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NUR MISC Exam STUDY GUIDE

NUR MISC EXAM 3 CH. 36 Antihistamines, Decongestants, Antitussives, & Expectorants Antihistamines • Drugs that directly compete with histamine for specific receptor sites • Two histamine receptors o H1 (histamine1): smooth muscle contraction and capillaries o H2 (histamine2): GI and HR acceleration • H1 antagonists (H1 Blockers  antihistamines o Examples: chlorpheniramine, fexofenadine (Allegra), loratadine (Claritin), cetirizine, diphenhydramine (Benadryl) • Antihistamine Properties o Antihistaminic o Anticholingeric o Sedative • H2 blockers or H2 antagonists o Used to reduce gastric acid in peptic ulcer disease (PUD) o Examples: cimetidine, ranitidine, famotidine, nizatidine Antihistamines: Mechanism of Action • Block action of histamine at H1 receptor sites • Compete with histamine for binding at unoccupied receptors • Cannot push histamine off the receptor if already bound • The binding of H1 blockers to the histamine receptors prevents the adverse consequences of histamine stimulation o Vasodilation o Increased gastrointestinal (GI) and respiratory secretions o Increased capillary permeability • More effective in preventing the actions of histamine rather than reversing them • Should be given early in treatment, before all the histamine binds to the receptors Histamine vs. Antihistamine Effects • Cardiovascular (small blood vessels) o Histamine effects  Dilation and increased permeability (allowing substances to leak into tissues) o Antihistamine effects  Reduce dilation of blood vessels  Reduce increased permeability of blood vessels • Smooth muscle (on exocrine glands) o Histamine effects  Stimulate salivary, gastric, lacrimal, and bronchial secretions o Antihistamine effects  Reduce salivary, gastric, lacrimal, and bronchial secretions • Immune system (release of substances commonly associated with allergic reactions) o Histamine effects  Mast cells release histamine and other substances, resulting in allergic reactions o Antihistamine effects  Binds to histamine receptors, thus preventing histamine from causing a response Antihistamines: Other Effects • Skin o Reduce capillary permeability, wheal-and-flare formation, itching • Anticholinergic o Drying effect that reduces nasal, salivary, and lacrimal gland secretions (runny nose, tearing, and itching eyes) • Sedative o Some antihistamines cause drowsiness Antihistamines: Clinical Indications • Management of: o Nasal allergies o Seasonal or perennial allergic rhinitis (hay fever) o Allergic reactions o Motion sickness o Parkinson’s disease o Sleep disorders • Also used to relieve symptoms associated with the common cold o Sneezing, runny nose o Palliative treatment, not curative Antihistamines: Contraindications • Known drug allergy • Narrow-angle glaucoma • Cardiac disease, hypertension (HTN) • Kidney disease • Bronchial asthma, chronic obstructive pulmonary disease (COPD) • Peptic ulcer disease (PUD) • Seizure disorders • Benign prostatic hyperplasia (BPH) • Pregnancy Antihistamines: Adverse Effects • Anticholinergic (drying) effects, most common o Dry mouth o Difficulty urinating o Constipation o Changes in vision • Drowsiness o Mild drowsiness to deep sleep Antihistamines: Two Types • Traditional o Brompheniramine, chlorpheniramine, dimenhydrinate, meclizine, and promethazine • Nonsedating o Loratadine, cetirizine, and fexofenadine Nonsedating: Peripherally Acting Antihistamines • Developed to eliminate unwanted adverse effects, mainly sedation • Work peripherally to block the actions of histamine  fewer CNS adverse effects • Longer duration of action (increases compliance) Traditional Antihistamines • Older • Work both peripherally and centrally • Have anticholinergic effects, making them more effective than nonsedating drugs in some cases Antihistamines: Nursing Management • Assess for allergic reactions that required treatment, including drug allergies • Instruct patients o Report excessive sedation, confusion, or hypotension o Avoid driving or operating heavy machinery, consuming alcohol or other CNS depressants o Not to take these medications with other prescribed or over-the-counter medications without checking with prescriber • Best tolerated when taken with meals  reduces GI upset • If dry mouth occurs, teach patient to perform frequent mouth care, chew gum, or suck on hard candy (preferably sugarless) to ease discomfort • Monitor for intended therapeutic effects Nasal Congestion • Excessive nasal secretions • Inflamed and swollen nasal mucosa • Primary causes o Allergies o Upper respiratory infections (URIs; common cold) Decongestants: Types • Three main types are used o Adrenergics  Largest group  Sympathomimetics o Anticholinergics  Less commonly used  Parasympatholytics o Corticosteroids  Topical, intranasal steroids Oral Decongestants • Prolonged decongestant effects, but delayed onset • Effect less potent than topical • No rebound congestion • Exclusively adrenergics • Example: pseudoephedrine Topical Nasal Decongestants • Topical adrenergics o Prompt onset o Potent o Sustained use over several days causes rebound congestion, making the condition worse • Examples o Adrenergics: ephedrine, oxymetazoline, and tetrahydrozoline o Others: phenylephrine Inhaled Intranasal Steroids and Anticholinergic Drugs • Not associated with rebound congestion • Often used prophylactically to prevent nasal congestion in patients with chronic upper respiratory tract symptoms • Examples o Intranasal steroids: beclomethasone dipropionate, budesonide, flunisolide, fluticasone, triamcinolone, ciclesonide o Intranasal anticholinergic: ipratropium Nasal Decongestants: Mechanism of Action • Site of action: blood vessels surrounding nasal sinuses • Adrenergics o Constrict small blood vessels that supply upper respiratory tract structures o As a result these tissues shrink  nasal secretions in the swollen mucous membranes are better able to drain • Nasal steroids o Anti-inflammatory effect o Work to turn off the immune system cells involved in the inflammatory response o Decreased inflammation results in decreased congestion o Shrink engorged nasal mucous membranes o Relieve nasal stuffiness Nasal Decongestants: Clinical Indications • Relief of nasal congestion associated with o Acute or chronic rhinitis o Common cold o Sinusitis o Hay fever o Other allergies o Used to reduce swelling of the nasal/pharyngeal membranes before surgery or diagnostic procedures Nasal Decongestants: Contraindications • Drug allergy • Narrow-angle glaucoma • Uncontrolled cardiovascular disease, HTN • Diabetes and hyperthyroidism • History of cerebrovascular accident (CVA) or transient ischemic attacks (TIAs) • Long-standing asthma • BPH Nasal Decongestants: Adverse Effects • Adrenergics o Nervousness o Irritation o Insomnia o Palpitations o Tremors • Steroids o Local mucosal dryness and irritation • Systemic sympathomimetic drugs and sympathomimetic nasal decongestants are likely to cause drug toxicity when given together. Nasal Decongestants: Interactions • Systemic sympathomimetic drugs and sympathomimetic nasal congestant are likely to cause drug toxicity when given together • Monoamine oxidase inhibitors and sympathomimetic nasal decongestants raise blood pressure. • Methyldopa • Urinary acidifiers and alkalinizers Nasal Decongestants: Nursing Management • Assess for drug allergies • Decongestants  hypertension, palpitations, CNS stimulation o Avoid in patients with these conditions • Patients on medication therapy for hypertension should check with their HCP before taking OTC decongestants • Avoid caffeine and caffeine-containing products • Report a fever, cough, symptoms lasting longer than a week • Monitor for intended therapeutic effects Cough Physiology • Respiratory secretions and foreign objects are naturally removed by the cough reflex o Induces coughing and expectoration o Initiated by irritation of sensory receptors