Atheroma (Pathophysiology) Flashcards

1
Q

What is an atheroma?

A

A formation of focal elevated lesions in the intima of large and medium arteries

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2
Q

What is arteriosclerosis?

A

Agee related change to muscular arteries

Muscle hypertrophy and duplication of the IEL (fibrosis)

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3
Q

What does arteriosclerosis cause?

A

Cerebral, colonic and renal ischaemia in the elderly

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4
Q

What is the first stage of atheroma?

A

Fatty Streak

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5
Q

What follows the fatty streak?

A

Early atheromatous plaque

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6
Q

What follows the Early atheromatous plaque?

A

Fully developed atheromatous plaque

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7
Q

What follows the Fully developed atheromatous plaque?

A

Complicated atheroma

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8
Q

How does the fatty streak look like?

A

Yellow lipid-laden streak

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9
Q

What is contained within a fatty streak?

A

Masses of lipid-laden macrophages

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10
Q

What is contained within an atheromatous plaque?

A

Lipid core
Dead macrophage (foamy macrophages)
Extensive calcification

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11
Q

What are foamy macrophages?

A

Lipid laden macrophages containing oxidised lipoproteins

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12
Q

What is a complicated atheroma?

A

A FDAP with ruptured plaque leading to thrombosis

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13
Q

What causes the development of atheromatous plaque?

A

Endothelial damage with chronic inflammation

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14
Q

What changes to injured cells to increase the likelihood of atheroma formation?

A

Increased cell adhesion molecule expression
(ICAM-1, E-selectin)
Increased LDL permeability

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15
Q

What causes endothelial injury?

A

Turbulent flow
Hypercholesterolaemia
Increased free radicals
Growth factor release

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16
Q

What is the prevalence of hypercholesterolaemia in caucasians?

A

1/500

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17
Q

What are the signs of hypercholesterolaemia?

A

Family history of MI, atheroma
High blood LDL, HDL, total cholesterol
Corneal arcus
Xanthalasmata

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18
Q

What are biggest risk factors of atheroma?

A
Smoking
Hypertension
DM
Male
Age
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19
Q

Which plaques are most vulnerable?

A

Thin caps
Large lipid cores
Prominent inflammation

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20
Q

Primary prevention of atheroma

A
Smoking cessation
Control BP
Lose weight
Exercise
Diet control
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21
Q

Drug prevention of atheroma

A

Statins

Aspirin

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22
Q

Normal blood flow is what?

A

Laminar

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23
Q

What changes make up Virchow’s Triad?

A

Blood vessel wall
Blood constituents
Pattern of blood flow

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24
Q

What are Virchow’s triad?

A

Factors causing thrombosis

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25
Q

What is thrombosis?

A

Formation of a solid mass from the constituents of blood within the vascular system during life

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26
Q

What is the relationship between atheroma and thrombosis?

A

Arterial thrombosis most commonly superimposed on atheroma

27
Q

What are the outcomes of thrombosis?

A

Resolution
Organisation
Recanalisation
Propagation

28
Q

What is an embolism?

A

Movement of abnormal material in the bloodstream and its impaction in a vessel, blocking its lumen

29
Q

What factors effect the consequences of systemic thromboembolus?

A

Size of occluded vessel

Collateral circulation

30
Q

Where do venous thromboembolus most commonly travel to?

A

Pulmonary circulation

31
Q

Multiple PE over time lead to what?

A

Pulmonary Hypertension

RVF

32
Q

Risk factors for PTE, DVT?

A
Cardiac Failure
Severe trauma
Post-partum
Nephrotic syndrome
Malignancy
Oral contraceptive
Immobilisation
Obesity
PMH
33
Q

Prophylaxis for surgical patients at risk of PTE/DVT

A

Compression stockings

Herparin

34
Q

When can fat emboli occur?

A

After major fractures

35
Q

What is effected by fat emboli?

A

Brain
Kidneys
Skin

36
Q

When can cause gas emboli?

A

Air embolus

Decompression sickness

37
Q

What causes air embolus?

A

Head and neck wounds
Surgery
CV lines

38
Q

What is a trophoblastic emboli? Where does it effect?

A

Material from placenta

Lungs

39
Q

What are the different types of embolus?

A
Fat
Gas
Tumour
Bone marrow
Foreign Bodies
Amniotic Fluid
Trophoblastic material
Septic material
40
Q

What are the presenting features of Rheumatic Fever?

A
Flitting polyarthritis of large joints
Rashes
Fever
Pancarditis 
Heart Murmurs
41
Q

Most common bacteria in Rheumatic fever?

A

Group A Beta-haemolytic streptococci

42
Q

What are Aschoff bodies?

A

Foci of chronic inflammation, necrosis and activated macrophages
Seen in acute Rheumatic Fever

43
Q

What is the most common cause of mitral regurgitation?

A

Ischaemic heart disease

44
Q

What is hypoxic hypoxia?

A

Low inspired O2

(or) Low PaO2

45
Q

What is anaemic hypoxia?

A

Abnormal blood with normal inspired O2

46
Q

What is stagnant hypoxia?

A

Abnormal delivery

  • local (occlusion)
  • systemic (shock)
47
Q

What is cytotoxic anaemia?

A

Tissue level disorder

48
Q

Complicated atheroma in the coronary arteries leads to what?

A

Unstable angina

49
Q

Ulcerated/fissured plaques of the coronary arteries lead to what?

A

Thrombosis –> MI

50
Q

What is ischaemia?

A

Lack of blood supply to a tissue relative to demand, leading to hypoxia

51
Q

What factors affect Oxygen supply to tissues?

A
Inspired O2
Pulmonary function
Blood flow/constituents
Integrity of vasculature 
Tissue mechanisms
52
Q

What are the clinical presentations of ischaemia?

A

Cell dysfunction
Pain
Damage (specialised cells)

53
Q

The scale of damage in infarction is dependent on what?

A

Duration
Tissue being cut off
Collateral blood supply
Previous disease

54
Q

How long does ATP depletion take post MI?

A

Seconds

55
Q

How long does loss of contractility take post MI?

A

<2 minutes

56
Q

How long do reversible changes take post MI?

A

Minutes

57
Q

How long do irreversible changes take post MI?

A

20-30 minutes

58
Q

How long does myocyte necrosis onset take post MI?

A

20-40 minutes

59
Q

How long does microvascular injury take post Infarct?

A

1hr

60
Q

How long do swollen mitochondria take to appear post infarct (electron microscopy)?

A

3-12 hours

61
Q

Where do pale infarcts occur?

A

Myocardium
Spleen
Kidney

62
Q

Where do red infarcts form?

A

Loose tissues
Liver
Lung

63
Q

How long does chronic inflammation/granulation tissue onset take post infarct?

A

72hrs

64
Q

What are the end results of infarcts?

A

Scar

Reperfusion injury