Pharmacology Final Exam Study Guide, Exams of Nursing

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UNRS 113 Pharmacology Final Exam Study Guide 1 PHARMACOLOGY FINAL EXAM STUDY GUIDE Please know the mechanism of action, drug effects, indications (may have more than one indication), contraindications, adverse effects, antidotes for toxicity (if any), desired therapeutic effect, significant drug-drug interactions, nursing implications, and important patient education for each of the following classes of drugs: PHARM PRINCIPLES Pharmaceutics (compare and contrast the different routes including enteral, parental, topical, and transdermal routes) The science of preparing and dispensing drugs, including dosage form design ● Science of “dosage form” design ● Dosage form design determines the rate at which drug dissolution occurs ● A variety of dosage forms exist to provide both accurate and convenient drug delivery systems Enteral: ● Absorbed through mucosa of stomach or intestine o Oral (PO) medications ▪ Tablet ● Powdered medication compressed into hard disk ● Are often scored so a half-dose can be given ▪ Capsules ● Medication encased in gelatin shell ● May contain sustained or extended release granules ▪ Enteric coated tablets ● Tablets are coated so that they do not break down in the stomach ● Absorption of the drug takes place in the small intestine ● Cannot be divided into smaller doses ▪ Chewable tablets ● Can be chewed ● Used for children and other clients who have a hard time swallowing pills ● Break down of the drug starts in the mouth ▪ Sublingual (SL) ● The tablet is put under the tongue ▪ Liquids, elixirs, and syrups ● Already dissolved and are usually absorbed more quickly than solid dosage forms Parenteral: ● Refers to injection o Intradermal, subcutaneous, intramuscular, intravenous ▪ Intradermal (ID) UNRS 113 Pharmacology Final Exam Study Guide 2 ● Injection into the dermis just below the epidermis o TB UNRS 113 Pharmacology Final Exam Study Guide 5 ▪ Other metabolic tissue include – skeletal muscle, kidneys, lungs, plasma and intestinal mucosa ● Biotransformation capabilities of the liver can vary considerably from patient to patient: o Age o Genetics (CYP 450 system) o Disease o Concurrent use of other medications ● Biochemical alteration of a drug into an inactive metabolite, a more soluble compound, a more potent active metabolite ● Enzyme inhibitors Excretion ● Elimination of drugs from the body; primarily by the kidney, or liver and bowel ● Excretion refers to the elimination of the drug from the body ● Requires adequate functioning of the circulatory system and organs of excretion: o Kidneys via urine o Liver via bile and into the feces o Lungs via exhaled air o Saliva, tears, and sweat or skin Onset of action, peak effect, duration of action, half-life, and peak and trough Onset of action: the time required for a drug to elicit a therapeutic response after dosing Peak effect: the time required for a drug to reach its maximum therapeutic response in the body ● Corresponds to increasing drug concentrations at site of action Duration of action: the length of time the concentration of a drug in the blood or tissues is sufficient to elicit a response ● How long it’s in your system Half-life: in pharmacokinetics, the time required for half of an administered dose of drug to be eliminated by the body, or the time it takes for the blood level of a drug to be reduced by 50% (also called elimination half-life) ● Example: a given drug is 100 mg/L in 8 hours the drug level is 50 mg/L, 8 hours= half-life of that drug ● Half-life is useful for determining when steady state will be reached o Steady state: physiologic state in which the amount of drug removed via elimination is equal to the amount of drug absorbed with each dose UNRS 113 Pharmacology Final Exam Study Guide 6 Peak level: the maximum concentration of a drug in the sample for therapeutic drug monitoring ● Highest blood level o Drug toxicity occurs if peak blood level is too high Trough level: the