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Pharmacology- Block 2 > 3-Antithrombotic Agents > Flashcards

3-Antithrombotic Agents Flashcards

1
Q

Aspirin (MOA, dose dep effects)

A
  1. MOA: irreversible acetylation of serine residue of COX-1
  2. Dose Dep:
    - Low dose = COX 1 specific inhibitor (only decreases TXA2 synthesis)
    - High dose = binds other COX forms (decrease synthesis of other PGs as well)
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2
Q

Thienopyridines (MOA & Name 4 types)

A

MOA: Antiplatelet drugs: Irreversibly inhibit ADP receptors on platelets (thus inhibit activation of GPIIb/IIIa receptors/platelet aggregation)

  1. Ticagrelor
  2. Ticlopidine
  3. Clopidogrel
  4. Prasugrel
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3
Q

Ticlopidine (Class, MOA, Metabolism)

A
  1. Class: Antiplatelet: irreversibly inhibit ADP receptors
  2. MOA: P2Y12 ADP platelet receptor
  3. Metabolism: Prodrug (parent drug inactive)
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4
Q

Clopidogrel (Class, Metabolism)

A

Plavix:
1. Class: Antiplatelet: irreversibly inhibit ADP receptors
2. Metabolism: Primarily metabolized by CYP 2C19
(Some genetic populations lack this enzyme: drug stuck in prodrug form)

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5
Q

Ticagrelor (Class, Metabolism, Other)

A
  1. Class: Antiplatelet: REVERSIBLY inhibit ADP platelet receptor
  2. Metabolism: NOT a prodrug (direct acting)
  3. Other: Faster onset/Greater inhibition of platelet aggregation than Clopidogrel
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6
Q

Name 3 GPIIb/IIIa Antagonists

A
  1. Abciximab (monoclonal antibody)
  2. Tirofiban (fibrinogen analogue)
  3. Eptifibatide (fibrinogen analogue

(inhibit final common pathway for platelet aggregation)

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7
Q

What 3 situations are Anti-Platelet drugs used for?

A
  1. MI prophylaxis
  2. Arterial occlusions leading to stroke
  3. Arterial platelet issues (venous platelets like DVT would use Warfarin)
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8
Q

Which GPIIb/IIIa antagonist is not specific for GPIIb/IIIa & undergoes clearance via reticuloendothelial cells?

A

Abiciximab

Eptifibatide & Tirofiban are cleared renally and are specific

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9
Q

What are GP2b/3a antagonists indicated (2)?

A
  1. Treatment of unstable coronary syndromes

2. Adjunct to reduce risk of periprocedural MI following percutaneous coronary interventions

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10
Q

Warfarin (MOA)

A

Anti-Coagulant:

  • Inhibits VitK-epoxide reductase -> decreases Vit-K dep molecules:
  • Coagulation factors II, VII, IX & X
  • Protein C & S (which inhibit factors V & VIII)
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11
Q

How is Warfarin transported throughout the blood? Significance?

A
  • 99% plasma protein bound (inactive)
  • 1% free (active)
  • Drugs w/ high plasma protein binding capacity (DM drug Sulfonylureas) kick Warfarin off plasma proteins and increase free, active Warfarin = increased bleeding risk
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12
Q

Warfarin (metabolism & 3 associated alleles)

A

Metabolism: CYP 2C9
Alleles:
- 1* = normal warfarin metabolized
- 2** = 70% warfarin metabolized (30% less warfarin broken down) = increased risk of bleeding
- 3*** = 10% warfarin metabolized (90% less warfarin broken down) = super increased risk of bleeding

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13
Q

When would you use Warfarin?

A

Venous thrombolytic issues (DVT)

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14
Q

Warfarin (advantages & disadvantages)

A 
Advantages: 
- Oral
- Cheap
Disadvantages: 
- Bleeding
- Cross placenta (switch pregnant women to Heparin)
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15
Q

What 2 products would you administer for Warfarin reversal? Which has a more immediate action?

A
  • Fresh Frozen Plasma + Vitamin K

- FFP = more immediate action (Vit K takes time to induce synthesis of coagulation factors)

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16
Q

What is the HASBLED score?

A
  • Used in clinic to measure risk of warfarin
  • Max score of 9
  • Score over 3 = high risk of bleeding
  • HASBLED = Hypertension (1), Abnormal renal/liver fxn (2), Stroke (1), Bleeding (1), Labile INRs (1), Elderly (1), Drugs/Alcohol (2)
17
Q

Name 7 drugs that inhibit CYP 2C9? Significance w/ relation to Warfarin?

A

“Pams Off”

  1. Paroxetine
  2. Amiodarone
  3. Metronidazole
  4. Sulfonamides
  5. Omeprazole
  6. Fluconazole
  7. Fluoxetine

Decrease metabolism, thus increase active blood levels of Warfarin = increase risk of bleeding

18
Q

Name 3 drugs that induce CYP 2C9? Significance w/ relation to Warfarin?

A

RPC

  1. Rifampin
  2. Phenobarbital
  3. Carbamazepine

Increase metabolism, thus decrease active blood levels of warfarin = decrease risk of bleeding

19
Q

4 herbals that potentiate warfarin effects?

A
  1. Garlic
  2. Ginger
  3. Ginko
  4. Feverfew
20
Q

What is INR? Target INR?

A
  • INR = normalizes PT ratio by adjusting for the variability in the sensitivity of different thromboplastins
  • Target INR: 2-3
21
Q

Name 3 Warfarin dosing recommendations

A
  1. Individualize dose according to INR
  2. Loading dose controversial (may increase bleeding/may offer more rapid protection)
  3. Low initiation doses are recommended for elderly/frail/hepatic failure/malnourished patients
22
Q

Heparin (MOA, Conventional vs. LMWH)

A
  1. MOA: bind/enhance Antithrombin III (inhibits FII (thrombin) & X)
  2. Conventional Heparin aka Unfractionated Heparin (UFH):
    - Binds ATIII & Thrombin directly
  3. Low molecular weight heparin (LMWH):
    - Only binds ATIII
    - Higher specificity for Factor X
23
Q

How would you reverse Heparin?

A

Protamine Sulfate

PS is a base & Heparin is an acid

24
Q

Name 3 Low Molecular Weight Heparins (LMWH)

A

TED

  1. Tinzaparin
  2. Enoxaparin
  3. Dalteparin
25
Q

Which LMWH has a lower incidence of Hep-Induced-Thrombocytopenia?

A

Enoxaparin

26
Q

Fondiparinux (Class/Target)

A
  1. Class: Synthetic Heparin

2. Accelerates ATIII binding to FX ONLY (not FII)

27
Q

Name 3 Direct Thrombin Inhibitors (DTI)

A

BALD

  1. Bivalrudin (derived from saliva of leech)
  2. Argatroban
  3. Dabigatran (Pradaxa)
28
Q

How do you reverse Direct Thrombin Inhibitors?

A

You don’t. They have no antidotes.

29
Q

Name 2 oral Xa antagonists. When are these indicated?

A
  1. Roxirivaban
  2. Abixaban

Indications:

  1. Thromboprophylaxis in A-fib
  2. Reduce recurrent events after acute coronary syndromes
30
Q

Name 3 examples of fibrinolytic drugs.

A

TUS

  1. tPA
  2. Urokinase
  3. Streptokinase
31
Q

Name 2 anti-fibrinolytic drugs

A
  1. Aminocaproic acid

2. Tranexamic acid

Pharmacology- Block 2 (5 decks)

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