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Pharmacology > Antiplatelet agents > Flashcards

Antiplatelet agents Flashcards

1
Q

Antiplatelet agents are used for prevention and treatment of:

A

thrombotic disease (CVA, MI)

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2
Q

How is ASA different from other NSAIDs?

A

Irreversibly bind and inhibits COX enzyme for life of the platelet (7-10days)

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3
Q

What is the MOA of COX inhibitors?

A

Inhibit the COX enzyme which inhibits TxA2 which usually causes platelet aggregation

(also inhibits prostacyclin, which has a natural antiplt effect, in endothelial cells. Endothelial cells are able to synthesize new COX enzymes)

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4
Q

COX inhibitors include:

A

NSAIDs, ASA

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5
Q

What is the MOA of ADP Receptor Inhibitors?

A

Irreversibly inactivates or antagonizes the platelet P2Y (ADP) receptors which inhibits platelet activation

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6
Q

ADP Receptors Inhibitors include:

A

Ticlodipine (Ticlid)
Clopidogrel (Plavix)
Prasurgurel (Effient)
Ticragrelor (Brillanta)

All prodrugs and irreversible except Ticragrelor
Can be used with ASA

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7
Q

Ticlodipine (Ticlid):

A

ADP Receptor Inhibitor

  • Prodrug
  • Maximal plt inhibition within 8-11days, or 4-7 days with ASA
  • Loading dose often given
  • AE: neutropenia, thrombocytopenia, TTP
  • Monitor CBC frequently
  • Less tolerable and slower onset than clopidogrel
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8
Q

Clopidogrel (Plavix)

A

ADP Receptor Inhibitor
-Prodrug
**Metabolized to its active form by CYP 2C19
(poor met by genetic predisposition=less effective; drugs like omeprazole can inhibit CYP2C19= can’t activate prodrug)
-Loading dose often given
-Less AE
-GI AE similar to ASA

**Omeprazole inhibits CYP induction, Rotonavir induces

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9
Q

Prasugrel (Effient)

A

ADP receptor inhibitor

  • Prodrug
  • More complete inhibition of P2Y(ADP) receptor; efficiently metabolized=higher concentration of active drug= increased risk of bleeding
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10
Q

Ticagrelor (Brilinta)

A

ADP Receptor Inhibitor

  • Active form (not a prodrug) with active metabolites
  • Reversible and noncompetitive inhibition of P2Y (ADP) receptors (recovery of plt function depends on serum concentration of drug and its active metabolites)
  • Metabolized by CYP 3A4
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11
Q

What is the MOA of GPIIb/IIIa Antagonists?

A

Inhibit the GPIIb/IIIa receptors on platelets which link together to cause aggregation (final pathway/step)

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12
Q

What is the route of administration of GPIIb/IIIa antagonists?

A

IV

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13
Q

The most common AE of GPIIb/IIIa antagonists:

A

Bleeding

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14
Q

Abciximab: Class, AE

A

GPIIb/IIIa antagonist

Bleeding: Irreversible, fresh platelet infusion needed

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15
Q

Eptifibatide, tirofiban: Class, AE

A

GPIIb/IIIa antagonists
Bleeding: Reversible, drug greatly outnumbers receptors. Wait for drug clearance, do not immediately transfuse platelets = drug will attach to new platelets as well.

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16
Q

What is the MOA of Phosphodiesterase inhibitors?

A

Inhibit breakdown of cAMP which decreases platelet activation. These drugs are uses in combination with another antiplatelet therapy

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17
Q

Dipyridamole:

A

Phosphodiesterase inhibitor

Weak plt inhibitor

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18
Q

Vit K is required for normal hepatic synthesis of what coagulation factors and proteins?

A

Factors, II, VII, IX, X

Protein C and S (body’s natural anticoagulants- balance)

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19
Q

Vit K in its inactive form is activated or regenerated by what and how is this related to warfarin’s MOA?

A

Epoxide reductase

Warfarin inhibits the C1 subunit of vitamin K epoxide reductase (VKORC1) enzyme complex

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20
Q

Warfarin can also be called a____ _______.

A

Vit K antagonist

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21
Q

Degree of depression of VKORCI is dependent on:

A

Dosage

Patient’s VKORC1 genotype: sensitive/resistant

22
Q

What are the half life of the clotting factors and proteins that warfarin affects?

A 
Factor II: 60hrs
Factor VII: 4-6hrs
Factor IX: 24hrs
Factor X: 48hrs
Protein C: 8hrs
Protein S: 30hrs
23
Q

What is warfarin’s onset, peak, and duration of a single dose?

A

Onset: 24 hours
Peak: 72-96 hours
Duration of single dose: 2-5 days

24
Q

Roughly how many days should you wait to check a warfarin level after a dose has been changed?

