Atherosclerosis Flashcards

1
Q

What is atherosclerosis

A

Buildup of fatty plaques on arterial walls

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2
Q

Modifiable risk factors of atherosclerosis - 4

A
  • Smoking
  • Hypertension
  • Hyperlipidemia
  • Diabetes
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3
Q

Hyperlipidemia as a risk factor of atherosclerosis

A

Hypercholesterolaemia

High density lipoprotein = good
Low density lipoprotein = bad

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4
Q

Diabetes as a risk factor of atherosclerosis

A

Makes blood vessels more rigid - Advanced glycoprotein end products (AGE)

Abnormal cross linking traps LDL

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5
Q

Non-modifiable risk factors - 3

A
  • Genetics
    • variation in cholesterol metabolism, inflammatory response, control of BP
  • Male
    • likely due to oestrogen
  • Age
    • 40s to 60s
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6
Q

6 stages of formation of atherosclerotic plaque

A
  1. Primary endothelial injury
  2. Uptake of LDL from blood into intima of artery where it is oxidised to become OXLDL
  3. Macrophages migrate across the endothelium into intima where they take up OXLDL to become foam cells + form fatty streak
  4. Activated macrophages release cytokines and growth factors particularly Platelet derived growth factor (PDGF) resulting in proliferation of smooth muscle layer and deposition of collagen forming a scab
  5. As plaque enlarges Blood flow is compromised
  6. Unstable angina / MI result when large enough plaque ruptures activating clotting cascade and thrombus formed occludes artery
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7
Q

Causes of primary endothelial injury

A

Smoking
Hypertension

Bifurcations are more susceptible

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8
Q

Complications of atheroma - 3

A

Aneurysm
Stenosis
Dissection

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9
Q

What is stenosis + what can it cause

A

Narrowing and reduced elasticity of the arterial lumen
:. Reduced flow in systole

Can cause ischaemia in some tissues

Arterial stenosis can affect any artery

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10
Q

What is an Aneurysm

A

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

Most common in abdominal aorta

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11
Q

Complications of aneurysm - 5

A
  • Rupture
  • Thrombosis
  • Embolism
  • Pressure erosion of adjacent structures
  • Infection
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12
Q

What is Dissection

A

Splitting within the media by flowing blood
Splits into lanes through vessel walls

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13
Q

What is haemostasis

A

The arrest of bleeding and the maintenance of vascular patency

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14
Q

Requirements of haemostasis - 4

A

Permanent state of readiness
Prompt response
Localised response
Protection against unwanted thrombosis

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15
Q

What is primary haemostasis

A

Formation of platelet plug

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16
Q

What is secondary haemostasis

A

Formation of fibrin clot

17
Q

What is Fibrinolysis

A

Breakdown of fibrin clot

18
Q

Components of haemostatic system - 4

A

Primary haemostasis
Secondary haemostasis
Fibrinolysis
Anticoagulant defences

19
Q

Platelets - what + lifespan

A

Small anucleate discs

Mean lifespan of 7-10 days

20
Q

How and where are platelets formed

A

In the marrow by budding from megakaryocytes

21
Q

What is Von Willebrand factor (VWF) and how does it affect platelets

A

Released when endothelium is damaged

Platelets have receptors for it so stick to site of injury

Platelets secrete various chemicals which leads to platelet aggregation of platelets

22
Q

Causes of failure of platelet plug formation - 3

A
  • Vascular
  • Platelets
  • VWF deficiency
23
Q

Vascular causes of failure of platelet plug formation

A

Can be hereditary e.g. Marfans
Can be aquired - age related, vitamin C deficiency, vasculitis

24
Q

What is thrombocytopenia and reasons

A

Reduced number of platelets

Marrow problem - reduced production
Increased destruction - coagulopathy - autoimmune conditions

25
Q

What causes reduced function of platelets

A

Drugs
- Aspirin
- NSAIDS

Renal failure

26
Q

Von Willebrand factor deficiency

A

Can be aquired but mostly hereditary

27
Q

Consequences of failure of platelet plug formation - 4

A

Spontaneous bruising and purpura
Mucosal bleeding
- epistaxis
- gastrointestinal
- conjunctival
- menorrhagic
Intercranial haemorrhage
Retinal haemorrhage

28
Q

Screening test for primary haemostasis

A

Platelet count

29
Q

3 pathways in formation of fibrin clot

A

Intrinsic pathway
Extrinsic pathway
Final common pathway

30
Q

What activates the intrinsic pathway of fibrin clot formation

What clotting factors are involved

A

Activated by contact with a damaged surface

Factor XII -> XI -> IX -> common pathway

31
Q

What activates the extrinsic pathway of fibrin clot formation

What clotting factors are involved

A

Pathway activated by release of tissue factors

Factor VII -> common pathway

32
Q

What actives the final common pathway and what molecules are involved

A

Proceeds the intrinsic or extrinsic pathways

Factor X causes prothrombin (factor II) to be converted to thrombin (factor IIa)

Thrombin converts Fibrinogen (factor I) to Fibrin (factor II)
Also converts factor XIII to XIIIa (fibrin mesh)

33
Q

What are the causes of failure of fibrin clot formation (3)

A

Single clotting factor deficiency - hereditary

Multiple clotting factor deficiencies - aquired

Increased Fibrinolysis

34
Q

What are two reasons for multiple clotting factor deficiency

A

Liver failure - all coagulation factors are synthesised in the liver

Vitamin K deficiency - require to synthesise factors 2,7,9,10

35
Q

What are the tests for fibrin clot formation deficiency

A
  • Prothrombin time
    • extrinsic pathway
  • Activate partial thromboplastin time
    • intrinsic pathway
36
Q

What is the difference between an arterial and venous thrombus

A

Arterial
- white thrombus
- embolis lodges in artery in brain
- treated with anti platelets

Venous
- red thrombus
- embolis lodges in lung
- treated with anti-coagulants