Heme Pharm Flashcards
(31 cards)
What enzyme does ASA inhibit
What is the result of the enzyme inhibition?
-COX 1 & 2 are irreversibly inhibited
-This will reduce the amount of thromboxane A2 that is released by platelet dense bodies
-Platelets that are passing the injury have receptors for TXA2 & ADP = less TXA2 = less platelet activation for the plug
What does Plavix inhibit?
-Inhibitor of the ADP receptor P2Y12
-Dense bodies contain ADP along with TXA2 & both of these help with platelet activation for forming the platelet plug
-CAD + stent/bypass or PVD = dual-antiplatelet therapy
-Only adjusted if there is bleeding
-Plavix, prasugrel, or ticagrelor
What does Abciximab inhibit?
List drugs with similar mechanism of action
-Inhibits Gp2b/3a
-Prevents fibrinogen (unactive F1) from binding & helping neighboring platelets adhere together in the formation of the platelet plug
-Tirofiban
-Eptifibatide
-Highly specific use, like coronary angioplasty
What enzymes do NSAIDs bind?
-NSAIDs reversibly bind COX 1 & 2
-Not antiplatelet drugs
-There is risk of bleeding, but NSAIDs are used as fever & pain reducers (anti-inflammatory)
-Ibuprofen competes with ASA & decreases its cardioprotective effects
-Celecoxib & meloxicam = selective COX2 inhibitors
What drug can be used to induce more release of von willebrand factor from WPDs in times of hemorrhage?
Desmopressin (DDAVP)
Treatment for chronic Immune/ Idiopathic thrombocytopenia purpura (ITP)?
-Short-term options = steroids or IVIG (saturated Fc potion of macrophages so unable to find platelets)
-Refractory = splenectomy
-Rituximab
What is Rituximab & what does it do/ can be used for?
-Anti-CD20 mab that reduces B-cell immunity
-Can be used for Chronic ITP
Treatment for TTP
-Plasma exchange to remove von willebrand multimers (to prevent death)
-Do NOT give platelets
-Steroids, IVIG, & plasmapheresis can be attempted if pt cannot accept blood products
Treatment for HUS (in kids)
-Ate beef (E.coli O157:H7) or Dysentery at daycare (Shigella)
-Bloody diarrhea followed by renal failure
-Supportive care
Treatment of DIC
-Treat underlying cause + supportive care
-cryoprecipitate = repletes fibrinogen (F1)
-PRBCs = increases Hgb
-Platelets & FFP (for factors)
Mechanism of Warfarin (anticoagulant)
-Inhibitor of Vitamin K epoxide reductase (decrease in factors 10, 9, 7, 2, proteins C & S)
-Decreased protein C/S = temporary hypercoagulable state
-Antidote = oral vitamin K or fresh frozen plasma if pt is bleeding, or 4F PCC
-Monitor with PT/INR
-Goal = 2-3, with mechanical valve 2.5-3.5
-Narrow therapeutic window drug
-SEs = bleeding, drug interactions, skin necrosis (protein C deficiency)
-DO NOT give to pregnant women = hemorrhagic disease of baby & bone malformations
What is Warfarin metabolized by?
-CYP2C9
-Inducers = Phenytoin, EtOH, St. John’s Wart, Rifampin, Carbamazepine
Barbs, cholestyramine
-Inhibitors = Cimetidine (H2 blocker), Ketoconazole/azoles, Grapefruit, Sulfa abx/ TMP-SMX, Isoniazid, Ciprofloxacin, Amiodarone, Chloramphenicol
Mechanism of Heparin & what is it considered?
-Heparin induces antithrombin 3 to inactivate factor 10 & factor 2
-Common path is affected = PTT increased
-Anti-coagulant
What is the difference between unfractionated/High molecular weight heparin, Low molecular weight heparin (LMWH), & pentasaccharide/ fondaparinux
-UFH = large molecule
-Continuous heparin drip (needs monitoring, PTT)
-Chosen when there is high chance of bleeding or needed bridge to Warfarin
-Can be used in pregnancy & CKD
-Reversal = protamine sulfate
-SEs = HIT, hyperkalemia
-LMWH:
-Enoxaparin & Dalteparin
-Injection form, monitoring not needed
-DVT/PE prophylaxis or as therapeutic
-Partial reversal with protamine sulfate
-fondaparinux = smallest molecule, synthetic
-F10 inhibition only
-No reversal available
3 Categories of anti-platelets for primary hemostasis (or platelet plug formation)
usually needed for arterial clots/ atherosclerosis
& so anti-platelets cause platelet bleeding
-ASA = nonselective COX-1 affected decreasing TXA2 = reduced platelet activation
-also fever & pain reducer because of the arachidonic acid path
-SEs = anion gap metabolic acidosis, respiratory alkalosis
-ADP-P2Y12 antagonists = preventing platelet aggregation
-Gp3a/2b inhibitors = fibrinogen unable to bind = prevention of platelet aggregation
What do anti-coagulants target?
-Secondary hemostasis or preventing the normal functioning of coagulant factors
-Used in DVT & PE
-Can result in factor bleeding
List the different P2Y12 Antagonists
-Clopidogrel/ Plavix
-Prasugrel
-Ticagrelor/ Brilinta (reversible)
What are the drugs Apixaban/Eliquis & Rivaroxban?
-Direct 10-a inhibitors or DOACs
-X looks like roman 10
-Inhibiting the common pathway for factor clotting
-No bridge or monitoring needed
-Reversal = Andexanet-alfa
What are the drugs Argatroban & Dabigatran?
-Direct 2-a inhibitors
-Inhibiting the common pathway for factor clotting
-Argatroban (used for HIT) & Bivalirudin (stents) (injectable)
-No reversal
-Oral = dabigatran/ Pradaxa
-Reversal = Idarucizumab/ Praxbind
Explain the mechanism of thrombolytics
-Dissolving existing clots by catalyzing the existing mechanism
-plasminogen is converted to plasmin by tPA, plasmin breaks down fibrin into split products
-Examples:
-Streptokinase
-Alteplase, Tenecteplase, or Reteplase (2 dose regimen)
-Used in stroke, MI when PCI isn’t feasible, & PE
-Remember there is a long criteria checklist for these drugs
What drugs are available to reverse tPA in the case of excess med effect?
-Supportive cryoprecipitate & FFP given 1st
-Aminocaproic acid or tranexamic acid
Drug options used for cytoreduction in ET & PV?
-Hydroxyurea
-Interferon-alpha
-Ruxolitinib
What can be given for sideroblastic anemia?
-Vit B6 or pyridoxine
-Need to also supplement when giving Isoniazid
Treatment options for lead poisoning
-Eliminate exposure
-Lead encephalopathy = IV EDTA or parenteral dimercaprol for 5 days, then oral succimer (DMSA)
-Lead anemia = oral succimer (DMSA)
