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CVS Pharmaco > Antiplatelets and Antithrombotics > Flashcards

Antiplatelets and Antithrombotics Flashcards

1
Q

Name 3 classes of anti clotting drugs

A
  1. Antiplatelets
  2. Anticoagulants
  3. Thrombolytics
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2
Q

Name 4 classes of antiplatelets

A
  1. NSAIDs
  2. Platelet GPIIB/IIIA receptor blockers
  3. ADP receptor blockers
  4. Phosphodiesterase (PDE) inhibitors
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3
Q

Name an example of a NSAID antiplatelet

A

Aspirin

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4
Q

Name 3 examples of platelet GPIIB/IIIA receptor blockers

A
  1. Abciximab
  2. Tirofiban
  3. Eptifibatide
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5
Q

Name 2 examples of ADP receptor blockers

A
  1. Ticlopidine
  2. Clopidogrel
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6
Q

Name a PDE inhibitor

A

Dipyridamole

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7
Q

MOA of aspirin

A

COX 1 and COX 2 inhibitor, which reduces conversion of arachidonic acid to eicosanoids. Acts as an anti platelet

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8
Q

3 clinical uses of aspirin

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

2 ADRs of aspirin use

A
  1. Bleeding (PGI2)
  2. GI effects: gastric upset, ulcers, GI bleeding (PGE2)
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10
Q

State the normal function of GPIIb/IIIa receptor

A

A platelet membrane surface protein.
GPIIb/IIIa complex functions as a receptor for mainly fibrinogen and vitronectin, and also fibronectin and vWF.
Activation of the complex is the final common pathway for platelet aggregation

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11
Q

Structure of abciximab

A

Chimeric monoclonal antibody that reversibly inhibits the GPIIb/IIIa receptor complex

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12
Q

Structure of eptifibatide

A

Structural analogue of the carboxyl terminal of fibrinogen, thus binds reversibly to the GPIIb/IIIa receptor complex

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13
Q

2 clinical uses of platelet GPIIb/IIIa receptor blockers

A
  1. Prevent restenosis after coronary angioplasty
  2. Treatment of acute coronary syndrome
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14
Q

MOA of clopidogrel and ticlopidine

A

ADP receptor inhibitor. Prevent binding of ADP, reduce platelet aggregation

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15
Q

MOA of dipyridamole

A

Inhibits PDE which prevents conversion of cAMP to AMP, thus reducing platelet aggregation

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16
Q

Name the 4 drug classes for anticoagulants

A
  1. Heparin derivatives
  2. Coumarin derivatives (Warfarin)
  3. Lepirudin, Hirudin
  4. Antithrombin III
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17
Q

Outline 4 physiological actions / effects of thrombin

A
  1. Activates upstream proteins (esp factor V, VIII and XI) which increases thrombin generation
  2. Cleaves fibrinogen into fibrin which polymerises
  3. Activates factor XIII to factor XIIIa which stabilises the fibrin-fibrin linkages
  4. Increases platelet aggregation, stimulates smooth muscle contraction and increases cell proliferation
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18
Q

MOA of antithrombin III

A

Endogenous anticlotting protein that irreversibly binds and inactivates clotting factor proteases, especially IIa (thrombin), IXa and Xa by forming equilimolar stable complexes with them

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19
Q

Heparin is a family of sulfated…

A

Glycosaminoglycans

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20
Q

State 2 PK advantages of low molecular weight heparin (LMWH) compared to regular heparin

A
  1. Higher bioavailability
  2. Longer half-life
21
Q

MOA of heparin on factor IIa (thrombin)

A

Binds tightly to ATIII, causing a conformational change which exposes its active site for more rapid interaction with the protease
Must bind to BOTH ATIII and factor IIa to inhibit thrombin

22
Q

MOA of heparin on factor Xa

A

Binds tightly to ATIII, causing a conformational change which exposes its active site for more rapid interaction with the protease
Only needs to bind to ATIII to inhibit factor Xa

