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Principles > Pathology: Atheroma and Thrombosis > Flashcards

Pathology: Atheroma and Thrombosis Flashcards

1
Q

What are the risk factors for atheroma?

A 
Smoking 
Diabetes
Hypertension
Hyperlipidemia 
Hypercholesterolaemia
Age
Gender
Genetics
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2
Q

Why does diabetes as an independent risk factor increase your risk of endothilial injury?

A

1) Increases cholesterol levels
2) Increased sugar levels => Advanced Glycation End Products
3) Abnormal cross linking in the vessel wall making it stiff (loss of elasticity increases the impact of injury
4) Traps LDL cholesterol

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3
Q

Why does being male as an independent risk factor increase your risk of atherosclerosis?

A

Oestrogen has a protective effect- therefore there is no difference after the menopause

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4
Q

What is the pathogenisis of atheroma?

A

1) Endothelial injury
2) Accumulation of lipids and macrophages
3) Migration of smooth muscle cells
4) Progression and increase in size. Fatty streak, fatty plaque, complicated plaque

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5
Q

Pathogenesis of atheroma: Explains what follows endothilial injury?

A

1) Endothilial dysfunction. Increased permeability
2) Increase WBC adhesion due to increased expression of VCAM/ICAM. Monocytes adhere and trans-endothilially migrate to become macrophages.

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6
Q

Pathogenesis of atheroma: Explains what causes accumulation of lipid and macrophages?

A

1) Macrophages engulf cholesterol that cannot be easily digested
2) While the volume of cholesterol is low it remains in the cell but when it increases LDL is deposited => fatty streak
3) HDL cholesterol shuttles back to the liver

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7
Q

Pathogenesis of atheroma: Explains what causes migration of smooth muscle cells?

A

1) Smooth muscle migrates from the tunica media to the tunica intima => expansion of intima
2) In response to cytokines, it creates an extracellular matrix of collagen
3) Fatty streak becomes a fibrofatty plaque

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8
Q

Pathogenesis of atheroma: What does progression and more cholesterol, macrophages, smooth muscle and collogen cause?

A

A pool of extracellular collagen at the centre of the plaque

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9
Q

What is a complicated plaque?

A

Atheroma with overlying thrombosis

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10
Q

How does the flow rate through a vessel vary with the radius of the vessel?

A

Radius to the power 4. A small change in radius will dramatically reduce flow.

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11
Q

When is critical arterial disease more common?

A

When its the only artery supplying an organ (no collateral circulation)
The artery diamer is small
Overall blood flow is reduced

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12
Q

What is arterial stenosis?

A

Narrowing of the arterial lumen

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13
Q

What are the consequences of arerial ischemia?

A

Reduced elasticity, reduced flow in systole and tissue ischemia

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14
Q

What are the clinical effects of cardiac ischemia?

A

Reduced exercise tolerance
Angina (stable -> unstable)
MI and cardiac failure

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15
Q

What are the clincial effects of cardiac fibrosis?

A

Loss of cardiac myocytes and replacement by fibrous tissue

Loss of contractility and elasticity and reduced filling

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16
Q

What is an aneurysm?

A

Abnormal and persistent dilation of an artery due to a weakness in its wall.

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17
Q

What are the causes of aneurysm?

A

Atheroma, congenital, dissection, mycotic, traumatic

18
Q

Where is the most common site for aneurysm formation?

A

Abdominal aorta

19
Q

What is arterial dissection?

A

Splitting within the media by flowing blood creating a false lumen within the media but the media doesn’t rupture through to the outside

20
Q

What are the symptoms of aortic dissection?

A

Sudden death/collapse

Very acute excrutating pain

21
Q

What conditions predispose you to arterial dissection?

A

Hypertension, trauma, pregnancy, marfans syndrome, coarctation

22
Q

What is coarctation?

A

Congenital narrowing of the aorta?

23
Q

What is a clot?

A

Extravascular coagulation- bruising

24
Q

What is a thrombus?

A

Intravascular coagulation

25
Q

What is exanguination?

A

blood loss

26
Q

How do you measure the intrinsic pathway of the coagulation cascade?

A

PT- prothrombin time

27
Q

How do you measure the extrinsic pathway of the coagulation cascade?

A

aPTT- activated partial prothrombin time

28
Q

What is the precursor to thrombin?

A

Prothrombin

29
Q

What is the function of thrombin?

A

To convert fibrinogen to fibrin

30
Q

What is Virchows triad?

A

1) Endothilial injury
2) Turbulent blood flow
3) Hypercoaguable blood

31
Q

What is primary vasculitis?

A

Inflammation of vessel walls (increases thrombophilic tendencies)

32
Q

What are some of the primary causes of increased viscosity?

A 
Factor V (Leiden)
Protein C deficiency
Protein S deficiency
Antithrombin deficiency
33
Q

What is an embolism?

A

Obstruction of an artery?

34
Q

What is the typical CXR sign of PE a few hours after the event?

A

Wedged shaped infarct

35
Q

What is ischemia?

A

Insufficient blood supply

36
Q

What is infarction?

A

Death of a tissue as a result of ischemia

37
Q

What are the different types of emboli?

A

Air, Amneotic fluid, fat, tumour, septic and thrombo

38
Q

Explain the bends?

A

Breathing at high pressure results in more disolved gas in the blood. As the pressure reduces (coming up from the dive) nitrogen comes out of solution forming multiple bubbles => decompression sickness

39
Q

How does an amneotic fluid emboli occur?

A

Tear in the placenta or uterine vessels with secondary infusion of amneotic fluid or foetal material. Identify fetal skin and hair in pulmonary vessels

40
Q

How does a fat embolism occur?

A

Large skeletal injuries where marrow contents are embolised. Delayed onset of 1-3 days post major trauma

41
Q

When does septic emboli occur?

A

Specific intravascular infections. Thrombus froms in association with an infectious agent. Infective endocarditis or mycotic aneurysm

Principles (12 decks)

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