Study guide for EXAM 1 EMR (diana) (1).docx

Study Guide for Exam 1 Please remember that this is just a study guide; you must review the chapters and power points. For all medications, you will need to know: Classification and Prototypes the purpose mechanism of action side effects/adverse reactions 6 rights of preparation and administration I...

Study Guide for Exam 1 Please remember that this is just a study guide; you must review the chapters and power points. For all medications, you will need to know: Classification and Prototypes the purpose mechanism of action side effects/adverse reactions 6 rights of preparation and administration Indications/nursing Implications Patient Education Chapter 1: Safety Medication Practice Error-reduction strategies during medication administration include the following: Having a “quiet zone” to prepare medications. Placing “quiet zone” signs at the entrance to medication room or above the automated medication-dispensing system. Following protocols and checklist outlining medication administration. Wearing a sash or vest to signal others to avoid interrupting the nurse during medication administration. Educating staff to reduce interruptions of nurses administering medications. Having a drug guide available during drug administration. Trade/Generic Names Drug names Generic name: related to the chemical or official name and is independent of the manufacturer. Often indicates the drug group. Brand (trade) name: designed and patented by the manufacturer. Scheduled Drugs/Narcotics Categories of Controlled Substances Schedule I: not accepted, lack of safety, and high abuse potential. Example: heroin, LSD, ecstasy, and peyote. Schedule II: used medically and have high abuse potentials. Example: opioid analgesics (codeine, hydromorphone, morphine, and oxycodone) Schedule III: less potential for abuse than I and II; they may lead to psychological or physical dependence. Example: androgens and anabolic steroids, some depressants. Schedule IV: accepted medically but with some potential for abuse. Example: diazepam, lorazepam. Schedule V: containing moderate amounts of controlled substances. Dispensed by the pharmacists without a physician’s prescription but some restrictions. The Drug Enforcement Administration (DEA) enforces the Controlled Substances Act. They keep accurate records of all transactions, provide for secure storage. Nurses are responsible for strong controlled substances in locked containers, administering them only to people for whom are prescribed recording each dose given and documenting or reporting discrepancies to the proper authorities. Chapter 2: Pharmacokinetics/Pharmacodynamics - Medications effects in body Absorption, Distribution, Metabolism, Excretion of Prototypes Pharmacokinetics Involves drug movement through the body to reach sites of action, metabolism, and excretion. Specific processes are absorption, distribution, metabolism, and excretion. Absorption The process that occurs from the time a drug enters the body to the time it enters the bloodstream to be circulated. Most oral drugs must be swallowed, dissolved in gastric fluid, and delivered to the small intestine before they are absorbed. Drugs injected into the subcutaneous or intramuscular (IM) tissues are usually absorbed more rapidly than are oral drugs because they move directly to the bloodstream. Distribution Involves the transport of drug molecules within the body. Depends largely on the adequacy of blood circulation. Drugs are distributed rapidly to organs receiving a large blood supply, such as the heart, liver, and kidneys. Metabolism Metabolism, or biotransformation, is the method by which drugs are inactivated or bio transformed by the body. Most often, an active drug is changed into inactive metabolites, which are then excreted. The kidneys can excrete only water-soluble substances. One function of metabolism is to convert fat-soluble drugs into water-soluble metabolites. CYP enzymes are complex proteins with binding sites for drug molecules. They catalyze the chemical reactions of oxidation, reduction, hydrolysis. This enzyme induction accelerates drug metabolism because larger amounts of the enzymes allow larger amounts of a drug to be metabolized during a given period. As a result, larger doses of the rapidly metabolized drug may be required to produce or maintain therapeutic effects. Metabolisms also can be decreased or delayed in a process called enzyme inhibition, which most often occurs with concurrent administration of two or more drugs that compete for the same metabolizing enzymes. Excretion Refers to elimination of a drug from the body. Effective excretion requires adequate functioning of the circulatory system and the organs of excretion (kidneys, bowel, lungs, and skin). Factors impairing excretion: severe renal disease, which leads to accumulation of numerous drugs and may cause severe adverse effects of dosage is not reduced. Chapter 3: Overall information of antibiotic classifications Routes of medications/Protypes Chapter 9: Medications: Vitamin K (anticoagulant) Vitamin K Antagonists / Warfarin (PROTOTYPE) PHARMACOKINETICS Administration with food may delay the rate but not the extent of absorption. The drug is highly bound to plasma proteins (98%), mainly albumin. Metabolism takes place in the liver. Excretion, primarily as inactive metabolites, occurs in the kidneys. Renal impairment does not affect drug metabolism but may decrease excretion of the drug. VITAMIN K: ANTIDOTE Vitamin K is the antidote for warfarin and may be administered if the INR level is 5 or more and signs of bleeding are present. ACTION Warfarin acts in the liver to prevent synthesis of vitamin K–dependent clotting factors (i.e., factors II, VII, IX, and X). Similar to vitamin K in structure, warfarin therefore acts as a competitive antagonist to hepatic use of vitamin K Warfarin has no effect on circulating clotting factors or on platelet function, so the anticoagulant effects do not occur for 3 to 5 days after warfarin is started because clotting factors already in the blood follow their normal pathway of elimination. USE Warfarin is most useful in long-term prevention or management of venous thromboembolic disorders, including DVT, pulmonary embolism, and embolization associated with atrial fibrillation and prosthetic heart valves After cardiac surgery, children receive warfarin to prevent thromboembolism, but there are no established doses and guidelines for safe, effective use. (monitor blood coagulation tests) Warfarin metabolism may be altered in older adults. As patient age increases, a lower dose of warfarin is usually required to produce a therapeutic effect. likely to cause bleeding in patients with hepatic disease because of decreased synthesis of vitamin K and decreased plasma proteins. In addition, only the liver eliminates warfarin; thus, it may accumulate in people with hepatic impairment, and dosage adjustment may be necessary. Because the anticoagulant and antithrombotic effects of warfarin take several days to occur, (LONG TERM THERAPY) patients who are critically ill require concurrent treatment with other anticoagulants, such as heparin or LMWHs. Heparin is usually continued until the international normalized ratio (INR) is the therapeutic range. ADVERSE EFFECTS: The primary adverse effect associated with warfarin therapy is hemorrhage. Additionally, nausea, vomiting, abdominal pain, alopecia, urticaria, dizziness, and joint or muscle pain may occur. CONTRAINDICATIONS The US Food and Drug Administration (FDA) has issued a BLACK BOX WARNING ♦ for warfarin because of the risk of its causing major or fatal bleeding. PREGNANCY CATEGORY X Alteplase (thrombolytic drug) Alteplase (PROTOTYPE) PHARMACOKINETICS Administration of alteplase is by IV infusion. Metabolism occurs predominantly in the liver. Following discontinuation of the infusion, more than 50% of the drug is cleared, with more than 80% clearance within 10 minutes. Excretion takes place in the urine. Whether alteplase crosses the placenta or is excreted into breast milk is unknown. ACTION Alteplase is a protein that lyses unwanted fibrin blood clots by catalyzing the conversion of plasminogen to plasmin. USE Indications for alteplase include lysis of acute coronary arterial thromboembolism associated with evolving transmural myocardial infarction or acute pulmonary thromboembolism. Clinicians also considered it as first-line therapy for the treatment of acute ischemic stroke in selected people. Caution is warranted in older patients (65–80 years of age).Alteplase is not recommended in people older than 80 years of age. Caution is necessary in patients with significant hepatic impairment. ADVERSE EFFECTS As with other anticoagulants and antiplatelet agents, bleeding is the main adverse effect of alteplase. To minimize this risk, it is important to select recipients carefully, avoid invasive procedures when possible, and omit anticoagulant or antiplatelet drugs (except for aspirin) while thrombolytics are being given CONTRAINDICATIONS Due to an increased risk of bleeding, alteplase is contraindicated in patients with uncontrolled severe hypertension, aneurysm, arteriovenous malformation, known coagulopathy or internal bleeding, intracranial or intraspinal surgery or trauma within the past 3 months, intracranial mass, recent major surgery, or current use of oral anticoagulants. Only experienced personnel in an emergency department, a critical care unit, or diagnostic/interventional setting with cardiac and other monitoring devices in place should perform thrombolytic therapy. It is necessary to minimize intramuscular injections in patients who are receiving systemic thrombolytic therapy, because bleeding, bruising, or hematomas may develop. ADMINISTERING THE MEDICATION Before a thrombolytic agent is begun, it is essential to check INR, aPTT, platelet count, and fibrinogen