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55 Cards in this Set
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- Back
bronchial asthma - pathology
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Increased airway reactivity
increased bronchoconstrictor response to stimuli (allergens, pollen, chemicals, stress, cold, exercise, infection, unknown factors?) trigger release of proinflammatory mediators (prostoglandins, histamine, leukotrienes) irritation of respiratory epithelium leads to contraction of bronchiole smooth muscle and narrow airway |
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clinical features of asthma
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wheezing, secretions
dyspnea, increased accessory muscle use anxiety,tachycardia, tachypnea, hypoxemia with cyanosis often see GERD with asthma (not sure which comes first) |
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Treatment of asthma
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Inhaled steroids (Pulmicort) to reduce inflammation
May add-Leukotriene inhibitors (Singular) to decrease inflammation, helps lower the steroid dose needed Short acting Beta 2 agonists MDIs(Albuterol) as rescue therapy |
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treatment of chronic asthma
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If not responding to other treatments:
Long acting beta 2 agonists (Advair) may be used to supplement glucocorticoids Xanthines (Theophylline) in lowest possible doses to supplement glucosteroids – watch for toxicity Use meds cautiously if cardiovascular disease present – common side effect tachycardia |
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rehab goals for asthma
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Patient Education: teach strategies to avoid triggers, breathing exercises
Encourage aerobic exercise (such as swimming) if exercise is not a trigger Environmental modifications |
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COPD
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COPD affects more than16 million in USA, increasing mortality and prevalence
Emphysema (pink puffers): destruction of alveolar walls, enlarged terminal air spaces, CO2 retention causes flushing) Bronchitis (blue bloaters): cyanosis/ hypoxemia due to long standing bronchial tree inflammation with hypersecretion of mucus |
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COPD Pathology
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Chronic airflow obstruction due to air trapped in lungs
Airways are narrowed (bronchial smooth muscle spasm), further narrowing when exhale Lungs are hyperinflated which leads to barrel chest deformity Diaphragm is flattened - disturbed length-tension relationship causes diaphragm to be less effective Accessory muscle use increases Determine stage by % air expired with forced exhalation (FEV1) |
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COPD classic symptoms
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chronic cough, increased mucus production and viscosity
wheezing, dyspnea on exertion hyperventilation (overbreathing) causes decreased carbon dioxide levels-dizziness |
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COPD pt education
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Pursed lip breathing
with trunk flexion/leaning forward: improves diaphragm length-tension relationship to help force air out with weight on arms: stabilizes arms to allow more efficient accessory muscle use and improved rib movement Pacing/Energy Conservation |
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COPD bronchiodilators
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Anticholinergics (Spiriva, Atrovent inhalers)
Long acting Beta 2 agonists (Advair) Theophylline (Theo-Dur) oral for acute exacerbations Glucocorticoids (Pulmicort inhaler) for severe exacerbations |
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COPD oxygen therapy
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COPD breathing is triggered by O2 levels, not CO2 as it is in “normals” ( they have grown accustomed to elevated CO2)
Goal of O2 therapy: Reach PaO2 (oxygen level in blood) of 60mmHG SaO2 (hemoglobin saturated with O2) of 89-92% (don’t want too high O2 levels as it suppresses urge to breathe in COPD patients) |
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COPD oxygen therapy - treatment implications
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rapid drop in O2 with activity-may need to increase oxygen only during activity.
