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Pharm. Hemo
| Question | Answer |
|---|---|
| Hemostasis | physiologic process by which bleeding is stopped. 1) formation of platelet plug 2) coagulation (fibrin) |
| Platelet aggregation | platelets come into contact with collagen on exposed surface of a damaged blood vessel. Platelrts adhere to site of injury and initiate platelet activation, which leads to massive platelet aggregation |
| GP IIb/IIIa receptors | located on platelets. Fibrinogen forms bridges between them on adjacent platelets. Must be activated by multiple facotrs including thromboxane A2, thrombin, collagen, platelet activation factor, ADP. Once bridges form, aggregated platelets constitute plug |
| Coagulation | production of fibrin, a thread like protein that reinforces the platelet plug |
| Factor X | catalyzes conversion of prothrombin into thrombin |
| thrombin | catalyzes conversion of fibrinogen into fibrin, catalyzes conversion of factor V into active form Va (increases activity of factor X), catalyzes conversion of factor VIII into VIIIa (increases activity of IXa in intrinsic pathway) |
| Vitamin K dependent coagulation factors | VII, IX, X, prothrombin |
| Thrombosis | pathologic functioning of hemostatic mechanisms |
| Antithrombin | forms complexes with clotting factors and inhibits their activity |
| Plasmin | enzyme responsible for fibrin degradation |
| plasminogen | precursor of plasmin (thrombolytics promote conversion of plasminogen to plasmin) |
| Anticoagulants | drugs that reduce the formation of fibrin; inhibit synthesis of clotting factors and inhibit activity of clotting factors |
| Heparin (unfractioned)- MOA | binds antithrombin producing a conformational change that enhances its ability to inactivate both thrombin and factor Xa, thereby suppressing formation of fibrin. Very short half life- effect develop quickly |
| Heparin- Indications | pregnancy and situation that requires rapid onset of effects (stroke, pulmonary embolism, VTE), adjunct to thrombolytic in MI, surgical prophylaxis |
| Heparin- Adverse Effects | Hemorrhage, heparin induced thrombocytopenia |
| Heparin- monitoring | to avoid spontaneous bleedin- test aPTT (activated partial thromboplastin time) q 4-6 hrs |
| Low Molecular Weight Heparins - MOA | molecules are shorter than unfractioned heparin; bind antithrombin and factor Xa- less ability to inactivate thrombin- suppresses formation of fibrin |
| LMWH- drugs | Enoxaparin (Lovenox) |
| LMWH- Indications | first line for treatment and prevention of DVT, management of unstable angina |
| LMWH Advantages | equal efficacy to UFH, increased bioavailability (dont bind to protein and tissue), longer half life (less frequent dosing), more predictable (no monitoring aPTT) |
| Warfarin (coumadin)- MOA | vitamin K antagonists- blocks synthesis of vitamin K dependent clottin gfactors (prothrombin, VII, IX, X)- inhibits the enzyme that is needed to covnert Vitamin K to its active form. Very long half life (37 hours) |
| Warfarin (coumadin)- indications | prevention of DVT, prevention of systemic arterial embolism, prevention ofMI and stroke, prosthetic heart valves, prevention of atrial fibrillation |
| Warfarin (coumadin)- Adverse effects | Bleeding (can be reversed with vitamin K supplements), teratogenesis, measure prothrombin time to monitor |
| Warfarin (coumadin)- drug interactions | foods rich in Vitamin K (lessens effects), enzymatic inhibitors (increase effects of warfarin, promote bleeding), enzymatic inducers (decrease effects of warfarin) |
| Dabigatran (Pradaxa)- MOA | new oral anticoagulant; directly inhibits thrombin |
| dabigatran (Pradaxa) - uses | decreases risk of stroke and systemic embolism in patients with atrial fibrillation |
| Dabigatran (Pradaxa)-adverse effects | bleeding, GI, increased risk of MI |
| Rivaroxaban (Xarelto)- MOA | new oral agent; direct inhibitor of Factor Xa |
| Rivaroxaban (Xarelto)- uses | o Athropaty of knee, prophylaxis of post op DVT o DVT o Afib- prophylaxis of systemic embolism o Pulmonary embolism |
| Antiplatelet Drugs | suppress platelet aggregation, principal indication is prevention of thrombus in ARTERIES |
| 3 categories of antiplatelet drugs | Aspirin, ADP antagonists, GO IIb-IIIa Receptor Antagonists |
| Aspirin- MOA | at low doses (75-325 mg), irreversibly inhibits COX, which synthesizes thromboxane A2 in platelets (activates GP IIb-IIIa and promote vasoconstriction)-- lasts entire platelet lifetime (~10 days) |
| Aspirin- Uses | primary prevention of MI |
| ADP Antagonists- MOA | inhibit the binding of ADP to its platelet receptor and subsequent ADP-mediated activation of GPIIb-IIIa complex, thereby inhibiting platelet aggregation |
| ADP Antagonists- drugs | Clopidogrel (Plavix) Ticegrelor (Brilinta) Prasugrel (Effient) |
| ADP Antagonists- Uses | secondary prevention of MI or ASA intolerant patients. Prevent blockage of coronry artry stents, reduce thrombotic events in arteries in patients with ACS and in those with atherosclerosis documented by recent MI, stroke or PAD |
| ADP Antagonists- Adverse effects | abdominal pain, dyspepsia, diarrhea, rash |
| GP IIb/IIIa Receptor Antagonists- MOA | GPIIb/IIIa receptor inhibition (final step in platelet aggregation)- platelets cant aggregate through fibrinogen (IV ONLY) |
| GP IIb/IIIa Recpetor Antagonists- drugs | Amciximab (ReoPro), Integrilin, aggrastat |
| GP IIb/IIIa Recpetor Antagonists- uses | used to prevent ischemia in patients with Acute coronary syndromes, usually added to ASA and UFH/LMWH to reduce risk of complications, used in PCI, expensive |
