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Pharmacology-PA
Hematology
| Question | Answer |
|---|---|
| 1. Is laying down after taking your Fe a good idea? | No, do not lay down for 1 hour. |
| 2. What is recommended to do when taking Fe? | Full glass of water, |
| 3. How long does it take before Hgb rise is noticed after Fe treatment? | 2months |
| 4. What happens if you take Fe with meals? | Absorption decreases |
| 5. When is paraenteral Fe therapy is used? | When there’s a large deficit, when oral absorption is decreased, when pt simply doesn’t want to |
| 6. What needs to be considered when Fe is administered IV? | Consider weight of pt, calculate Fe deficit, and do a test dose |
| 7. What is the relationship between alcoholics and Folic acid? | Alcoholics don’t eat a lot and don’t get the folic acid from their diet |
| 8. How does the use of antibiotics affect folic acid deficiency? | Frimellaprin decrases Folic acid absorption |
| 9. Are folic acids sensitive to meals? | Yes, after a meal a person may appear to have enough folic acid, may not seem like Folic acid anemic |
| 10. Where do people get their B12? | From animal products |
| 11. How are B12 found in the system? | B12 is found bound to intrinsic factors produced in the stomach (not sure) |
| 12. Where is B12 absorbed? | Absorbed in the ileum |
| 13. What interferes with B12 absorption? | lack of intrinsic factors, illeum sectioned off in surgery, bacterial overgrowth and competition for B12 |
| 14. For how long do you take B12 and what frequency? | |
| 15. What produces EPO? | Renal cortex |
| 16. What increases EPO? | High altitudes |
| 17. What is Darbepoetin? | A modified version of EPO which has an increased half life |
| 18. What type of patients should be put on Darbepoetin? | Pts with kidney renal insufficiency, renal failure, and dialysis are on this drug |
| 19. What is EPO administered with EPO? | |
| 20. How is BP affected by EPO? | Increased bp |
| 21. Chemotherapy suppresses dividing cells, stem cells, and marrow cells. HIV pts on AZT (anti HIV agent which inhibits DNA replication) are affected by this. What should they be treated with? | EPO |
| 22. What are some ADRs of EPO? | GI, nausea, vomiting, and HTN |
| 23. What is hemostasis? | Body’s normal process of preventing bleeding |
| 24. What is the first degree hemostasis? | Local vasoconstriction and making a platelet clot |
| 25. What is the second degree hemostasis? | Clotting plasma, fibrin deposition |
| 26. What is vit K required for? | K is required by hepatocytes to complete synthesis of clotting factors 2,7,9,10 and anticoagulant protein C and S |
| 27. What causes K deficiency? | Malabsorption states, poor dietary intake combined with anti biotic associated loss of intestinal bacterial production |
| 28. Who receives K treatment? | Bleeding or asymptomatic pts with a prolonged PT |
| 29. What is K treatment? | Phytonadione, which can be administered PO, SC or IV |
| 30. What is factor 8 bound to in circulation? Bound to vWF while inactive in circulation | |
| 31. What happenes to factor 8 when not bound vWF? | Degrades rapidly |
| 32. What causes the release of factor 8 from vWF? | Thrombin |
| 33. What else does vWF bind to? | Exposed collagen binds to vWF |
| 34. What is the most common type of Hemophilia? | A |
| 35. What type of disorder is Hemophilia A? | Inherited disorder of protein required to form blood clot is missing or reduced |
| 36. Can spontaneous gene mutation cause hemophila A? | Yes |
| 37. What is mild hemophilia A? | Problems with bleeding only after serious injury or trauma or surgery |
| 38. What is moderate hemophilia A? | Bleeding episodes after injuries and occasional spontaneous bleeding episodes |
| 39. What is severe hemophilia A? | Bleeding following an injury and may have frequent spontaneous bleeding episodes, often into the joints and muscles. |
| 40. What happens in vWF deficiency or dysfunction? | Leads to bleeding tendency, which is most apparent in tissues having high blood flow shear in narrow vessels. |
| 41. How is hemophilia A managed? | Primary therapy is replacement of factor 8 |
| 42. How is factor 8 levels increase? | 2% for every 1unit/kg factor 8 concentrate infused |
| 43. How is hemostasis restored in hemophiliacs? | By giving concentrated F8 from donated blood plasma or giving recombinant F8 |
| 44. When is home therapy of F8 allowed? | For minor bleeding in out pt therapy |
| 45. How is life threatening bleeds treated? | 100unites/kg porcrine F8 followed by IV infusion of 4 units/kg/hr |
| 46. How is less severe bleeds be treated? | With 100 units/kg IV bolus human F8 followed by infusion of 10units/kg/hr |
| 47. What was the problem of plasma transfusion in early days? | Transmission of HIV, HBV, HCV |
| 48. What was the role in pharmaceutical companies in reducing transmission of diseases when blood transfusion took place? | They produced recombinant synthesized factor products |
| 49. What is a major concern for pts receiving therapy against bleeding? | Antibody formation |
| 50. What is it dependent on? | Various factors including F8 product |
| 51. What are anticoagulants? | Drugs that interfere with clotting cascade and thrombin formation |
| 52. Do anticoagulants dissolve existing clots? | Nope |
| 53. What’s heparin? | Naturally occurring polysaccharide that inhibits coagulation |
| 54. What is natural heparin consisted of? | Varying molecular chains of varying lengths and molecular weights |
| 55. Where is heparin obtained from? | porcine or bovine intestinal mucosa. |
| 56. What is MOA for heparin? | Heparin catalyzes inactivation of thrombin and factor Xa prolonging aPTT |
| 57. What are the benefits of giving heparin parenterally? | Immediate effect and short plasma half life |
| 58. What happens when heparin is given SC? | Delayed effect and prolonged effect |
| 59. When heparin is administered full dose what should be done? | Must be monitored daily and dose adjusted to the target therapeutic range due to the 10 fold intersubject variability in response to a given dose of heparin |
| 60. What is antithrombin? | Small serine protease inhibitor produced by the liver and found in the plasma that degrades the serine protease; thrombin 2a, 9a, 10, 11a, 12a |
| 61. What happens to anti thrombin 3 in the presence of heparin sulfate? | Its adhesion to thrombin factors increased in the presence of heparins |
| 62. Can heparin be used prophilactically to prevent clot formation? | Yes |
| 63. What is heparin combined with? | Antithrombin 3 which inactivated thrombin |
| 64. What is MOA of Thrombin? | Converts fibrinogen to fibrin |
| 65. What forms fibrin clots? | Conversion of fibrinogen to fibrin form fibrin clots |
| 66. What antagonizes the fibrin clot formation? | Heparin |
| 67. Why are pregnant pts able to take heparin? | Heparin is a large molecule to cross the placenta |
| 68. What are the ADRs of heparin? | Bleeding episodes, thrombocytopenia, pruritis, hypersensitivity rxns, chills, fever, urticaria, anaphylaxis |
| 69. What is aPTT? | Functional measure of intrinsic pathway |
| 70. How is aPTT measured? | Blood is collected with oxalate or citrate to prevent coagulation, specimen is delivered to the lab. Activator (such as silica, celite, kaolin, ellagic acid) is added to activate intrinsic pathway and calcium is added to reverse the effect of oxalate. The |
| 71. When heparin is administered what signs be monitored? | Hematuria, epistaxis, echymoses, hypotension, occult blood in stool |
| 72. What is administered in heparin over dose? | Protamin sulfate |
| 73. What are the indications for heparin? | Prevent extension of DVT, pulmonary embolism, coronary thrombosis, in pt with artificial heart valves or suffering from stroke |
| 74. What are the contraindications of heparin? | Do not administer to pts with bleeding disorders, PUD, recent eye, brain, spinal surgery, sever liver/renal disease, hemophilia |
| 75. Will IV heparin have immediate onset of action? | Yes, SC is 20-60 mins |
| 76. When is heparin clearance prolonged? | Jin liver/renal failure |
| 77. What is the standard dosage and high risk pt dosage? | 5000units |
| 78. What are complications of heparin? | Bleeding, concomitant antiplatelet use result in increased risk of bleeding - therefore avoid, GI bleeding is contraindication for heparin therapy, osteoporosis result in long term therapy |
| 79. What is protamine sulfate used for? | To reverse heparin effects or overdose of heparin |
| 80. What are the considerations when using protamine sulfate? | Reserved for major bleeding due to risk of anaphylaxis |
| 81. What is an antidote for dalteparin & enoxaparin? | Protamine sulfate |
| 82. What are low molecular weight heparins LMWH consist of? | Only short chain polysaccharide |
| 83. What is a property of LMWH? | Heparin salts having an average molecular weight of less than 8000Da |
| 84. How are LMWH obtained? | Various methods of fractionation or depolymerization of polymeric heparin |
| 85. What are some examples of LMWH? | Dalteparin, Enoxaparin, Ardeparin |
| 86. What is Enoxaparin? | LMWH that inactivates factor Xa and into some extent fibrin |
| 87. What are the clinical use of LMWH? | Arterial thrombosis, venous thromboembolism, thrombophlebitis, DVT, calf vein thrombosis, DVT prophylaxis |
| 88. What are the advantages of having LMWH as opposed to unfractionated? | Once daily rather than continuous infusion, no need for monitoring of the aPTT coagulation, smaller risk of bleeding, smaller risk of osteoporosis, smaller risk of thrombocytopenia |
| 89. What is the protamine sulfate effect on LMWH? | Limited reversibility |
| 90. how does LMWH effect thrombin compared to heparin? | Less effect |
| 91. How does LMWH effect on factor Xa compared to heparin? | Same as heparin |
| 92. What do oral anticoagulants do? | Inhibit liver synthesis of Vitamin K, the depending clotting factors are 2,7,9,10 |
| 93. What are the indications of oral anticoagulants? | Prevent clotting in thrombophlebitis, PE and embolism related to AFib |
| 94. What are the contraindications of oral anticoagulants? | Bleeding disorders, peptic ulcers, severe renal disease, severe liver disease, blood dycrasia, teratogenic |
| 95. How are oral anticoagulants different? | Prolongs clotting time and adjusted upward or downward accordingly |
| 96. What is Warfarin? | Another name for Coumadin, with onset of 2-7 days and half life of .5-3 days |
| 97. What does Warfarin do? | Inhibits vitamin K conversion to active form and will lead to depletion of clotting factors 2,7,9,10 |
| 98. Is it well absorbed orally? | Yes, but takes 4-5 days for full effect |
| 99. What should you avoid when taking Warfarin? | Foods high vitamin K |
| 100. Chronic warfarin therapy pts should discontinue warfarin for what reason? | |
| 101. What are complications of warfarin? | life threatening hemorrhage, bleeding in 5% pts, skin necrosis, thrombocytopenia, GI anorexia, N/V, alopecia, rash |
| 102. A bleeding pt on Warfarin should be treated with what? | Vitamin K |
| 103. What is the warfarin indications for nursing and pregnant pts? | Contraindicated for 1st trimester of pregnancy, safe for nursing mothers |
| 104. What needs to be monitored for oral anticoagulants? | Hematuria, epistaxis, black tarry stool, echymoses, hypotension, Vitamin K overdose |
| 105. What is recombinant hirudin? | Lepirudin, a thrombin specific inhibitor used in the management of heparin induced thrombocytopenia (HIT) |
| 106. How do you monitor Lepirudin? | Monitored aPTT |
| 107. What should be considered when treating Lepirudin? | Adjust with renal compromise |
| 108. Platelet activation and degranulation result in local accumulation of what molecules? | TBXA2 and ADP |
| 109. What is the importance TBXA2 and ADP? | For further recruitment of platelets as wells as the amplification of activation signals as described above. The secreted agonists activate their respective G protein coupled receptors. This interaction counteracts the stimulation of cAMP formation by end |
| 110. What consisted of formation of platelet plug? | Platelet adhesion, cytoskeletal reorganization, degranulation, and amplification loops |
| 111. What results in platelet plug formation cascade? | Activation of fibrinogen receptor GP2b/3a expressed on platelet cells. This activation develops binding sites for fibrinogen, which are not available in inactive platelets |
| 112. What results in binding of fibrinogen? | Linkage of activated platelets through fibrinogen leads to aggregation |
| 113. What happens when the Fibrinogen receptor is inhibited? | Glycoprotein 2b/3a inhibitors blocks platelet aggregation |
| 114. What do platelet aggregation inhibitors do? | Decrease formation or the action of chemical signals that promote platelet aggregation |
| 115. What are some examples of platelet aggregation inhibitors? | Aspirin, ticlopidine, dipyridamole, clopidogrel, sulfinpyrazone |
| 116. What are some glycoprotein receptor antagonists? | Abciximab, eptifibatide, tirofiban |
| 117. What are the functions of platelet aggregation inhibitors? | Prevention and treatment of occlusive cardiovascular disease, maintenance of vascular grafts and arterial patency |
| 118. What is sulfinpyrazone? | It’s a uricosuric acid used to treat gout, and to reduce platelet aggregation by inhibiting degranulation of platelets which reduces the release of ADP and thromboxane |
| 119. What is aspirin used for? | It is the mainstay of primary and secondary heart disease prevention, is an irreversible inhibitor of platelet cyclooxygenase and platelet thromboxane A2 production |
| 120. What type of platelet aggregation is not prevented by aspirin? | Aggregation due to thrombin, epinephrine, serotonin, because they are alternate pathways of platelet aggregation and activation |
| 121. What is pt response to aspirin? | 5% resistance, 25% partial response |
| 122. What is clopidogrel? | A thienopyridine derivative closely related to ticlopidine in chemical structure and function |
