Pharm Exam 4 study guide .

Drugs for Thromboembolism Alteplace (tPA): (Activase, Cathflo activase) also known as tissue plasminogen activation. Identical to human tPA. Binds with plasminogen to form an active complex • Used by RNS • Clearance of CVC: LOW dose alteplase: dilute solutions with dwell time according to policy Action: alteplase-plasminogen complex then catalyzes the conversion of other plasminogen molecules into plasmin, an enzyme that digests the fibrin meshwork of cloths. risk of hemorrhage. Use: MI, Ischemic Stroke, Massive PE Adverse Effects: o Bleeding • Reasons = pre-existing clots, re-bleed or new clots cannot form • risk for intracranial bleeding with streptokinase • Rx: give whole blood or blood products • IF bleeding cannot be controlled: IV aminocaproic acid (Amicar) (inhibits plasmin) o Fever Advantages: Does NOT cause allergic reactions. Does NOT induce hypotension Nursing Implications: monitor for subtle signs & symptoms of bleeding, Intracranial hemorrhage is our greatest concern, change in LOC = immediate STOP of drug, tarry stools, PINK urine, look at joints for swelling (hematoma), NO venipunctures or insertion of tubes after administering the drug YOU MUST DO INSERTION FIRST BEFORE ADMINISTRATION. Aminocaprioc Acid (Amicar): MOA: inhibits activation of plasminogen, thereby reducing conversion of plasminogen to plasmin (fibrinolysin), an enzyme that degrades fibrin clots as well as fibrinogen and other plasma proteins including the procoagulant factors V and VIII. Aminocaproic acid ALSO directly inhibits plasmin activity, but higher doses are required. Adverse effects: myocardial necrosis, hemorrhage, thrombosis, anaphylaxis, muscle necrosis, rhabdomyolysis, pulmonary embolism, urinary tract obstruction, intracranial hypertension, CVA, renal failure. Anticoagulants: Disrupt coagulation cascade; prevent venous thrombus • Heparin • LMWH - Enoxaparin • Vitamin K Antagonist Warfarin • Direct thrombin inhibitors Dabigastran, Argatroban • Factor Xa Inhibitor - Rvaroxaban (Xarelto), Apixiban (Eliquis) *Anticoagulants are more effective in venous thrombosis Antiplatelets: inhibit platelet aggregation and arterial thrombus. • Aspirin (ASA) • Clopidogrel (Plavix) • Abciximab (ReoPro) *Antiplatelet are most effective in arterial thrombosis Thrombolytics: promote “lysis” of fibrin, “clot busters” break up clots after it has been formed by speeding up the conversation of plasminogen to plasmin. Fibrinolytics - alteplase, reteplase, tenecteplase Andexnet (Andexxa): medication that has been FDA approved for patients treated with rivaroxaban and apixaban when reversal of anticoagulant is needed due to lifethreatening or uncontrolled bleeding occurs. MOA: recombinantly produced, inactive form of factor Xa that acts as a decoy binding to factor Xa and neutralizing anticoagulant effect of Rivaroxaban/Xarelto and Eliquis/Apixaban. Adverse Effects: infusion reaction, urinary tract infectious disease, pneumonia, acute myocardial infarction, cardiac arrest, DVT, ischemic stroke, PE Apixiban (Eliquis): factor Xa inhibitor, anti-coagulant MOA: acts as a selective site inhibitor of factor Xa inhibiting both free and bound factor. Decreasing thrombin generation and development. Adverse effects bleeding Side effects bleeding, anaphylaxis Nursing Considerations assess for bleeding, assess for stroke, DVT, PE or Peripheral Vascular Disease, Stop 24 hrs before surgery Argatroban: direct thrombin inhibitor, IV anticoagulant MOA: direct inhibition of thrombin USE: indicated for prevention of DVT in patients undergoing elective HIP replacement surgery, prophylaxis and treatment of thrombosis in patients with HIT ADR: bleeding, hematuria, allergic reactions in some with meds for coronary angioplasty. Aspirin: ASA, antiplatelet agent MOA: irreversible inhibition of cyclooxygenase (COX) COX enzyme required in synthesis TXA2 • Inhibition of cyclooxygenase • risk of GI bleeding & hemorrhagic stroke 1. TXA2 is necessary to activate platelet 2. TXA2 also promotes vasoconstriction on VSM, both actions promote hemostasis, creates the stickiness of the vessel walls. ASA inhibits this process = so it inhibits platelet aggregation and the vasoconstriction, permanently alters the platelet. Indications: Ischemic stroke and TIA (reduced risk of death & nonfatal stroke), chronic stable or unstable angina, prophylaxis of MI in patients with angina, acute MI – bypass surgery, Coronary Stenting, HX of MI, Primary Prevention of MI. Abciximab (ReoPro): antiplatelet drug, purified fragment of Monoclonal antibody MOA: binds to platelets GP IIb/IIIa receptors, preventing the receptors from binding fibrinogen, used in conjunction with aspirin and heparin. USE: approved for IV therapy of ACS and for patients undergoing PCI – can accelerate revascularization in patients undergoing thrombolytic therapy for acute MI, antiplatelet effects 24 to 48 hrs after the infusion is stopped. Chlorothiazide (Diuril): thiazide diuretic; antihypertensive MOA: increase excretion of Na and H2O by inhibiting Na reabsorption in the disal tubule. Promotes excretion of Cl, K, Mg, and HCO3. Indications: management of mild to moderate hypertension. Treatment of edema associated with heart failure, renal dysfunction, cirrhosis, glucocorticoid therapy. Contraindications: hypersensitivity, cross-sensitivity with thiazides and sulfonamides, lactation. Adverse Effects: dizziness, headache, blurred vision, sun sensitivity, Steven-Johnson Syndrome. Nursing Interventions: monitor BP, I/O and daily weight. Assess feet and legs for edema. Consider potassium supplement. Assess for skin rash. Clopidogrel (Plavix): antiplatelet, ADR receptor antagonist, used alone or in conjuctive with ASA. Prodrug: converted to active form of CYP2C19 Action: ADP Antagonist – blocks P2Y12 ADP receptor on platelet surface, prevents ADP stimulated PLT aggregation. • Reduction or prevention of clots in stents • Reduction in incidence of cerebral vascular accident (CVA), and acute coronary syndrome, MI • Effective in peripheral arterial disease (PAD) ADR: common abdominal pain, dyspepsia, diarrhea & rash. Bleeding hemorrhage (less than aspirin), stop med 5-7 days prior to surgery. Interactions: all other anticoags, and CYP2 inhibitors, herbal drugs (chamomile, clove, garlic, ginger, ginkgo, ginseng, anise) PPI: may reduce GI bleed but also reduces clopidogrel effectiveness. *poor metabolizers* = genetic inability to convert clopidogrel to active form; blood/saliva tests are available - in 2012, evidence that it may only be effective in smokers Dabigatran (Pradaxa): direct thrombin inhibitor, oral anticoagulant MOA: PO-prodrug undergoes conversion to dabigatran, direct thombin inhibitor – reversible, combines with free thrombin & thrombin in clots, prevents conversion of fibrinogen to fibrin, prevents activation of Factor VIII. USE: Afib- reduces the risk of stroke in patient with non-valvular Afib, DVT & PE, Prevention for hip/knee surgery ADR: bleeding – lower risk than warfarin, GI Disturbances – dyspepsia, gastritis Monitoring: infrequent aPTT, check LFTs Drug-to-Drug: ketoconazole, amiodarone, verapamil, no food interactions, not for mechanical valve convertase Antidote: idarucizumab (praxbind)- Fa15 PO Dose: standard dose, DO NOT CHEW OR CRUSH, also very expensive Direct Thrombin Inhibitor: MOA: direct inhibition of thrombin PO - Dabigatran