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Systemic Pharmaco > Anti-Platelets & Anti-Thrombotics > Flashcards

Anti-Platelets & Anti-Thrombotics Flashcards

1
Q

Review the process of haemostasis

A
  1. Vasoconstriction, vascular spasm
  2. Primary haemostasis (platelet adhesion, activation, aggregation)
  3. Secondary haemostasis (coagulation cascade, fibrin clot formation)
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2
Q

What are the 3 main classes of anti-clotting drugs?

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

What are the 4 classes of anti-platelet drugs?

A
  1. NSAIDs
  2. GPIIb/IIIa receptor blockers
  3. ADP receptor blockers
  4. Phosphodiesterase inhibitor
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4
Q

Briefly explain the events involved in platelet activation and aggregation, starting from what the healthy endothelium produces

A
  1. Healthy endothelium releases prostacyclin (activates adenylyl cyclase, cAMP, inhibits platelet degranulation)
  2. Thrombin, thromboxane A2, exposed collagen of damaged endothelium releases arachidonic acid from platelet membrane (synthesise more TXA2)
  3. TXA2 binds receptors on other platelets (stimulate degranulation)
  4. Balance btwn levels of prostacyclin & TXA2 determines platelet aggregation or free circulation
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5
Q

What is the MOA of aspirin?

A

Irreversibly inhibit COX enzymes

  • Decrease conversion of arachidonic acid to PGG2 (early PGE2)
  • Decrease TXA2, PGI2, PGE2
  • Decrease degranulation of other platelets by TXA2
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6
Q

How long does the inhibitory effect of aspirin last? Why?

A

Rapid and lasts for life of the platelet (irreversible) approx. 7-10d

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7
Q

What are the clinical uses of aspirin?

A
  1. Prophylactic treatment of transient cerebral ischaemia
  2. Reduce incidence of recurrent MI
  3. Decrease mortality in post MI pt
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8
Q

What are the adverse effects of aspirin?

A

Gastric upset & ulcers (decreased protective fn of gastric mucosa by PGE2)

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9
Q

What are the GP IIb/IIIa receptor blockers?

A

Abciximab
Eptifibatide
Tirofiban

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10
Q

What is the general function of GP IIb/IIIa receptor blockers?

A

Blocks platelet aggregation with fibrinogen

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11
Q

What is the MOA of abciximab? Can it be overcome?

A

(Humanized monoclonal Ab against GP IIb/IIIa complex)

Reversibly inhibits binding of fibrinogen & other ligands to GP IIb/IIIa
- Can be overcome by increased fibrinogen

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12
Q

What is the MOA of eptifibatide?

A

(Analog of fibrinogen)

Mediates binding of fibrinogen to the receptor
- Prevents actual fibrinogen from binding

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13
Q

What is the MOA of tirofiban?

A

Small molecule blocker of GP IIb/IIIa

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14
Q

What are the clinical uses of GP IIb/IIIa receptor inhibitors?

A
  1. Prevent restenosis after coronary angioplasty

2. Used in acute coronary syndromes

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15
Q

What are the ADP receptor blockers?

A

Clopidogrel

Ticlopidine

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16
Q

What is the MOA of ADP receptor blockers?

A

Prevent binding of ADP to ADP receptor

- Prevent platelet degranulation

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17
Q

What is the phosphodiesterase (PDE) inhibitor?

A

Dipyridamole

18
Q

What is the MOA of PDE inhibitors?

A

Inhibits PDE

  • Inhibits breakdown of cAMP to AMP
  • Accumulation of cAMP (negative, “everything’s fine!!!” signal)
  • Inhibits platelet degranulation
19
Q

What are the types of anti-coagulants?

A

Heparin
Warfarin
Antithrombin III

20
Q

What is the MOA of heparin?

A

Active heparin binds ATIII and cause a conformational change

  • Exposes active site for more rapid interaction w proteases (potentiates ATIII fn)
  • To inhibit IIa (thrombin): must bind IIa + ATIII
  • To inhibit Xa: only need to bind to ATIII
21
Q

What is the MOA of low molecular weight heparin? How is it different from normal heparin?

