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semester 4 - CPT & Prescribing > 11. Antiplatelets and fribrinolytics > Flashcards

11. Antiplatelets and fribrinolytics Flashcards

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1
Q

what are common Thromboembolic diseases ?

A
  • deep vein thrombosis (DVT) and pulmonary embolism (PE)
  • consequence of atrial fibrillation (AF)
  • transient ischaemic attacks (TIA), ischaemic stroke - myocardial infarction (MI)
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2
Q

define thrombus and embolus

A

Thrombus - a clot adhered to vessel wall

Embolus - intravascular clot distal to site of origin

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3
Q

Describe a venous thrombosis.

A
  • associated with stasis of blood and or damage to the veins - less likely to see endothelial damage
  • High red blood cell and fibrin content, low platelet content evenly distributed
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4
Q

Describe a arterial thrombosis.

A
  • usually forms at site of atherosclerosis following plaque rupture
  • Lower fibrin content and much higher platelet content
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5
Q

What do endothelial cells produce to inhibit platelet aggregation?

A

Prostacyclin (PGI2)

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6
Q

How does prostacyclin inhibit platelet aggregation?

A
  • PGI2 binds to platelet receptors → ↑[cAMP] in platelets
  • ↑[cAMP] → ↓calcium release preventing platelet aggregation
  • ↓in platelet aggregatory agents
  • Stabilises GPIIb/IIIa receptors
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7
Q

describe the process of platelet activation and aggregation

A

damaged endothelium –> activated platelets adhere to exposed subendotheial surface of damaged endothelium –> activated platelets release chemical mediators –>initiates further platelet activation –> platelet plug

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8
Q

What do platelet granules contain? (5)

A

ADP, thromboxane A2, serotonin, platelet activation factor, thrombin

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9
Q

What are the effects of substances from the platelet granules?

A
  • bind to receptors on platelets
  • ↑calcium and ↓cAMP in platelets
  • activation of the platelets (GPIIb/IIIa receptors, which bind to fibrinogen to bind to other platelets)
  • calcium release cause further granule release and thromboxane A2 synthesis activation
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10
Q

What drugs are used for arterial and venous thrombi?

A
  • “white” Arterial thrombi: platelet rich - antiplatelet and fibrinolytics
  • “red” Venous thrombi: high blood, fibrin rich: parenteral anticoagulants heparins etc. and oral anticoagulants warfarin
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11
Q

when may a combination of antiplatelet and anticoagulant be used?

A

A combination of both may be used in some patients often in secondary prevention – targeting multiple sites and mechanisms of thromboembolic cascades

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12
Q

Name some classes of antiplatelets. (4)

A
  • cyclo-oxygenase inhibitors
  • ADP receptor antagonists
  • GPIIb/IIIa inhibitors
  • Phosphodiesterase inhibitors
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13
Q

Give an example of a Cyclo-oxygenase inhibitor.

A

Aspirin

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14
Q

How does aspirin work?

A
  • Potent platelet aggregating agent thromboxane A2 (TXA2) formed from arachidonic acid by COX-1
  • Aspirin - inhibits COX-1 mediated production of TXA2 and reduces platelet aggregation – irreversible
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15
Q

how does the dose of aspirin affect its use?

A 
low dose (baby aspirin) used for antiplatelet effect - 75mg
high dose used for analgesic affect - 300-900 mg

in MI, stroke, TIA - given at 300mg doses acutely

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16
Q

What does aspirin inhibit at higher doses?

A

Endothelial prostacyclin (PGI2 - inhibits activation of platelets and a vasodilator) - reduced vasodilation so less inflammatory effect

Irreversible COX-1 and COX-2 inhibition → inhibition of prostacyclin and prostaglandin synthesis → antipyretic, anti-inflammatory, and analgesic effect

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17
Q

What is aspirin metabolised into?

A

Hepatic hydrolysis to salicylic acid

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18
Q

adverse effects of aspirin?