delayed drop in O2 such as at the end of the 6 min walk test, problem is CO2 build up - focus on pursed lip breathing rather than increasing O2 |
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GI disorders: a challenge to rehab
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GI problems result from:
Damage caused by gastric acid secretion Abnormal GI motility (constipation, diarrhea, emesis) Goals of GI Meds: decrease acid help protect and heal the mucosal lining restore normal motility |
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GI disorders: special concerns in rehab pts
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PT routinely ordered for post op GI surgeries:
Goals: Decrease pain Increase peristalsis Early foley removal Decrease chances for pneumonia Decrease length of stay GI issues can decrease participation in therapy and lead to slow recovery: Constipation is a significant problem for rehab patients due to bedrest, pain medications Nausea is common with cancer patients, post-surgical patients due to pain meds Exercise tends to increase gastric acid, may exacerbate symptoms |
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GI disorders: acid base diseases - GERD, gastritis, ulcer disease
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GERD
Damage to lower esophageal sphincter from irritants, infection Reflux of pepsin/bile into esophagus Effects 20% of Americans Gastritis Inflammation of stomach mucosa Intense pain, nausea Ulcer Disease Disruption of the gastric or duodenal mucosa Causes bleeding, pain |
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Acid bases disorders - treatments (antacids)
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Antacids (Tums, Rolaids)
Chemically neutralize stomach acids Promote healing of gastric ulcers Used to treat minor dyspepsia/heartburn Side effects: depend on composition constipation – aluminum based diarrhea – magnesium based Acid rebound (calcium based products - Tums, Rolaids) Altered drug metabolism/excretion |
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Acid base disorders - treatments (H2 receptors)
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H2 receptor blockers (Tagamet, Pepcid, Zantac)
Used for acute/ long term care of GERD, ulcers Blocks H2 receptor (increase gastric acid secretion) on GI smooth muscle Side effects: dizziness, diarrhea, headache, arthralgia, acid rebound, can cause B vitamin deficiencies *Not as effective as proton pump inhibitors in acid control and healing |
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acid based disorders - treatments (2) NSAIDS
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NSAID-Induced Ulcers (Cytocec- misoprostol)
Long-term NSAID use leads to gastritis and ulcerations Inhibit gastric acid secretion, stimulate mucus secretion and mucosal blood flow. Less effective than PPIs Side Effects: diarrhea and abdominal cramping |
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acid base pump disorders - treatment 3 - proton pump inhibitors
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Proton pump inhibitors (Prilosec, Nexium, Prevacid, Protonix)
Effective treatment of GERD and ulcers Less risk of esophageal damage/cancer Inhibits the proton pump on the parietal cell membrane of the gastric mucosa to completely block all gastric acid secretion* Side Effects: dizziness, fatigue, may have acid rebound when discontinued, B vitamin deficiencies with long term use *may lead to more GI infections |
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acid base disorders - treatments - proton pumps continued
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Inhibition of gastric acid secretion by PPI’s may increase incidence of C-difficile infection
Vegetative form of C difficile can survive in gastric contents with a raised pH Patients using PPIs may be prone to colonization with C difficile. |
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C diff colitis
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Increasing incidence in young as well as old
Usually related to antibiotic use, PPIs may predispose Infection releases toxins that damage the protective lining of the large intestine, this produces severe diarrhea, pain, fever Treat with Flagyl for 10 days if mild, severe disease requires vancomycin and possible surgery consult for colon resection Eating yogurt daily recommended Florastor – probiotic in oral form (better than yogurt, OTC) |
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C diff colitis transmission prevention
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Transmission Prevention
Fecal-oral transmission-spore remains for 30+days! Alcohol waterless handwashes don’t break down the spore, must use soap and water Keep on contact isolation until 2 negative stool cultures |
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acid base disorder treatments - H. Pylori
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H. Pylori is a bacteria found in upper GI tract may cause or potentiate ulcers via mucosal breakdown leading to chronic gastritis, PUD, GERD and gastric CA-very undiagnosed
Triple therapy used: 2 antibiotics and one PPI, include bismuth with diarrhea Successful eradication of this infection may eliminate need for antiulcer meds |
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acid base disorder treatments - Mucosal Protectors: Bismuth Chelate
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Mucosal Protectors: Bismuth Chelate
Coats the base of the ulcer, increases gastric mucous epithelial cell growth Offers protective properties against H. pylori Side Effects: blackening of the tongue & feces, nausea, vomiting |
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acid base disorder treatments - Mucosal Protectors: Sucralfate (Sulcrate)
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Forms a protective coating over an ulcer
Used for stress ulcers and chronic peptic ulcer disease Stays local, does not interact with other drugs Side effects: constipation, nausea, can decrease the absorption of other meds |
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abnormal GI motility - Antiemetic drugs
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Prokinetic Drugs: Reglan (metoclopramide)
Stimulates peristalsis, facilitating gastric emptying Moves contents away from esophagus which decreases GERD irritation Used for chemotherapy-related vomiting Side Effects: CNS/dopamine antagonist, motor restlessness, fatigue, diarrhea, weakness, parkinsonlike tremor (long term), hypotension, HTN, tachycardia |
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Abnormal GI motility - antiemetic drugs: anticholinergics, antihistamines, neuropleptics
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Anticholinergics (Scopolamine)- motion sickness
Side effects: dizziness, drowsiness, blurred vision, dilated pupils, dry mouth, difficulty urinating Antihistamines (Antivert, Benadryl, Dramamine)-motion sickness Side effects: diziness and sedation Neuroleptics (Compazine, Phenergan)- immediately post-op Side effects: orthostatic hypotension, tachycardia, blurred vision, dry eyes, urinary retention |