in the respiratory tract o Two basic types of cough  Productive: congested; removes excessive secretions  Nonproductive: dry cough • Coughing is mostly beneficial, but can be harmful in certain situations Antitussives • Drugs used to stop or reduce coughing • Opioid and non-opioid • Used only for nonproductive coughs! • May be used in cases where coughing is harmful Antitussives: Mechanism of Action • Opioids o Suppress the cough reflex by direct action on the cough center in the medulla o Analgesia, drying effect on the mucosa of the respiratory tract, increased viscosity of respiratory secretions, reduction of runny nose and postnasal drip o Examples:  codeine  hydrocodone • Nonopioids o Suppress the cough reflex by numbing the stretch receptors in the respiratory tract  preventing the cough reflex from being stimulated o No analgesic properties  no CNS depression o Examples:  benzonatate (Tessalon pearls)  dextromethorphan (Rubitussin DM or DXM) Antitussives: Indications and Contraindications • Indications o Used to stop the cough reflex when the cough is nonproductive harmful • Contraindications o Drug allergy o Opioid dependency o Respiratory depression Antitussives: Adverse Effects • benzonatate (Tessalon p) o Dizziness, headache, sedation, nausea, and others • dextromethorphan (R DM) o Dizziness, drowsiness, nausea • Opioids (Codeine) o Sedation, nausea, vomiting, lightheadedness, constipation Antitussives: Nursing Management • Perform respiratory, cough assessment, & allergies • Instruct patients to avoid driving or operating heavy equipment because of possible sedation, drowsiness, or dizziness • Report the following: o Cough that lasts more than a week o A persistent headache o Fever o Rash • Patients taking chewable tablets or lozenges should not drink liquids for 30 to 35 minutes afterward • Monitor for intended therapeutic effects Expectorants • Drugs that aid in the expectoration (removal) of mucus • Reduce the viscosity of secretions: drink fluids! • Disintegrate and thin secretions o Example: guaifenesin (Mucinex) Expectorants: Mechanism of Action • Reflex stimulation o Drug causes irritation of the GI tract o Loosening and thinning of respiratory tract secretions occur in response to this irritation • Direct stimulation o The secretory glands are stimulated directly to increase their production of respiratory tract fluids • Result  thinner mucus that is easier to remove • Drug Effect: by loosening and thinning sputum and bronchial secretions  indirectly diminishes coughing Expectorants: Clinical Indications • Used for relief of productive coughs o Common colds o Bronchitis o Laryngitis o Pharyngitis o Coughs  chronic paranasal sinusitis o Pertussis o Influenza o Measles Expectorants: Nursing Management • Use cautiously in the older patients or those with asthma or respiratory insufficiency • Encourage fluid intake  loosen and liquefy secretions • Report: fever, cough, or other symptoms longer than a week • Monitor for intended therapeutic effects Supplements and Herbal Products • Vitamin C • Goldenseal • Echinacea o Herbal plant (daisy family ) o Reduces symptoms of the common cold and recovery time o Adverse effects  Dermatitis  GI disturbances  Dizziness  Headache Respiratory Drugs Lower Respiratory Tract Diseases: Asthma • Persistent and present (air flow obstruction) most of the time despite treatment • Recurrent and reversible shortness of breath • Occurs when the airways of the lungs become narrow as a result of: o Bronchospasms o Inflammation of the bronchial mucosa o Edema of the bronchial mucosa o Production of viscous mucus • Alveolar ducts/alveoli remain open, airflow to them is obstructed • Symptoms o Wheezing o Difficulty breathing • Four categories o Intrinsic: idiopathic o Extrinsic: allergen o Exercise induced o Drug induced: NSAIDs, beta blocker, sulfites, etc • Status asthmaticus** o Prolonged asthma attack that does not respond to typical drug therapy o May last several minutes to hours o Medical emergency**: open airway asap rocky, give a short acting inhaled beta 2 agonist Lower Respiratory Tract Diseases: Chronic Obstructive Pulmonary Disease (COPD) • Chronic bronchitis o Continuous inflammation and low-grade infection of the bronchi o Excessive secretion of mucus and certain pathologic changes in the bronchial structure o Often occurs as a result of prolonged exposure to bronchial irritants • Emphysema o Air spaces enlarge as a result of the destruction of alveolar walls o The surface area where gas exchange takes place is reduced o Effective respiration is impaired Bronchodilators • Relax the bronchial smooth muscle  dilation of the bronchi and bronchioles that are narrowed as a result of the disease process • Three classes o Beta-adrenergic agonists o Anticholinergics o Xanthine derivatives Beta-Adrenergic Agonists: Short and Long-Acting Examples • Short-acting beta agonist (SABA) inhalers (given in asthma attacks) o albuterol (Ventolin)* know o levalbuterol (Xopenex)* know o pirbuterol o terbutaline o metaproterenol (Alupent)* know • Long-acting beta agonist (LABA) inhalers (given in maintenance) o arformoterol (Brobana)* know o formoterol o salmeterol (severent)* know o indacterol o vilanterol in conjunction  fluticasone (Breo Ellipta)  umeclidinium (anticholinergic; Anoro Ellipta) Beta-Adrenergic Agonists • Used during acute phase of asthmatic attacks • Quickly reduce airway constriction and restore normal airflow • Three Types know these o Nonselective adrenergic agonists  Stimulate alpha, beta1 (cardiac), and beta2 (respiratory) receptors  Example: epinephrine o Nonselective beta-adrenergics  Stimulate both beta1 and beta2 receptors  Example: metaproterenol o Selective beta2 drugs  Stimulate only beta2 receptors  Example: albuterol Beta-Adrenergic Agonists: Mechanism of Action • Activation of beta2 receptors activates cyclic adenosine monophosphate (cAMP)  relaxes smooth muscle in the airway  bronchial dilation and increased airflow Beta-Adrenergic Agonists • Indications o Relief of bronchospasm related to asthma, bronchitis, and other pulmonary diseases o Used in treatment and prevention of acute attacks o Used in hypotension and shock • Contraindications o Known drug allergy o Uncontrolled HTN* o Cardiac dysrhythmias* o High risk of stroke  Related to vasoconstrictive drug action** • Adverse Effects o Alpha and beta (epinephrine)  Insomnia  Restlessness*  Anorexia  Vascular headache  Hyperglycemia  Tremor  Cardiac stimulation o Beta1 and beta2 (metaproterenol)  Cardiac stimulation  Tremor*  Anginal pain  Vascular headache  Hypotension o Beta2 (albuterol)  Hypotension or HTN  Vascular headache  Tremor Beta-Adrenergic Agonists: Interactions • Diminished bronchodilation when nonselective beta blockers are used with the beta agonist bronchodilators • Monoamine oxidase inhibitors (enhance HTN crisis) • Sympathomimetics • Monitor patients with diabetes; an increase in blood glucose levels can occur. Beta-Adrenergic Agonists • Albuterol o Short-acting beta2-specific bronchodilating beta agonist o Most used drug in this class o Must not be used too frequently** o Oral and inhalational use o Including metered-dose inhalers (MDIs)** • Salmeterol o Long-acting beta2 agonist bronchodilator o Never to be used for acute treatment o Used for the maintenance treatment of asthma and COPD and in conjunction with an inhaled corticosteroid o Should never be given more than twice daily nor should the maximum daily dose (one puff twice daily) be exceeded Beta-Adrenergic Agonists: Nursing Implications • Albuterol, if used too frequently, loses its beta2-specific actions at larger doses  stimulates beta1 receptors  causing nausea, increased anxiety, palpitations, tremors, and increased heart rate • Ensure that patients take medications exactly as prescribed, with no omissions or double doses • Inform patients to report insomnia, jitteriness, restlessness, palpitations, chest pain, or any change in