lowest concentration of drug reached in the bod after it falls from its peak level, usually measured in a blood sample for therapeutic drug monitoring ● Lowest blood level o Drug may not produce a response if trough blood level is too low Safety considerations (e.g. black box warnings, pregnancy categories, look-alike sound-alike drugs, high alert medications, double check medications) Black box warning: a type of warning that appears in a drug’s prescribing information and is required by the U.S. Food and Drug Administration (FDA) to alert prescribers of serious adverse events that have occurred with the given drug. ● Strictest warning o Reasonable evidence of an association of a serious hazard with the drug ▪ Benefit outweigh the risk Pregnancy categories: the fetus is at greatest risk for drug-induced developmental defects during the first trimesters. ● Category A→ No risk to human fetus ● Category B → No risk to animal fetus, information on humans not available ● Category C → Adverse effects reported in animal fetus, information on humans not available ● Category D → Possible fetal risk in humans ● Category X → Fetal abnormalities; these drugs are not to be used on pregnant women Look-alike sound-alike drugs (LASA): confusing one medication for another that is spelled or sounds similar to a different medication High alert medications: drugs that bear a heightened risk of causing significant patient harm when used in error. Double check medications: medications that must be checked by two licensed registered nurses to verify correct dose/medication ● Heparin ● Insulin AUTONOMIC NERVOUS SYSTEM DRUGS UNRS 113 Pharmacology Final Exam Study Guide 7 The autonomic nervous system is part of the peripheral nervous system. The autonomic nervous system controls everything that is involuntary and subconscious. ● Regulation of the heart ● Regulation of secretory glands (salivary, gastric, sweat, and bronchial glands) ● Regulation of smooth muscles (muscles of bronchi, blood vessels, urogenital system, and GI tract) Further divided into: ● Parasympathetic nervous system (rest-and-digest): primarily concerned with the “housekeeping” chores of the body (digestion of food and excretion of wastes). Controls vision and conserves energy (by reducing cardiac work) o Constricted pupil o Decreased heart rate o Contracted bronchi o Increased gastric secretions o Increased GI peristalsis o Emptying bowel o Empting bladder ● Sympathetic nervous system (fight-or-flight): regulates the cardiovascular system and body temperature and implements the fight or flight reaction. By influencing the heart and blood vessels, the SNS can achieve three homeostatic objectives: 1) maintenance of blood flow to the brain 2) redistribution of blood flow during exercise 3) Compensation for loss of blood. Primarily by causing vasoconstriction. o Dilated pupils o Increased heart rate o Increased blood pressure o Dilated bronchi o Stored energy mobilized o Blood shunted from skin and viscera into skeletal muscles o Temperature regulation Alpha-adrenergic (epinephrine, levophed) ● Sympathomimetics: Drugs that stimulate the sympathetic nervous system by mimicking the effects of the SNS neurotransmitters (mimes the sympathetic nervous system) o These drugs are also known as adrenergic agonists Mechanism of action ● Direct-acting sympathomimetic o Binds directly to the receptor and causes a physiologic response ● Indirect-acting sympathomimetic o Causes release of neurotransmitter from storage sites (vesicles) in nerve endings UNRS 113 Pharmacology Final Exam Study Guide 10 ● Take medications as prescribed and do not abruptly stop o Rebound hypertension or chest pain ● Change positions slowly ● Avoid activates that precipitate hypotension o Avoid extreme heat such as hot tub or sauna Beta-adrenergic (albuterol) Beta1- one heart Beta2-two lungs Mechanism of action ● Stimulate beta2-adrenergic receptors on bronchial smooth muscles which causes muscle relaxation and bronchodilation ● Direct-acting sympathomimetic o Binds