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Abnormal GI motility - antiemetic drugs: serotonin blockers, cannabinoids, neurokinin 1 receptor agonists
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Antiemetic Drugs - chemotherapy-related
Serotonin Blockers (Zofran) Side effects: headache, dizziness, diarrhea Cannabinoids (Marinol) Side effects: ataxia, light-headedness, blurred vision, dry mouth, weakness, tachycardia or bradycardia, CNS effects, munchies Neurokinin 1 receptor antagonists (Aprepitant) in combination w/corticosteroids and serotonin blockers Side effects: Hiccups |
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Abnormal GI motility - antidiarrheal drugs
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Slow GI mobility, enhance absorption of nutrients/water, provide bulk to stool
Prolonged diarrhea can cause dehydration, a common admitting diagnosis in the elderly |
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abnormal GI motility - antidiarrheal drugs: absorbents and opoid derivatives
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Antidiarrheal Drugs
Adsorbents (Pepto-Bismol*, Kaopectate) Coat GI tract wall, bind to bacteria & carry them out Decrease effectiveness of many drugs (digoxin, hypoglycemic drugs, oral anticoagulants) *Aspirin product Opiod derivatives (Immodium) decreases GI motility, increases absorption of electrolytes and water Side effects: nausea, fatigue, addiction? |
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abnormal gi motility: laxatives
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Promote bowel evacuation when there is decreased GI motility due to bed rest, medications, surgery, SC injuries
Frequently abused, dependence develops Teach patients to focus on high fiber diet, hydration, exercise |
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abnormal GI motility: laxative meds: bulk forming & emollient/lubricant
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Bulk forming (Metamucil, Citrucel)
Absorb water, increases bulk of intestinal contents, stretch stimulates BM Emollient/Lubricant (Colace, mineral oil) Side effects: decreased absorption of vitamins, cramps, nausea, electrolyte imbalances |
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Abnormal GI motility: laxative meds - hyperosmotics: saline & stimulants
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Laxative Meds
Hyperosmotics (Milk of Magnesia) Saline (Fleet Enema) Enhance peristalsis by osmotically increasing the bowel fluid volume Stimulants (Correctol, Dulcolax) Irritate GI mucosa, nerve stimulus for BM |
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Anticholinergics - decrease bronchospasm
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- Block acetylcholine receptors on airway smooth muscle; leading to bronchodilation. Max bronchodilation occurs in 30 minutes, duration up to 5 hours.
Atrovent (ipratropium) Oxitropium Spiriva (tiotropium) *First choice for COPD because they also decrease mucous secretion. Effective in asthma when combined with beta 2 agonist |
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Corticosteroids - decrease inflammation
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Inhibit production of pro-inflammatory products which trigger exaggerated response in respiratory passages
Also increase anti-inflammatory proteins Inhalation preferred – goes directly to mucosa, fewer systemic side effects Given by IV during severe attacks |
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Corticosteroids - Pulmocort & Flovent - decrease inflammation
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Side Effects: Steroid catabolic effect on support tissues -
osteoporosis, weakening muscles, ligaments, skin tears cataracts , glaucoma (with inhaler use) hypergylcemia, hypertension, fluid retention adrenal suppression Oral thrush – rinse mouth after use |
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Cromones (inhaled non-steroids) - descrease inflammation (respiratory)
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Intal, Tilade
Must be taken prior to the onset of bronchoconstriction Prevents bronchospasm by inhibiting release of inflammatory mediators (histamine, leukotrienes) Used with allergies and asthma to prevent response to pets etc- take before you go Administered by MDI, nebulizer, or nonprescription nasal spray (Nasalcrom) |
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leukotriene inhibitors - decrease inflammation (respiratory)
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Leukotriene Inhibitors - Blocks the inflammatory effects of leukotrienes which cause bronchial constriction and mucus production
Singular (montelukast) - blocks the respiratory tissue receptor for leukotrienes Zyflo (zileuton) – inhibits the production of leukotrienes Can be combined with beta agonists and steroids for optimal treatment for COPD and asthma Side effects: Safer than other anti-inflammatory agents, low side effects |
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Durg Nomenclature
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Trade name always capitalized (Tylenol)
Generic (non-proprietary) in lower case letters (acetaminophen) |
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pharmacokinetics: why imp. for PTs
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So we can schedule our therapy for desired effect, therapists need to understand:
What the medication is used for How it works How it is absorbed, distributed and eliminated |
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Administration and Absorption: Enteral
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Absorbed by GI tract
Oral (p.o.) - depending on med - take with food to buffer or no food for absorption. Sublingual (sl.) - Large vein under tongue - fast to venous system Rectal (p.r.) - unconscious or vomiting |
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Parenteral
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Inhalation – rapid absorption due to large surface area of alveoli (respiratory MDI, nebs)
Injection - IV (reaches target quickly), IM (local or prolonged systemic release, subq (local response, slow systemically) Transdermal - topical (skin or mucous problems) Intrathecal - bypasses blood-brain barrier to reach CNS |
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pharmacokinetic Considerations
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Age: metabolism slows with age
Medical History: liver, kidney, cardiac disease Gender/Genetics: hormones may influence Diet: foods/other meds may interact Body Composition: fat cells may store meds Mode of Delivery: IV=100%, Inhalation-blocked if congested, oral depends on stomach absorption, liver metabolism |
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distribution and Timing
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How long before it starts working?
