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Semester 2 Pathological Processes > L11: Athersclerosis > Flashcards

L11: Athersclerosis Flashcards

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?

A

Legs—> peripheral vascular disease, gangrene

20
Q

What are the risk factors for athersclerosis?

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?

A

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

22
Q

How are lipids metabolised?

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?

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?

A

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

25
Q

What is familial hyperlipidaemia? What are the associated physical signs?

A

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
Q

How does cigarette smoking increase risk of atherosclerosis formation?

A

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
Q

How does hypertension increase risk of atherosclerosis formation?

A

Mechanism unclear

Increase pressure damage BV walls–> predisposes plaque formation

28
Q

How does diabetes mellitus increase risk of atherosclerosis formation?

A

Double ischaemic heart disease risk
High risk of cerebral vascular and peripheral vascular disease
Related to hyperlipidaemia and hypertension

29
Q

How does alcohol consumption increase risk of atherosclerosis formation?

A

> 5 units per day increased risk

Small amount of alcohol throught to be protective

30
Q

What are the theories around the pathogenesis of atherosclerosis?

A
  1. Thrombogenic theory
  2. Insudation theory
  3. Encrustation theory
  4. Reaction to injury hypothesis
  5. The monoclonal hypothesis
31
Q

What is the thrombogenic theory?

A

Plaques formed by repeated thrombosis
Lipid derived from thrombi
Overlying firbous cap on plaque

32
Q

What is the insudation theory?

A

Endothelial injury
Inflammation
Increased permeability to lipid from plasma

33
Q

What is the encrustation theory?

A

Model plaques are formed by repeated thrombi overlying thrombi
Lipid core is derived from thrombi

34
Q

What is the reaction to injury hypothesis?

A

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
Q

What is the monoclonal hypothesis?

A

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
Q

What processes are involved/ appear to be involved?

A

Thrombosis
Lipid accumulation
Production of intracellular matrix
Interaction between cell types

37
Q

What are the cells involved?

A 
Endothelial cells 
Platelets
SMC
Macrophages 
Lymphocytes
Neutrophils
38
Q

What role do the endothelial cells play in atherosclerosis formation?

A

Haemostasis
Altered permeability to lipoproteins
Production of collagen
Stimulation of proliferation and migration of SMC

39
Q

What role do the platelets play in atherosclerosis?

A

Haemostasis

Stimulate proliferation and migration of SMC through platelet derived growth factor

40
Q

What role do the SMC play in atherosclerosis?

A

Take up LDL–> Foam cells

Synthesis of collagen and proteoglycans

41
Q

What do the macrophages do in atherosclerosis?

A

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
Q

What role do lymphocytes play in atherosclerosis?

A

Tumour necorsis factor may affect lipid metabolism

Stimulate proliferation and migration of SMC

43
Q

What do neutrophils do in atherosclerosis?

A

Secrete proteases leading to continued local damage and infection

44
Q

What is the unifying hypothesis of how atherosclerosis develops?

A
  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
Q

How can atherosclerosis be prevented?

A 
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
Q

What intervention strategies are there to treat atheroscleoris?

A

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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