CVS Flashcards

1
Q

What is atherosclerosis?

A

A chronic inflammatory disease influenced by many factors involving a vast array of inflammatory cells and cytokines. Disease of the intima

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2
Q

List 5 risk factors of atherosclerosis

A
Age
Tobacco Smoking
High Serum Cholesterol
Obesity
Diabetes
Hypertension
Family History
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3
Q

What is an atherosclerotic plaque

A

A plaque is a complex lesion of lipid, necrotic core, connective tissue, fibrous cap found focally distributed along the length of an artery

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4
Q

Where are atherosclerotic plaques found

A

In peripheral and coronary arteries

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5
Q

key cells involved in atherosclerotic plaque

A

endothelial cells, smooth muscle cells, macrophages, fibroblasts

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6
Q

two main outcomes of plaque?

A

Vessel occlusion

Rupture and embolism

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7
Q

What id the response to injury hypothesis?

A

Atherosclerosis is Initiated by an injury to the endothelial cells which leads to endothelial dysfunction.
Signals sent to circulating leukocytes which then accumulate and migrate into the vessel wall.
Inflammation ensues

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8
Q

Whi is LDL important in atherosclerosi

A

It can pass in and out the arterial wal and can undergo oxidation and glycation. This damages the intima

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9
Q

5 stages of atherosclerosis progression

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaques or advanced lesion
  4. Plaque rupture
  5. Plaque erosion
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10
Q

What is characteristic of fatty streaks

A

Consist of aggregations of lipid–laden macrophages and T lymphocytes within the intimal layer of the vessel wall

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11
Q

What is characteristic of intermediate lesions

A
Composed of layers of :
	Lipid laden macrophages (foam cells) 
	Vascular smooth muscle cells 
  	T lymphocytes
	Adhesion and aggregation of platelets to 	vessel wall
	Isolated pools of extracellular lipid
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12
Q

What is characteristic of an intermeduate lesion

A

Impedes blood flow
Prone to rupture
Covered by dense fibrous cap made of ECM proteins including collagen (strength) and elastin (flexibility) laid down by SMC that overlies lipid core and necrotic debris
May be calcified
Contains: smooth muscle cells, macrophages and foam cells and T lymphocytes

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13
Q

What is plaque rupture

A

Plaques constantly growing and receding.
Fibrous cap has to be resorbed and redeposited in order to be maintained.
If balance shifted eg in favour of inflammatory conditions (increased enzyme activity), the cap becomes weak and the plaque ruptures.
Basement membrane, collagen, and necrotic tissue exposure as well as haemorrhage of vessels within the plaque
Thrombus (clot) formation and vessel occlusion

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14
Q

What is plaque erosion?

A

Second most prevalent cause of coronary thrombosis
Lesions tend to be small ‘early lesions’
Fibrous cap does not disrupt
Luminal surface underneath the clot may not have endothelium present but is smooth muscle cell rich.
There may be a prominent lipid core

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15
Q

How can coronary artery disease be treated?

A

PCI - ppercutaneous coronary intervention (sent)

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16
Q

Pharmacological interventions imp in CAD. Why?

A
  1. aspirin, inhibits COX therefore prevens platelet aggregation
  2. Clopidogrel/Ticagrelor – inhibitors of the P2Y12 ADP receptor on platelets
  3. Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis