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NUR MISC EXAM 3 CH. 36 Antihistamines, Decongestants, Antitussives, & Expectorants

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NUR MISC EXAM 3 CH. 36 Antihistamines, Decongestants, Antitussives, & Expectorants Antihistamines  Drugs that directly compete with histamine for specific receptor sites  Two histamine recep... tors 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 mucosao 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 impairedBronchodilators  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  Hypotensiono 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 symptomsAnticholinergics  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 dypillineXanthine 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 Restlessnesso 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 betaadrenergic 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 41Antitubercular 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) casesMultidrug-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 groupso 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 throughacetylation—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, antiinflammatory, 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 antiinflammatory 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 paino 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 inhibitorso 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 CBCo 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  Hormoneso 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 osteoclastmediated 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 muscleso 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 neuronsCOMT 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 levodopao 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 ability to perform ADLs, to concentrate, and to think clearly o Less intense parkinsonian manifestations, such as less tremor, shuffling gait, muscle rigidity, and involuntary movements Antiepileptic Drugs Epilepsy  Seizure o Brief episode of abnormal electrical activity in nerve cells of the brain  Convulsion o Involuntary spasmodic contractions of any or all voluntary muscles throughout the body, including skeletal, facial, and ocular muscles  Epilepsy o Chronic, recurrent pattern of seizures  Primary (idiopathic) o Cause cannot be determined o Roughly 50% of epilepsy cases  Secondary (symptomatic) o Distinct cause is identified  Trauma, infection, cerebrovascular disorder  Febrile in young children Classification of Epilepsy  Generalized onset seizures o Formerly known as grand mal seizures o Tonic-clonic seizures: contractions throughout the body o Aclonic: o Myoclonic o Absence seizures  Partial onset seizures o Simple (formerly known as petit mal seizures)o Complex o Secondary generalized tonic-clonic  Unclassified seizures Status Epilepticus  Multiple seizures occur with no recovery between them  Result: o Hypotension o Hypoxia o Brain damage o Death  True medical emergency Antiepileptic Drugs (AEDs)  Also known as anticonvulsants  Goals of therapy o To control or prevent seizures while maintaining a reasonable quality of life o To minimize adverse effects and drug-induced toxicity  AED therapy is usually lifelong  Combination of drugs may be used  Single-drug therapy started before multiple-drug therapy is tried  Serum drug concentrations must be measured o Therapeutic drug monitoring o Serum concentrations of phenytoin, phenobarbital, carbamazepine, levetiracetam, and primidone correlate better with seizure control and toxicity than do those of valproic acid, ethosuximide, and clonazepam  Antiepileptic drugs traditionally used to manage seizure disorders include: o Barbiturates o Hydantoins o Iminostilbenes plus valproic acid o Second- and third-generation antiepileptics Mechanism of Action and Drug Effects  Exact mechanism of action is not known  Pharmacologic effects: o Reduce nerve’s ability to be stimulated o Suppress transmission of impulses from one nerve to the next o Decrease speed of nerve impulse conduction within a neuron  Antiepileptic Drugs: Indications  Prevention or control of seizure activity  Long-term maintenance therapy for chronic, recurring seizures  Acute treatment of convulsions and status epilepticus  Other uses Antiepileptic Drugs: Adverse Effects  Numerous adverse effects—vary per drug  Adverse effects often necessitate a change in medication Black box warning as of 2008 