directly to the receptor and causes a physiologic response ● Indirect-acting sympathomimetic o Causes release of neurotransmitter from storage sites (vesicles) in nerve endings o Neurotransmitter then binds to receptors and causes a physiologic response Drug effects ● Stimulation of beta2-adrenergic receptors on the airways results in o Relaxation of the smooth muscle around bronchi o Bronchodilation o Ease of breathing ● Other effects of beta2-adrenergic stimulation o Uterine relaxation o Glycogenolysis in liver o Enhanced skeletal muscle contraction Indications ● Treatment of asthma o Bronchodilators are drugs that stimulate beta2-adrenergic receptors on bronchial smooth muscles causing relaxation and bronchodilation Adverse effects ● CNS o Tremors, headache, nervousness, dizziness ● Cardiovascular o Palpitations, tachycardia, dysrhythmia, angina ● Other o Sweating, nausea, vomiting, muscle cramps Drug-drug interactions ● Antihypertensive ● Anticholinergic antihistamines ● Thyroid hormone replacement Nursing implications UNRS 113 Pharmacology Final Exam Study Guide 11 ● Complete medical history and medication list o Assess for contraindications such as angina, dysrhythmias, hypertension, history of MI/CVA o Assess for use of antihypertensive, adrenergic blockers or anticholinergics, thyroid drugs ● Current vital signs o Especially blood pressure and heart rate ● Current labs including liver and kidney function ● Assess for therapeutic and adverse responses Patient educations ● Take exactly as prescribed ● Do not stop abruptly ● Report worsening symptoms to provider ● OTC medications and herbals require prescriber’s approval due to increased risk of drug-drug interactions Beta-blockers (atenolol, metoprolol) GENERIC BETA BLOCKERS –OLOL Beta1- one heart Beta2- two lungs Mechanism of action ● Interrupts stimulation of the SNS as the alpha 1-adrenergic receptors work by either direct competition with norepinephrine or by non- competitive process Drug effects ● Reduce SNS stimulation of the heart o Decrease heart rate o Decrease force of contraction o Decrease conduction rate through the AV node ● Decrease renin release from kidneys Indications ● Angina o Beta blockers decrease demand for myocardial oxygen ● Cardio-protective S/P MI o Beta blockers inhibit stimulation from circulation catecholamine’s ● Hypertension o Beta blockers decrease contractility which decreases stroke volume Contraindications ● Contraindicated in clients who have AV block and sinus bradycardia Adverse effects ● Cardiovascular UNRS 113 Pharmacology Final Exam Study Guide 12 o Bradycardia, atrioventricular (AV) block, decreased cardiac output and worsening heart failure, rebound myocardium excitation (black box warning) ● Respiratory o Bronchoconstriction, wheezing ● Metabolic o Masks signs of hypoglycemia, inhibition of Glycogenolysis Nursing implications ● Assess for underlying heart and pulmonary disease ● Assess pulse and B/P prior to administration ● Hold beta-blocker and contact MD for bradycardia Patient education ● Take medications as prescribed and do not abruptly stop o Rebound hypertension or chest pain ● Change positions slowly ● Avoid activities that precipitate hypotension o Avoid extreme heat such as hot tub or sauna Cholinergics (bethanechol) Mechanism of action ● Direct-acting cholinergic agonist Drug effects ● Increases the tone of the detrusor urinary muscle ● Stimulates gastric and intestinal motility ● Increases lower esophageal sphincter pressure ● Cardiovascular and nicotinic activity are minimal Indications ● Post-op urinary retention-direct acting muscarinic agonist stimulate receptors of the bladder o Contraction of the detrusor muscle o Relaxing of the sphincter allowing urine to flow Contraindications ● Drug allergy ● Active bronchial asthma ● Epilepsy ● Hyperthyroidism ● Parkinson’s ● Peptic ulcer ● Cardiac disease /CAD Adverse effects ● Syncope ● Seizure ● Hypotension with reflex tachycardia ● GI upset ● Headache UNRS 113 Pharmacology Final Exam Study Guide 15 ● Anticholinergics