symptoms Anticholinergics • Used to prevent bronchoconstriction/bronchospasm associated with COPD • NOT used for acute exacerbations! • Examples o Ipratropium (Atrovent)**similar to atropine o Tiotropium (Spiriva)** o Aclidinium (Tudorza) Anticholinergics: Mechanism of Action • Acetylcholine (ACh) causes bronchial constriction and narrowing of the airways  anticholinergics bind to the ACh receptors  prevents ACh from binding  airways dilate preventing bronchoconstriction • Indirectly cause airway relaxation and dilation • Help reduce secretions in COPD patients • Used to prevent bronchospasm associated with COPD not for acute symptoms Anticholinergics: Adverse Effects • Dry mouth or throat • Nasal congestion • Heart palpitations • Gastrointestinal (GI) distress • Headache • Coughing • Anxiety Anticholinergics: Ipratropium • Oldest and most commonly used anticholinergic bronchodilator • Available both as a liquid aerosol for inhalation and as a multidose inhaler • Usually dosed twice daily • Others: o tiotropium (Spiriva) o aclidinium (Tudorza) o umeclidinium Xanthine Derivatives • Plant alkaloids o Caffeine, theobromine, and theophylline o Only theophylline is used as a bronchodilator  Used in COPD patients as a last resource • Synthetic xanthines o Aminophylline (it has to change to thophyline before it affects body) and dypilline Xanthine Derivatives: Mechanism of Action • Increase levels of energy-producing cAMP  inhibiting phosphodiesterase (PDE), the enzyme that breaks down cAMP  increased cAMP intracellular levels causes: smooth muscle relaxation, bronchodilation, and increased airflow • Drug Effects: Cause bronchodilation by relaxing smooth muscle in the airways  relief of bronchospasm and greater airflow into and out of the lungs o CNS stimulation: into the medullary respiratory center o CV stimulation  positive inotropic effect, positive chronotropic effect  increased cardiac output and blood flow to the kidneys (diuretic effect) Xanthine Derivatives: Indications • Dilation of airways in asthmas, chronic bronchitis, and emphysema • Mild to moderate cases of acute asthma • NOT for management of acute asthma attack • Adjunct drug in the management of COPD • Not used as frequently because of potential for drug interactions and variables related to drug levels in the blood Xanthine Derivatives: Adverse Effects • Nausea, vomiting, anorexia • Gastroesophageal reflux during sleep • Sinus tachycardia, extrasystole, palpitations, ventricular dysrhythmias ** • Transient increased urination * • Hyperglycemia Xanthine Derivatives • Caffeine o Used without prescription as a CNS stimulant or analeptic to promote alertness (for long-duration driving or studying) o Cardiac stimulant in infants with bradycardia * o Enhancement of respiratory drive in infants • Theophylline o Most used xanthine derivative o Oral, rectal, injectable (as aminophylline), and topical dosage forms o Aminophylline: intravenous (IV) treatment of patients with status asthmaticus who have not responded to fast-acting beta agonists (epinephrine) ** o Therapeutic range for theophylline blood level is 10 to 20 mcg/mL (most clinicians now advise levels between 5 and 15 mcg/mL) Xanthine Derivatives: Nursing Implications • Contraindications: history of PUD or GI disorders** • Cautious use: cardiac disease • Timed-release preparations should not be crushed or chewed  causes gastric irritation • Report to prescriber: o Nausea o Vomiting o Restlessness o Insomnia o Irritability o Tremors Xanthine Derivatives: Nursing Implications • Be aware of drug interactions with cimetidine, oral contraceptives, allopurinol, certain antibiotics, influenza vaccine- can increase Xanthine levels (decrease dose) • Cigarette smoking, Rifampin & St Johns wart enhances xanthine metabolism which decrease theopilline levels (increase dose) • Interacting foods include charcoal-broiled, high-protein, and low-carbohydrate foods o May reduce serum levels of xanthines through various metabolic mechanisms Nonbronchodilating Respiratory Drugs • Leukotriene Receptor Antagonists (LTRAs): (monteluksat, zafirkulast and zileuton) • Corticosteroids: (beclomethasone, budesonide,… • Mast Cell stabilizers: rarely used cromolyn and nedocromil, which are sometimes used for exercise-induced asthma Leukotrienes & LTRAs • Leukotrienes are substances released when a trigger, such as cat hair or dust, starts a series of chemical reactions in the body o Leukotrienes  inflammation, bronchoconstriction, and mucus production  coughing, wheezing, shortness of breath • LTRAs mechanism of action  prevent leukotrienes from attaching to receptors on cells in the lungs and circulation  inflammation in lungs is blocked  relieving asthma symptoms • Nonbronchodilating • Newer class of asthma medications • Currently available drugs o montelukast ** o zafirlukast o zileuton LRTAs: Drug Effects • By blocking leukotrienes: o Prevent smooth muscle contraction of the bronchial airways o Decrease mucus secretion o Prevent vascular permeability o Decrease neutrophil and leukocyte infiltration to the lungs  preventing inflammation LRTAs: Indications & Contraindications • Indications o Prophylaxis and long-term treatment and prevention of asthma in adults and children 12 years and older o NOT meant for management of acute asthmatic attacks o Montelukast is approved for treatment of allergic rhinitis o Improvement with use is typically seen in 1 week * • Contraindications o Known drug allergy o Previous adverse drug reaction o Allergy to povidone, lactose, titanium dioxide, or cellulose derivatives  These are inactive ingredients in these drugs LRTAs: Adverse Effects • zileuton o Headache, nausea, dizziness, insomnia • zafirlukast and montelukast o Headache, nausea, diarrhea • Montelukast (PO) has fewer interactions o Phenobarbital and rifampin decrease the concentration of this LRTAs: Nursing Implications • Ensure that the drug is being used for chronic management of asthma, not acute asthma • Teach the patient the purpose of the therapy • Improvement should be seen in about 1 week • Advise patients to check with prescriber before taking over-the-counter (OTC) or prescribed medications to determine drug interactions • Assess liver function before beginning therapy and throughout • Teach patient to take medications every night on a continuous schedule, even if symptoms improve*** Corticosteroids (Glucocorticoids) • Antiinflammatory properties • Used for chronic asthma • Do not relieve symptoms of acute asthmatic attacks • Oral or inhaled forms o Inhaled forms reduce systemic effects • May take several weeks before full effects are seen Corticosteroids: Mechanism of Action • Stabilize membranes of cells that release harmful bronchoconstricting substances (leukocytes or white blood cells) • Increase responsiveness of bronchial smooth muscle to beta-adrenergic stimulation • Dual effect of both reducing inflammation and enhancing the activity of beta agonists • Shown to restore in increase the responsiveness of bronchial smooth muscle to beta-adrenergic receptor stimulation  more pronounced stimulation of beta2 receptors by beta agonist drugs (albuterol) Inhaled Corticosteroids • beclomethasone dipropionate (Beclovent)* • budesonide (Pulmicort Turbuhaler)* • ciclesonide • flunisolide • fluticasone (Flovent- oral inhaler, Flonase- nose inhaler) • mometasone • triamcinolone acetonide (Azmacort)** Corticosteroids: Indications • Treatment of bronchospastic disorders to control the inflammatory response that cause these disorders • Used for persistent asthma • Often used concurrently with beta-adrenergic agonists • Systemic corticosteroids are used only to treat acute exacerbations or severe asthma • IV corticosteroids: acute exacerbation of asthma or COPD Corticosteroids: Contraindications • Drug allergy • Not intended as sole therapy for acute asthma attacks • Hypersensitivity to glucocorticoids • Patients whose sputum tests positive for Candida organisms • Patients with systemic fungal infection • Causes immune suppressions Inhaled Corticosteroids: Adverse Effects • Pharyngeal irritation • Coughing • Dry mouth • Oral fungal infections • Systemic effects are rare because low doses are used for inhalation therapy Inhaled Corticosteroids: Drug Interactions • Drug interactions are more likely to occur with systemic (versus inhaled) corticosteroids • May increase serum glucose levels, possibly requiring adjustments in dosages of antidiabetic drugs • Cyclosporine and tacrolimus • Itraconazole • Phenytoin, phenobarbital, and rifampin Inhaled Corticosteroids: Nursing Implications • Teach patients to gargle and rinse the mouth with lukewarm water afterward to prevent the development of oral fungal infections • Teach patients to monitor disease with a peak flow meter • Encourage use of a spacer device to ensure successful inhalations • Teach patient how to keep inhalers and nebulizer equipment clean after uses • If a beta agonist bronchodilator and corticosteroid inhaler are both ordered, the bronchodilator should be used several minutes before the corticosteroid to provide bronchodilation before administration of the corticosteroid Phosphodiesterase-4 Inhibitor • roflumilast (Daliresp) o Indicated to prevent coughing and excess mucus from worsening and to decrease the frequency of life-threatening COPD exacerbations** o Adverse effects include nausea, diarrhea, headache, insomnia, dizziness, weight loss, and psychiatric symptoms Monoclonial Antibody Antiasthmatic • omalizumab, mepolizumab, reslizumab o Add-on therapy for treatment of asthma o Selectively binds to the immunoglobulin IgE, which in turn limits the release of mediators of the allergic response o Given by injection** o Potential for producing anaphylaxis o Monitor closely for hypersensitivity reactions Nursing Implications: All Respiratory Drugs • Encourage patients to take measures that promote a generally good state of health to prevent, relieve, or decrease symptoms of COPD o Avoid exposure to conditions that precipitate bronchospasm (allergens, smoking, stress, air pollutants) o Adequate fluid intake o Compliance with medical treatment o Avoid excessive fatigue, heat, extremes in temperature, caffeine • Encourage patients to get prompt treatment for flu or other illnesses, and to get vaccinated against pneumonia or flu • Encourage patients to always check with their physician before taking any other medication, including OTC medications • Perform a thorough assessment before beginning therapy, including: o Skin color o Baseline vital signs o Respirations (should be between 12 and 24 breaths/min) o Respiratory assessment, including pulse oximetry o Sputum production o Allergies o History of respiratory problems o Other medications o Smoking history • Teach patients to take bronchodilators exactly as prescribed • Ensure that patients know how to use inhalers and MDIs, and have patients demonstrate use of the devices • Monitor for adverse effects • Monitor for therapeutic effects • Decreased dyspnea • Decreased wheezing, restlessness, and anxiety • Improved respiratory patterns with return to normal rate and quality • Improved activity tolerance • Decreased symptoms and increased ease of breathing Inhalers: Patient Education • Ensure that the patient can self-administer the medication • Provide demonstration and return demonstration • Ensure that the patient knows the correct time intervals for inhalers • Provide a spacer if the patient has difficulty coordinating breathing with inhaler activation • Ensure that the patient knows how to keep track of the number of doses in the inhaler device Antitubercular Drugs- Chapter 41 Antitubercular Drugs • Tuberculosis (TB) o Caused by Mycobacterium tuberculosis (MTB) • Antitubercular drugs treat all forms of Mycobacterium • TB is most characterized by granulomas in the lungs • Common infection sites o Lung (primary site) o Brain (cerebral cortex) o Bone (growing end) o Liver o Kidney Mycobacterium Infections • Aerobic bacillus** • Passed from infected: o Humans o Cows (bovine) o Birds (avian)  Much less common • Tubercle bacilli (MTB) o Droplet transmission  enter body by inhalation  spread to other organs via blood & lymphatic systems o May become dormant or walled off by calcified or fibrous tissue • Very slow-growing organism** • More difficult to treat than most other bacterial infections • First infectious episode: primary TB infection • Reinfection: chronic form of the disease • Dormancy: may test positive for exposure but are not necessarily infectious because of this dormancy process Incidence/Timeline • 1950s TB in the United States • TB incidence decreased in most years until about 1985 • 1985: TB incidence began to rise for the first time in 20 years because of the development of TB in patients coinfected with HIV • 1992: There was a resurgence peak in the United States, but it has decreased since that time o Decline is attributed to intensified public health efforts aimed at preventing, diagnosing, and treating TB as well as HIV infection • Concern now: increasing number of multidrug-resistant tuberculosis (MDR-TB) cases Multidrug-Resistant Tuberculosis (MDR-TB) • TB infects one third of the world’s population. • MDR-TB that is resistant to both isoniazid (INH) and rifampin • Extensively drug-resistant tuberculosis (XDR-TB): relatively rare type of MDR-TB, resistant to almost all drugs used to treat TB, including the two best first-line drugs, INH and rifampin, as well as to the best second-line medications • XDR-TB is of special concern for patients who have AIDS or are otherwise immunocompromised. • Use of multiple medications to treat TB due to increasing presence of resistance TB Diagnosis Antitubercular Drugs • First-line drugs o isoniazid (INH)* o rifapentine o ethambutol o rifabutin o pyrazinamide (PZA) o rifampin o streptomycin o *Primary drug used • Second-line drugs o capreomycin o cycloserine o levofloxacin o ethionamide o ofloxacin o kanamycin o para-aminosalicyclic acid (PAS) Tuberculosis-Related Injections • Purified protein derivative (PPD) • A diagnostic injection given intradermally in doses of 5 tuberculin units (0.1 mL) to detect exposure to the tuberculosis (TB) organism • Positive result is indicated by induration (not erythema) at the site of injection • Bacille Calmette-Guérin (BCG) o A vaccine injection derived from an inactivated strain of Mycobacterium bovis o Used in much of the world to vaccinate young children against TB o Does not prevent infection o Reduces active TB by 60% to 80% o Effective at preventing more severe cases involving dissemination of infection throughout the body o Can cause false-positive results on the tuberculin skin test o Not done in the us o Will give a false positive test if test given after this injection Antitubercular Therapy Considerations • Major effects: reduction of cough and reduction of infectiousness o Normally occurs within 2 weeks of initiation of drug therapy if TB strain is drug sensitive** • Most cases of TB can be cured • Successful treatment: several antibiotic drugs for at least 6 months and sometimes for as long as 12 months • Perform drug-susceptibility testing on the first Mycobacterium spp. that is isolated from a patient specimen to prevent the development of multidrug-resistant TB (MDR-TB) • Even before the results of susceptibility tests are known, begin a regime with multiple antitubercular drugs  to reduce the chances of resistance • Adjust drug regimen after the results of susceptibility testing are known • Monitor patient compliance closely during therapy • Problems with successful therapy occur because of patient nonadherence to drug therapy and the increased incidence of drug-resistant organisms Mechanism of Action • Three groups o Protein wall synthesis inhibitors: streptomycin, kanamycin, capreomycin, rifampin, rifabutin, others o Cell wall synthesis inhibitors: cycloserine, ethionamide, INH o Other mechanisms of action: ethambutol, INH, PAS Antitubercular Therapy • Effectiveness depends on: o Type of infection o Adequate dosing o Sufficient duration of treatment o Adherence to drug regimen o Selection of an effective drug combination • Problems: o Drug-resistant organisms o Drug toxicity o Patient nonadherence • MDR-TB Bedaquiline (Sirturo) • First drug approved in over 40 years • Treatment of multidrug-resistant TB • Inhibits mycobacterial ATP synthase • Adverse effects: headache, chest pain, nausea, and QT prolongation** • Interactions: alcohol, mifepristone, other drugs with high risk for causing QT prolongation • Administer with food** Ethambutol (Myambutol) • First bacteriostatic drug used in treatment of TB • Diffuses into the mycobacteria and suppresses RNA synthesis, inhibiting protein synthesis • Used in combination with other actions • Contraindications: optic neuritis, pediatric patients (younger than 13) • Adverse effects: retrobulbar neuritis, blindness Isoniazid (INH) • Drug of choice for TB • Resistant strains of Mycobacterium emerging • Metabolized in the liver through acetylation—watch for “slow acetylators” (adjust dose downwards) • Used alone or in combination with other drugs • Contraindicated with liver disease • Black-box warning regarding possible hepatitis • Adverse effects: peripheral neuropathy, hepatotoxicity • Pyridoxine (Vitamin B6) may be used to combat neuropathy adverse effects * Pyrazinamide (PZA) • Bacteriostatic or bactericidal • Used in combination with other agents • Inhibits lipid and nucleic acid synthesis in mycobacteria • Contraindications: • Severe hepatic disease • Acute gout Rifabutin , Rifampin, and Rifapentine • Rifamycin antibiotic • Also used to treat infections caused by non-TB mycobacterial species • Adverse effects o Turns urine, feces, saliva, skin, sputum, sweat, and tears a red-orange-brown color (know! It is specific for these three meds) o Tell patient that they can keep taking pills but to use other forms of brith control as they are more likely to get pregnent o Hepatitis*** • Causes oral contraceptive to become ineffective  another form of birth control needed Streptomycin • Aminoglycoside antibiotic • Used in combination with other agents • Injectable form only Nursing Management • Obtain a thorough medical history and assessment • Perform liver function studies in patients who are to receive INH or rifampin (especially in elderly patients or those who use alcohol daily) • Assess for contraindications to the various drugs, conditions for cautious use, and potential drug interactions • Patient education is critical • Therapy may last for up to 24 months • Take medications exactly as ordered, at the same time, every day • Emphasize the importance of strict adherence to regimen for improvement of condition or cure • Remind patients that they are contagious during the initial period of their illness—instruct in proper hygiene and prevention of the spread of infected droplets • Teach patients to take care of themselves, including adequate nutrition and rest • Patients should not consume alcohol while on these medications or take other medications, including over-the-counter (OTC) medications, unless they check with their prescriber • Oral preparations may be given with meals to reduce gastrointestinal upset, even though recommendations are to take them 1 hour before or 2 hours after meals • Monitor for adverse effects: o Instruct patients on the adverse effects that should be reported to the prescriber immediately: fatigue, nausea, vomiting, numbness and tingling of the extremities, fever, loss of appetite, depression, jaundice • Monitor for therapeutic effects: o Decrease in symptoms of TB, such as cough and fever (and weight gain) o Lab studies (culture and sensitivity tests) and chest x-ray should confirm clinical findings o Watch for lack of clinical response to therapy, indicating possible drug resistance Anti-inflammatory and Antigout Drugs Nonsteroidal Anti-inflammatory Drugs (NSAIDs) • Large and chemically diverse group of drugs with the following properties: o Analgesic o Anti-inflammatory o Antipyretic o Aspirin-platelet inhibition • Properties all NSAIDs share: o Antipyretic o Analgesic o Anti-inflammatory NSAIDs • NSAIDs are also used for the relief of: o Mild to moderate headaches o Myalgia o Neuralgia o Arthralgia o Alleviation of postoperative pain o Relief of the pain in arthritic disorders  Rheumatoid arthritis, juvenile arthritis, ankylosing spondylitis, and osteoarthritis o Treatment of gout and hyperuricemia** NSAIDs: Mechanism of Action • Inhibition of the leukotriene pathway, the prostaglandin pathway, or both  blocking the chemical activity of cyclooxygenase (COX) o Cyclooxygenase-1 (COX-1)  Maintains normal lining of the stomach (GI mucosa)  Involved in kidney and platelet function o Cyclooxygenase-2 (COX-2)  Present primarily at sites of inflammation • Aspirin o Irreversible inhibitor of COX-1 receptors within the platelets  reduces formation of thromboxane A2 (promotes platelet aggregation) o Other NSAIDs lack these antiplatelet effects NSAIDs: Contraindications and Interactions • Contraindications o Known drug allergy o Patients with documented aspirin allergy must not receive NSAIDs o Conditions that place the patient at risk for bleeding:  Vitamin K deficiency  Peptic ulcer disease (PUD) o Risk for maternal bleeding and neonatal toxicity o Watch for syncope!! • Interactions o Serious interactions can occur when given with: o Anticoagulants and aspirin: increased risk of bleeding o Corticosteroids and other ulcerogenic drugs: increased risk of GI ulceration o Protein bound drugs such as warfarin, sulfonylureas, methotrexate o Diuretics o ACE inhibitors: NSAIDs block production of vasodilator/natriuretic prostaglandins; hyperkalemia, bradycardia  syncope NSAIDs: Adverse Effects • Misoprostol o Many of the adverse effects of NSAIDs are secondary to their inactivation of protective prostaglandins that help maintain the normal integrity of the stomach lining. o Prevents GI bleeding** o Synthetic prostaglandin E1 analogue inhibits gastric acid secretion  cytoprotective component o Mechanism of action: unclear • Gastrointestinal o Dyspepsia, heartburn, epigastric distress, nausea o GI bleeding*  misoprostol can be used to reduce these dangerous effects o Mucosal lesions* (erosions or ulcerations) • Acute renal failure (if dehydration exists) • Noncardiogenic pulmonary edema • Increased risk of myocardial infarction (MI) and stroke (Black-box warning) except aspirin*** o NSAIDs may counteract cardioprotective effects of aspirin • Altered hemostasis • Hepatotoxicity (acute reversible) • Skin eruption, sensitivity reaction • Tinnitus, hearing loss NSAIDs and Renal Function • Renal function depends partly on prostaglandins • Disruption of prostaglandin function by NSAIDs is sometimes strong enough to precipitate acute or chronic renal failure • Use of NSAIDs can compromise existing renal function • Renal toxicity can occur in patients with dehydration, heart failure, liver dysfunction, or use of diuretics or ACE inhibitors NSAIDs: Chemical Categories • Salicylates • Acetic acid derivatives • Cyclooxygenase-2 (COX-2) inhibitors • Enolic acid derivatives • Propionic acid derivatives Salicylates • Salicylic acid (Aspirin)- 81-325mg prophylactic o Inhibits platelet aggregation o Antithrombotic effect: used in the treatment of MI and other thromboembolic disorders o Patients with the lower dose usually is given because they are taking other blood thinners • Examples: aspirin, diflunisal, choline magnesium trisalicylate, and salsalate • Indications o Headache (HA), neuralgia, myalgia, arthralgia o Pain syndromes as a result of inflammation: arthritis, pleurisy, pericarditis o Systemic lupus erythematosus (SLE) o Antipyretic action Aspirin: Reye’s Syndrome • Acute and potentially life-threatening condition involving progressive neurologic deficits that can lead to coma and may also involve liver damage • Triggered by viral illnesses such as influenza as well as by salicylate therapy itself in the presence of a viral illness • Survivors of this condition may or may not have permanent neurologic damage • Do not give to children and teenagers Salicylate Toxicity • Cardiovascular (CV): increased heart rate • Central nervous system (CNS): tinnitus, hearing loss, dimness of vision, HA, dizziness, mental confusion, lassitude, drowsiness • Gastrointestinal (GI): nausea, vomiting, diarrhea • Metabolic: sweating, thirst, hyperventilation, hypo- or hyperglycemia Acetic Acid Derivatives (analgesic, anti-inflammatory, antirheumatic and antipyretic) • diclofenac sodium • indomethacin (Indocin)** • sulindac • etodolac • ketorolac (Toradol)** o patient comes in after surgery is given morphine max limit for pain. And the pain is not being relieved. You should give this med for anti-inflammatory purpose. • meclofenamate • mefenamic acid • Indomethacin o Uses: rheumatoid arthritis, osteoarthritis, acute bursitis or tendonitis, ankylosing spondylitis, acute gouty arthritis, and treatment of preterm labor o Promote closure of patent ductus arteriosus (PDA), a heart defect that sometimes occurs in premature infants o Oral, rectal, intravenous (IV) use • Ketorolac o Some antiinflammatory activity o Used primarily for its powerful analgesic effects (comparable to narcotic drugs) o Indication: short-term use (up to 5 days) to manage moderate to severe acute pain o Adverse effects: renal impairment, edema, GI pain, dyspepsia, and nausea COX-2 Inhibitors • celecoxib o First and only remaining COX-2 inhibitor o Indicated: osteoarthritis, rheumatoid arthritis, acute pain symptoms, ankylosing spondylitis, and primary dysmenorrhea o Adverse effects: headache, sinus irritation, diarrhea, fatigue, dizziness, lower extremity edema, and hypertension o Little effect on platelet function o Celecoxib is not to be used in clients with known sulfa allergy*** Enolic Acid Derivatives • piroxicam (Feldene)** o used to treat RA, gouty arthritis and osteoarthritis o assess GI system before you give it • meloxicam (Mobic) o used to treat RA, gouty arthritis and osteoarthritis • nabumetone (Relafen) o better tolerated by GI system than other NSAIDs o used for OA and RA Propionic Acid Derivatives o fenoprofen o flurbiprofen o Ibuprofen (Motrin, Advil)  Most commonly used o ketoprofen o Naproxen  Second most commonly used o oxaprozin • Uses: analgesic effects in the management of RA, OA, primary dysmenorrhea, gout, dental pain, musculoskeletal disorders, antipyretic actions Gout • Gout: condition that results from inappropriate uric acid metabolism o Underexcretion of uric acid o Overproduction of uric acid • Uric acid crystals are deposited in tissues and joints, resulting in pain • Hyperuricemia Antigout Drug Examples • allopurinol (Zyloprim) • febuxostat (Uloric) • colchicine* • probenecid • lesinurad • sulfinpyrazone Antigout Drugs: Indications • allopurinol (Zyloprim) 200-600 mg/day (800mg) o Prevents uric acid production** o Prevents acute tumor lysis syndrome • Probenecid (250 to 500 mg PO BID) o Inhibits the reabsorption of uric acid in the kidneys  increases the excretion of uric acid  Must have good renal function** • Febuxostat (Uloric) (40-80/day max 120 mg) o Nonpurine selective inhibitor of xanthine oxidase o More selective for xanthine oxidase than allopurinol o May pose a greater risk of CV events than allopurinol • colchicine o Reduces inflammatory response to the deposits of urate crystals in joint tissue o Used for short-term management or prevention of gout  For acute gout: • Initial dose of 0.6-1.2 mg, followed by 0.6 mg/hr until: • Pain is relieved • Severe nausea and diarrhea occur • Total of 6 mg has been administered o May cause short-term leukopenia and bleeding into the gastrointestinal or urinary tracts • Lesinurad (Zurampic) o Uric acid transporter inhibitors o Inhibits the transporter proteins involved in renal uric acid reabsorption resulting in lower serum uric acid levels and increase renal clearance of uric acid o Given in combination with xanthine oxidase inhibitor o Teaching: at least 2 liters of fluid a day to get rid of the uric acid o Dose: 200mg/day taking with food* Herbal Products: Glucosamine and Chondroitin • Used to treat the pain of osteoarthritis • Adverse effects o GI discomfort o Drowsiness, headache, skin reactions (glucosamine) • Drug interactions o Enhances effects of warfarin o May increase insulin resistance(glucosamine) NSAIDs & Antigout: Nursing Implications • Before beginning therapy, assess for conditions that may be contraindications to therapy, especially: o GI lesions or PUD o Bleeding disorders • Assess for conditions that require cautious use • Perform laboratory studies as indicate: o Cardiac, renal, and liver function studies o Complete blood count (CBC) o Platelet count • Perform a medication history to assess for potential drug interactions • Several serious drug interactions exist • Because these drugs generally cause GI distress, they are often better tolerated if taken with food, milk, or an antacid to avoid irritation • Explain to patients that therapeutic effects may not be seen for 3 to 4 weeks • Educate clients about the various adverse effects of NSAIDs, and inform them to notify their prescriber if these effects become severe or if bleeding or GI pain occurs • Inform clients to watch closely for the occurrence of any unusual bleeding • Advise patients that enteric-coated tablets should not be crushed or chewed • Monitor for therapeutic effects, which vary according to the condition being treated o Decrease in swelling, pain, stiffness, and tenderness of a joint or muscle area Musculoskeletal Agents: Antirheumatic & Osteoporosis Rheumatoid Arthritis vs. Osteoarthritis • Rheumatoid Arthritis o Autoimmune disorder causing inflammation and tissue damage in joints o Diagnosis primarily symptomatic o Treatment consists of nonsteroidal anti-inflammatory drugs (NSAIDs) and DMARDs  NSAIDs  DMARDs (Disease-Modifying Antirheumatic Arthritis Drugs) • Osteoarthritis o Another type of arthritis o Age-related degeneration of joint tissues o Pain and reduced function Disease-Modifying Antirheumatic Drugs (DMARDs) • Modify the disease of RA • Exhibit anti-inflammatory, antiarthritic, and immunomodulating effects • Inhibit the movement of various cells into an inflamed, damaged area, such as a joint • Slow onset of action of several weeks, versus minutes to hours for NSAIDs • Also referred to as slow-acting antirheumatic drugs (SAARDs) DMARDs • Traditional/Nonbiologic o Methotrexate ** o Leflunomide (Arava)* o sulfasalazine o hydroxychloroquine • Biologic Agents o adalimumab (Humira)** o anakinra o etanercept (Enbrel) o infliximab (Remicade) ** o adalimumab o Abatacept (Orencia) ** o rituximab o tocilizumab (Actemra) o tofacitinib (Xeljanz) **  newest med DMARDs • DMARDs provide anti-inflammatory and analgesic effects and can arrest or slow disease processes associated with RA • Current recommendation of first-line therapy in clients with RA** Methotrexate: Non-biologic DMARD • Used as baseline therapy in most RA clients • Long acting medication • Typical dose 7.5-25 mg orally or injection once per week (7.5-10mg) o Always ask when was the last time they took the medication. Specially if you are a nurse in the emergency room. • Labs: (done prior to starting and then every 2-3 months) o Hepatitis serologies o LFTs o CBC o Creatinine • Adverse effects: (bone marrow suppression*) o Nausea, diarrhea, fatigue, mouth ulcers, rash, alopecia, pneumonitis, sepsis, liver disease, Epstein-Barr virus-related lymphoma • Must be taken with folic acid supplements to counteract the bone marrow suppression • May take 3-6 weeks to see onset of antirheumatic action Leflunomide: Non-biologic DMARD • Treatment of active RA (oral form) • Modulates or alters the responses