Lect 13 - Atheroma, Thrombosis & Embolism Flashcards

(29 cards)

1
Q

what is Atherosclerosis

A

“Degeneration of arterial walls characterised by fibrosis, lipid deposition and inflammation which limits blood circulation and predisposes to thrombosis”

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2
Q

what vessels are commonly affected by Atherosclerosis

A
Bifurcations (sites of turbulent flow)
Abdominal aorta 
Coronary arteries
Popliteal arteries
Carotid vessels
Circle of Willis
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3
Q

What are the common nonmodifiable risk factors for Atherosclerosis

A

Age
Male
FH
Genetic

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4
Q

what are the modifiable risk factors for atherosclerosis?

A

Hyperlipidaemia (LDL:HDL)
Hypertension
Smoking
Diabetes

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5
Q

talk though the Pathophysiology of Atherosclerosis formation, up to the point of fatty streak formation.

A

endothelial injury -> lipid accumulates in intima ->Monocytes come and ingest the lipid becoming foam cells

FORMS FATTY STREAK

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6
Q

what do foam cells do?

A

secrete chemokines attracting more monocytes/macrophages, lymphocytes and smooth muscle cells

CONSTITUENTS OF THE ATHEROSCLEROTIC PLAQUE

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7
Q

What different zones within the plaque form?

A

the edges = “shoulders”
the top = “fibrous cap”
the middle = “necrotic core”

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8
Q

what tends to happen after atherosclerosis formation?

A

Occlusion

Weakening of vessel walls
Aneurysm formation

Erosion
Thrombosis formation?

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9
Q

what is a Thrombosis

A

Solidification of blood contents formed in the vessel during life.

it is different to a clot in pathogenesis and morphology.

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10
Q

what factors make up virchow’s triad

A

The intimal surface of the vessel
The pattern of blood flow
Blood constituents

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11
Q

what are platelets fragments of?

A

Fragments of megakaryocytes in the bone marrow

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12
Q

what do Platelets release?

A

Alpha granules: fibrinogen, fibronectin, PDGF

Dense granules: chemotactic chemicals

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13
Q

why would plaque rupture lead to arterial thrombus?

A

causes turbulent flow and intimal change. also Hyperlipidaemia – change in blood constituents

Platelets bind and fibrin is produced entrapping RBC

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14
Q

what is Venous thrombosis caused by?

A

Intimal change: valves

Change in blood flow: Immobile

Change in blood constituents:
Inflammatory mediators (infection, malignancy)
factor V leiden
Oestrogen

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15
Q

what is a thrombi in the heart known as?

A

mural thrombi

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16
Q

where do mural thrombi form?

A

over areas of endomyocardial injury:
MI
Myocarditis

NOTE : Can also occur with arrhythmias and cardiomyopathy

17
Q

what is the major risk of thrombosis?

18
Q

what is an Embolus

A

A mass of material in the vascular system able to lodge in a vessel and block it

19
Q

what is the most common type of emboli?

A

PE.

Very common cause of hospital morbidity and mortality

20
Q

what are the clinical effects of a small PE

A

initially asymptomatic, if multiple may result in pulmonary hypertension

21
Q

what are the clinical effects of a medium PE

A

Cause acute respiratory and cardiac failure (V/Q mismatch, RV strain)

22
Q

what are the clinical effects of a large (saddle) PE

23
Q

what are the types of emboli? (6)

A
infective
tumour
gas
Amniotic fluid embolism
Fat embolism
Foreign body embolism
24
Q

where do Infective emboli come from?

A

Usually from the vegetations on infected heart valves

Effects compounded by the infective nature – may lead to mycotic aneurysm formation

25
where do Tumour emboli come from?
Bits may break off as tumours penetrate vessels Do not usually cause immediate physical problems
26
where do Gas emboli come from?
Air (vessel opened into the air) ``` Nitrogen Decompression sickness (“the bends”) ```
27
where do Amniotic fluid emboli come from?
Increased uterine pressure during labour may force AF into maternal uterine veins (1:50,000 deliveries)
28
where do fat emboli come from?
Microscopic fat emboli found in 80% patients with significant trauma at PM Sudden onset of respiratory distress
29
where do foreign body emboli come from?
Particles injected intravenously E.g. talc in IVDU’s Leads to a granulomatous reaction