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Pharm. Hemo

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