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Hematology

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Question
Answer
show No, do not lay down for 1 hour.  
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show Full glass of water,  
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show 2months  
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show Absorption decreases  
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show When there’s a large deficit, when oral absorption is decreased, when pt simply doesn’t want to  
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show Consider weight of pt, calculate Fe deficit, and do a test dose  
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7. What is the relationship between alcoholics and Folic acid?   show
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8. How does the use of antibiotics affect folic acid deficiency?   show
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show Yes, after a meal a person may appear to have enough folic acid, may not seem like Folic acid anemic  
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10. Where do people get their B12?   show
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11. How are B12 found in the system?   show
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12. Where is B12 absorbed?   show
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13. What interferes with B12 absorption?   show
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show  
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15. What produces EPO?   show
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16. What increases EPO?   show
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show A modified version of EPO which has an increased half life  
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18. What type of patients should be put on Darbepoetin?   show
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show  
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show Increased bp  
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show EPO  
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show GI, nausea, vomiting, and HTN  
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show Body’s normal process of preventing bleeding  
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24. What is the first degree hemostasis?   show
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show Clotting plasma, fibrin deposition  
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show  
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26. What is vit K required for?   show
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27. What causes K deficiency?   show
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show Bleeding or asymptomatic pts with a prolonged PT  
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29. What is K treatment?   show
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30. What is factor 8 bound to in circulation? Bound to vWF while inactive in circulation   show
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show Degrades rapidly  
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show Thrombin  
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show Exposed collagen binds to vWF  
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34. What is the most common type of Hemophilia?   show
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show Inherited disorder of protein required to form blood clot is missing or reduced  
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36. Can spontaneous gene mutation cause hemophila A?   show
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show Problems with bleeding only after serious injury or trauma or surgery  
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38. What is moderate hemophilia A?   show
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show Bleeding following an injury and may have frequent spontaneous bleeding episodes, often into the joints and muscles.  
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40. What happens in vWF deficiency or dysfunction?   show
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41. How is hemophilia A managed?   show
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42. How is factor 8 levels increase?   show
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43. How is hemostasis restored in hemophiliacs?   show
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44. When is home therapy of F8 allowed?   show
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45. How is life threatening bleeds treated?   show
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show With 100 units/kg IV bolus human F8 followed by infusion of 10units/kg/hr  
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47. What was the problem of plasma transfusion in early days?   show
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48. What was the role in pharmaceutical companies in reducing transmission of diseases when blood transfusion took place?   show
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show Antibody formation  
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50. What is it dependent on?   show
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51. What are anticoagulants?   show
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52. Do anticoagulants dissolve existing clots?   show
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show Naturally occurring polysaccharide that inhibits coagulation  
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show Varying molecular chains of varying lengths and molecular weights  
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show porcine or bovine intestinal mucosa.  
