Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Antiplatelet agents > Flashcards

Antiplatelet agents Flashcards

1
Q

Antiplatelet agents are used for prevention and treatment of:

A

thrombotic disease (CVA, MI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is ASA different from other NSAIDs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

COX inhibitors include:

A

NSAIDs, ASA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the MOA of ADP Receptor Inhibitors?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The most common AE of GPIIb/IIIa antagonists:

A

Bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Abciximab: Class, AE

A

GPIIb/IIIa antagonist

Bleeding: Irreversible, fresh platelet infusion needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Dipyridamole:

A

Phosphodiesterase inhibitor

Weak plt inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Warfarin can also be called a____ _______.

A

Vit K antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

25
Warfarin is a racemic mixture of R- and S-enantiomers; which is the more active and how is it metabolized?
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
Two main genetic important components related to warfarin?
VKORC1 | CYP 2C9 allele
27
What percentage of warfarin is albumin/protein bound and why is this important?
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
How do broad spectrum abx affect warfarin?
Eliminate gut bacteria which decreases availability of vit K that is usually present in the GI tract, enhancing the effects of warfarin
29
Examples of vit K rich foods and how patients should be counseled about their intake:
Green, leafy vegetables, beef/pork liver, legumes. | Keep intake consistent
30
What is the most common AE of warfarin and how is it treated?
Bleeding Hemorrhage: administer FFP (contains II, VII, IX, X) Minor: vit K administration
31
How can warfarin cause skin necrosis?
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
Purple toe syndrome caused by warfarin is related to the breakage of ________ which travel to the feet.
Small cholesterol deposits
33
How does warfarin causes osteoporosis?
Reduced dietary intake of vit K (misconception) | Inhibition of vit K mediated bone formation/maintenance
34
Goal INRs are generally:
2-3 or 2.5-3.5 | standardized PT
35
Why is warfarin frequently monitored (4)?
1. Narrow TI 2. Drug interactions 3. Pharmacogenetics (CYP2C9 and VKORC1) 4. Toxicity risks
36
Unfractionated heparin catalyzes inactivation of:
Less selective: Thrombin (IIa) Xa
37
How is unfractioned heparin monitored?
aPTT (activated partial thromboplastin time) High levels= prolonged time to fibrin clot formation
38
LMWH includes which drugs and is more selective for inactivation of what?
Exoxaparin, dalteparin, tinzaprin | More selective for inactivation of Factor Xa>thrombin (3:1)
39
Why is monitoring of LMWH less necessary than heparin?
Larger TI | Could measure antifactor Xa activity
40
How is LMWH eliminated?
Renally
41
What is the difference between UF and LMWH in respect to half life and therefore administration?
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
What is HIT? | What are the 2 types?
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
What is the antidote for heparin?
Protamine chemically antagonizes heparin | some effect on LMWH, none on fondaprinux
44
Factor Xa inhibitors include:
Fondaparinux- IV | Rivaroxaban (Xarelto), apixaban (Eliquis)- oral
45
Direct thrombin inhibitors (Lepirudin, hirudin, desirudin, bivalirudin, argatroban, dabigatran) are often used to treat:
HIT | Prevent further reduction of plt count while preventing thrombosis
46
Dabigatran (Pradaxa):
Oral direct thrombin inhibitor Prodrug, active drug binds competitively to active site of thrombin No frequent laboratory monitoring ? Significant bleeding, MI risk increased
47
MOA of thrombolytics:
Lysis of existing clot | Restore patency of obstructed tissue and prevent distal tissue necrosis
48
Thrombolytics works as _________ activators.
Plasmin | which degrades cross-linked fibrin polymers which are essential to the formation of a stable clot
49
Clinical indications for thrombolytic administration:
Acute MI Acute ischemic stroke (NOT hemorrhagic) Massive PE Central line occlusion (local application)
50
AE of thromboyltics include:
Dissolution of pathologic thrombi or physiologically appropriate fibrin clots =Bleeding/Hemorrhage

Pharmacology (48 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions