NRSG 2350 Exam 2 Meds Questions with Correct Answers Latest Update

NRSG 2350 Exam 2 Meds Questions with Correct Answers Latest Update ferrous sulfate - Answers WHY: treatment for IDA MOA: Replaces serum iron concentration for hemoglobin production ADE: constipation, darkened stool, staining of teeth, NVD CI: children toxicity, hemochromatosis, peptic ulcers D-D: antacids, tetracyclines, ascorbic acid cyanocobalamin (synthetic form of B12) - Answers WHY: pernicious anemia, essential for cell growth and division - necessary for myelin sheath MOA: replacement of essential vitamin B12 ADE: NVD, injection site reaction, itching CI: alleries, thickened blood folic acid (vitamin B9) - Answers WHY: folic acid deficiency anemia, prophylaxis during pregnancy (prevent neural tube defects) MOA: water soluble, essential for cell growth and division, replacement of essential vitamin ADE: NVD, no known because it is something we already have CI: allergy, methotrexate hydroxyurea (droxia) - Answers WHY: sickle cell anemia, increase fetal hemoglobin in the bone marrow MOA: increase fetal hemoglobin in the bone marrow ADE: NVD, HA, disorientation, chills, increase risk of cancer, bone marrow suppression CI: allergy, severe anemia / leukopenia, pregnancy, liver/kidney impairment D-D: warfarin, uricosuric agents epoetin alfa (Epogen), erythropoiesis stimulating agent - Answers WHY: treat anemia of chronic disease, reduce the need for pRBC transfusions MOA: stimulates bone marrow to make more RBCs (erythropoiesis) ADE: seizures, HA, dizzy, NVD, HTN, edema, chest pani CI: uncontrolled HTN D-D: do not mix with other drugs antihemophilic - Answers WHY: replace factor VIII in patients with hemophilia A, prevent blood loss from injury, surgery or to treat disorder MOA: replaced blood clotting factors - genetically missing or low ADE: HA, flushing, chills, lethargy, NV, site reaction CI: allergy, inhibitors of factor VIII, factor IX with liver disease, lactation antiocoagulants - Answers -prevents clots and prevents from getting bigger -does not get rid of a clot - heparin - warfarin heparin - Answers - suppresses intrinsic pathway - monitor PTT levels every ~4-6 hours - IV: bolus then continuous drip; unfractional - SQ: LMW, doesn't require monitoring of PTT levels at low doses - inactivator: protamine sulfate - therapeutic action within seconds - dosing is weight based low molecular weight heparins - Answers - more predictable and longer half life - as effective as unfractionated heparin - no need to monitor PTT - SQ only -ADE: bleeding, thrombocytopenia, neurologic injury - most common: enoxaparin (lovenox) warfarin - Answers - suppresses extrinsic pathway - long term systemic therapy - PO - bridge heparin to warfarin - need to monitor INR (time it takes blood to clot: 2-3 ideal) - reduces risk of stroke, systematic embolism, & given prophylaxis for major procedures - prevent DVT, PE, thrombus - Reversal: vitamin K antiplatelet - aspirin - Answers WHY: decrease platelet aggregation MOA: irreversibly inhibits COX-1, suppression of platelet aggregation - use low dose 81mg/day for MI prophylaxis - use medium dose 162-325 mg/day for acute MI ADE: GI irritation thrombolytics - Answers - break down of existing clots