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56. What is MOA for heparin?   show
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57. What are the benefits of giving heparin parenterally?   show
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show Delayed effect and prolonged effect  
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show 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  
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60. What is antithrombin?   show
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show Its adhesion to thrombin factors increased in the presence of heparins  
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show Yes  
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show Antithrombin 3 which inactivated thrombin  
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show Converts fibrinogen to fibrin  
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show Conversion of fibrinogen to fibrin form fibrin clots  
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show Heparin  
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67. Why are pregnant pts able to take heparin?   show
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68. What are the ADRs of heparin?   show
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69. What is aPTT?   show
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show 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  
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71. When heparin is administered what signs be monitored?   show
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72. What is administered in heparin over dose?   show
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73. What are the indications for heparin?   show
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show Do not administer to pts with bleeding disorders, PUD, recent eye, brain, spinal surgery, sever liver/renal disease, hemophilia  
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show Yes, SC is 20-60 mins  
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76. When is heparin clearance prolonged?   show
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77. What is the standard dosage and high risk pt dosage?   show
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show 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  
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show To reverse heparin effects or overdose of heparin  
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80. What are the considerations when using protamine sulfate?   show
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show Protamine sulfate  
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show Only short chain polysaccharide  
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83. What is a property of LMWH?   show
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84. How are LMWH obtained?   show
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show Dalteparin, Enoxaparin, Ardeparin  
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86. What is Enoxaparin?   show
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show Arterial thrombosis, venous thromboembolism, thrombophlebitis, DVT, calf vein thrombosis, DVT prophylaxis  
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88. What are the advantages of having LMWH as opposed to unfractionated?   show
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show Limited reversibility  
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show Less effect  
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show Same as heparin  
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show Inhibit liver synthesis of Vitamin K, the depending clotting factors are 2,7,9,10  
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show Prevent clotting in thrombophlebitis, PE and embolism related to AFib  
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94. What are the contraindications of oral anticoagulants?   show
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show Prolongs clotting time and adjusted upward or downward accordingly  
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show Another name for Coumadin, with onset of 2-7 days and half life of .5-3 days  
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show Inhibits vitamin K conversion to active form and will lead to depletion of clotting factors 2,7,9,10  
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98. Is it well absorbed orally?   show
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show Foods high vitamin K  
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show  
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101. What are complications of warfarin?   show
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show Vitamin K  
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103. What is the warfarin indications for nursing and pregnant pts?   show
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104. What needs to be monitored for oral anticoagulants?   show
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105. What is recombinant hirudin?   show
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106. How do you monitor Lepirudin?   show
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107. What should be considered when treating Lepirudin?   show
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show TBXA2 and ADP  
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show 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  
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show Platelet adhesion, cytoskeletal reorganization, degranulation, and amplification loops  
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111. What results in platelet plug formation cascade?   show
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show Linkage of activated platelets through fibrinogen leads to aggregation  
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113. What happens when the Fibrinogen receptor is inhibited?   show
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show Decrease formation or the action of chemical signals that promote platelet aggregation  
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show Aspirin, ticlopidine, dipyridamole, clopidogrel, sulfinpyrazone  
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116. What are some glycoprotein receptor antagonists?   show
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show Prevention and treatment of occlusive cardiovascular disease, maintenance of vascular grafts and arterial patency  
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118. What is sulfinpyrazone?   show
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show It is the mainstay of primary and secondary heart disease prevention, is an irreversible inhibitor of platelet cyclooxygenase and platelet thromboxane A2 production  
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120. What type of platelet aggregation is not prevented by aspirin?   show
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show 5% resistance, 25% partial response  
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122. What is clopidogrel?   show
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123. How do ticlopidine and clopidogrel block ADP induced platelet activation?   show
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124. What is Abciximab?   show
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show 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  
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show Fibrinogen, von Willebrand factor, vitronectin, and other adhesive molecules from binding to the receptor.  
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show 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  
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show 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  
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129. How does tirofiban inhibits platelet aggregation?   show
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130. What is tirofiban indicated for?   show
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131. What is eptifibatide indicated for?   show
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132. What is ADR for eptifibatide?   show
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133. What is MOA for eptifibatide?   show
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134. What is MOA of aspirin?   show
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show Prophylactic treatment of transiet cerebral ischemia  
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show Prolongs bleedings times, may cause additional complications  
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show Inhibits platelet aggregation through decreasing the binding of platelets to fibrinogen and to each other, reduce incidence of thrmbotic stroke. What is an ADR?  
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show Ticlopidine is more effective than aspirin in preventing initial stroke in pts with stoke precursors, but causes significantly more ADR than asprin.  
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show 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  
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show 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.  
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show Coronary vasodilator, prophylaxis against angina pectoris usually given with combination with aspirin  
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show Inhibits thromboxane A2, synthesis and may decrease platelet adhesion through potentiation of prostacyclin PG12  
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143. What dipyridamine is given in combination?   show
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show 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  
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show 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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