o Suicidal thoughts and behavior  Long-term therapy with phenytoin may cause gingival hyperplasia, acne, hirsutism, and Dilantin facies Antiepileptic Drugs: Interactions  Drug interactions are numerous  Many antiepileptic drugs interact with each other  Induce hepatic metabolism resulting in reduction of effects of other drugs  Interfere with birth control  Avoid grapefruit with carbamazepine Antiepileptic Drug Listing  Valproic acid  Gabapentin  Lamotrigine  Felbamate  Levetiracetam  Topiramate  Zonisamide  Tiagabine  Pregabalin  Perampanel  Ezogabine  Vigabatrin  Eslicarbazepine  Clobazam  Brivaracetam Barbiturates: Phenobarbital and Primidone  Primidone is metabolized in the liver to phenobarbital  Most common adverse effect: sedation  Therapeutic effects: serum levels of 10-40 µg/mL  Contraindications: known allergy, porphyria, liver or kidney impairment, and respiratory illness  Adverse effects: cardiovascular, CNS, GI, and dermatologic reactions Hydantoins: Phenytoin  Phenytoin has been used as a first-line drug for many years and is a prototypical drug  Adverse effects: gingival hyperplasia, acne, hirsutism, Dilantin facies, and osteoporosis  Therapeutic levels are usually 10-20 µg/mL  Highly protein bound: binds to protein, you will have little protein if at first they had too much and now it binds to the medication  Intravenous (IV) administration o Very irritating to veinso Slow IV directly into a large vein through a large-gauge (20-gauge or larger) venous catheter o Diluted in normal saline (NS) for IV infusion o Filter must be used o Saline flush  Fosphenytoin is an injectable water-soluble prodrug of phenytoin that can be given IM or IV without causing burning on injection associated with phenytoin Iminostilbenes: Carbamazepine  Second most prescribed antiepileptic in US after phenytoin  Autoinduction of hepatic enzymes o Autoinduction is a process in which, over time, a drug stimulates the production of enzymes that enhance its own metabolism, which leads to lower than expected drug concentrations  Oxcarbazepine – chemical analogue of carbamazepine; for partial seizures o Adverse reactions: headache, dizziness, nausea Ethosuximide  Used in the treatment of uncomplicated absence seizures  Not effective for secondary generalized tonic-clonic seizures  Contraindication: known allergy  Adverse effects: GI and CNS effects  Drug interactions: hepatic enzyme-inducing drugs Miscellaneous Drugs  Gabapentin o Chemical analogue of GABA (a neurotransmitter that inhibits brain activity) o Works by increasing the synthesis and synaptic accumulation of GABA between neurons o Used in the treatment of partial seizures and neuropathy  Lamotrigine o Used for simple or complex partial seizures; also used in treatment of bipolar disorder o Common adverse effects: relatively minor CNS and GI symptoms and possible Stevens-Johnson syndrome  Levetiracetam o Adjunct therapy for partial seizureso Contraindication: known allergy o Mechanism of action: unknown o Adverse effects: generally well tolerated, CNS o No drug interactions  Pregabalin o Schedule V controlled substance o Indication: adjunct therapy for partial seizures o Other common uses: neuropathic pain, postherpetic neuralgia, and fibromyalgia  Tiagabine o Adjunct therapy for partial seizures o Beneficial effects by inhibiting the reuptake of GABA o Avoid off label use of this drug it can cause paradoxical seizures o Adverse effects: CNS and GI symptoms  Topiramate o Adjunct therapy for partial and generalized seizures o Mechanism of action unknown o Adverse effects: CNS related, angle-closure glaucoma  Valproic Acid o Treatment of generalized seizures, bipolar disorder, and controlling partial seizures o Highly protein bound o Adverse effects: drowsiness, GI disturbances, tremor, weight gain, hair loss, hepatotoxicity, pancreatitis  Zonisamide o Sulfonamide derivative o Used for a variety of seizure types o Adverse effects: CNS and GI symptoms Nursing Implications  Assessment o Health history, including current medications o Drug allergies o Liver function studies, CBC o Baseline vital signs  Oral drugs o Take regularly, same time each day o Take with meals to reduce GI upset o Do not crush, chew, or open extended-release forms o If patient is NPO for a procedure, contact prescriber regarding AED dosage  Intravenous forms o Follow manufacturer’s recommendations for IV delivery—usually given slowly o Monitor vital signs during administration o Avoid extravasation of fluids o Use only normal saline with IV phenytoin (Dilantin) Teach patients that therapy is long term and possibly lifelong (not a cure)  Monitor for therapeutic effects o Decreased or absent seizure activity  Monitor for adverse effects o Mental status changes, mood changes, changes in level of consciousness or sensorium o Eye problems, visual disorders o Sore throat, fever (blood dyscrasias may occur with Dilantin) Ophthalmic Drugs Drugs That Affect the Eye  Mydriatics (apraclonidine) o Dilate the pupil  Miotics (acetylcholine, pilocarpine) o Constrict the pupil  Cycloplegics (atropine, cyclopentolate) o Paralyze the ciliary body o Have mydriatic properties o Cycloplegia: paralysis of accommodation Ocular Drugs Antiglaucoma drugs  Antimicrobial and anti-inflammatory drugs  Topical anesthetics  Diagnostic drugs  Antiallergic drugs  Lubricants and moisturizers Glaucoma  Inhibition of the normal flow and drainage of aqueous humor  Results in increased intraocular pressure (IOP)  Pressure against the retina destroys neurons, leading to impaired vision and eventual blindness Types of Glaucoma  Angle-closure glaucoma  Open-angle glaucoma  Also characterized by underlying cause o Primary o Secondary o Congenital Drugs Used to Reduce IOP  Direct-acting cholinergics  Indirect-acting cholinergics  Adrenergics: sympathomimetics  Anti-adrenergics: beta blockers  Carbonic anhydrase inhibitors (CAIs)  Osmotic diuretics  Prostaglandin agonists Cholinergic Drugs  Mimic the PSNS neurotransmitter acetylcholine  Also called miotics, cholinergics  Direct-acting and indirect-acting drugs  Cause pupillary constriction (miosis), which leads to reduced IOP caused by increased outflow of aqueous humor  Direct-acting drugs o acetylcholine o carbachol o pilocarpine  Indirect-acting drugs o echothiophate  Indications o Open-angle glaucoma o Angle-closure glaucoma o Ocular surgery o Convergent strabismus (“cross-eye”)o Ophthalmologic exams Cholinergic Drugs: Adverse Effects  Most limited to local effects  If sufficient amounts enter the bloodstream, systemic effect may occur (most likely with indirect acting) o Hypotension, bradycardia, or tachycardia o Headache, nausea, vomiting, diarrhea, abdominal cramps, asthma attacks o Others Sympathomimetics  Mimic the sympathetic neurotransmitters epinephrine and norepinephrine  Stimulate the dilator muscle to contract o Result is increased pupil size (mydriasis)  Enhance aqueous humor outflow through the canal of Schlemm o IOP is reduced  apraclonidine  brimonidine  dipivefrin o Prodrug of epinephrine o When applied topically  Hydrolyzed to epinephrine  Penetrates tissues better  Indications o Chronic, open-angle glaucoma (to reduce IOP) o Reduction of perioperative IOP o Reduction of ocular hypertension Sympathomimetics: Adverse Effects  Primarily limited to ocular effects o Burning o Eye pain o Lacrimation  Rare systemic effects o Hypertension o Tachycardia o Extrasystoles o Headache o Faintness Beta-Adrenergic Blockers  betaxolol  carteolol  levobetaxolol  metipranolol  timolol  Reduce IOP by:o Reducing aqueous humor formation o Increasing aqueous humor outflow  Does not affect pupil size, accommodation, or night vision Beta-Adrenergic Blockers: Indications  Reduction of elevated IOP o Chronic open-angle glaucoma o Ocular hypertension  Treatment of some forms of angle-closure glaucoma  Administration of systemic beta blockers with high doses of ophthalmic beta blockers may result in additive effects Beta-Adrenergic Blockers: Adverse Effects  Primarily ocular effects o Transient burning and discomfort o Blurred vision o Pain o Photophobia o Others  Limited systemic effects o Headache o Dizziness o Cardiac irregularities o Bronchospasm Carbonic Anhydrase Inhibitors  brinzolamide (Azopt)  dorzolamide (Trusopt)  Inhibit the enzyme carbonic anhydrase, which reduces aqueous humor formation in the eye  Ask for any allergies to sulfide  Result is decreased IOP Carbonic Anhydrase Inhibitors: Indications  Treatment of glaucoma o Open angle o Angle closure  Preoperatively to reduce intraocular pressure Carbonic Anhydrase Inhibitors: Adverse Effects  Oral forms can produce systemic effects o Drowsiness, confusion o Transient myopia, tinnitus o Anorexia, vomiting, diarrhea o Several others  Patients with sulfa allergies may develop cross-sensitivities Osmotic Diuretics  Create ocular hypotension by producing an osmotic gradient Water is forced from the aqueous and vitreous humors into the bloodstream  Result is reduced volume of intraocular fluid, thus reduced IOP  