pharm - hematology.txt

Card Set Information

Author:
tallone4830
ID:
164477
Filename:
pharm - hematology.txt
Updated:
2012-07-30 19:03:02
Tags:
pharm hematology
Folders:

Description:
pharm - hematology.txt
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user tallone4830 on FreezingBlue Flashcards. What would you like to do?


  1. UFH MOA
    amplifies the anticuagulant effect of antithrombin III (inhibits factors IIa and Xa).
  2. LMWH MOA
    not big enough to bind both antithrombin III and factor IIa at the same time, only AT III (so effect largely due to influence on factor Xa)
  3. UFH monitoring
    PTT guides UFH dosing (ideally 1.5 to 2.3 times normal)
  4. LMWH monitoring
    more predicitable than UFH and doesn't mess with PTT, so no routine monitoring required. can look at antifactor Xa activity if needed.
  5. heparin contraindications
    previous HIT, thrombocytopenia, active bleeding
  6. heparin SE
    HITS (antibodies against platelet factor 4 produced, bind to platelets, activating them = thromboses, thrombocytopenia (being used up), excessive bleeding (being used up)). osteoporosis, hyperkalemia.
  7. heparin or warfarin in pregnancy?
    heparin. warfarin not safe, revaroxaban also not safe.
  8. HIT and heparinoids
    danaparoid has similar MOA, but not structurally related so safe to use in pts c HIT hx.
  9. heparin OD
    UFH reversible c protamine (binds), LMWH has no antidote.
  10. direct factor Xa inhibitors MOA
    factor Xa converts factor II to IIa (thrombin). inhibitors stop this conversion without using antithrombin III as an intermediary (like heparins)
  11. direct factor Xa inhibitors indications
    postsurgical VTE prophylaxis, alternative to heparin in pts with severe HIT
  12. direct thrombin inhibitors MOA
    binds to thrombin (factor IIa), inhibiting the conversion of fibrinogen to fibrin.
  13. direct thrombin inhibitors indications
    postsurgical VTE prophylaxis. bivalirudin HIT.
  14. direct thrombin inhibitors reversible?
    univalent inhibitors ("-gatr-") and bivalirudin are reversible, other bivalents are irreversible
  15. direct thrombin inhibitors advantage?
    considered more predictable for anticoagulation as they are not bound to plasma proteins (heparin), are not neutralized by platelet factor 4 (heparin), and because they directly inhibit fibrin formation.
  16. direct thrombin inhibitors monitoring
    bivalirudin can be monitored using PTT.
  17. vitamin K antagonists MOA
    vitamin K is a key cofactor for the activation of factors II, VII, IX, and X. To work, it must be reduced by vitamin K epoxide reductase. warfarin inhibits VKOR.
  18. vitamin K antagonists kinetics
    PO (unlike heparins). takes 2-3 days of tx before anticoagulation takes effect (because the inhibited proteins take that long to be cleared from the system)
  19. vitamin K contraindications
    platelet disorders (if you have dysfunctional clotting cells and dysfunctional clotting proteins, you'll be in real trouble if you need a clot)
  20. why bridge warfarin therapy with heparin?
    temporary hypercoaguable state due to inhibition of proteins C and S when first given
  21. warfarin target INR
    2 to 3
  22. warfarin pharmacogenomics
    there is significant genetic variability in response to warfarin owing to variants in 2C9 that metabolize the drug less efficiently and due to variants in VKOR
  23. salicylates MOA
    like NSAIDS, salicylates inhibit cyclooxygenase (COX) enzymes, specifically irreversibly inhibiting COX-1's formation of cyclic endoperoxide
  24. salicylates contraindications
    not for use in children (Reye's syndrome)
  25. salicylates SE
    GI (reduced PG levels causes reduced mucous -> ulcers), bleeding, tinnitus (high doses)
  26. salicylates kinetics
    ASA binds to platelets irreversibly, so duration of action is 5-7 days (lifespan of a platelet)
  27. salycilates and respiration
