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Semester 2 Pathological Processes > L11: Athersclerosis > Flashcards

L11: Athersclerosis Flashcards

(46 cards)

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1
Q

Define atheroma?

A

Necrotic core

Consists of dead cells, debris and cholesterol crystals

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2
Q

Define atherosclerosis?

A

Disease of large and medium sized arteries
Begins in the intima
Plaques accumulate in the artery wall filled with atheromas
Often calcify—> harden

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3
Q

Define arteriolosclerosis?

A

Hardening of arterioles
Thickening of the walls of the arteries and arterioles
Result of hypertension or diabetes mellitus

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4
Q

Define arteriosclerosis?

A

Hardening of the arteries
Thickened wall
Reduced elasticity
Includes: Atherosclerosis, arteriolosclerosis, Monkeberg’s disease (uncommon disease, calcification of the media of large arteries)

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5
Q

What are the basic components of an atherosclerotic plaque?

A

Cells—> macrophages (foam cells), leukocytes (WBCs) and smooth muscle cells

Intra and extracellular lipid

Extracellular matrix—> collagen, elastin and proteoglycans

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6
Q

What are the macroscopic features of atherosclerosis?

A

Fatty streak
Simple plaque
Complicated plaque

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7
Q

What are the macroscopic features of a fatty streak?

A 
Flat (slightly raised)- no disturbance to blood flow 
Lipid deposit in intima
Foam cells 
Smooth muscle cells 
Extracellular lipid
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8
Q

What are the macroscopic features of a simple plaque?

A

Fatty streak grows
White/yellow
Impinge on lumen of artery
Widely distributed

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9
Q

What are the macroscopic features of a complicated plaque?

A
  • Ulceration—> fibrous cap eroded
  • Thrombosis—> exposed plaque thrombogenic, non-exposed can occur, may occlude vessel lumen
  • Spasm—> caused by vasoconstrictors released by thrombosis
  • Embolism—> exposed atheroma or thrombus
  • Calcification—> in and around, makes it hard
  • Haemorrhage—> new vessel into plaque, expands plaque causing vessel occlusion or pressure can result in haemorrhage of plaque
  • Aneurysm formation—> elastic tissue destroyed by plaque, wall weaker, dilation of wall
  • Rupture of atherosclerotic artery—> bleeding, result of weakened media seen in cerebral arteries when patient has hypertension in addition to atherosclerosis
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10
Q

What are the common sites for atherosclerosis formation?

A 
Elastic arteries
- Aorta (abdominal)
- Carotid
- Iliac 
Large and medium sized muscular arteries
- Coronary 
- Popliteal
  • Cerebral
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11
Q

What is the normal arterial structure?

A
  • Endothelium (Tunica Intima)
  • Sub-endothelial connective tissue
  • Internal elastic membrane/lamina
  • Smooth muscle cells and elastic fibres (Tunica Media)
  • External elastic lamina
  • Connective tissue (Tunica Adventitia)
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12
Q

What are the microscopic changes that appear in the early stags of atherosclerosis formation?

A

Proliferation of smooth muscle cells
Accumulation of foam cells (macrophages containing lipid)
Extracellular lipid

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13
Q

What are the microscopic changes that appear in the late stags of atherosclerosis formation?

A

Fibrosis
Necrosis
Cholesterol clefts—> cholesterol crystals
+/- inflammatory cells (different stages of evolution)
Disruption of internal elastic lamina
Damage extends into TM
In growth of BV
Plaque fissuring—> rupture of cap—> bleeding into plaque or thrombosis

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14
Q

What are the clinical effects of atherosclerosis?

A

Symptoms usually in heart, brain, kidneys, legs or bowel

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15
Q

What are the clinical effects of atherosclerosis on the heart?

A

Heart—> Ischaemic heart disease, MI, angina pectoris, arrhythmias, cardiac failure,sudden death

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16
Q

What are the clinical effects of atherosclerosis on the brain?

A

Brain—> cerebral ischaemia, transient ischaemic attack, cerebral infarction (stroke) and mutli-infarct dementia

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17
Q

What are the clinical effects of atherosclerosis on the bowel?

A

Bowel—> mesenteric ischeamia, ischaemic colitis, malabsorption, intestinal infarction

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18
Q

What are the clinical effects of atherosclerosis on the kidneys?

A

Kidneys—> hypertension, renal failure

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19
Q

What are the clinical effects of atherosclerosis on the legs?

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A

Legs—> peripheral vascular disease, gangrene

20
Q

What are the risk factors for athersclerosis?

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A

Non modifiable

  • Age
  • Gender –> more common in males, incidence increase in famales after menopause
  • Genetic predisposition

Modifiable

  • Hyperlipidaemia
  • Cigarette smoking
  • Hypertension
  • Obesity
  • Georgraphy
  • Diabetes Mellitus
  • Alcohol
  • Infection
21
Q

How does hyperlipidaemia increase your risk of developing artheresclerosis?

Study These Flashcards
A

High plasma cholesterol
LDL most significant
LDL delivers cholesterol to peripheral tissue

22
Q

How are lipids metabolised?

