Brainscape's Knowledge GenomeTM

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


See full index

B and L exam 4 > Pharmacology of anticoagulation > Flashcards

Pharmacology of anticoagulation Flashcards

1
Q
  1. Describe the mechanism of action and pharmacokinetics of heparin and low molecular weight heparins, and differences in management of patients on these therapies.

Heparin

MOA: heparin potentiates the action of _______ to inactivate ___, ____, _____, ____ and _____.

Do you need to adjust dose in renal dysfunction?

A
  • Molecule
  • 3000-30,000 kilodaltons (mean 15,000 kDa)
  • 1/3 of molecules possess a pentasaccharide sequence capable of binding to antithrombin (AT).
  • very negatively charged
  • **Porcine product
  • MOA:
  • potentiates the action of antithrombin inactivating IIa (thrombin), Xa, IXa, XIa, and XIIa
  • inactivates IIa via heparin cofactor II independent of pentasaccharide (requires very high doses)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. Describe the mechanism of action and pharmacokinetics of heparin and low molecular weight heparins, and differences in management of patients on these therapies.

Low molecular weight heparins:

By potentiating the action of Antithrombin they inactivate factors ______ and ______.

Clearence is ________.

Is the outcome more or less predicatable than that of heparin?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Describe the complications associated with heparin therapy, including excessive bleeding and heparin-induced thrombocytopenia with associated thrombosis.

For bleeding, _____ is used to reverse heparin.

No reversal available for ____, ____, _____.

What is heparin induced thrombocytopenia?

What are the four Ts to condiser in HIT?

What alternatives to use other than heparin?

A

i.Complications of parenteral anticoagulants

Bleeding

-Protamine sulfate to reverse heparin.

No reversal available for *fondaparinux, *bivalirudin, or *argatroban

Heparin induced thrombocytopenia (HIT)

  • 50% decrease in platelets usually 5-10 days of heparin start
    i. Consider 4Ts (Thrombocytopenia, Timing, Thrombosis, oTher cause for thrombocytopenia)
    ii. Presence of platelet-activating anti-PF4 antibodies

Discontinue all heparin

High risk of thrombosis (arterial or venous)

i.Treat with non-heparin, use instead:

1.Direct thrombin inhibitor

2.Fondaparinux

3.Warfarin (once platelets >150k)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. Describe the alternative anticoagulant therapies used for patients with heparin-induced thrombocytopenia.

Fondaparinux

It is a synthetic version of ________ AT binding ________ that is modified to increase affinity for AT.

Explain its MOA:

Is it derived from porcine?

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

Fondaparinux indications include:

A
  • Venous thromboembolism (VTE)
  • VTE prophylaxis
  • Arterial clots
  • Acute coronary syndrome
  • Percutaneous coronary intervention
  • Bridge anticoagulation to warfarin, dabigatran, edoxaban
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the differences between heparin and LMWH:

Which one is cleared via non-kidney mechanisms?

Which one is has more unpredictable side effects and a shorter half-life?

Which one requires frequent lab monitoring?

Which one can be used during pregnancy?

Which one has complete reversal of its effects?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. Describe the alternative anticoagulant therapies used for patients with heparin-induced thrombocytopenia

Bivalirudin:

Binds to active site of thrombin via ______ residues and interacts with exocite 1 on thrombin.

It increases ______.

Used to treat_______.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Describe the alternative anticoagulant therapies used for patients with heparin-induced thrombocytopenia

Argatroban:

It is very small around_____ kDa

Increases INR and it is used to treat ________.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. Describe the mechanism of action, pharmacokinetic and uses of oral anticoagulant warfarin.

Warfarin is a _____ analogue.

MOA: interferes with cyclic interconversion of ____ and vitamin K epoxide which modulates the gamma-carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins.

Why is carboxylation important?

Which warfarin has a half-life of 45 hours? 29 hours?

Which warfarin is metabilized by CYP3A4?

Which warfarin is metabolized by CYP2C9 (VKOR)?

A

Molecule: vitamin K analogue

  • MOA: interferes with cyclic interconversion of vitamin K and vitamin K epoxide which modulates the y-carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins
  • carboxylation is required for a *calcium-dependent conformational change in coagulation proteins that promotes binding to cofactors on phospholipid surfaces.
  • Half-life:
  • R-warfarin 45 hours
  • S-warfarin 29 hours
  • Metabolism:
  • R-warfarin CYP3A4
  • S-warfarin CYP2C9 (VKOR) enzyme mutations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. Describe the mechanism of action, pharmacokinetic and uses of oral anticoagulant warfarin.
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Direct Oral anticoagulants:

  • Dabigatran, apixaban, rivaroxaban, and edoxaban approved for ___1____ and _____2______ treatment
  • ___3____ only for VTE prophylaxis
A

1- venous thromboembolism

2- non-valvular atrial fibrillation

3- Betrixaban

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

Efficacy of Direct Oral Anticoagulant vs. Vitamin K antagonist in treating atrial debrifillation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. Describe the adverse effects and potential complications associated with use of warfarin.
A

•Heparin induced thrombocytopenia (HIT)

  • 50% decrease in platelets usually 5-10 days of heparin start
  • Discontinue all heparin
  • High risk of thrombosis (arterial or venous)

Skin necrosis/limb gangrene

•warfarin

Purple toe syndrome

•warfarin

Bone abnormalities

  • Heparin
  • Warfarin

Bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. Describe the mechanisms of action and uses of fibrinolytic agents

Which has the shortest half-life?

Clearence of which one is by antibodies and renal?

A

Uses:

  • Acute Ischemic Stroke
  • Pulmonary Embolism
  • Myocardial infarction
  • Limb ischemia
  • Frostbite
  • Parapneumonic effusion and empyema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. Describe the mechanisms of action and uses of fibrinolytic agents
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. Describe the mechanisms of action and uses of antiplatelet agents.
A

Antiplatelet agents

  • Inhibits formation of platelet products
  • Inhibits platelet activation and aggregation (ADP receptor antagonists)
  • Inhibits adhesion proteins (glycoprotein IIb/IIIa inhibitors)
  • Inhibits protease-activated receptor-1 (PAR-1)
17
Q
  1. Describe the mechanisms of action and uses of antiplatelet agents.
A

Oral agents

Aspirin and thienopyridines

  • Acute coronary syndrome
  • If stent, ADP receptor antagonist combination with aspirin
  • Prevention of myocardial infarction
  • Prevention of acute ischemic stroke

Dipyridamole

•Adjunct therapy for prevention of acute ischemic stroke

Cilostazol

  • Intermittent claudication
  • If unable to tolerate other oral antiplatelet agents, could use for stroke or following stent

Intravenous agents (abciximab, eptifibatide, tirofiban)

  • Angioplasty after myocardial infarction
  • Unstable angina

B and L exam 4 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions