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GEP Pulmonary

GEP Pulmonary Flash Cards Week 5 2009

QuestionAnswer
Asthma (Basic Definition + Symptoms) Chronic Inflammatory Disorder of the airways. <BR> Unlike COPD, it is reversible. <BR> Symptoms - Cough, wheezing, S.O.B., chest tightness
Extrinsic vs Intrinsic Asthma Extrinsic - early childhood onset, IgE-mediated. <BR> <BR> Intrinsic - adult onset, not IgE-mediated, less positive prognosis
Asthma Pathology Denudation (erosion) of airway epithelium <BR> Collagen deposition beneath basement memb. <BR> Edema (mucosal due to goblet cells replace epithelium) <BR> Mast cell activation <BR> Inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes)
Innate Asthma Cause? Th1 vs Th2 T-helper (Th1) - immune response that fights infection <BR> T-helper (Th2) - leads to expression of allergic diseases and asthma <BR> Genetic or environmental ("hygiene hypothesis") - Th1 downregulated so Th2 dominates (causes inflammation)
Asthma - Role of Eosinophils Allergen -> Mast cells -> release cytokines including IL-5 -> Eosinophils released from bone marrow travel to airways. <BR> <BR> Eosinophils release granular proteins that injure epithelium and enhance bronchial responsiveness
Asthma Treatments - Beta2 Agonists Mechanism of Action Activate beta2 receptors in smooth muscle of lungs -> bronchodialation. <BR> <BR> Also suppress histamine release and increase ciliary motility
Asthma Treatments - Beta2 Agonists - Drugs Short Acting (SABA) - <BR> Inhaled - albuterol, levalbuterol, pirbuterol <BR> <BR> Long Acting (LABA) - <BR> Inhaled - formoterol, salmeterol <BR> Oral - albuterol, terbutaline
Asthma Treatments - Methylxanthines Theophylline & Aminophylline <BR> Bronchodialators, probably inhibit phosphodiesterase & elevate levels of cAMP <BR> Can be toxic to CNS and heart, many drug interactions including caffeine <BR> Oral or IV routes
Asthma Treatments - Anticholinergics Ipratropium & Tiotropium <BR> Block muscarinic receptors in bronchi -> bronchodialation <BR> Only approved for COPD, but used for asthma when other meds aren't enough
Asthma Treatments - Glucocorticoids Mechanism of Action Suppress Inflammation <BR> Decrease synthesis & release of mediators <BR> Decrease infiltration & activity of inflammatory cells <BR> Decrease edema of airway mucosa
Asthma Treatments - Glucocorticoids - Drugs Inhaled - futicason, budesonide, beclomethasone, triamcinolone, flunisolide, mometasone <BR> Oral - prednisone <BR> IV - methylprednisolone
Asthma Treatments - Combo Inhaled Glucocorticoid + LABA Low dose ICS + LABA more effective than higher dose ICS alone <BR> Glucocorticoid causes increased synthesis of Beta2 receptors <BR> Advair - fluticasone + salmeterol <BR> Symbicor - budesonide + formoterol
Asthma Treatments - Mast Cell Stabilizers Cromolyn & Nedocromil <BR> Stabilize mast cell memb. & inhibit IgE-mediated release of histamine & other mediators <BR> Used as inhaler <BR> Not useful during attack
Asthma Treatments - Leukotriene Modifiers Zileuton - blocks leukotriene synthesis <BR> Zafirlukast & Montelukast - block leukotriene receptors <BR> All are given orally <BR> Montelukast (Singulair) - safest one
Asthma Treatments - Omalizumab IgG monoclonal antibody <BR> Binds IgE to inhibit it binding to mast cells <BR> Given Sub Q <BR> Very expensive <BR> only used in pts with moderate to severe asthma that can't be controlled with inhaled corticosteroids <BR> observe pts for anaphylaxis
COPD - Definition Airflow limitation that is NOT fully reversible <BR> Progressive disease associated w/ abnormal inflammatory response to noxious particles or gases <BR> 90% of COPD cases are smokers, 15% of smokers get COPD
Bronchitis vs Emphysema Chronic Bronchitis - the "blue bloater"; hypersecretion of bronchial mucus and chronic cough, inflammation narrows airways, polycythemia <BR> Emphysema - the "pink puffer", destruction of alveoli and small airways
COPD Treatment - Inhaled Bronchodilators anticholinergic - ipratropium bromide <BR> SABAs <BR> LABAs <BR> improve symptoms and exercise tolerance
COPD Treatment - Corticosteroids Inhaled Corticosteroids (ICS) - for pts with moderate to severe COPD and frequent exacerbations <BR> Oral Steroids - only for short bursts
COPD Treatment - Theophylline & Antibiotics Theophylline - use for pts when other therapies don't work; use sustained release for sleep-related breathing disorders <BR> <BR> Antibiotics - for treatment of acute exacerbations (change in quantity or character of sputum)
COPD Prognosis - BODE Index Body mass index + airway obstruction + dyspnea score + exercise capacity <BR> <BR> predicts death and hospitalization better than FEV1 alone
Smoking Cessation - First-Line Pharmacotherapies Bupropion SR (Zyban) - antidepressant, unknown mechanism, pts think cigs taste bad <BR> Varenicline (Chantix) - alpha-4, beta-2 partial agonist, watch for mood changes <BR> Nicotine Replacement Therapies
Smoking Cessation - Second-Line Pharmacotherapies Clonidine - antihypertensive, useful for alcohol and heroin w/drawal <BR> Nortriptyline - antidepressant
Upper Respiratory Infections - Characteristics Rhinovirus = most common pathogen <BR> Incubation = 1-10 days; onset of symptoms = 1-2 says after viral infection (peak 2-4 days); virus may remain 1 week after symptoms start
Upper Respiratory Infections - Decongestants Topical - Nasal Sprays - Oxymetazoline <BR> stimulate alpha andrenergic receptors, vasoconstriction <BR> <BR> Oral - pseudoephedrine (often combined w/ antihistamine) <BR> increase BP, HR; don't use w/ meds that increase serotonin
Upper Respiratory Infections - Expectorants Guaifenesin <BR> Increase output of respiratory tract fluid by decreasing adhesiveness and surface tension
Upper respiratory Infections - Antitussives Inhibit cough center in medulla <BR> non-narcotic and narcotic options <BR> Dextromethorphan (can cause hallucinations at high doses), codeine, hydrocodone
Upper Respiratory Infections - Anticholinergic Atrovent Nasal Spray <BR> Inhibits vagally mediated reflexes by antagonizing acetylcholine action, inhibits secretions from serous and seromucous glands
Upper Respiratory Infections - Antihistamines (H1 Receptor Blockers) competitive inhibition of histamine <BR> Non-sedating - peripheral H1 receptors (selective) <BR> Sedating - central and peripheral H1 receptors (non-selective)
Tuberculosis "Primary TB" - radiographicallly and clinically silent <BR> "Latent TB" - can lie dormant for years, can't transmit to others
Tuberculosis - Drugs Must use multiple drugs in treatment <BR> Isoniazid - bacteriocidal, hepatotoxic, causes B6 deficiency <BR> Rifampin - bacteriocidal, watch for hepatitis, bleeding problems, renal failure, turns pee orange
Tuberculosis - Drugs, continued Atrovent Nasal Spray <BR> Inhibits vagally mediated reflexes by antagonizing acetylcholine action, inhibits secretions from serous and seromucous glands
Created by: frolickinglizard
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