A

Low molecular weight heparin (LMWH) increase action of ATIII only on Xa but NOT on IIa (thrombin)

  • LMWH have longer durations of action than heparin
22
Q

How is heparin administered?

A

Given IV or S.C

23
Q

Which method of administration cannot be used for heparin?

A

NEVER GIVEN IM (CAUSE HEMATOMAS!!)

24
Q

What are the clinical uses of heparin? What other drugs is it used in combination with?

A
  1. Treatment of DVT, PE, AMI (prevent further worsening & spread but does not resolve the existing thrombus)
  2. Used in combination w thrombolytics for revascularization
  3. Used in combination w GP IIb/IIIa inhibitors during angioplasty & placement of coronary stents
  4. Used when an anti-coagulant must be used in pregnancy
25
Q

What are the adverse effects of heparin? How can it be reversed?

A
  1. Haemorrhage
    - Stop heparin therapy + give protamin sulfate (heparin chelator)
  2. Thrombosis & thrombocytopenia
26
Q

What is the purpose of vit. K in clotting factors?

A

(Fat-soluble vitamin essential for II, VII, IX, X)

Reduced vit. K essential cofactor in the carboxylation (post-translational modification) of glutamate residues

  • Activates factors II, VII, IX, X
  • Increase clotting
27
Q

What are the clinical uses of vit. K?

A
  1. Treatment and/or prevention of bleeding
    - Resulting from use of oral anticoagulant (eg. warfarin): give *reduced vit. K
    - In babes: To prevent haemorrhagic disease of newborn
  2. For vit. K deficiencies in adults
28
Q

What is the MOA of warfarin?

A

Inhibits reduction of vit K. required for carboxylation of clotting factors

  • Reduced active clotting factors II, VII, IX, X
  • Decrease clotting
29
Q

How is warfarin administered?

A

Orally

30
Q

How is warfarin eliminated?

A

Elimination by hepatic cytochrome p450

31
Q

What is the Vd of warfarin?

A

Small Vd (strongly bound to plasma albumin >99%)

32
Q

What are the clinical uses of warfarin?

A

(same as heparin but not used in pregnant women)

  1. Treatment of DVT, PE, AMI (prevent further worsening & spread but does not resolve the existing thrombus)
  2. Used in combination w thrombolytics for revascularization
  3. Used in combination w GP IIb/IIIa inhibitors during angioplasty & placement of coronary stents
33
Q

What are the adverse effects of warfarin?

A
  1. Haemorrhage
  2. NEVER ADMINISTERED IN PREGNANCY
    - Cross placenta readily & can cause haemorrhagic disorder in fetus
    - Fetal proteins w ∂-carboxyglutamate residues found in bone & blood may be affected
  3. DDIs w CYP450 inducers (barbiturates, carbamazepine, phenytoin) & inhibitors (amiodarone, cimetidine, disulfiram, imipramine) – will need dose adjustment
34
Q

What are the contraindications for warfarin? What can be used instead?

A

Pregnant women

use heparin instead

35
Q

What is the MOA of antithrombin III?

A

(Endogenous anti-clotting protein)

Irreversibly inactivates clotting factor proteases esp. IIa (thrombin), IXa, Xa by forming stable complexes w them

36
Q

What are the 4 thrombolytic agents?

A

t-PA (Alteplase)
Urokinase
Streptokinase
Anistreplase

37
Q

What is the MOA of thrombolytic agents?

A

(All function as tissue plasminogen activator but only alteplase is called that)

Stimulates conversion of plasminogen to plasmin
- Degrades fibrin to fibrin degradation products

38
Q

How are thrombolytic agents administered?

A
  1. Intracoronary injection

2. Intravenous injection

39
Q

What are the clinical uses of thrombolytic agents?

A
  1. Emergency treatment of coronary artery thrombosis

2. Peripheral arterial thrombosis and emboli

40
Q

What are the adverse effects of thrombolytic agents?

A

Bleeding (aft. removal of clot)

41
Q

What are the contraindications of thrombolytic agents?

A
  1. Healing wound (clotting is to allow for wound healing, decreased clotting will impair healing)
  2. Pregnant women

Systemic Pharmaco (6 decks)

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