A

Gastrointestinal irritation, GI bleeding (peptic ulcer), haemorrhage (stroke) hypersensitivity

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19
Q

warnings, contraindications of aspirin?

A
  • Reye’s syndrome – avoid <16 years
  • Hypersensitivity
  • 3rd trimester – premature closure of ductus arteriosus
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20
Q

What is Reye’s syndrome?

A

A rare syndrome of rapid liver degeneration and encephalitis in children treated with aspirin during a viral infection

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21
Q

Why is there premature closure of the ductus arteriosus when using aspirin in 3rd trimester?

A

Inhibition of production of prostaglandins, reduction in prostaglandins cause closure.

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22
Q

important drug reactions of aspirin?

A

Δ caution - other antiplatelet and anticoagulants (additive/synergistic action)

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23
Q

Why does inhibition last lifespan of platelet (7-10 days)?

A

Platelets do not have nuclei, cannot produce more enzymes. Aspirin irreversibly binds to COX1

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24
Q

What are the indications for use of aspirin?

A
  • Atrial fibrillation (AF) before considering anticoagulants
  • Secondary prevention of stroke and TIA
  • Secondary prevention of acute coronary syndromes (ACS)
  • Post primary percutaneous coronary intervention (PCI) and stent to reduce ischaemic complications
  • Often co prescribed with other antiplatelet agents
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25
Q

what are the doses for aspirin for NSTEMI/STEMI and acute ischaemic stroke?

A

• NSTEMI/STEMI - initial once only 300 mg loading dose – chewable is best!
acute ischaemic stroke initial 300 mg daily 2 weeks

26
Q

What may have to be given with aspirin?

A

Gastric protection required for long term use in at risk patients (proton pump inhibitor)

27
Q

after an MI, which dual anti platelet are given and which one is dropped?

A

dual anti platelet therapy of aspirin an clopidogrel and then clopidogrel dropped

28
Q

Give 3 examples of ADP receptor antagonists.

A

clopidogrel, prasugrel, ticagrelor

29
Q

How do ADP receptor antagonists work?

A

Inhibit binding of ADP to P2Y12 receptor → inhibit activation of GPIIb/IIIa receptors → reduced platelet aggregation (independent of COX pathway)

30
Q

What type of receptor is P2Y12?

A

Gi, coupled GPCR

- when activated decreased intracellular [cAMP] thereofre leading to increase Ca++ and activation of the GPIIb/IIIa

31
Q

What is the difference in speed of action between the different ADP antagonists?

A
  • Clopidogrel has slow onset (without loading dose)

- prasugrel and ticagrelor have more rapid onset

32
Q

Which ADP antagonists are prodrugs?

A
  • Clopidogrel and prasugrel are prodrugs -they have active hepatic metabolites
  • ticagrelor has active metabolites
33
Q

Which ADP antagonists are irreversible and reversible?

A
  • Clopidogrel and prasugrel are irreversible inhibitors of P2Y12
    Ticagrelor acts reversibly at different site to clopidogrel
34
Q

adverse effects of ADP antagonists?

A

Bleeding! GI upset – dyspepsia and diarrhoea rarely - thrombocytopenia

35
Q

warnings, contraindications of ADP antagonists?

A

caution in high bleed risk patients with renal and hepatic impairment

36
Q

important drug interactions of ADP antagonists?

A

clopidogrel requires CYPs for activation
CYP inhibitors – omeprazole, ciprofloxacin, erythromycin, some SSRIs
- need to consider use of other PPIs with clopidogrel
- ticagrelor can interact with CYP inhibitors and inducers
- caution when co prescribed with other antiplatelet and anticoagulant agents or NSAIDs – increased bleeding risk

37
Q

When should ADP antagonists be stopped before surgery?

A
  • clopidogrel needs stopping ~ 7 days prior to surgery (risk vs. benefit)
38
Q

What are the indications for use of ADP antagonists?

