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heme/onc > anticoagulation: pharm > Flashcards

anticoagulation: pharm Flashcards

1
Q

Three major natural anticoagulant pathways

A
  1. Tissue factor pathway inhibitor (TFPI)
  2. Protein C / Protein S pathway
  3. Anti-thrombin III ** (AT-III)
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2
Q

antithrombin AT inhibits coagulation:

A
  1. thrombin IIa
  2. FIXa
  3. FXa
  4. FXIa
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3
Q

what accelerates AT inhibitor function by more than 1000x

A

heparin sulphate

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4
Q

Heparin (3)

A
  1. unfractionated heparin
  2. low molecular weight heparins
  3. synthetic pentasacchardie
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5
Q

vitamin K antagonist

A

warfarin

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6
Q

direct thrombin inhibitors do not need _____ to work

A

AT-III

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7
Q

unfractionated heparin

  1. bioavailability
  2. administration
  3. half-life
  4. induces conformational change in _____ and augments it for neutralization of (4)
  5. impairs ____ function
  6. major adverse rxn
A
  1. low bioavailability
  2. poorly absorbed through GI thus it needs to be with SQ or IV
  3. 1-2 hr. half life
  4. induces conformational change in AT-III and augments it for neutralization of thrombin, Xa, IXa, XIa
  5. impairs platelet function
  6. HIT- heparin induced thrombocytopenia
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8
Q

HIT

  1. immune mediated?
  2. occurs
  3. happens more in
  4. males vs females
  5. thrombocytopenia
  6. b/c ab complex activated endothelial cells it leads to
  7. treatment
A
  1. yep- IgG against heparin PF4 complex
  2. occurs 4-10 days after starting heparin
  3. UF> LMWH
  4. females>males
  5. low platelet count
  6. thrombosis
  7. stop all heparin and give a direct thrombin inhibitor instead until platelet count is normal and then we can start warfarin
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9
Q

heparin neutralizing protein in alpha granules

A

platelet factor 4

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10
Q

LMWH

  1. common example
  2. synthetic analogue
  3. difference to UFH
  4. fondaparinux? significance?
  5. PTT prolongation?
  6. monitoring?
  7. platelet effect
A
  1. enoxaprin-lovenox
  2. pentasaccharide
  3. b/c chains are smaller than UFH, LMWH inhibits factor Xa» IIa-thrombin
  4. fondaparinux is a pure anti-Xa inhibitor which mediates effects through AT-III but there is no affinity for PF4 thus no HIT
  5. PTT is minimally prolonged b/c thrombin is not max. inhibited
  6. monitor- anti-Xa assay
  7. less anti-platelet effect than UFH
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11
Q

Anti- Xa: anti-IIa

UFH vs LMWH

A

UFH- 1:1

LMWH: 2:1 or 4:1

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12
Q

monitoring

UFH vs LMWH

A

UFH: APTT
LMWH: anti-Xa assay

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13
Q

frequency of HIT

UFH vs LMWH

A

UFH: high
LMWH: low

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14
Q

fondaparinux has an antidote

A

nope

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15
Q

reversal of heparin (2)

A
  1. discontinue drug

2. protamine sulphate UFH»LMWH

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16
Q

oral agent approved for stroke prevention in non-valvular atrial fibrillation; DVT, PE

A

dabigatran (direct thrombin inhibitor)

17
Q

direct thrombin inhibitor

  1. hepatic clearance
  2. renal clearance
  3. how does it work?
  4. chances of HIT
  5. true or false: anticoag. response if predictable since they do not bind to endothelium or plasma proteins
  6. drug interactions
  7. antidote
  8. monitoring
A
  1. argatroban
  2. bivalirudin- off label for HIT
  3. inactivates thrombin bound to fibrin
  4. not neutralized by PF4 released from platelets thus no HIT or thrombocytopenia
  5. true
  6. no know drug interactions
  7. no antidote
  8. no monitoring
18
Q

