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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
what are the doses for aspirin for NSTEMI/STEMI and acute ischaemic stroke?
• NSTEMI/STEMI - initial once only 300 mg loading dose – chewable is best! acute ischaemic stroke initial 300 mg daily 2 weeks
26
What may have to be given with aspirin?
Gastric protection required for long term use in at risk patients (proton pump inhibitor)
27
after an MI, which dual anti platelet are given and which one is dropped?
dual anti platelet therapy of aspirin an clopidogrel and then clopidogrel dropped
28
Give 3 examples of ADP receptor antagonists.
clopidogrel, prasugrel, ticagrelor
29
How do ADP receptor antagonists work?
Inhibit binding of ADP to P2Y12 receptor → inhibit activation of GPIIb/IIIa receptors → reduced platelet aggregation (independent of COX pathway)
30
What type of receptor is P2Y12?
Gi, coupled GPCR | - when activated decreased intracellular [cAMP] thereofre leading to increase Ca++ and activation of the GPIIb/IIIa
31
What is the difference in speed of action between the different ADP antagonists?
- Clopidogrel has slow onset (without loading dose) | - prasugrel and ticagrelor have more rapid onset
32
Which ADP antagonists are prodrugs?
- Clopidogrel and prasugrel are prodrugs -they have active hepatic metabolites - ticagrelor has active metabolites
33
Which ADP antagonists are irreversible and reversible?
- Clopidogrel and prasugrel are irreversible inhibitors of P2Y12 Ticagrelor acts reversibly at different site to clopidogrel
34
adverse effects of ADP antagonists?
Bleeding! GI upset – dyspepsia and diarrhoea rarely - thrombocytopenia
35
warnings, contraindications of ADP antagonists?
caution in high bleed risk patients with renal and hepatic impairment
36
important drug interactions of ADP antagonists?
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
When should ADP antagonists be stopped before surgery?
- clopidogrel needs stopping ~ 7 days prior to surgery (risk vs. benefit)
38
What are the indications for use of ADP antagonists?
• 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
in patients who have had strokes, which dual antiplatelet therapy is given and which is stopped later?
aspirin and clopidogrel and aspirin stopped
40
Give an example of a phosphodiesterase inhibitor.
dipyridamole
41
How do phophodiesterase inhibitors work?
acts as phosphodiesterase inhibitor which prevents cAMP degradation → inhibit expression of GPIIb/IIIa (increase in [cAMP])
42
Other than its action as a phosphidiesterase inhibitor, how does dipyridamole work?
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
adverse effects of dipyridamole?
V+D, dizziness
44
important drug interactions of dipyridamole?
antiplatelets and anticoagulants, adenosine
45
What are the indications for use of phosphodiesterase inhibitors?
- Secondary prevention of ischaemic stroke and TIAs | - Adjunct for prophylaxis of thromboembolism following valve replacement
46
Give an example of a Glycoprotein IIb/IIIa inhibitor.
abciximab (monoclonal antibodies)
47
How do GP IIb/IIIa inhibitors work? Size of effect?
Blocks binding of fibrinogen and von Willebrand factor (vWF) | - >80% reduction in aggregation - bleeding risk
48
How are are GPIIb/IIIa administered?
I.V. is a protein digested by P.O??
49
adverse effects of Glycoprotein IIb/IIIa inhibitor?
Bleeding! dose adjustment for body weight
50
important drug interactions of Glycoprotein IIb/IIIa inhibitor?
caution with other antiplatelet and anticoagulant agents
51
What are the indications for use of Glycoprotein IIb/IIIa inhibitor?
Specialist use in high risk percutaneous transluminal coronary angioplasty patients with other drugs
52
Give 2 examples of fibrinolytic agents.
- streptokinase, | - alteplase (plasminogen activator)
53
how do fibrinolytic agents work?
Fibrinolytics “clot busters” dissolve the fibrin meshwork of thrombus alteplase acts as tissue plasminogen activator - convert plasminogen to plasmin --> fibrinolysis
54
WHat are indications for use of alteplase?
Alteplase in acute ischaemic stroke <4.5 hours from symptoms Following STEMI diagnosis acutely vs. primary PCI
55
what is a disadvantage of streptokinase?
Streptokinase can only be used once as antibodies develop
56
adverse effect of fibrinolytic?
Bleeding!
57
important drug interactions of fibrinolytic?
antiplatelets and anticoagulants
58
What is best practise for treatment in acute STEMI?
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
what should be offered to all patients post MI?
ACEi should be offered to all patients post MI once haemodynamically stable
60
Why is clopidogrel contraindicated in hepatic failure?
prodrug so converted to active metabolite in liver so if hepatic failure cannot be effective
61
Why do GP IIb/IIIa inhibitors afford more complete platelet aggregation than other agents?
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
What is tranexamic acid used for?
inhibits fibrinolysis so stops bleeding

semester 4 - CPT & Prescribing (25 decks)

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