Arterial Thrombosis and Anti-platelet drugs Flashcards

1
Q

arterial thrombotic events

A

coronary, cerebral, peripheral

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2
Q

arterial thrombosis treatment

A
  • aspirin and other anti-platelet drugs
  • modify risk factors for atherosclerosis (smoking, BP, diabetes)
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3
Q

atherosclerosis- what happens/pathophysiology

A

damage to endothelium

‘foamy’ macrophages rich in cholesterol are recruited to the damage

forms plaques rich in cholesterol

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4
Q

stable atherosclerotic plaques

A

Hyalinised and calcified

Stable plaques: stable angina (coronary artery), intermittent claudication (leg artery)

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5
Q

unstable atherosclerotic plaques

A

Plaques rupture, platelets are recruited and cause acute thrombosis

Sudden onset of symptoms

Unstable angina or myocardial infarction (coronary arteries)

Stroke (cerebral arteries)

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6
Q

Unstable atherosclerotic plaques - gradual or sudden onset of symptoms?

A

sudden

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7
Q

are plaque ruptures more likely in veins or arteries

A

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

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8
Q

Factors that cause damage to endothelium, increase in foamy macrophages and platelet activation:

A

Factors that cause damage to endothelium, increase in foamy macrophages and platelet activation:
- Hypertension (damage to endothelium,
platelet activation)

- Smoking (endothelium, platelets)

- High cholesterol (accumulated in plaque)

- Diabetes mellitus (endothelium, platelets, 
  cholesterol)
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9
Q

prevention of arterial thrombosis

A

Stop smoking
Treat hypertension
Treat diabetes
Lower cholesterol
Anti-platelet drugs

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10
Q

platelets are formed in the ____ _____ by ‘budding’ from ___________

A

bone marrow
megakaryocytes

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11
Q

what is the mean lifespan of platelets

A

7-10 days

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12
Q

what do platelets releasee to further stimulate platelet activation in order to recruit more platelets

A

Thrombin,Thromboxane A2 and ADP

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13
Q

Aspirin inhibits __________ which is necessary to produce Thromboxane A2 (a platelet agonist released from granules on activation).

A

cyclo-oxygenase

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14
Q

Aspirin inhibits cyclo-oxygenase which is necessary to produce ____________ (a platelet agonist released from granules on activation).

A

Thromboxane A2

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15
Q

side effects of aspirin

A
  1. Bleeding
  2. Blocks production of prostaglandins:
    • GI ulceration
    • Bronchospasm
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16
Q

how does clopidogrel work

A

blocks ADP receptor

17
Q

Dipyridamole mechanism of action

A

Phosphodiesterase inhibitor - increases production of cAMP which inhibits platelet aggregation.

18
Q

GP IIb/IIIa inhibitors example

A

abciximab

19
Q

GP IIb/IIIa inhibitors mechanism of action

A

inhibit aggregation

20
Q

Platelets attach to each other via ________ and _________.

A

GPIIbIIIa
fibrinogen

21
Q

How long before elective operations should anti-platelet agents be stopped

A

7 days

22
Q

If serious bleeding, how could we potentially reverse

A

platelet transfusion

23
Q

arterial thrombosis conclusions

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 conclusions

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