Administered IV, PO, or topically  Glycerin usually tried first o Can cause hyperglycemia  Mannitol used if glycerin is unsuccessful  Isosorbide and urea may also be used  Indications o Acute glaucoma episodes o Before and after ocular surgery to reduce IOP  Adverse effects o Nausea, vomiting, headache o May cause fluid and electrolyte imbalance Prostaglandin Agonists  Newest class of drugs for glaucoma  Three drugs o latanoprost (Xalatan) o travoprost (Travatan-Z) o bimatoprost (Lumigan)  Reduce IOP by increasing the outflow of aqueous fluid  Increase uveoscleral outflow of fluid  Used in the treatment of glaucoma  Most drugs allow for single daily dosing because of effects lasting for 20 to 24 hours  Effects on eye color o In some persons with hazel, green, or blue/brown eyes, eye color will change permanently to brown o Color change occurs even if medication stopped Ocular Antimicrobial Drugs  Topical and systemic administration o Antibacterial o Antiviral o Antifungal o Topical application may cause transient and local inflammation, burning, and stinging  Use of ophthalmic antibiotics with corticosteroids may make it more difficult to rid the eye of infection  Aminoglycosides o Antibacterial o gentamicin (Garamycin) , tobramycin (Tobrex)  Macrolides o Antibacterial o erythromycin, azithromycin, otherso Erythromycin also is used for prevention of Neisseria gonorrhoeae eye infections in newborns o Treatment of neonatal conjunctivitis caused by Chlamydia trachomatis o Polypeptides o Antibacterial o bacitracin (AK-Tracin), polymyxin B  Quinolones o ciprofloxacin (Ciloxan) o gatifloxacin (Zymar) o moxifloxacin (Vigamox) o levofloxacin (Quixin) o ofloxacin (Ocuflox)  Sulfonamides o sulfacetamide (Bleph-10) o sulfisoxazole (Gantrisin) Ocular Antifungal Drugs  natamycin (Natacyn) o Used topically to treat  Blepharitis  Conjunctivitis  Keratitis  ganciclovir (Vitrasert) o Treatment of ocular cytomegalovirus (CMV) o Administered by surgical implant in the eye  fomivirsen (Vitravene) o Treatment of ocular CMV o Administered by surgical implant in the eye  trifluridine (Viroptic,1% ophthalmic drops) o Used for ocular infections (keratitis and keratoconjunctivitis) caused by types 1 and 2 of the herpes simplex virus o Applied topically as drops o Significant adverse effects include secondary glaucoma, corneal punctate defects, uveitis, and stromal edema (edema in the tough, fibrous, transparent portion of the cornea known as the stroma) Ocular Anti-inflammatory Drugs  NSAIDs o ketorolac (Acular) o flurbiprofen (Ocufen) o bromfenac (Xibrom) o diclofenac (Voltaren)  Corticosteroids o dexamethasone (Decadron, AK-Dex) o fluocinonide (Retisert)o fluorometholone (Fluor-Op) o loteprednol (Lotemax) o medrysone (HMS) o prednisolone (Pred Forte) o rimexolone (Vexol)  Act on various parts of the arachidonic acid metabolic pathway  Reduce the production of various inflammatory mediators  As a result, pain, erythema, and other inflammatory processes are reduced  Used prophylactically after surgery to prevent inflammation and scarring  NSAIDs used for symptomatic treatment of seasonal allergic conjunctivitis Topical Ophthalmic Anesthetics  tetracaine  proparacaine (Alcaine)  Used to prevent eye pain during o Surgery o Ophthalmic examinations o Removal of foreign bodies or sutures o Diagnostic testing and procedures  Short-term use only  Not for self-administration Ophthalmic Diagnostic Drugs  Cycloplegic mydratics  atropine sulfate (Isopto Atropine) o Results in  Mydriasis  Cycloplegia o Used for  Ophthalmic examinations  Uveitis (which benefits from pupillary dilation)  Cycloplegic mydratics (cont’d)  cyclopentolate (Cyclogyl) o Causes mydriasis and cycloplegia o Used for diagnostic examinations o Not used for uveitis  Other cycloplegic mydriatics o scopolamine (Isopto Hyoscine) o homatropine (Isopto Homatropine) o tropicamide (Mydriacyl)  Ophthalmic dye o fluorescein (AK-Fluor)  Diagnostic dye used to identify corneal defects and to locate foreign objects in the eye  Used in fitting hard contact lenses Various defects are highlighted in either bright green or yellow-orange, and foreign objects have a green halo around them Ophthalmic Antiallergic Drugs  Ophthalmic antihistamines o Used to treat symptoms of allergic conjunctivitis (“hay fever”) o azelastine (Optivar) o olopatadine (Patanol) o emedastine (Emadine) o ketotifen (Zaditor) o epinastine (Elestat)  Used for seasonal allergy symptoms o Mast cell stabilizers  cromolyn sodium (Crolom)  pemirolast (Alamast)  nedocromil (Alocril)  lodoxamide (Alomide) o Decongestants  Tetrahydrolozine (Visine)  phenylephrine (Neo-Synephrine)  oxymetazoline (Visine LR)  naphazoline (Clear Eyes) Ophthalmic Lubricants and Moisturizers  Artificial tears o Over-the-counter products o Provide lubrication or moisture for dry or irritated eyes o Available in drops or ointment o Brand names include: Murine, Nu-Tears, Moisture Drops, Tears Plus, Akwa Tears  Restasis o Ophthalmic form of cyclosporine o Immunosuppressant drug o Used to treat keratoconjunctivitis sicca (dry eyes) o It can be used together with artificial tears, if the drugs are given 15 minutes apart Nursing Implications  Assess the patient’s history, including medication history  Assess patient’s baseline vital signs and visual acuity, and perform a physical assessment of the eye and surrounding structures  Assess for contraindications to specific drugs  Follow specific guidelines for administration of ophthalmic drugs  Avoid touching the eye with the tip of the dropper or container  Apply ointments as a thin layer in the conjunctival sac  When applying eyedrops, have the patient look up to the ceiling, and place the drop in the conjunctival sac Pressure may be applied to the inner canthus for at least 1 minute to reduce systemic absorption of the drug  If more than one eye medication is ordered, clarify the correct order and intervals for administration  If the patient wears contact lenses, check to see if they should be removed during therapy with eye medications  Provide patient/family education on correct procedures for administration of eye medications  Monitor for adverse effects  Monitor for therapeutic response to therapy Otic Drugs Structure of the Ear Ear Disorders  Bacterial and fungal infections  Inflammatory disorders that cause pain  Earwax accumulation  External ear: physical trauma, dermatitis  Middle ear: otitis media o Most often afflicts children, following a respiratory tract infection o In adults usually results from foreign objects or water sportso Symptoms include pain, fever, malaise, pressure, sensation of fullness in the ears, hearing loss o If untreated, tinnitus, nausea, vertigo, mastoiditis may occur o Hearing deficits and hearing loss may result if prompt therapy not started Otic Drugs for External and Middle Ear Disorders  Antibiotics  Antifungals  Antiinflammatory drugs  Local analgesics  Local anesthetics  Steroids  Wax emulsifiers Antibacterial and Antifungal Otic Drugs  Topical formulations applied to the external ear  Often combined with steroids for antiinflammatory, antipruritic, and antiallergic drug effects  Middle ear infections generally require systemically administered antibiotics  Antibiotics o neomycin and polymyxin B plus hydrocortisone combination (Cortisporin Otic) o Others containing ciprofloxacin and dexamethasone (Ciprodex) o Fluroquinolone: Ofloxacin  Antifungals o Cortic (combination of antifungal drugs and hydrocortisone) o Acetasol HC (hydrocortisone, local anesthetic, antiseptic, antifungal, emulsifier, and antiseptic preservative)  Wax Emulsifiers  carbamide peroxide (Debrox)  Combined with other drugs, such as glycerin, to work together to loosen and help remove cerumen  Ear canal irrigation with water may be required  Other names include: Debrox Drops, Murine Ear Drops, Auro Ear Drops Nursing Implications  Assess baseline hearing or auditory status  Evaluate patient’s symptoms  Assess drug and food allergies  Assess for contraindications  Perforated eardrum(s) may be a contraindication to these drugs o ciprofloxacin and ofloxacin can be used with perforated ear drums  If necessary or if ordered, remove cerumen before instilling ear drops by irrigation Cleanse outer ear thoroughly  Ear drops should be warmed to approximately body temperature before instillation  Allow refrigerated solutions to warm to room temperature.  Cold solutions may cause vomiting and dizziness  For adults, drops should be given while holding the pinna up and back  For children younger than 3 years, hold the pinna down and back when giving ear drops  Allow the drops time to flow down into the ear canal  Patients should lie on the side opposite to the side of the affected ear for about 5 minutes after instillation of the drug  A small cotton ball may be gently inserted into the ear canal to keep the drug in, but do not force the cotton into the ear canal  Gently massage the tragus of the ear to encourage flow of medication [Show More]

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