to establish baseline values and to determine whether a blood coagulation disorder is present. Two or three hours after thrombolytic therapy is started, the nurse must ensure that the fibrinogen level is measured to determine that fibrinolysis is occurring. Alternatively, he or she can check INR or aPTT for increased values because the breakdown products of fibrin exert anticoagulant effects. Administration is IV as a bolus injection or infusion. The nurse administers all infusions using an IV infusion device. It is necessary to reconstitute alteplase as indicated and not to shake it. Clopidogrel (antiplatelet) Adenosine diphosphate receptor antagonists clopidogrel (PROTOTYPE) Clopidogrel and the other ADP receptor antagonists, prasugrel and ticagrelor, have antiplatelet effects similar to aspirin and inhibit the ADP receptor on the surface of platelets. Clopidogrel has three shortcomings: delayed onset of action, irreversible inhibitory effects on platelets with no reversing agent or antidote, and significant individual variability in platelet response. PHARMACOKINETICS Clopidogrel is rapidly absorbed after oral administration and undergoes extensive first-pass metabolism in the liver. Clopidogrel is a prodrug and is converted to its active form by hepatic CYP2C19 (an isozyme of the cytochrome P-450 system). To a lesser extent, activation of the drug also occurs via CYP3A4 enzymes. Platelet inhibition may occur 2 hours after a single dose, but the onset of action is slow, so that an initial loading dose is usually administered. The drug has a half-life of about 8 hours. The drug is excreted in the urine and feces. D ACTION Clopidogrel irreversibly blocks the ADP receptor on platelet cell surface. Effective dose-dependent prevention of platelet aggregation can be seen within 2 hours of a single oral dose, but the onset of action is slow, so that a loading dose of 300 to 600 mg is usually administered. Platelet inhibition essentially lasts for the lifespan of the platelet (7–10 days). With repeated doses of 75 mg/d, maximum inhibition of platelet aggregation is achieved within 3 to 7 days. Platelet aggregation progressively returns to baseline about 5 days after discontinuing clopidogrel. (SLOW) USE Indications for use include reduction of myocardial infarction, stroke, and vascular death in patients with atherosclerosis and in those after placement of coronary stents. Specific uses include prevention of vascular ischemic events in patients with symptomatic atherosclerosis or with acute coronary syndrome (with or without ST-segment elevation) In acute coronary syndrome, clopidogrel is given with aspirin (dual antiplatelet therapy). Patients may also take clopidogrel in conjunction with aspirin to prevent thrombosis following placement of an intracoronary stent. People with atrial fibrillation who are unable to take vitamin K antagonists take clopidogrel instead. Adding clopidogrel to aspirin in people with atrial fibrillation reduces the rate of major vascular events compared with aspirin alone but is associated with a greater risk of bleeding. Prescribers also order clopidogrel as an alternative antiplatelet drug for patients who cannot tolerate aspirin. (ALTERNATIVE OPTION) safety in kids not established Older adults are more likely than younger ones to experience bleeding and other complications of antiplatelet drugs. Clopidogrel is commonly used to prevent thrombotic stroke but can increase the risk of hemorrhagic stroke. A safe loading dose for clopidogrel in patients 75 years of age and older has not yet been established. Because clopidogrel is metabolized in the liver, it may accumulate in people with hepatic impairment. Caution is necessary. ADVERSE EFFECTS The most common adverse effects associated with clopidogrel are pruritus, rash, purpura, and diarrhea. (LECTURE POINT) Thrombotic thrombocytopenic purpura, hemorrhage, and severe neutropenia have also occurred. People with variant forms of CYP2C19 may be poor or ultrarapid metabolizers of clopidogrel. Ultrarapid metabolizers of clopidogrel may have an increased risk of bleeding. With poor metabolizers, the benefits of the drug may not be adequate recommend an alternative antiplatelet therapy (e.g., prasugrel, ticagrelor) for CYP2C19 poor or intermediate metabolizers if there are no contraindications. CONTRAINDICATIONS Contraindications to clopidogrel include hypersensitivity to the drug or any other component. It should not be used in patients with active bleeding in conditions such as intracranial hemorrhage or peptic ulcer disease. A category B medication, the drug requires cautious use in pregnant and lactating women. ADMINISTERING THE MEDICATION Patients take clopidogrel once daily without regard to food intake. As previously stated, although the drug may be effective 2 hours after a single dose, the onset of action is slow, and an initial loading dose is usually administered. The FDA has approved a 300-mg tablet as