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7 Cards in this Set
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1. For the drugs listed below, describe the approved use/indication and how the drug works (mechanism of action).
Desvenlafaxine (Pristiq) (2008) |
Desvenlafaxine (Pristiq) was approved for the treatment od major depressive disorder. Desvenlafaxine is the active metabolite of venlafaxine (Effexor®). Both agents inhibit the reuptake of serotonin and norepinephrine and are referred to as serotonin/norepinephrine reuptake inhibitors (SNRIs).
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1. For the drugs listed below, describe the approved use/indication and how the drug works (mechanism of action).
Fospropofol (Lusedra) (2008) |
Fospropofol (Lusedra) is a new intravenous anesthetic approved for use in monitored anesthesia care sedation in patients undergoing diagnostic or therapeutic procedures. (22) Fospropofol disodium is a prodrug of propofol. (22) Propofol interacts with the GABAA receptor, which is the presumed mechanism of action whereby it produces a sedative/hypnotic effect. (22) Propofol is an alkyl-phenolic compound with intravenous general anesthetic properties. The drug is unrelated to any of the currently used barbiturate, opioid, benzodiazepine, arylcyclohexylamine, or imidazole intravenous anesthetic agents.
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1. For the drugs listed below, describe the approved use/indication and how the drug works (mechanism of action).
Minacipran (Savella) (2009) |
Milnacipran (Savella) is a new antidepressant within the class of serotonin/norepinephrine reuptake inhibitors and is approved for the management of fibromyalgia.
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1. For the drugs listed below, describe the approved use/indication and how the drug works (mechanism of action).
Prasugrel (Effient) (2009) |
Prasugrel (Effient) is an antiplatelet agent approved to reduce the rate of thrombotic cardiovascular events (eg, stent thrombosis) in patients with unstable angina, non-ST-segment elevation MI, or ST-elevation MI (STEMI) managed with percutaneous coronary intervention (PCI). Prasugrel is a prodrug that is metabolized to both active and inactive metabolites.(27) The active metabolite irreversibly blocks the P2Y12 component of ADP receptors on the platelet, which prevents activation of the GPIIb/IIIa receptor complex, thereby reducing platelet activation and aggregation. Platelet aggregation returns to baseline within 5-9 days of discontinuation.
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1. For the drugs listed below, describe the approved use/indication and how the drug works (mechanism of action).
Telavancin (Vibativ) (2009) |
Telavancin (Vibativ) is a glycopeptides-type antibacterial. It gained FDA approval for the treatment of complicated skin and skin structure infections caused by susceptible gram-positive organisms including methicillin-susceptible or -resistant Staphylococcus aureus, vancomycin-susceptible Enterococcus faecalis, and Streptococcus pyogenes, Streptococcus agalactiae, or Streptococcus anginosus group. Telavancin exerts concentration-dependent bactericidal activity . (30) It inhibits bacterial cell wall synthesis by blocking polymerization and cross-linking of peptidoglycan by binding to D-Ala-D-Ala portion of cell wall. (30) Unlike vancomycin, additional mechanism involves disruption of membrane potential and changes cell permeability due to presence of lipophilic side chain moiety.
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1. For the drugs listed below, describe the approved use/indication and how the drug works (mechanism of action).
Dabigatran etexilate mesylate (Pradaxa) |
Dabigatran etexilate mesylate (Pradaxa) was approved for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Dabigatran etexilate is a prodrug lacking anticoagulant activity that is converted in vivo to the active dabigatran, a specific, reversible, direct thrombin inhibitor that inhibits both free and fibrin-bound thrombin. The druh inhibits coagulation by preventing thrombin-mediated effects, including cleavage of fibrinogen to fibrin monomers, activation of factors V, VIII, XI, and XIII, and inhibition of thrombin-induced platelet aggregation. It is taken orally in twice daily doses.
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1. For the drugs listed below, describe the approved use/indication and how the drug works (mechanism of action).
Denosumab (Prolia) |
Denosumab (Prolia) was approved for the treatment of osteoporosis in postmenopausal women at high risk for fracture; for prevention of skeletal-related events (eg, fracture, spinal cord compression, bone pain requiring radiation therapy) in patients with bone metastases from solid tumors. Denosumab is a monoclonal antibody with affinity for nuclear factor-kappa ligand (RANKL). Osteoblasts secrete RANKL; RANKL activates osteoclast precursors and subsequent osteolysis which promotes release of bone-derived growth factors, such as insulin-like growth factor-1 (IGF1) and transforming growth factor-beta (TGF-beta), and increases serum calcium levels. Denosumab binds to RANKL, blocks the interaction between RANKL and RANK (a receptor located on osteoclast surfaces), and prevents osteoclast formation, leading to decreased bone resorption and increased bone mass in osteoporosis. In solid tumors with bony metastases, RANKL inhibition decreases osteoclastic activity leading to decreased skeletal related events and tumor-induced bone destruction
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