| GP IIb/IIIa Recpetor Antagonists- Adverse Effects | double risk of major bleeding, but no risk of fatal hemorrhage |
| thrombolytic Agents- MOA | plasminogen activators- convert plasminogen (precursor) into plasmin, an enzyme that digests fibrin clots |
| thrombolytic Agents- drugs | Streptokinase, Alteplase (tPA), Tenecteplase |
| thrombolytic Agents- uses | Acute MI and acute ischemic stroke treatment (within 3 hours), pulmonary embolus, central deep venous thrombosis |
| thrombolytic Agents-adverse effects | bleeding, hypersensitivity, hypotension |
| Anemia | decrease i normal number, size, or hemoglobin content of red blood cells |
| Uptake and distribution of iron | uptake into mucosal cells in small intestine, undergo storage as ferritin within mucosal cells, undergo binding to transferrin |
| Utilization and Storage of Iron | • Taken up by cells of the bone marrow for incorporation into hemoglobin • Taken up by liver and other tissues for storage as ferritin • Taken up by muscle for production of myoglobin |
| Iron deficiency- causes | caused by imbalance in iron uptake and iron demand (increased demand) -Pregnancy -Infancy/early childhood -chronic blood loss |
| Consequence of Iron deficiency | Microcytic, Hypochromic anemia |
| Microcytic, Hypochromic anemia | cells are small(microcytic) and low in hemoglobin levels (hypochromic/pale). Results from inadequate intake of iron or excessive blood loss |
| symptoms of microcytic, hypochromic anemia | less oxygen = listlessness, fatigue, pallor of skin/mucus membranes. Behavioral and learning problems in children |
| Oral Iron- 3 preparations | Ferrous Sulfate, Ferrous Fumarate, Ferrous Gluconate |
| Ferrous Sulfate | 20% iron |
| Ferrous Fumarate | 33% iron |
| Ferrous Gluconate | 12% iron |
| What 2 things increase absorption of oral iron? | ascorbic acid and food |
| drug interactions with oral iron | tetracycline and antacids decrease iron absorption |
| Adverse effects of oral iron | staining of teeth, poisoning in children |
| Parenteral iron (drug name) | Iron Dextran (INFeD, DexFerrum) |
| Parenteral Iron - clinical use | given to severely deficient patients unable to tolerate or absorb oral iron, or in cases of extensive chronic blood loss. |
| Parenteral iron- adverse effects | dangerous, fatal anaphylaxis |
| Vitamin B12 | essential for synthesis of DNA- catalyzes the conversion of folic acid into its active form, active folic acid participates in several reactions essential for DNA synthesis |
| causes of vitamin B12 deficiency | impaired absorption (regional enteritis, celiac disease, absence of intrinsic factor needed for absorption= pernicious anemia) |
| Megaloblastic (macrocytic) anemia | wihtout proper DNA synthesis, growing cells are unable to divide. Cause oversized cells |
| Which vitamin deficiency may have irreversible neurologic effects? | Vitamin B12 Deficiency |
| Why does deficiency of B12 cause neurologic damage? | deficiency of B12 causes demyelination of neurons, primarily in spinal cord and brain= paresthesias, reduction in deep tendon reflexes, loss of memory, mood changes, hallucinations, psychosis (can be permanent) |
| B12 deficiency- adverse effects | affects all tissues in cells that are undergoing growth and division- prevents bone marrow from making wbcs and platelets (increases infection and bleeding), suppresses cells that form epithelial linings (oral ulcerations, GI disturbance) |
| B12- IM or SubQ | for patients with impaired B12 absorption |
| Moderate B12 deficiency- tx | B12 alone |
| severe B12 deficiency- tx | IM injection of B12 and folic acid, administration of 2-3 units of packed rbcs, transfusion of platelets, antibiotic therapy for infection |
| folic acid (folate, B9) | essential factor for DNA synthesis, DNA replication, cell division. Absorbed in early segment of small intestine, dietary sources |
| Folic Acid Anemia- causes | poor diet (alcoholism), malabsorption syndrome (sprue=celiac disease) |
| consequences of folic acid anemia | Megaloblastic (macrocytic) anemia, may be indistinguishable from B12 deficiency, but occurs more rapidly, neural tube defects |
| Hematopoietic growth factors | hormones tht stimulate proliferation of blood cells by binding to receptors on progenitor cells in bone marrow |
| Erythropoietin (EPO,epoetin alfa, epogen) - MOA | glycoprotein hormone that stimulates production of RBCs, binds to receptors on RBC progenitors |
| Epogen- uses | used for anemia of chronic disease, exogenous EPO used as performance enhancing drug |
| Epogen- adverse effects | hypertension, Black Box: increased mortality, serious CV and thromboembolic events. Rate of HgB rise of >1g/dL over 2 weeks may contribute to these risks |
| Filgrastim (Neupogen)- MOA | leukocyte growth factor, granulocyte colony stimulating factor. Stimulate WBC production through receptors on progenitors |
| Pegfilgrastim (Neulasta) | pegylated for of filgrastim - long acting, increases half life, single dose instead of one dose every day for 2 weeks |
| Filgrastim (Neupogen)-clinical use | bone marrow transplants, used following chemo to reduce febrile neutropenia, decreases hospitalization and infection, HIV, aplastic anemia |
| GM-CSF, Sargramostim (Leukin) | o Accelerates bone marrow recovery following transplant |
| - IL-11, Oprelvekin | thrombopoietic growth factor o stimulates platelet production in chemotherapy |
Created by:
alexadianna
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