of the immune system to RA • Antiproliferative, antiinflammatory, and immunosuppressive activity • Adverse effects: diarrhea, respiratory tract infection, alopecia, elevated liver enzymes, rash • Contraindicated in women who are or may become pregnant Biologic DMARDs: Can be administered in combination with methotrexate • Abatacept o Caution if the patient has a history of recurrent infections or chronic obstructive pulmonary disease o Patients must be up to date on immunizations before starting therapy. o May increase risk of infections associated with live vaccines o May decrease response to vaccines o IV- q 4 weeks, use filter • Etanercept o Erelzi is the approved biosimilar product for etanercept. o Patients must be screened for latex allergy (some dosage forms may contain latex). o Onset of action: 1 to 2 weeks o Contraindicated in presence of active infections  Reactivation of hepatitis and tuberculosis has been reported  SQ Nursing Implications • Assess for allergies, specifically allergies to egg proteins, IgG, or neomycin • Assess for conditions that may be contraindications • Assess baseline blood counts; perform cardiac, renal, and liver studies • Assess for presence of infection • Do not give medication to the pt if they are currently sick • Follow specific guidelines for preparation and administration of drugs • Monitor the client’s response during therapy • Teach clients to report signs of infection immediately o Sore throat o Vomiting/diarrhea o Fever over 100.5°F (38.1°C) or higher • Monitor for therapeutic responses o Decrease in growth of lesion or mass o Improved blood counts o Absence of infection, anemia, and hemorrhage • Monitor for adverse effects Osteoporosis • Age-related degeneration of joint tissues  pain and reduced function • Low bone mass  increased risk of fractures • Primarily affects women o 40% of women over 50 years will develop osteoporotic fracture • 20% with this condition are men Osteoporosis: Risk Factors • European/Asian descent • Slender body build • Early estrogen deficiency • Smoking • Alcohol consumption • Low-calcium diet • Sedentary lifestyle • Family history Drug Therapy for Osteoporosis • Calcium supplements and vitamin D may be recommended for women at high risk for osteoporosis • Current recommendations are that women, especially those older than age 60, consider taking calcium and vitamin D supplements for bone health • Bisphosphonates o Alendronate, ibandronate, risedronate, zoledronic acid • Selective estrogen receptor modifiers (SERMs) o Raloxifene, tamoxifen • Hormones o Calcitonin, teriparatide, denosumab Bisphosphonates • Work by inhibiting osteoclast-mediated bone resorption  indirectly enhances bone mineral density  preventing bone loss • Can reverse lost bone mass and reduce fracture risk • Prevention and treatment of osteoporosis and Paget’s Disease • Examples o alendronate (Fosamax)* o ibandronate (Boniva) o risedronate (Actonel) o zoledronic acid (Reclast) Bisphosphonates: Mechanism of Action • Highly selective inhibitor of bone resorption o Resorption occurs following activation of osteoclasts  to breakdown bone and releases from bone to the blood • Reduction in bone resorption  decreased serum calcium & phosphate concentrations • Increased bone mineral density to reverse progression of osteoporosis • Absorbed orally - decreased absorption by 40% if taken with food & beverages (other than plain water) • Stored in skeleton (not metabolized after absorption)  slow release  urinary excretion Bisphosphonates: Contraindications & Interactions • Drug hypersensitivity • Hypocalcemia • Esophageal dysfunction • Inability to sit or stand upright for at least 30 minutes after taking the medication • Known drug interactions o Ranitidine: doubles bioavailability of alendronate o Calcium supplements & antacids: separate doses by 2 hours o Aspirin: increased risk of GI effects • Advise client to wait at least 30 minutes after taking alendronate before taking any other drug Bisphosphonates: Adverse Effects • Headache, GI upset, joint pain • Risk of esophageal burns if medication lodges in esophagus before reaching the stomach o GI irritation more likely if client does not take with full glass of water • Risk of osteonecrosis of the jaw o Always tell the dentist you take bisphosphonates as they cannot perform dental procedures with this. Must run labs first. • Possible severe (incapacitating) bone, joint, or muscle pain Alendronate (Fosamax) • Oral bisphosphonate • First nonestrogen nonhormonal option for preventing bone loss • Inhibits or reverses osteoclast-mediated bone resorption • Indications: prevention and treatment of osteoporosis in men and in postmenopausal women as well as treatment of glucocorticoid-induced osteoporosis in men and for the treatment of Paget disease in women Bisphosphonates: Nursing Implications • Ensure that patients have no esophageal abnormalities and can remain upright or in a sitting position for 30 minutes after the dose • Instruct patients to take medication upon rising in the morning, with a full glass of water, and 30 minutes before eating. • Emphasize that patients should sit upright for at least 30 minutes after taking the medication Selective Estrogen Receptor Modifiers (SERMs) • Stimulate estrogen receptors on bone and increase bone density (protectors of the bones) • Drugs o raloxifene (Evista) o tamoxifen (Nolvadex) • Indications o Prevention of postmenopausal osteoporosis** • Stimulate estrogen receptors on bone and increase bone density SERMs: Contraindications • Women with known allergy • Women who may become pregnant** • Venous thromboembolic disorder or history o Deep vein thrombosis (DVT) o Pulmonary embolus (PE) o Retinal vein thrombosis SERMs: Adverse Effects • Hot flashes • Leg cramps • Increase risk of venous thromboembolism • Teratogenic • Leukopenia SERMs: Nursing Indications • Instruct clients that the medication will need to be discontinued 72 hours before and during any prolonged immobility (such as surgery or a long trip)** with doctor approval Hormones: Calcitonin • Indications: treatment of osteoporosis • Mechanism of actions: Directly inhibits osteoclastic bone resorption • Contraindications: drug allergy or salmon allergy • Adverse effects o Flushing of the face o Nausea/diarrhea o Reduced appetite • Nasal spray most used Hormones: teriparatide (Forteo) • Mechanism of action: Stimulates bone formation** • Contraindications: drug allergy • Adverse effects o Chest pain o Dizziness o Hypercalcemia o Nausea o arthralgia Hormones: denosumab (Prolia) • Mechanism of action o Blocks osteoclast activation  prevents bone resorption by blocking osteoclast activation • Given as a subcutaneous injection once every 6 months with daily calcium and vitamin D • Contraindications o Hypocalcemia o Renal impairment or failure o Infection • Adverse effects: infections Herbal Products: Soy • Relief of menopausal symptoms, osteoporosis prevention • Estrasorb, applied as a lotion • Adverse effects o Nausea o Diarrhea o Abdominal pain o Estrasorb remains on skin for 8 hours Nursing Implications • Assess baseline vital signs, weight, blood glucose levels, and renal and liver function study results. • Assess whether the patient smokes. • Assess history and medication history. • Assess contraindications, including potential pregnancy. • Monitor for therapeutic responses. • Monitor for adverse effects. Anti-parkinson Drugs Parkinson’s Disease (PD) • Chronic, progressive, degenerative disorder • Affects dopamine-producing neurons in the brain • Caused by an imbalance of two neurotransmitters o Dopamine: inhibits excitement o Acetylcholine (ACh): excites cells Neurotransmitter Abnormality in Parkinson’s Disease • Symptoms occur when about 80% of the dopamine stored in the substantia nigra of the basal ganglia is depleted • Symptoms can be partially controlled if there are functioning nerve terminals that can take up dopamine • Classic symptoms