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CPT > Antiplatelet + Firbinolytic Drugs > Flashcards

Antiplatelet + Firbinolytic Drugs Flashcards

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1
Q

Compare venous and arterial thrombosis in relation to fibrin + platelet content

A
  • venous: high fibrin, low platelet
  • arterial: low fibrin, high platelet
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2
Q

What is virchows triad?

A

Blood vessel injury
Increased coaguability
Reduced blood flow

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3
Q

Outline how platelet aggregation is prevented in healthy endothelium

A

prostacyclin produced + released by endothelial cells > inhibition of platelet aggregation:
- PGI2 bind to platelet receptors > increase [cAMP] in platelets > decrease Ca2+
- decrease in platelet aggregatory agents
- stabilises inactive GPIIb/IIIa receptors

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4
Q

Lifespan of platelets

A

8-10 days

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5
Q

What type of drugs are used in platelet rich ‘white arterial thrombi?

A

Anti platelets
Fibrinolytic drugs

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6
Q

What types of drugs are used in lower platelet content ‘red’ venous thrombi?

A

Anticoagulants

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7
Q

What class of drug is aspirin?

A

Cyclo-oxygenase inhibitor
COX 1

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8
Q

What is the mechanism of action of aspirin?

A
  • irreversibly inhibits COX1 mediated production of thromboxane A2 from arachidonic acid
  • reduces platelet aggregation
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9
Q

Why does aspirin not completely inhibit all platelet aggregation?

A

There are other platelet aggregators
Aspirin only inhibits COX1

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10
Q

What dose is considered baby aspirin?

A

75mg

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11
Q

Describe baby aspirin

A

Low dose 75mg
Non analgesic dose

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12
Q

What is the loading dose of aspirin?

A

300mg

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13
Q

High vs low dose aspirin

A

high - 300mg
low - 75mg

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14
Q

Action of high dose aspirin

A

Inhibit endothelial prostacyclin

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15
Q

What are the adverse drug reactions for aspirin?

A
  • GI irritation
  • GI bleeding due to ulcer
  • Haemorrhage
  • Hypersensitivity
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16
Q

What are contraindication of aspirin?

A
  • Reye’s syndrome (avoid <16 years old)
  • hypersensitivity
  • 3rd trimester pregnancy
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17
Q

Why should aspirin not be given in 3rd trimester of pregnancy?

A

Premature closure of ductus arteriosus

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18
Q

What are important drug drug interactions of aspirin?

A

Other anti platelets + anticoagulants

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19
Q

What are uses of aspirin?

A
  • AF patients post stroke
  • secondary prevention of stroke + TIA + acute coronary syndromes
  • post primary percutaneous coronary intervention
  • NSTEMI/STEMI
  • pain relief
20
Q

Examples of ADP receptor antagonists

A

Clopidogrel
Prasugrel
Ticagrelor

21
Q

What is the mechanism of action of ADP receptor antagonists?

A
  • Inhibit binding of ADP to P2Y12 receptor
  • reduces Ca2+
  • this inhibits activation of GPIIb/IIIa receptors
22
Q

Examples of irreversible ADP receptor antagonists

A

Clopidogrel + prasugrel

23
Q

Example of reversible ADP receptor antagonist

A

Ticagrelor

24
Q

Route of administration of ADP receptor antagonists

A

P.O. - oral

25
Q

Difference in onset of action of different ADP receptor antagonists

A

slow onset - clopidogrel
fast onset - ticagrelor + prasugrel

26
Q

What are adverse drug effects of ADP receptor antagonists?

A
  • Bleeding
  • GI upset - dyspepsia + diarrhoea
  • thrombocytopenia
27
Q

What is dyspepsia?

A

Indigestion

28
Q

What are contraindications of ADP receptor antagonists?

A

Caution in high bleed risk patients with renal or hepatic impairment

29
Q

What are important drug drug interactions of ADP receptor antagonists

A
  • Clopidogrel need CYPs for activation (pro drug) - CYP inhibitors e.g. erythromycin, omeprazole
  • ticagrelor can interact with CYP inhibitors + inducers
  • other anti platelets
  • anti coagulants
  • NSAIDs
30
Q

What are uses of ADP receptor antagonists

A
  • ischaemic stroke + TIA
  • when aspirin is contraindicated
  • NSTEMI/STEMI alongside aspirin
31
Q

Example of phosphodiesterase inhibitors

A

Dipyridamole

32
Q

What is the mechanism of action of dipyridamole?

A
  • Phosphodiesterase inhibitor > prevents cAMP degradation > inhibit expression of GPIIb/IIIa
  • Inhibits cellular uptake of adenosine > increased [adenosine] > inhibits platelet aggregation via adenosine receptors
33
Q

Example of glycoprotein IIb/IIIa inhibitors

A

abciximab

34
Q

What is the mechanism of action of GPIIb/IIIa inhibitors?

A

Blocks binding of fibrinogen + Von Willebrand factor

35
Q

What are adverse effects of GPIIb/IIIa inhibitors?

A

Bleeding

36
Q

What are important drug drug interactions of GPIIb/IIIa inhibitors?

A

Other antiplatelets + anticoagulant agents

37
Q

Action of fibrinolytics

A

Dissolves fibrin meshwork of thrombus > fibrin degradation products

38
Q

Why does it take 7-10 days for anti platelet effects to cease after terminating aspirin treatment?

A
  • Aspirin is an irreversible COX inhibitor in platelets
  • need to wait for the lifespan of these platelets to end (8-10 days) before the effects stop
39
Q

What tranexamic acid used for?

A

Stops bleeding

40
Q

Examples of fibrinolytic agents

A

Streptokinase
Alteplase

41
Q

What are adverse effects of fibrinolytic agents?

A

Bleeding

42
Q

What is used in the secondary prevention for acute coronary syndrome

A

Once haemodynamically stable:
- ACEi
- B blockers
- dual anti platelets > 75mg aspirin + ADP receptor antagonist
- statin
+ cardiac rehab

43
Q

Outline platelet activation and aggregation

A
  • damaged endothelium
  • platelets adhere to exposed endothelium
  • release of platelet granules e.g. ADP, thromboxane A2, platelts activation factor, thrombin
  • activation + aggregation occurs through fibrinogen + GPIIb/IIIa receptors
  • increase in Ca2+ + decrease in cAMP in platelets
  • amplification from platelet to platelet
  • fibrin cap made
44
Q

What is Reye’s syndrome?

A

Rare but serious condition causing swelling of liver + brain

45
Q

What drug class should be co-prescribed with long term aspirin use?

A

Proton pump inhibitors
For gastric protection

46
Q

Administration of Abciximab

A

IV

47
Q

When can streptokinase be used?

A

Only once antibodies develop

CPT (28 decks)

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