A

4 days

25
Q

Warfarin is a racemic mixture of R- and S-enantiomers; which is the more active and how is it metabolized?

A

The S-enantiomer has 2-5x anticoagulant activity
Metabolized by CYP 2C9
Pts with variant CYP 2C9 alleles have decreased warfarin clearance
(R enantiomer also met by CYP pathway)

26
Q

Two main genetic important components related to warfarin?

A

VKORC1

CYP 2C9 allele

27
Q

What percentage of warfarin is albumin/protein bound and why is this important?

A

99%, this means most of drug is bound and not active in circulation.
Many drugs can displace warfarin from albumin and move to systemic circulation.
**Ex- amiodarone, chloral hydrate, clopiodogrel, alcohol

28
Q

How do broad spectrum abx affect warfarin?

A

Eliminate gut bacteria which decreases availability of vit K that is usually present in the GI tract, enhancing the effects of warfarin

29
Q

Examples of vit K rich foods and how patients should be counseled about their intake:

A

Green, leafy vegetables, beef/pork liver, legumes.

Keep intake consistent

30
Q

What is the most common AE of warfarin and how is it treated?

A

Bleeding
Hemorrhage: administer FFP (contains II, VII, IX, X)
Minor: vit K administration

31
Q

How can warfarin cause skin necrosis?

A

Microvascular thrombosis secondary to inhibition of Protein C & S (body’s natural anticoagulants). Many of the Factors have longer half lives. Protein C is inhibited earlier which causes thrombosis prior to other Factors being depleted.

**Bridge w/heparin

32
Q

Purple toe syndrome caused by warfarin is related to the breakage of ________ which travel to the feet.

A

Small cholesterol deposits

33
Q

How does warfarin causes osteoporosis?

A

Reduced dietary intake of vit K (misconception)

Inhibition of vit K mediated bone formation/maintenance

34
Q

Goal INRs are generally:

A

2-3 or 2.5-3.5

standardized PT

35
Q

Why is warfarin frequently monitored (4)?

A
  1. Narrow TI
  2. Drug interactions
  3. Pharmacogenetics (CYP2C9 and VKORC1)
  4. Toxicity risks
36
Q

Unfractionated heparin catalyzes inactivation of:

A

Less selective:
Thrombin (IIa)
Xa

37
Q

How is unfractioned heparin monitored?

A

aPTT (activated partial thromboplastin time)

High levels= prolonged time to fibrin clot formation

38
Q

LMWH includes which drugs and is more selective for inactivation of what?

A

Exoxaparin, dalteparin, tinzaprin

More selective for inactivation of Factor Xa>thrombin (3:1)

39
Q

Why is monitoring of LMWH less necessary than heparin?

A

Larger TI

Could measure antifactor Xa activity

40
Q

How is LMWH eliminated?

A

Renally

41
Q

What is the difference between UF and LMWH in respect to half life and therefore administration?

A

UF has a shorter half life and therefore needs to be administered continuously
LMWH’s half life is longer and injections usually need to be given twice a day

42
Q

What is HIT?

What are the 2 types?

A

Heparin induced Thrombocytopenia
Development of Ab to heparin bound platelets
More common with UF

Type 1:
Ab coated plts targeted for removal from circulation
50-75% reduction in plt count in 5days
Transient and reversible (stop heparin)

Type 2:
Also targets platelets for destruction
Ab also causes platelet activation and aggregation which would lead to fatal thrombosis

43
Q

What is the antidote for heparin?

A

Protamine chemically antagonizes heparin

some effect on LMWH, none on fondaprinux

44
Q

Factor Xa inhibitors include:

A

Fondaparinux- IV

Rivaroxaban (Xarelto), apixaban (Eliquis)- oral

45
Q

Direct thrombin inhibitors (Lepirudin, hirudin, desirudin, bivalirudin, argatroban, dabigatran) are often used to treat:

A

HIT

Prevent further reduction of plt count while preventing thrombosis

46
Q

Dabigatran (Pradaxa):

A

Oral direct thrombin inhibitor
Prodrug, active drug binds competitively to active site of thrombin
No frequent laboratory monitoring
? Significant bleeding, MI risk increased

47
Q

MOA of thrombolytics:

A

Lysis of existing clot

Restore patency of obstructed tissue and prevent distal tissue necrosis

48
Q

Thrombolytics works as _________ activators.

A

Plasmin

which degrades cross-linked fibrin polymers which are essential to the formation of a stable clot

49
Q

Clinical indications for thrombolytic administration:

A

Acute MI
Acute ischemic stroke (NOT hemorrhagic)
Massive PE
Central line occlusion (local application)

50
Q

AE of thromboyltics include:

A

Dissolution of pathologic thrombi or physiologically appropriate fibrin clots
=Bleeding/Hemorrhage

Pharmacology (48 decks)

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