a loading dose for appropriate patients. The effect of the drug is apparent as soon as 2 hours after the 300-mg dose. It is recommended that patients who receive implants with a bare-metal stent or a drug-eluting stent take dual antiplatelet therapy for at least 12 months. If well tolerated, dual antiplatelet therapy can be continued for another 18 months. Do not double a dose if missed. Coumadin Aspirin (antiplatelet) Heparin Heparins/ Heparin (PROTOTYPE) pharmaceutical preparation of the natural anticoagulant produced primarily by mast cells in pericapillary connective tissue, and it is the prototype anticoagulant. Endogenous heparin is found in various body tissues, most abundantly in the liver and lungs. ANTIDOTE: PROTAMINE SULFATE PHARMACOKINETICS give heparin intravenously or subcutaneously, because the gastrointestinal (GI) tract does not absorb the drug. After IV injection, the drug acts immediately. After subcutaneous injection, heparin acts within 20 to 30 minutes. Metabolism takes place in the liver and the reticuloendothelial system. Excretion, primarily in the form of inactive metabolites, occurs in the urine. Hemodialysis does not remove it. ACTION Heparin combines with antithrombin III (a natural anticoagulant in the blood) to inactivate clotting factors IX, X, XI, and XII; inhibit the conversion of prothrombin to thrombin; and prevent thrombus formation. After thrombosis has developed, heparin can inhibit additional coagulation by inactivating thrombin, preventing the conversion of fibrinogen to fibrin, and inhibiting factor XIII (fibrin-stabilizing factor). USE Prophylactically, patients at risk for certain disorders take low doses of heparin prophylactically to prevent DVT and pulmonary embolism. These disorders include the following: Major illnesses (e.g., acute myocardial infarction, heart failure, serious pulmonary infections, stroke) Major abdominal or thoracic surgery A history of thrombophlebitis or pulmonary embolism, including pregnant women Gynecologic surgery, especially in patients who have been taking estrogens or oral contraceptives or have other risk factors for DVT Restrictions such as bed rest or limited activity expected to last longer than 5 days patients receive heparin for management of acute thromboembolic disorders (e.g., DVT, thrombophlebitis, pulmonary embolism). In these conditions, the aim of therapy is to prevent further thrombus formation and embolization. Another use is in disseminated intravascular coagulation (DIC), a life-threatening condition characterized by widespread clotting, which depletes the blood of coagulation factors. The goal of heparin therapy in DIC is to prevent blood coagulation long enough for clotting factors to be replenished and thus be able to control hemorrhage. Heparin does not cross the placental barrier and is not secreted in breast milk, making it the anticoagulant of choice for use during pregnancy and lactation. Use in children based on weight for dosage. patients with renal or hepatic impairment may take usual doses but half-life may be affected. Used in critically ill patients. Patients may take standard heparin at home using the subcutaneous route, and use of LMWHs for home management of venous thrombosis has become standard practice. It is essential to take platelet counts before therapy begins and every 2 to 3 days during heparin therapy. If the platelet count falls below 100,000 platelets per microliter of blood or to less than half the baseline value, it is necessary to discontinue the heparin. ADVERSE EFFECTS Hemorrhage Heparin-induced thrombocytopenia (HIT) (type II) is a potentially life-threatening complication of heparin administration, leading to a decrease in platelet count and detectable HIT antibodies. CONTRAINDICATIONS Contraindications include GI ulcerations (e.g., peptic ulcer disease, ulcerative colitis), intracranial bleeding, dissecting aortic aneurysm, blood dyscrasias, severe kidney or liver disease, ADMINISTERING THE MEDICATION Traditional anticoagulants have two major limitations: a narrow therapeutic window of adequate anticoagulation without bleeding and a highly variable individual dose–response that requires monitoring by laboratory testing. use aPTT (activated partial thromboplastin time) to regulate heparin dosage During heparin therapy, the aPTT should be maintained at approximately 1.5 to 2.5 times the control or baseline value. The normal control value is 25 to 35 seconds; therefore, therapeutic values of adequate anticoagulation are 45 to 70 seconds, approximately. With continuous IV infusion, blood for the aPTT may be drawn at any time; with intermittent administration, blood for the aPTT should be drawn approximately 1 hour before a dose of heparin is scheduled. It is not necessary to monitor aPTT with low-dose standard heparin given subcutaneously for prophylaxis of thromboembolism or with the LMWHs (e.g., enoxaparin). Chapter 11: Medications: Epoetin The prototype recombinant form of human erythropoietin that helps the body produce more RBCs. The clinical benefit of treatment of anemia with an ESA is to reduce the need and cost of blood transfusions, lessen the risk of infectious diseases from transfusions, and potentially enhance the overall quality of life as anemia is relieved. Evidence indicates that the patients who benefit consistently from ESAs are prescribed epoetin alfa or another ESA for chemotherapy-associated anemia or those with anemia due to chronic kidney disease. The onset of action is 11 to 14 days. For cancer patients with chemotherapy-associated anemia who have a hemoglobin level that has decreased below 10 g/dL Treatment of anemia associated with chronic kidney disease. Premature infants should not receive epoetin alfa from multidose vials because they contain benzyl alcohol, which can be fatal. Patients with chronic kidney disease may also benefit from an ESA because they have reduced production of erythropoietin. Most common adverse effects are hypertension. Avoid using ESAs in patients with hemoglobin values of 12 g/dL or above. Bolus injection at the end of dialysis Epoetin alfa is not effective unless sufficient iron is present; therefore, patient teaching may need to emphasize the importance of taking an iron supplement. Darbepoetin is a relatively long-acting agent compared to epoetin alfa’s shorter-acting duration. Epoetin beta (Mircera) is used in the treatment of anemia associated with chronic kidney disease in adults—whether or not they require dialysis. BLACK BOX WARNING ♦ for epoetin beta, reporting that it is not indicated and is not recommended for treatment of chemotherapy-induced anemia. Interferon Interferons: alfa, beta, or gamma, are biologic response modifiers that bind to specific cell surface receptors and alter intracellular activities. In viral infections, these immunostimulants induce enzymes that inhibit protein synthesis and degrade viral RNA. As a result, viruses are less able to enter uninfected cells, reproduce, and release new viruses. In addition to their antiviral effects, interferons also have antiproliferative and immunoregulatory activities. Interferons ‘interfere’ with viruses. The virus tries to pass the ball (RNA) and the interferon goes, “nope,” and swats it out of their hands. Increase expression of major histocompatibility complex molecules Augment the activity of NK cells. Increase the effectiveness of antigen-presenting cells in inducing the proliferation of cytotoxic T cells. Aid the attachment of cytotoxic T cells to target cells. Inhibit angiogenesis (formation of blood vessels) Enhance the immune system. They upgrade all the soldiers. Prototype: Interferon alfa 2b (Intron A) Pharmacokinetics🔬 80% absorbed and widely distributed but does not cross the blood–brain barrier. Minimal hepatic metabolism. Excretion is primarily renal. Peak onset of action is 3 to 12 hours. Half-life is approximately 2 to 3 hours. Action 🏃 Both antiviral and antineoplastic activities. Exerts its cellular activities by binding to specific membrane receptors on cell surface enhancing immune response, inhibiting viral replication in virus cells. Enhances function of the immune system by increasing phagocytic activity of macrophages and monocytes, which augments cytotoxicity against cancer cells. Suppresses the growth and reproduction of similar cells by cell division. Use 👾 (Used to KILL) Hairy cell leukemia, chronic hepatitis B and C, Kaposi’s sarcoma, genital warts, malignant melanoma, lymphoma (follicular), and condyloma. Adverse Effects💀 Caution in patients with liver disease; raises their hepatic enzymes so monitor ALT, AST, etc. Flu-like symptoms 😷 (e.g., fever, chills, fatigue, muscle aches, headache, tachycardia. Chest pain and alopecia Hematologic effects include neutropenia, anemia, and thrombocytopenia. Teratogenic! 👶💀 Administering the Medication IV, Sub-Q, IM, or intralesionally. Three times weekly, on a regular schedule (e.g., Monday, Wednesday, and Friday), at about the same time of day, at least 48 hours apart, per manufacturer. Diagnostic Tests 🧪 Liver function tests and WBC, RBC, and platelet values. Chapter 13: Medications: Overall information regarding Immunosuppressants. Corticosteroids Chapter 14: Methotrexate Chemotherapy Chapter 15 Overall information of antibiotics Chapter 16: Medications: Tylenol Aspirin Opioids Ibuprofen Chapter 18: penicillin Concentrate on: High Alert Medications Generic and Trade Names Drug Sources Drug Approval Processes Serum Drug Levels Pharmacokinetics Cell Membranes and Receptors Serum Half-life Drug-related variables Patient-related variables Drug Preparations and Dosage Forms Drug dosage Calculations Routes of Administration Medication Administration Process Health Education on Medications to Adults and Geriatric Patients Physiological Changes in Geriatrics in Relationship with Medications Safety in Administering Medications to Adults and The Elderly