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A

Lipids carried in the blood on lipoproteins
Lipoproteins carry cholesterol and triglycerides
(Hydrophobic lipid core)
Hydrophilic outer layer of phospholipid and apoliopoprotein (A-E)

23
Q

What are the different types of cholesterol carriers?

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A

Chylomicrons–> lipid from intestine to liver
VLDL–> cholesterol and TG from liver–> TG removed leaving LDL
LDL–> rich in cholesterol, carry cholesterol to non-liver cells
HDL–> carry cholesterol from periphery back to liver

24
Q

How can genetics affect hyperlipidaemia?

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A

Genetic variation in ApoE associated with changes in LDL levels
At least 6 Apo E phenotypes

25
What is familial hyperlipidaemia? What are the associated physical signs?
Genetic predisposition Atherosclerosis at very young age Signs --> Corneal Arcus--> ring around the eye --> Tendon xanthoma--> nodules found in tendon on hand --> Xanthelasma--> deposit of cholesterol usually around the eye
26
How does cigarette smoking increase risk of atherosclerosis formation?
Risk factor for ischaemic heart disease Mode of action uncertain--> coagulation system, reduced PGI2, increased platelet aggregation, increase inflammation, predisposition to oxidation of lipids
27
How does hypertension increase risk of atherosclerosis formation?
Mechanism unclear | Increase pressure damage BV walls--> predisposes plaque formation
28
How does diabetes mellitus increase risk of atherosclerosis formation?
Double ischaemic heart disease risk High risk of cerebral vascular and peripheral vascular disease Related to hyperlipidaemia and hypertension
29
How does alcohol consumption increase risk of atherosclerosis formation?
>5 units per day increased risk | Small amount of alcohol throught to be protective
30
What are the theories around the pathogenesis of atherosclerosis?
1. Thrombogenic theory 2. Insudation theory 3. Encrustation theory 4. Reaction to injury hypothesis 5. The monoclonal hypothesis
31
What is the thrombogenic theory?
Plaques formed by repeated thrombosis Lipid derived from thrombi Overlying firbous cap on plaque
32
What is the insudation theory?
Endothelial injury Inflammation Increased permeability to lipid from plasma
33
What is the encrustation theory?
Model plaques are formed by repeated thrombi overlying thrombi Lipid core is derived from thrombi
34
What is the reaction to injury hypothesis?
Chronic inflammatory response of the arterial wall Hypercholesterolaemia --> endothelial damage Increases permability--> platelet adhesion Monocytes penetrate endothelium SMC proliferate and migrate Endothelial injury subtle and undetected visually LDL, especially oxidised may damage endothelium
35
What is the monoclonal hypothesis?
Crucial role for SMC proliferation Thought plaques were monoclonal Therefore atherosclerosis is abnormal growth control Each plaque benign growth induced by cholesterol or virus
36
What processes are involved/ appear to be involved?
Thrombosis Lipid accumulation Production of intracellular matrix Interaction between cell types
37
What are the cells involved?
``` Endothelial cells Platelets SMC Macrophages Lymphocytes Neutrophils ```
38
What role do the endothelial cells play in atherosclerosis formation?
Haemostasis Altered permeability to lipoproteins Production of collagen Stimulation of proliferation and migration of SMC
39
What role do the platelets play in atherosclerosis?
Haemostasis | Stimulate proliferation and migration of SMC through platelet derived growth factor
40
What role do the SMC play in atherosclerosis?
Take up LDL--> Foam cells | Synthesis of collagen and proteoglycans
41
What do the macrophages do in atherosclerosis?
Release free radical--> oxidise LDL Take up lipids to become foam cells Secrete proteases which modify the matrix Stimulate proliferation and migration of SMC
42
What role do lymphocytes play in atherosclerosis?
Tumour necorsis factor may affect lipid metabolism | Stimulate proliferation and migration of SMC
43
What do neutrophils do in atherosclerosis?
Secrete proteases leading to continued local damage and infection
44
What is the unifying hypothesis of how atherosclerosis develops?
1. Chronic endothelial insult--> hyperlipidaemia, hypertension, smoking, haemodynamic stress--> endothelial dysfunction 2. Platelet adhesion, PDGF release, SMC proliferation and migration 3. LDLs (lipid droplets) and monocytes cross endothelium--> accumulated in intima 4. LDLs oxidised by free radical released from macrophages 5. Macrophages ingest the LDLs --> foam cells 6. Crowded foam cells cause the endothelium to bulge 7. SMC migrate into the lesion from media and proliferate--> fatty streak 8. SMC take up LDL--> foam cells 9. SMC secrete collage, elastin and other ECM--> fibrous cap 10. Cells in centre die--> necrosis--> dead cells release cholesterol --> cholesterol crystals 11. Small BV grow into the adventitia --> plaque undergoes calcification
45
How can atherosclerosis be prevented?
``` Decrease total and LDL cholesterol Stop smoking Control hypertension Control weight and regular exercise Sensible alcohol intake Treat diabetes mellitus Anti-oxidants --> Vit E maybe protective ```
46
What intervention strategies are there to treat atheroscleoris?
Lipid lowering drugs--> statins, aspirin and prophylaxis Stop smoking Modify diet Treat hypertension Treat diabetes Thrombolysis, angioplasty, stents and coronary artery bypass grafts

Semester 2 Pathological Processes (16 decks)

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