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Pathological Processes > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

What is the definition of “Atherosclerosis”?

A

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

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2
Q

What are the clinical effects of atherosclerosis?

A

Ischaemic heart disease and stroke

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3
Q

What is the fundamental lesion in atherosclerosis?

A

The plaques - initially discrete but gradually enlarge and coalesce

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4
Q

What things might the plaques be complicated by?

A

Calcification, thrombosis, haemorrhage and aneurysm formation

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5
Q

Name some risk factors for atherosclerosis

A

Age - increases with age
Gender - women protected before menopause
Hyperlipidemia - LDL, sign: tendon xanthomas, xanthelasma
Genetics - apoE
Cigarette smoking- powerful risk factor for IHD
Hypertension
Diabetes mellitus - doubles IHD risk
Alcohol
Infection

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6
Q

Atherosclerosis of the coronary arteries may result in what?

Coronary thrombosis leads to what?

A

Angina or heart failure

MI

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7
Q

Atherosclerosis of the carotid arteries may result in what?

A

Formation of thrombus over the plaque followed by thromboembolism into the carotid arteries = stroke

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8
Q

What is atheroma?

A

The accumulation/deposition of intracellular and extracellular lipid in the intima and media or large and medium sized arteries

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9
Q

What is the definition of arteriosclerosis?

A

The thickening of the walls of arteries and arterioles usually as a result of hypertension or DM

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10
Q

What are the 3 fundamental macroscopic features of atherosclerosis?

A
  • Fatty streak: lipid deposits in the intima
  • Simple plaque: raised, yellow/white, irregular outline, enlarge and coalesce
  • Complicated plaque: thrombosis, haemorrhage into plaque, calcification, aneurysm formation
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11
Q

What are the early and later microscopic features of atherosclerosis?

A

Early: proliferation of smooth muscle, foam cells, extracellular lipid
Later: fibrosis, necrosis, cholesterol clefts +/- inflammatory cells, distruption of internal elastic lamina, damage to media, ingrowth of blood vessels, plaque fissuring

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12
Q

Describe the normal arterial structure

A 
Endothelium
Sub-endothelial connective tissue 
Internal elastic lamina 
Muscular media 
External elastic lamia 
Adventitia
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13
Q

What are the clinical consequences of atherosclerosis?

A

Ischaemic heart disease: MI, sudden death, angina, arrythmias, cardiac function
Cerebral ischaemia: TIA, Stoke, multi-infarct dementia
Mesenteric ischaemia: Ischaemic colitis, malabsotption, intestinal infarction
Peripheral vascular disease: intermittent claudication, Leriche syndrome, ischaemic rest pain, gangrene

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14
Q

Outline the 4 theories of pathogenesis

A
  1. Thrombogenic: released thrombi cause plaques as they release lipid
  2. Insudation: endothelial injury, inflammation, increased permeability to lipid from the plasma
  3. Reaction to Injury: accepts some of 1 and 2, endothelial injury, hypercholesterolaemia leading to endothelial damage, increased permeability, oxidised LDL=damage
  4. The monoclonal hypothesis: smooth muscle proliferation, each plaque is monoclonal, possible role of infection
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15
Q

What cells are involved in atherosclerosis?

A

Endothelial cells- haemostasis, proliferation and migration of smooth muscle cells
Platelets- haemostasis, proliferation and migration of smooth muscle cells (PDGF)
Smooth muscle cells- take up LDL and become foam cells, synthesise collagen and proteoglycans
Macrophages- oxidise LDL, proliferation and migration of smooth muscle cells
Lymphocytes- TNF may affect lipoprotein metabolism, proliferation and migration of smooth muscle cells
Neutrophils- secrete proteases, local damage and inflammation

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16
Q

What is the unifying hypothesis of atherosclerosis?

A

Endothelial injury due to LDL, ‘toxins’, hypertension, haemodynamic stress which casues platelet adhesion, PDGF release, SMC proliferation and migration, LDL oxidation, uptake of lipid by SMC, migration of monocytes into intima
Stimulated SMC produce matrix material, foam cells secrete cytokines causing further stimulation and recruitment of inflammatory cells

17
Q

Give some ways that atherosclerosis can be prevented

A 
No smoking 
Reduce fat intake 
Treat hypertension
Not too much alcohol 
Regular exercise/weight control

Pathological Processes (9 decks)

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