    salycilates can stimulate respiratory centers directly or by increasing CO2 production, causing a potential acid/base issue (respiratory alkalosis)
  28. diflunisal
    salicylate derivative that is a more potent analgesic and antiinflammatory, but isn't antipyretic
  29. adenosine diphosphate blockers MOA
    inhibit the ADP-dependent pathway of platelet activation and subsequent sequestration.
  30. adenosine diphosphate blockers kinetics
    clopidogrel slow, takes 5 days to achieve plateau
  31. ticlopidine contraindications (ADP blocker)
    hematopoietic disorders (particularly neutropenia), thrombotic thrombocytopenic purpura (TTP)
  32. adenosine diphosphate blockers reversible?
    ticagrelor reversible. all others irreversible (therefore long biologic T1/2, 5-7 day life of platelet)
  33. adenosine diphosphate blockers pharmacogenetics
    various responses, from "clopidogrel unresponsive" (<10%) to 90% platelet inhibition, thought to be due to alterations in PGY12 receptor (VerifyNow P2Y12 assay).
  34. clopidogrel BBW
    pts with CYP2C19*2 and CYP2C19*3 variants that there is reduced conversion of clopidogrel to its active thiol metabolite, resulting in ineffective protection.
  35. antiplatelet IIb/IIIa inhibitors MOA
    fibrinogen and vWF bind to IIb/IIIa receptors, causing platelet binding and aggregation (activation and binding of other platelets). these drugs prevent this.
  36. antiplatelet IIb/IIIa inhibitors kinetics
    IV. adciximab has the shortest T1/2 (10 min), but the longest effect (1 day) because it binds to the platelets
  37. fibrinolytics MOA
    cleave plasminogen (endogenous) to form plasmin, a protease that digests fibrin, breaking up the clot. fibrin selective drugs require the presence of fibrin to cleave plasminogen, localizing their effects to the clot (in theory).
  38. fibrinolytics SE
    non-selectives (streptokinase/urokinase) are both antigenic, so multiple uses are discouraged due to hypersensitivity reactions
  39. fibrinolytics bonus
    tenecteplase more fibrin-specific than alteplase. reteplase works faster than alteplase.
  40. erythropoietins MOA
    stimulates the production of RBCs (endogenous, targets progenitor cells in bone marrow, typically produced in the kidneys but a little bit in the liver)
  41. erythropoietins kinetics
    epoetin has a shorter T1/2 (4-8h) vs darbepoetin (24h -- due to AA modifications)
  42. erythropoietins contraindications
    uncontrolled HTN
  43. erythropoietins SE
    iron deficiency (use an iron supplement), thrombosis (particularly c dialysis), HTN, seizures
  44. erythropoietins monitoring
    Hem, aim for 10 (less chance of side effects). b/c RBCs have a long T1/2, dosing adjustments won't be seen for 2-6 wks.
  45. colony-stimulating factors MOA
    stimulates the production of neutrophils and monocytes by binding to myeloid progenitor cells
  46. G-CSFs vs GM-CSFs?
    G-CSFs stimulate neutrophils. GM-CSFs stimulate neutrophils and monocytes, as well as the actions (phagocytosis, superoxide production, cell-mediated toxicity) or neutrophils, monocytes, and eosinophils
  47. colony-stimulating factors kinetics
    filgrastim T1/2 is 3-5h, the PEGgylated pegfilgrastim has an extended T1/2 of 40h (less easily titrated, but better for prophylaxis).
  48. colony-stimulating factor SE
    bone loss, joint pain, renal dysfunction, acute respiratory distress, splenomegaly, sickle cell crisis
  49. ferrous iron vs ferric iron?
    ferrous iron (Fe2+, from animals) is better absorbed than ferric iron (Fe3+, from veggies) in duodenum
  50. iron contraindications
    previous anaphylaxis-like rxn to IV formulation (particularly iron dextran - test dose!)
  51. iron SE
    GI including black stool.
  52. iron kinetics
    take on an empty stomach, as many foods mess with absorption. ascorbic acid (Vit C) enhances absorption
  53. iron toxicity
    deferoxamine (chelators), phlebotomy

What would you like to do?

Home > Flashcards > Print Preview