A

• ADP receptor antagonists used for wide variety of presentations where antiplatelet needed
• Clopidogrel
mono therapy where aspirin is contraindicated
NSTEMI patients – 3 months
STEMI patients - up to 4 weeks
Ischaemic stroke and TIA long term secondary prevention
• Prasugrel and ticagrelor with aspirin in ACS patients (undergoing PCI) for up to 12 months

39
Q

in patients who have had strokes, which dual antiplatelet therapy is given and which is stopped later?

A

aspirin and clopidogrel and aspirin stopped

40
Q

Give an example of a phosphodiesterase inhibitor.

A

dipyridamole

41
Q

How do phophodiesterase inhibitors work?

A

acts as phosphodiesterase inhibitor which prevents cAMP degradation → inhibit expression of GPIIb/IIIa
(increase in [cAMP])

42
Q

Other than its action as a phosphidiesterase inhibitor, how does dipyridamole work?

A

Inhibits cellular reuptake of adenosine → increased plasma adenosine → adenosine binds to and therefore inhibits platelet aggregation via A2 receptors
(A2a receptors - Gs increase in cAMP)

43
Q

adverse effects of dipyridamole?

A

V+D, dizziness

44
Q

important drug interactions of dipyridamole?

A

antiplatelets and anticoagulants, adenosine

45
Q

What are the indications for use of phosphodiesterase inhibitors?

A
  • Secondary prevention of ischaemic stroke and TIAs

- Adjunct for prophylaxis of thromboembolism following valve replacement

46
Q

Give an example of a Glycoprotein IIb/IIIa inhibitor.

A

abciximab (monoclonal antibodies)

47
Q

How do GP IIb/IIIa inhibitors work? Size of effect?

A

Blocks binding of fibrinogen and von Willebrand factor (vWF)

- >80% reduction in aggregation - bleeding risk

48
Q

How are are GPIIb/IIIa administered?

A

I.V. is a protein digested by P.O??

49
Q

adverse effects of Glycoprotein IIb/IIIa inhibitor?

A

Bleeding! dose adjustment for body weight

50
Q

important drug interactions of Glycoprotein IIb/IIIa inhibitor?

A

caution with other antiplatelet and anticoagulant agents

51
Q

What are the indications for use of Glycoprotein IIb/IIIa inhibitor?

A

Specialist use in high risk percutaneous transluminal coronary angioplasty patients with other drugs

52
Q

Give 2 examples of fibrinolytic agents.

A
  • streptokinase,

- alteplase (plasminogen activator)

53
Q

how do fibrinolytic agents work?

A

Fibrinolytics “clot busters” dissolve the fibrin meshwork of thrombus

alteplase acts as tissue plasminogen activator - convert plasminogen to plasmin –> fibrinolysis

54
Q

WHat are indications for use of alteplase?

A

Alteplase in acute ischaemic stroke <4.5 hours from symptoms

Following STEMI diagnosis acutely vs. primary PCI

55
Q

what is a disadvantage of streptokinase?

A

Streptokinase can only be used once as antibodies develop

56
Q

adverse effect of fibrinolytic?

A

Bleeding!

57
Q

important drug interactions of fibrinolytic?

A

antiplatelets and anticoagulants

58
Q

What is best practise for treatment in acute STEMI?

A

PCI if presentation is within 12 hours of onset of symptoms and primary PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given - otherwise fibrinolytics given (?)

59
Q

what should be offered to all patients post MI?

A

ACEi should be offered to all patients post MI once haemodynamically stable

60
Q

Why is clopidogrel contraindicated in hepatic failure?

A

prodrug so converted to active metabolite in liver so if hepatic failure cannot be effective

61
Q

Why do GP IIb/IIIa inhibitors afford more complete platelet aggregation than other agents?

A

Target final common pathway so unlike other pathways that are affected that may have an alternative route, this one ensures reduction in platelet aggregation

62
Q

What is tranexamic acid used for?

A

inhibits fibrinolysis so stops bleeding

semester 4 - CPT & Prescribing (25 decks)

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