| 123. How do ticlopidine and clopidogrel block ADP induced platelet activation? | By irreversible inhibition of one of the three platelet ADP receptors. This prevents upregulation of the glycoproetein 2b/3a receptor involved with the final common pathway for platelet activation |
| 124. What is Abciximab? | Chimeric human murine monoclonal antibody Fragmant antigen binding fragment |
| 125. What does abciximab do? | It inhibits platelet aggregation by specifically binding to the glycoproteins GP2b/3a receptor, the major surface receptor involved in the final common pathway for platelet aggregation |
| 126. Abciximab binding to GP2b/3a receptor prevents platelet aggregation of what? | Fibrinogen, von Willebrand factor, vitronectin, and other adhesive molecules from binding to the receptor. |
| 127. What is abciximab indicated for? | As an adjunct to aspirin and heparin for the prevention of acute cardiac ischemic complications not responding to conventional medical therapy or when percutaneous coronary intervention is planned w/in 24hrs |
| 128. What are some ADR of abciximab? | Human anti chimeric antibody (HACA) development may occur secondary to abciximab therapy. HACA titers may have allergic or hypersensitivity rxns when treated with other diagnostic or therapeutic monoclonal antibodies, include bleeding, orthostatic hypoten |
| 129. How does tirofiban inhibits platelet aggregation? | Reversibly bindng to the platelet receptor glycoprotein 2b/3a of human platelets, thus preventing the binding fibrinogen |
| 130. What is tirofiban indicated for? | In combination with heparin for the prevention of acute cardiac ischemic complications in patients with acute coronary syndrome, unstable angina, or non Q wave MI |
| 131. What is eptifibatide indicated for? | Usually as an adjunct to aspring and heparin, for the prevention of acute cardiac ischemic complications in patients with acute coronary syndrome, (unstable angina or non Qwave MI) |
| 132. What is ADR for eptifibatide? | Pts are at high risk for MI and sudden death due to progression of totally coronary artery occlusion, whether managed medically or with PCI |
| 133. What is MOA for eptifibatide? | It inhibits platelet aggregation by reversibly binding to the platelet receptor glycoprotein 2a/3a of human platelet, thus preventing the binding of fibrinogen, vWF and other adhesive ligands |
| 134. What is MOA of aspirin? | Blocks thromboxane A2 synthesis form arachidonic acid in platelets by irreversible acetylation and inhibition of cyclooxygenase |
| 135. What is the indication? | Prophylactic treatment of transiet cerebral ischemia |
| 136. ADRs of aspirin? | Prolongs bleedings times, may cause additional complications |
| 137. Indication of ticlopidine? | Inhibits platelet aggregation through decreasing the binding of platelets to fibrinogen and to each other, reduce incidence of thrmbotic stroke. What is an ADR? |
| 138. Compare ticlopidine with aspirin? | Ticlopidine is more effective than aspirin in preventing initial stroke in pts with stoke precursors, but causes significantly more ADR than asprin. |
| 139. What are the ADRs of ticlopidine? | Neutropenia, agranulcytosis, aplastic anemia and thrombotic thrombocytopenic purpura. Reserved for pts unable to take aspirin or who develop strokes despite aspirin therapy, and only when close hematologic monitoring is possible |
| 140. MOA of ticlopidine? | Inhibits ADP induced binding of fibrinogen to GP2b/3a complex, inhibits release of platelet granule constituents, platelet platelet interactions, and platelet adehesion to the endothelium and to atheromatous plaque. |
| 141. What is dipyridamole? | Coronary vasodilator, prophylaxis against angina pectoris usually given with combination with aspirin |
| 142. What is MOA for Dipyridamole? | Inhibits thromboxane A2, synthesis and may decrease platelet adhesion through potentiation of prostacyclin PG12 |
| 143. What dipyridamine is given in combination? | Warfarin, dipyridamole inhibits the embolization form prostetic heart valves |
| 144. What is clopidogrel indicated? | Reducing the risk of atherosclerotic events (MI, stroke, and vascular death) in patients with atherosclerosis documented by recent MI, recent stroke, or established peripheral arterial disease |
| 145. MOA of clopidogrel? | Inhibits ADP binding to its platelet receptor and activation of the glycoprotein GP2b/3a, because clopidogrel irreversibly modifies the ADP receptor, platelets are affected for the remainder of their life span. Platelet aggregation induced by agonists oth |
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