
  • Hypertension- increased BP damages vessels
  • Cigarette smoking
  • Geography (lower incidence in South America, Africa and Asia)
  • Obesity
  • Infection (with chlamydia pneumoniae or CMV)
  • Alcohol consumption (>5 units p/day)
  • lack of excercise
  • some oral contraceptives
29
Q

What genetic variations can predispose someone to atherosclerosis

A
  • Variations in LDL receptors are associated with increased LDL levels as less is taken up into the liver
  • Genetic variation in Apo E
30
Q

What 2 things can be used as intervention strategies for atherosclerosis?

A
  • Lipid lowering drugs (statins, aspirin)
  • Surgery (thrombolysis, angioplasty, stents, CABG)
31
Q

What 3 signs are associated with familial hyperlipidaemia?

A
  • Corneal Arcus
  • Xanthelasma
  • Tendon Xanthomas

Path Processes (12 decks)

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