23
Q

LMWHs increase the action of ATIII on factor ___ but not on factor ___

A

Increase action on factor Xa but not on factor IIa

24
Q

State 4 clinical uses of heparin

A
  1. Treatment of DVT, pulmonary embolism, acute myocardial infarction
  2. Combine with thrombolytics for revascularisation
  3. Combine with GPIIb/IIIa blockers during angioplasty and inserting coronary stents
  4. Used as an anticoagulant in certain pregnancies for treating venous thromboembolism (VTE)
25
Q

Is heparin / LMWH safe to use in pregnant patients?

A

Yes

26
Q

2 routes of administration for heparin

A
  1. Intravenous
  2. Subcutaneous
27
Q

Heparin must NEVER be administered ___ as it can cause ___

A

Intramuscularly
Hematomas

28
Q

State 2 ADRs of heparin use

A
  1. Haemorrhage
  2. Thrombocytopenia
29
Q

Outline the treatment for heparin induced haemorrhage

A

Stop heparin therapy
Give protamine sulfate (cationic peptide): Forms an inactive ionic complex with heparin

30
Q

Name the 4 clotting factors that require vitamin K

A

Factors II, VII, IX, X

31
Q

Functioning / activated vitamin K needs to be in the reduced or oxidised state?

A

Reduced state

32
Q

Name the enzyme that reduces oxidised vitamin K into its reduced form

A

Vitamin K reductase

33
Q

Name the type of reaction that reduced vitamin K is used in activating factors II, VII, IX, X

A

Carboxylation of glutamate residues in clotting factors

34
Q

State 3 clinical uses of vitamin K

A
  1. Treatment and prevention of bleeding from the use of oral anticoagulants
  2. Babies: Used to prevent haemorrhagic disease of the newborn
  3. Adults: For patients with vitamin K deficiency
35
Q

MOA of warfarin

A

Vitamin K reductase inhibitor.
Inhibits the reduction of oxidised vitamin K, thus reduces the carboxylation of glutamate residues in clotting factors II, VII, IX, X, thus inhibiting their coagulation function

36
Q

State 3 clinical uses of warfarin

A

*same as heparin
1. Treat DVT, PE, AMI
2. Combine with thrombolytics for revascularisation
3. Combine with GPIIb/IIIa during angioplasty and for inserting coronary stents

37
Q

Warfarin is administered

A

Orally

38
Q

Does warfarin bind to albumin in the blood?

A

Yes

39
Q

Where is warfarin metabolised?

A

Liver by CYP450

40
Q

State an adverse effect of warfarin use

A

Bleeding

41
Q

Warfarin is contraindicated in ___ because ___

A

Pregnancy
Crosses the placental barrier readily and causes haemorrhagic disease of the foetus.
It also affects fetal proteins containing gamma-carboxyglutamate residues

42
Q

Name 4 thrombolytic agents

A
  1. tPA (alteplase)
  2. Urokinase
  3. Streptokinase
  4. Anistreplase
43
Q

MOA of thrombolytic agents

A

Plasminogen activators which increase the conversion of plasminogen to plasmin, and thus increases fibrinolysis of fibrin clots / mesh, thus dissolving blood clots

44
Q

State 3 clinical uses of thrombolytics

A
  1. Emergency treatment in coronary artery thrombosis
  2. Peripheral artery thrombosis and emboli
  3. Ischaemic stroke
45
Q

Administering thrombolytics for ischaemic stroke must be done within (time window)

A

Less than 4.5 hours

46
Q

Can thrombolytics be used in haemorrhagic stroke?

A

No

47
Q

State 2 routes of administration for thrombolytics

A
  1. Intracoronary
  2. Intravenous
48
Q

State an adverse effect of thrombolytics

A

Bleeding

49
Q

Thrombolytics are contraindicated in 2 kinds of patients

A
  1. Healing wounds
  2. Pregnancy

CVS Pharmaco (6 decks)

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