Haematological agents Flashcards
Filgrastim
A= Biosynthetic hematopoietic agent, recombinant granulocyte colony stimulating factor (G-CSF) B= filgratim agonizes G-CSF receptors on neutrophil progenitor cells to stimulate production of neutrophils in BM + controls proliferation of progenitor cells & reduces their maturation time. Also increases the phagocytic activity of mature neutrophils & influences leukopoiesis C= acute myeloid leukemia ( chemotherapy induced neutropenia ), cancer patients receiving BM transplant, severe chronic neutropenia, Myelodysplastic Syndromes and Aplastic Anemia, Leukemias
Epoetin alfa
A= recombinant human erythropoietin, biosynthetic hemopoietic agent B= binds to and activates erythropoietin receptors on red blood cell progenitors --> stimulates erythroid prolieration and differentiation + induces release of reticulocytes from BM C= anemia of chronic renal failure, chronic anemia ass with malignancy, anemia ass with RA and rheumatic diseases
Darbepoeitin alfa
A= recombinant human erythropoietin, biosynthetic hemopoietic agent
B= binds to and activates erythropoietin receptors on red blood cell progenitors –> stimulates erythroid prolieration and differentiation + induces release of reticulocytes from BM
C= anemia of chronic renal failure, chemotherapy-induced anemia, chronic anemia ass with malignancy
(more heavily glycosylated due to changes in aa residues–> has a longer half life than epoA)
Factor VIII
A= hemostatic agent B= replacement therapy of factor VIII which is essential for blood clotting and maintenance of hemostasis. Administration of this preparation to patients with Hemophilia A results in increased plasma levels of factor VIII and temporarily corrects the coagulation defect. C= prevention and control of hemorrhagic episodes in patients with factor VIII deficiency. Prevention and treatment of hemophilia A and vW disease.
Tranexamic acid (aminocaproic acid)
A= antifibrinolytic agent
B= competitively inhibits activation of plasminogen (via binding to the kringle domain), thereby reducing conversion of plasminogen to plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, and other plasma proteins, including the procoagulant factors V and VIII. Tranexamic acid also directly inhibits plasmin activity, but higher doses are required than are needed to reduce plasmin formation.
C=patients with bleedings due to elevated fibrinolytic activity; hemophilia for short term use to reduce or prevent bleeding.
Desmopressin
A= vasopressin receptor agonist, synthetic analogue of ADH B= binds to and agonizes vasopressin2 receptors in the nephrons of collecting ducts to decrease excretion of water (ADH effect) + agonizes extrarenal V2 receptors to increase levels of factor VIII and vWF C= nocturnal enuresis, control of temporary polyuria and polydipsia following trauma/injury in pituitary region. Pituitary diabetes insipidus, hemophilia A and von Willebrand disease
Aspirin (low doses: antiplatelet (50-150 mg), high doses: antiinflammatory (500-1000mg))
A= NSAID, salicylate ester of acetic acid, antiplatelet, analgesic, antipyretic B= inhibits COX-1 and COX-2 activity. Irreversible acetylates and inactivates COX1 in platelets (Low doses) ---> inhibits synthesis of thromboxane A2 which is necessary for platelets to change their forms and release granules which leads to platelet aggregation. (In high doses also acts on COX enzymes in the endothelium--> blocks their action and subsequently decreases amount of inflammatory mediators & prostaglandins) C= TIA, stroke, primary and secondary prevention of CAD and MI, embolism ass with atrial fibrillation/flutter.
Clopidogrel (prodrug)
A=Antiplatelet B= the active metabolite binds selectively and noncompetitively to platelet surface P2Y12 ADP receptors, therefore inhibits ADP from bindint to the receptor and subsequent receptor activation of the platelet glycoprotein (GP IIb/IIIa) complex which is necessary for fibrinogen-platelet binding. Also inhibits ADP-mediated release of granules required for platelet aggregation C= to avoid thrombosis in patients with coronary stent placement, unstable angina, NSTEMI in combination with aspirirn, STEMI, recent MI, stroke, peripheral arterial disease,
Tirofiban
A= glycoprotein IIb/IIIa inhibitor, antiplatelet B= binds selectively to platelet GP IIb/IIIa receptors and reversibly inhibits platelet aggregation (by preventing binding of fibrinogen, vWF and other adhesive ligands to GP IIb/IIIa) C= acute coronary syndromes!!, venous thrombosis, pulmonary embolism, general sugery thromboprophylaxis
Heparin
A= anticoagulant, indirect thrombin inhibitor B= acts as a catalyst to accelerate the rate at which at which antithrombin III neutralizes thrombin and activated coagulation factor Xa. Low dose therapy neutralizes Xa which prevents the conversion of prothrombin to thrombin. Full-dose therapy neutralizes thrombin which prevents the conversion of fibrinogen to fibrin. Also prevents the formation of a stable fibrin clot by inhibitig activation of fibrin stabilizing factor (factor XIII) C= treatment of venous thrombosis or pulmonary embolism. Genar surgery thromboprophylaxis, thromboprophylaxis during cardioconversion of afib/flutter
Enoxaparin
A= anticoagulant, low molecular weight heparin B= has less effect on thrombin than unfractioned heparin. binds to and accelerates the activity of antithrombin III. By activating antithrombin III, enoxaparin preferentially potentiates the inhibition of coagulation factors Xa and IIa. Factor Xa catalyzes the conversion of prothrombin to thrombin, so enoxaparin’s inhibition of this process results in decreased thrombin and ultimately the prevention of fibrin clot formation. C= Hip/knee replacement surgery, general surgery thromboprophylaxis, medical conditions associated with thromboembolism, deep-vein thrombosis and pulmonary embolism, myocardial infarction
Warfarin
A= indirect acting
oral anticoagulant, a coumarin derivative
B= interferes with the hepatic synthesis of vit K dependent coagulation factors II (prothrombin), VII (proconvertin), IX(christmas factor) and X (Stuart-prower factor). Antithrombogenic effect generally occurs only after factors X and IX are diminished (usuall 2-7 days after initiation of therapy. [blocks gamma-carboxylation of several glutamine residues in these coag factors+ protein C and S –> results in inactive incomplete coag factors
C= For the treatment of retinal vascular occlusion, pulmonary embolism, cardiomyopathy, atrial fibrillation and flutter, cerebral embolism, transient cerebral ischaemia, arterial embolism and thrombosis
Rivaroxaban
A= oral anticoagulant, direct acting factor Xa inhibitor
B=Rivaroxaban competitively inhibits free and clot bound factor Xa. Inhibition of factor Xa interrups the intrinsic and extrinsic pathway of blood coagulation cascade, inhibiting both thrombin and formation and development of thrombi.
C= prevention of venous thromboembolism, thromboembolic prophylaxis in afib, pulmonary embolism, DVT, stroke prophylaxis
Dagibatran
A= oral anticoagulant, synthetic thrombin inhibitor B= D is a rapid-acting competitive and reversible direct inhibitor of thrombin. Thrombin, a serine protease, is responsible for the conversion of fibrinogen to fibrin in the coagulation cascade. Inhibition of thrombin consequently prevents thrombus development. Dabigatran inhibits free thrombin, fibrin-bound thrombin and thrombin-induced platelet aggregation. C= prevention of strokes in afib due to non heart valve causes
Alteplase
A= Human tissue plasminogen activator, thrombolytic agent
B= activate the plasminogen (hydrolyzes the arginine-valine peptide bond in plasminogen to form the active proteolytic enzyme plasmin) in thrombi, producing
trombolysis without development of general fibrinolysis
C = For management of acute myocardial infarction, acute ischemic stroke and for lysis of acute pulmonary embolism
