Arterial thrombosis Flashcards

1
Q

what is an arterial thrombosis

A

blood clot which forms in an artery

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2
Q

risk factors for arterial thrombosis

A

Factors that cause damage to endothelium, increase in foamy macrophages and platelet activation:
* Hypertension
* Smoking
* High cholesterol
Diabetes mellitus

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3
Q

management of arterial thrombosis

A

aspirin and other anti platelets
modify risk factors for atheroscleoriss

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4
Q

clinical presetation of arterial thrombosis

A

Peripheral arterial thrombosis: Sudden pain, pallor, coldness, pulselessness, and potential tissue necrosis in the limb.

Coronary thrombosis: Chest pain, shortness of breath, sweating, and possible heart attack (myocardial infarction).

Cerebral thrombosis: Sudden onset of weakness, speech difficulty, and loss of vision, possibly leading to a stroke.

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5
Q

atherosclerosis steps

A

damage to endothelium causes recruitment of foamy macrophages rich in cholesterol resulting in cholesterol rich plaques

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6
Q

what do stable plaques resul;t in

A

stable angina and intermittent claudicationwh

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7
Q

what do unsatble plaques result in

A

stroke, unstable angina or MI

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8
Q

durgs for arterial thrombosis

A

anti platelets

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9
Q

drugs for venous thrombosis

A

anti coags

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10
Q

characterisitcs of stable atherosclerotic plaques

A

hyalinsed and calcified

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11
Q

unstable atherosclerotic plaques steps

A

Plaques rupture, platelets are recruited and cause acute thrombosis
Sudden onset of symptoms
Unstable angina or myocardial infarction (coronary arteries)
Stroke (cerebral arteries)

leads to acute organ ischaemia and infarctionn

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12
Q

platelets and arterial thrombosis

A

Plaque ruptures – more likely in the high pressure environment of arteries

Platelet adheres to it – exposed endothelium and release of Von Willebrand factor

Platelets becomes activated - release granules that activate coagulation and recruit other platelets to developing platelet plug

Platelet aggregation via membrane glycoproteins

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13
Q

what are foamy macrophages rich in

A

cholesterol

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14
Q

what do platelets bind to subendothelial collagen via

A

glycoprotein 1b and vwf

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15
Q

what do platelets attach to each other via

A

GPIIbIIIa and fibrinogen

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16
Q

activation stage steps

A

Platelets alter their shape to expose more phospholipid on the surface-provides a greater surface area for coagulation activation and fibrin production to stabilise the clot.

Process is augmented by release of granules that further stimulate platelet activation eg Thrombin,Thromboxane A2 and ADP in order to recruit more platelets to the process.

This occurs via receptors to ADP etc on the platelet surface.

17
Q

MOA of aspirin

A

inhibits coco oxygenase which is necessary to produce thromboxane a2

18
Q

side effects of aspirin

A

. Bleeding

Blocks production of prostaglandins:

GI ulceration
Bronchospasm

19
Q

ADP receptor antagonists

A

clopidogrel, prasugrel

20
Q

Phosphodiesterase inhibitor

A

dipyridamole

increases production of camp which inhibits platelet aggregation

21
Q

GP IIb/IIIa inhibitors

A

abciximab

inhibit aggregation

22
Q

when should antiplatelets be stpped

A

7 days prior to elective operations

23
Q

arterial thrombosis conclusion

A

Causes organ ischaemia and is an inflammatory disorder instigated by damage to the endothelium

Platelets are central and are recruited to ruptured plaques

Antiplatelet drugs are useful in prevention

24
Q

venous thrombosis conclusion

A

Occurs in a low pressure system mainly by stasis

Platelets are not largely involved, and clots are rich in fibrin

Anticoagulants are useful in prevention

25
Q
A