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
What is thrombosis?
Formation of a solid mass from the constituents of blood within the vascular system during life
26
What is the relationship between atheroma and thrombosis?
Arterial thrombosis most commonly superimposed on atheroma
27
What are the outcomes of thrombosis?
Resolution Organisation Recanalisation Propagation
28
What is an embolism?
Movement of abnormal material in the bloodstream and its impaction in a vessel, blocking its lumen
29
What factors effect the consequences of systemic thromboembolus?
Size of occluded vessel | Collateral circulation
30
Where do venous thromboembolus most commonly travel to?
Pulmonary circulation
31
Multiple PE over time lead to what?
Pulmonary Hypertension | RVF
32
Risk factors for PTE, DVT?
``` Cardiac Failure Severe trauma Post-partum Nephrotic syndrome Malignancy Oral contraceptive Immobilisation Obesity PMH ```
33
Prophylaxis for surgical patients at risk of PTE/DVT
Compression stockings | Herparin
34
When can fat emboli occur?
After major fractures
35
What is effected by fat emboli?
Brain Kidneys Skin
36
When can cause gas emboli?
Air embolus | Decompression sickness
37
What causes air embolus?
Head and neck wounds Surgery CV lines
38
What is a trophoblastic emboli? Where does it effect?
Material from placenta | Lungs
39
What are the different types of embolus?
``` Fat Gas Tumour Bone marrow Foreign Bodies Amniotic Fluid Trophoblastic material Septic material ```
40
What are the presenting features of Rheumatic Fever?
``` Flitting polyarthritis of large joints Rashes Fever Pancarditis Heart Murmurs ```
41
Most common bacteria in Rheumatic fever?
Group A Beta-haemolytic streptococci
42
What are Aschoff bodies?
Foci of chronic inflammation, necrosis and activated macrophages Seen in acute Rheumatic Fever
43
What is the most common cause of mitral regurgitation?
Ischaemic heart disease
44
What is hypoxic hypoxia?
Low inspired O2 | (or) Low PaO2
45
What is anaemic hypoxia?
Abnormal blood with normal inspired O2
46
What is stagnant hypoxia?
Abnormal delivery - local (occlusion) - systemic (shock)
47
What is cytotoxic anaemia?
Tissue level disorder
48
Complicated atheroma in the coronary arteries leads to what?
Unstable angina
49
Ulcerated/fissured plaques of the coronary arteries lead to what?
Thrombosis --> MI
50
What is ischaemia?
Lack of blood supply to a tissue relative to demand, leading to hypoxia
51
What factors affect Oxygen supply to tissues?
``` Inspired O2 Pulmonary function Blood flow/constituents Integrity of vasculature Tissue mechanisms ```
52
What are the clinical presentations of ischaemia?
Cell dysfunction Pain Damage (specialised cells)
53
The scale of damage in infarction is dependent on what?
Duration Tissue being cut off Collateral blood supply Previous disease
54
How long does ATP depletion take post MI?
Seconds
55
How long does loss of contractility take post MI?
<2 minutes
56
How long do reversible changes take post MI?
Minutes
57
How long do irreversible changes take post MI?
20-30 minutes
58
How long does myocyte necrosis onset take post MI?
20-40 minutes
59
How long does microvascular injury take post Infarct?
1hr
60
How long do swollen mitochondria take to appear post infarct (electron microscopy)?
3-12 hours
61
Where do pale infarcts occur?
Myocardium Spleen Kidney
62
Where do red infarcts form?
Loose tissues Liver Lung
63
How long does chronic inflammation/granulation tissue onset take post infarct?
72hrs
64
What are the end results of infarcts?
Scar | Reperfusion injury