include: o Tremor o Rigidity o Akinesia o Postural instability o Staggering gait o Drooling • A progressive condition • Rapid swings in response to levodopa occur (“on-off phenomenon”) o PD worsens when too little dopamine is present o Dyskinesia occurs when too much dopamine is present • “Wearing-off phenomenon” • PD-associated dementia Dyskinesia • Difficulty in performing voluntary movements • Two common types o Chorea: irregular, spasmodic, involuntary movements of the limbs or facial muscles o Dystonia: abnormal muscle tone leading to impaired or abnormal movements, usually in feet Treatment of Parkinson’s Disease • Full explanation of disease to the patient • Treatment centers on drug therapy • PT, OT, speech therapy important • Severe cases; o Deep brain stimulation Pharmacology Overview • Aimed at increasing levels of dopamine • Antagonizes or blocks the effects of ACh • Slows the progression of the symptoms not the disease process • Indirect-Acting Dopaminergics: MAOIs • Dopamine Modulators • Catechol Ortho-Methyltransferase (COMT) Inhibitors • Direct-Acting Dopamine Receptor Agonists • Dopamine Replacements • Anticholinergic drugs • Antihistamines Indirect-Acting Dopaminergic Drugs • Monoamine Oxidase Inhibitors (MAOIs) break down catecholamines in the CNS, primarily in the brain • Selegiline and rasagiline are selective MAO-B inhibitors o Cause an increase in levels of dopaminergic stimulation in the CNS o Do not elicit the “cheese effect” of the nonselective MAOIs used to treat depression (if 10 mg or less is used) o Used as monotherapy or as adjuncts with levadopa o Contraindications  Known allergy  Concurrent use with meperidine • Adverse effects are usually mild o Dizziness, insomnia, nausea, diarrhea, chest pain, headache, weight loss o Doses higher than 10 mg/day may cause more severe adverse effects, such as hypertensive crisis Dopamine Modulator (indirect-acting) • amantadine o Antiviral drug used for treatment of influenza o Indirect acting o Causes release of dopamine and other catecholamines from storage sites at the end of nerve cells that have not yet been destroyed by the disease process o Blocks reuptake of dopamine into the nerve fibers o Result: higher levels of dopamine in the synapse between nerves and improved dopamine neurotransmission between neurons COMT Inhibitors • Tolcapone and entacapone • Block COMT, the enzyme that catalyzes the breakdown of the body’s catecholamines • Prolong the duration of action of levodopa; reduce wearing-off phenomenon • Adverse effects: o GI upset, urine discoloration, can worsen dyskinesia that may already be present o Tolcapone: severe liver failure Direct-Acting Dopamine Receptor Agonists • Two subclasses: o Nondopamine dopamine receptor agonists (NDDRAs) o Dopamine replacement drugs o Can be used in late or early stages Nondopamine Dopamine Receptor Agonists (NDDRAs) • Ergot derivatives: bromocriptine o Works by activating presynaptic dopamine receptors to stimulate the production of more dopamine o Inhibits the production of the hormone prolactin, which stimulates normal lactation and can be used to treat women with excessive or undesired breast milk production and prolactin-secreting tumors o Used with carbidopa-levadopa so that lower doses of levadopa are needed o Caution when used for patients with peripheral vascular disease o Adverse reactions: GI upset, dyskinesias, sleep disturbances o Drug interactions: erythromycin and adrenergic drugs • Nonergot drugs: pramipexole, ropinirole, and rotigotine o More specific antiparkinson effects with fewer adverse effects o Used in both early- and late-stage PD o May delay the need for levadopa o Monotherapy or adjunctive therapy o Also used for restless leg syndrome Dopamine Replacement Drugs • Dopamine replacement drugs o Levodopa, carbidopa, carbidopa-levodopa o Work presynaptically to increase brain levels of dopamine o Levodopa can cross the blood-brain barrier, and then it is converted to dopamine o However, large doses of levodopa needed to get dopamine to the brain also cause adverse effects o Carbidopa is given with levodopa o Carbidopa does not cross the blood-brain barrier and prevents levodopa breakdown in the periphery o As a result, more levodopa crosses the blood-brain barrier, where it can be converted to dopamine Levodopa Therapy • Levodopa is taken up by the dopaminergic terminal, converted into dopamine, and then released as needed • As a result, neurotransmitter imbalance is controlled in patients with early PD who still have functioning nerve terminals • As PD progresses, it becomes more difficult to control it with levodopa • Ultimately, levodopa no longer controls the PD, and the patient is seriously debilitated o Generally occurs between 5 and 10 years after the start of levodopa therapy • Adverse effects: o Confusion o Involuntary movements o GI distress o Hypotension o Cardiac dysrhythmias Carbidopa-Levodopa Therapy • Carbidopa: adjunct to treat nausea associated with Sinemet • Sinemet CR: increases “on” time and decreases “off” time • Drug interactions occur with tricyclic antidepressants and other drugs. • Carbidopa-levodopa: best taken on an empty stomach; to minimize GI side effects, it can be taken with food • Contraindicated in cases of angle-closure glaucoma • Use cautiously in patients with open-angle glaucoma • Adverse effects: cardiac dysrhythmias, hypotension, chorea, muscle cramps, and GI distress • Interactions: pyridoxine and dietary protein Anticholinergic Therapy • Anticholinergics block the effects of Ach • Used to treat muscle tremors and muscle rigidity associated with PD o These two symptoms are caused by excessive cholinergic activity • Does not relieve bradykinesia (extremely slow movements) • SLUDGE: Ach is responsible for causing increased salivation, lacrimation (tearing of the eyes), urination, diarrhea, increased GI motility, and possibly emesis (vomiting). • Anticholinergics have the opposite effects: dry mouth or decreased salivation, urinary retention, decreased GI motility (constipation), dilated pupils (mydriasis), and smooth muscle relaxation. • benztropine mesylate o Also used to treat extrapyramidal symptoms caused by use of antipsychotic drugs o Caution during hot weather or exercise; may cause hyperthermia o Adverse effects: tachycardia, confusion, disorientation, toxic psychosis, urinary retention, dry throat, constipation, nausea and vomiting o Avoid alcohol • trihexyphenidyl • Antihistamines also have anticholinergic properties o diphenhydramine (Benadryl) Nursing Implications • Perform a thorough assessment, nursing history, and medication history • Include questions about the patient’s: o CNS o GI and GU tracts o Psychologic and emotional status • Assess for signs and symptoms of PD o Masklike expression o Speech problems o Dysphagia o Rigidity of arms, legs, and neck • Assess for conditions that may be contraindications • Administer drugs as directed by manufacturer • Provide patient education regarding PD and the medication therapy o Don’t stop abruptly • Inform patient not to take other medications with PD drugs unless he or she checks with physician • When starting dopaminergic drugs, assist patient with walking because dizziness may occur • Administer oral doses with food to minimize GI upset • Encourage patient to force fluids to at least 3000 mL/day (unless contraindicated) • Taking levodopa with MAOIs may result in hypertensive crisis • Patient should be taught not to discontinue anti-parkinson drugs suddenly • Teach patient about expected therapeutic and adverse effects with anti-parkinson drug therapy • Entacapone may darken the patient’s urine and sweat. • Therapeutic effects of COMT inhibitors may be noticed within a few days; it may take weeks with other drugs. • Monitor for response to drug therapy o Improved sense of well-being and mental status o Increased appetite o Increased abili

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