taken by the elderly patient may lead to higher risk for heatstroke because of the effects on heat-regulating mechanisms ● Check with physician before taking any other medication, including OTC medications ● No double dosing ● Report blurred vision, chest pains, allergic reactions, constipation, and urinary retention ● Sunglass use to protect eyes ● Do not store in light or freezing PAIN MANAGEMENT AND ANTI-INFLAMMATORY DRUGS Analgesics: medications that relieve pain without causing loss of consciousness “Painkillers” Opioids (morphine, dilaudid) ● Opioid analgesic ● Synthetic drugs that bind to the opiate receptors to relieve pain Mechanism of action ● Agonists, similar to the body’s own endorphins o Bind to an opioid receptor in the brain o Cause an analgesic response (reduction of pain sensation) Drug effects ● Morphine: (strong agonist) severe pain, used to control postoperative and other types of pain. First line analgesics in immediate postoperative setting ● Dilaudid: (strong agonist) severe pain, also immediate postoperative, 7x’s stronger than Morphine Indications ● Main use: to alleviate moderate to severe pain ● Often given with adjuvant analgesic drugs to assist primary drugs with pain relief ● Opioids are also used for cough center suppression treatment of diarrhea and balance anesthesia Contraindications Adverse effects Antidotes for toxicity Therapeutic effect Drug-drug interactions Nursing implications Patient education Acetaminophen (Tylenol) ● Nonopiod analgesic ● Cyclooxygenase (COX) inhibitors o Lacks anti-inflammatory properties ● Cycolooxygenase-1 (COX-1) UNRS 113 Pharmacology Final Exam Study Guide 16 o “Good” COX o Located in stomach, platelets, kidney ● Cyclooxygenase-2 (COX-2) o “Bad” COX o Causes inflammation, pain, and fever o Located in blood vessels, kidney, colon/rectum, brain, injured tissues Mechanism of action ● Selective inhibition of cyclooxygenase (COX) in the CNS mostly (and perhaps in the periphery) Drug effects ● Analgesic (pain reliever) ● Antipyretic (fever reducer) Indications ● Fever ● Mild to moderate pain ● Alternative for those who cannot use aspirin Contraindications ● Drug allergy ● Severe liver disease ● G6PD disease o Caution ▪ Alcohol (ETOH) Adverse effects Toxicity & Management of Overdose ● Ingestion of large amounts of acetaminophen, as in acute intentional overdose or unintentional misuse can cause hepatic necrosis ● Acute ingestion of acetaminophen doses of 150 mg/kg or more may result in hepatic toxicity ● Antidote o Acetylcysteine (Mucomyst) ● Action o Substitute for depleted glutathione, prevents hepatotoxic metabolites of acetaminophen from forming ● Dosing o Loading dose of 140 mg/kg orally, followed by 70 mg/kg every 4 hours for 17 additional doses Therapeutic effect ● Decrease in pain ● Decrease in fever Drug-drug interactions Nursing implications ● Pre-administrations assessment o List of current medications o Assess comorbidities (liver disease, G6PD, ETOH) UNRS 113 Pharmacology Final Exam Study Guide 17 o Lab values (renal, liver, and CBC ● Monitor for therapeutic effects o Decrease in pain o Decrease in fever ● Monitor for adverse effects o S/S Chronic poisoning ▪ Rapid, weak pulse, dyspnea, and cold/clammy extremities o S/S Hepatotoxicity ▪ Dark urine, clay-colored stool, yellowing of skin and sclera, abdominal pain Patient education ● Teach NSAIDS (aspirin, ibuprofen) Mechanism of action Drug effects Indications Contraindications Adverse effects Antidotes for toxicity Therapeutic effect Drug-drug interactions Nursing implications Patient education CARDIAC AND RENAL DRUGS Angiotensin-converting enzyme inhibitors (lisinopril, benazepril) GENERIC ACE INHIBITORS OFTEN END IN -PRIL Mechanism of action Drug effects Indications Contraindications Adverse effects Antidotes for toxicity Therapeutic effect Drug-drug interactions Nursing implications Patient education Beta-blockers (see above) Calcium channel blockers (amlodipine, cardizem) GENERIC CCB OFTEN END IN -DIPINE Mechanism of action Drug effects