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CVS Pharmacology > Anti-platelets and anti-thrombotics > Flashcards

Anti-platelets and anti-thrombotics Flashcards

1
Q

Process of haemostasis?

A
  1. Vasoconstriction
  2. Platelet plug formation (adhesion, activation and aggregation)
  3. Coagulation cascade
  4. Fibrin mesh to stabilise platelet plug
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2
Q

Types of anti-clotting drugs

A
  1. Anti-platelets
  2. Anti-coagulants
  3. Thrombolytics
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3
Q

4 main classes of anti-platelets

A
  1. NSAIDs (e.g. aspirin)
  2. Platelet GP IIB/IIIA receptor blockers
  3. ADP receptor blockers
  4. PDE inhibitor
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4
Q

Role of prostacyclin in inhibiting platelet aggregation?

A
  • Prostacyclin (PGI2) binds to platelet membrane receptors causing synthesis of cAMP from ATP
    -cAMP inhibits release of granules containing platelet aggregating agents
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5
Q

Role of thromboxane A2 in activating platelet aggregation?

A

-Thromboxane A2 causes release of arachidonic acid from the platelet membrane
-Increased synthesis of TXA2
-Binds to receptors on neighbouring platelets, initiating release of aggregating agents

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6
Q

Mechanism of action of aspirin in inhibiting platelet aggregation

A

-Irreversible COX inhibitor that decreases the synthesis of TXA2 from arachidonic acid

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7
Q

How long does the effect of aspirin last?

A

-Lifespan of the platelet as it is an irreversible COX inhibitor (7-10 days)

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8
Q

Clinical uses of aspirin

A
  1. Prophylactic treatment of transient cerebral ischaemia
  2. Reduce incidence of recurrent myocardial infarction
  3. Decrease mortality in post myocardial infarction in patients
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9
Q

Adverse effects of aspirin

A
  1. Bleeding (PGI2)
  2. Gastric upset and ulcers / GI bleeding (PGE2)
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10
Q

What 4 molecules do GPIIB/IIIA bind to activate platelet aggregation?

A
  1. Fibronectin
  2. Fibrinogen
  3. Vitronectin
  4. von Willebrand factor
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11
Q

MOA of GP IIB/IIIA blockers?

A

-Bind to GPIIB/IIIA, preventing the binding of fibrinogen and other ligands that promote platelet aggregation

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12
Q

Name the 3 GPIIB/IIIA blockers.

A
  1. Abciximab (monoclonal antibody; reversible inhibitor)
  2. Eptifibatide (analogue of the sequence at the carboxyl terminal of the delta chain of fibrinogen)
  3. Tirofiban (small molecule blocker)
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13
Q

2 clinical uses of GP IIB/IIIA blockers

A
  1. Prevent restenosis after coronary angioplasty
  2. Acute coronary syndromes
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14
Q

Name the 2 ADP receptor blockers that inhibit platelet activation

A
  1. Clopidogrel
  2. Ticlopidine
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15
Q

Name the phosphodiesterase inhibitor.

A

Dipyridamole (increases cAMP which inhibits granule release)

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16
Q

Name the 4 types of anticoagulants.

A
  1. Heparin derivatives
  2. Warfarin
  3. Lepirudin, hirudin
  4. Antithrombin III
17
Q

Describe 4 actions of thrombin

A
  1. Further thrombin generation by activating FV, VIII and IX
  2. Cleaves fibrinogen, forming fragments that polymerise to fibrin
  3. Activates FXIII, a fibrinoligase that forms fibrin-fibrin links, stabilising coagulum
  4. Platelet aggregation, smooth muscle cell proliferation and contraction
18
Q

Function of antithrombin III

A

Irreversibly inactivates IIa, IXa and Xa by forming equilimolar stable complexes with them

19
Q

What are heparins?

A

Sulfated glycosaminoglycans (mucopolysaccharides)

20
Q

Do LMWHs or unfractionated heparins have a longer duration of action?

A

LMWHs

21
Q

MOA of heparin

A

-Binds to ATIII, induces a conformational change that exposes its active site for more rapid interaction with clotting factor proteases
-To inactivate IIa, needs to bind to IIa and ATIII
-To inactivate Xa, only needs to bind to ATIII

22
Q

MOA of LMWHs

A

-Increases action of ATIII on Xa but not IIa

23
Q

Clinical uses of heparin

A
  1. DVT, PE and AMI (Prevents worsening and spread of thrombus)
  2. Combined with thrombolytics for revascularisation
  3. Combined with GP IIa/IIIb inhibitors for angioplasty and placement of coronary stents
  4. Anticoagulant of choice in pregnancy
24
Q

How is heparin administered?

A

IV or subcutaneously (NO IM as it predisposes to haematoma formation)

25
Q

Two adverse effects of heparin

A
  1. Haemorrhage (Stop heparin and administer protamine sulfate)
  2. Thrombosis and thrombocytopaenia (Ig M and Ig G mediated)
26
Q

What is Vitamin K used for in the body?

A

Reduced vitamin K is an essential cofactor in the carboxylation (post-translational modification) of glutamate residues (FII, VII, IX and X)

27
Q

Two clinical uses of Vitamin K?

A
  1. Treatment and/or prevention of bleeding resulting from use of oral anticoagulants (e.g. warfarin) and prevention of haemorrhagic disease of the newborn; give reduced Vit K
  2. Vitamin K deficiencies in adults
28
Q

MOA of warfarin

A

Inhibits Vit K reductase, preventing the formation of reduced Vitamin K and thus the post-translational modification of FII, VII, IX and X

29
Q

Clinical uses of warfarin

A

Same as heparin but MUST NOT be used in pregnancy

30
Q

PK factors of warfarin

A
  1. Small and lipid-soluble, good oral bioavailbility
  2. Small Vd, >99% bound to plasma albumin
  3. Elimination by CYP450
31
Q

Three adverse effects of warfarin

A
  1. Bleeding
  2. Contraindicated in pregnancy due to fetal haemorrhagic disorder and effects on fetal proteins with gamma carboxyglutamate residues in bone and blood
  3. DDIs (CYP450)
32
Q

Name the 4 thrombolytic agents

A
  1. t-PA (alteplase)
  2. Urokinase
  3. Streptokinase
  4. Anistreplase
33
Q

MOA of thrombolytic agents

A

Activate plasminogen, forming plasmin which degrades fibrin to form fibrin degradation products

34
Q

Three clinical uses of thrombolytics

A
  1. Emergency treatment of coronary artery thrombosis
  2. Peripheral arterial thrombosis and emboli (e.g. PE)
  3. Ischaemic stroke (<4.5h)
35
Q

How are thrombolytic agents administered?

A

Intracoronary or IV injection

36
Q

Two adverse effects of thrombolytic agents?

A
  1. Bleeding
  2. CI: healing wound, pregnancy

CVS Pharmacology (3 decks)

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