DTIs inactivate thrombin but unlike heparin it does so in an

A

antithrombin -independent fashion

19
Q

Warfarin

  1. administration
  2. half life
  3. circulation
  4. activity
  5. inhibits
  6. VKORCI is a key enzyme in
  7. gamma carboxylation adds ____ which serve to
  8. variability
A
  1. oral- rapid absorption from gut
  2. 36-42 hr half life
  3. circulates free and bound to plasma proteins
  4. only free warfarin is active
  5. inhibits vit.k epoxide reductase subunit 1
  6. VKORCI is a key enzyme in recycling of Vit. K
  7. gamma carboxylation adds Gla residues to serve to anchor the clotting factors to phospholipid membranes via Ca2+ bridges
  8. variable response within a single patient
20
Q

warfarin has Dose variability amongst patients due to variable metabolism

A

yep

21
Q

Warfarin lab monitoring

  1. PT
  2. PTT
  3. Thrombin time
A
  1. PT- acute prolongation due to fall in FVII
  2. PTT- prolonged after a few days with decreased II, IX and X
  3. thrombin time is not affected by warfarin
22
Q

thromboplastin reagent used in the PT assay is assigned an ISI (International Sensitivity Index) calibrated against a primary WHO standard thromboplastin

A

INR

23
Q

Bridging from Heparin or DTI to Warfarin

A
  1. start warfarin while patient is still on heparin/DTI
  2. continue heparin/DTI doses until at least 5 days to ensure full anticoag.
  3. continue heparin/DTI until INR shows therapeutic levels
24
Q

complications of warfarin (3)

A
  1. bleeding- supratherapeutic INR
  2. skin necrosis in patients with protein C deficiency
  3. teratogenic avoid in pregnancy
25
Q

direct oral agent

  1. approved for use in stroke prevention in atrial fibrillation, DVT, PE
  2. antidote for 1
  3. monitoring
  4. direct factor Xa inhibitor and antidote and monitonring
A
  1. dabigatran
  2. idarucizumab–humanized monoclonal antibody fragment which binds to dabigatran
  3. no monitoring
  4. rivaroxaban- andexxa alpha is the antidote and for monitoring you can use anti-Xa levels for monitoring
26
Q

A human protein derived from tissue culture using recombinant technology
(a native protein so no immune response)

A

rtPA

27
Q

rtPA:

  1. act
  2. degrades
  3. cleared from plasma
A
  1. directly activates plasminogen
  2. degrades fibrin clot
  3. cleared from plasma in 4-8 minutes
28
Q

indications for trhombolytic therapy (2)

A
  1. occluded central venous catheters (alteplase)

2. life or limb threatening situations

29
Q

complications of thrombolytic therapy

A
  1. intracranial hemorrhage
30
Q

are there contraidications to thrombolytic therapy

A

yep, major bleeds

31
Q

Thromboxane A2 inhibitor

A

aspirin- anti-platelet agent

32
Q

ADP-receptor antagonists

A
  1. Clopidogrel (Plavix)
  2. Prasugrel (Effient)
  • anti-platelet agent
33
Q

GPIIb/IIIa blockers

A

eptifibatide (Integrilin)

  • anti-platelet blocker
34
Q

PAR-1 receptor antagonists (thrombin)

A

Vorapaxar (Zontivity)

  • antiplatelet agent
35
Q

irreversibly acetylates cyclooxygenase preventing arachidonic acid conversion to prostaglandin and Thromboxane; impaired platelet aggregation

** indicated by secondary stroke, TIA

A

aspirin

36
Q

via P2Y12 receptor – inhibits platelet aggregation

*indicated for ACS and PCI

A

ADP receptor antagonists

37
Q

These drugs reversibly inhibit platelet aggregation by binding of GPIIb/IIIa – the site fibrinogen binding between platelets

A

GPIIb-IIIa antagonists

38
Q

Thrombin receptor antagonists- thrombin activates platelets via PAR1 and 4

A

PAR-1 receptor antagonists (protease activated receptor)

heme/onc (30 decks)

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