When is the peak effect? (ie: Ativan peaks 6 hours later) How long will it last? Generally it takes 5 half- lives to clear a drug Example: Drug with 2 hour half- life takes 10 hours to clear. |
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metabolism and excretion
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Metabolism occurs in the liver-the drug is chemically changed to a less active state
Excretion of drug is primarily by the kidneys: Decreased drug clearance with kidney dysfunction- check creatine clearance labs, watch for toxicity |
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implications for PT
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Physical activity and modalities may affect absorption and bioavailability of the drug:
Heat and exercise increase blood flow and speeds absorption and dispersion away from the site Diabetics may become hypoglycemic if injected insulin is absorbed too fast Cold decreases dispersion, slows distribution |
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Pulmonary system function review
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Respiration is the exchange of O2 and CO2
Oxygen is needed to produce energy in cells Alveoli act as a “sponge” O2 exchanged between alveoli and capillaries O2 binds to HgB, transported in blood CO2 exchanged from blood to alveoli as bicarbonate (HCO3) and exhaled as waste gas Goal: maintain acid -base balance (kidneys,lungs) Level of H+ ions (C02) stimulates inspiration Excess retained CO2 leads to acidosis |
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Antitussives (Robitussin DM)
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- help annoying dry coughs
Side Effects: sedation, dizziness, GI upset, constipation |
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Decongestants
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Decongestants: Help thin AND clear secretions by drying up mucosal vasculature
Pseudo-epinephrine Sudafed: oral Afrin: spray (nasal sprays do not penetrate severe congestion) Systemic side effects: increases sympathetic drive (i.e.: headache, nervousness, nausea, increased blood pressure, palpitations; dangerous with prolonged use |
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Mucolytics and expectorants (thin and clear secretions
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- Used to prevent accumulation of thick secretions that can clog respiratory passages
Mucomyst or Mucosil (acetylcysteine): inhaled, decreases viscosity of secretions (may decrease free radical damage) |
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Antihistamines (thin and clear secrections)
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- compete with H1 receptor sites, not allowing histamine to attach. Decreases nasal congestion, discharge, coughing and sneezing
Side effects: sedation, fatigue, nausea |
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non-sedating antihistamines
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Zyrtec (cetirizine)
Claritin (loratadine) Allegra (fexofenadine) Clarinex (desloratidine) |
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Beta 2 Agonists - decrease bronchospasm
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- Promotes bronchodilation by relaxing smooth muscles and increasing mucociliary clearance. Delivery by MDI, DPI, nebulizer or oral*
Albuterol: rescue inhaler – rapid onset, duration 4 - 6 hours Advair: delayed onset, long acting – 12 – 15 hours *Inhalation preferred – fewer side effects and more effective however oral form may be needed to reach more distal branches if bronchioles constricted |
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Beta 2 Agonist Side Effects
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increases airway irritation and severity of attacks with prolonged use
May develop tolerance to drug CNS/cardiac irregularities: tachycardia, tremor, hypokalemia, hyperglycemia, increased BP and cardiac contractility |
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Xanthine derivatives - decreased bronchospasm
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Promotes respiratory smooth muscle relaxation
Increases contractility and endurance of the diaphragm Found in coffee, tea, and chocolate in small amounts Side effects: strong tachycardic and hypertensive effects, nausea, vomiting, headache, insomnia * Serious problems with toxicity due to narrow therapeutic range |