Chronic Obstructive Pulmonary Disease (Copd)


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  • Asthma just might pave the way for the development of chronic obstructive pulmonary disease (COPD), a much more serious lung condition.As a matter of fact, people with asthma are 12.5 times more likely to develop COPD later in life
  • Currently, three medications have been approved for smoking cessation: nicotine, bupropion, and varenicline.Nicotine replacement medications include 2- and 4-mg nicotine polacrilex gum, transdermal nicotine patches, nicotine nasal spray, the nicotine inhaler, and nicotine lozenges. All seem to have comparable efficacy but, in a randomized study, compliance was greatest for the patch, lower for gum, and very low for the spray and the inhaler.[93] A smoker should be instructed to quit smoking entirely before beginning nicotine replacement therapies.Optimal use of nicotine gum includes instructions to chew slowly, to chew 8 to 10 pieces/day for 20 to 30 minutes each, and to continue long enough for the smoker to learn a lifestyle without cigarettes, usually 3 months or longer. Side effects of nicotine gum are primarily local and can include jaw fatigue, sore mouth and throat, upset stomach, and hiccups.Several different transdermal nicotine preparations are marketed—three deliver 21 or 22 mg over a 24-hour period, and one delivers 15 mg over a period of 16 hours. Most brands have lower-dose patches for tapering. Patches are applied in the morning and removed either the next morning or at bedtime, depending on the patch. Patches intended for 24-hour use can also be removed at bedtime if the patient is experiencing insomnia or disturbing dreams. Full-dose patches are recommended for most smokers for the first 1 to 3 months, followed by one to two tapering doses for 2 to 4 weeks each. Nicotine nasal spray, one spray into each nostril, delivers about 0.5 mg nicotine systemically and can be used every 30 to 60 minutes. Local irritation of the nose commonly produces burning, sneezing, and watery eyes during initial treatment, but tolerance develops to these effects in 1 to 2 days. The nicotine inhaler actually delivers nicotine to the throat and upper airway, from where it is absorbed similarly to nicotine from gum. It is marketed as a cigarette-like plastic device and can be used ad libitum.Most recently, nicotine lozenges have been marketed over the counter. The lozenges are available in 2- and 4-mg strengths and are to be placed in the buccal cavity where they are slowly absorbed over 30 minutes.[94] Smokers are instructed to choose their dose according to how long after awakening in the morning they smoked their first cigarette (a measure of the level of dependence). Those who smoke within 30 minutes are advised to use the 4-mg lozenge, whereas those who smoke their first cigarette at 30 or more minutes are advised to use the 2-mg lozenges. Use is recommended every 1 to 2 hours.Nicotine medications seem to be safe in patients with cardiovascular disease and should be offered to them.[95–98] Although smoking-cessation medications are recommended by the manufacturer for relatively short-term use (generally 3–6 mo), the use of these medications for 6 months or longer is safe and may be helpful in smokers who fear relapse without medications.
  • Bupropion sustained release, a dopamine-norepinephrine reuptake inhibitor that also has nicotinic cholinergic receptor antagonist activity, was originally marketed and is still widely used as an antidepressant. Bupropion was found to aid smoking cessation independent of whether a smoker was depressed or not.[99] Hurt and coworkers[99] demonstrated that with a 300-mg sustained-release dose, 44% of patients quit at 7 weeks versus 19% of controls. n additional randomized, placebo-controlled trial demonstrated that the combination of bupropion with a nicotine patch is safe, and that bupropion alone or in combination was as effective or more effective than the patch alone.Bupropion in excessive doses can cause seizures and should not be used in an individual with a history of seizures or with eating disorders (bulemia or anorexia).Varenicline, available by prescription only, is a nicotinic receptor partial agonist that selectively binds to α4β2 nicotinic cholinergic receptors in the brain.[102] This receptor mediates dopamine release and is thought to be the major receptor involved in nicotine addiction. A partial agonist means that the drug both activates the receptor and blocks the effects of other agonists on the receptor. Varenicline activates the α4β2 nicotinic cholinergic receptor with a maximal effect about 50% that of nicotine and, at the same time, blocks effects of nicotine from tobacco use on the receptor. As a consequence of the receptor stimulation, nicotine withdrawal symptoms are relieved, and as a consequence of receptor blockade, the rewarding effects of smoking are diminished. The latter effect reduces the desire to smoke and, in the case of a lapse, may prevent continued smoking.Varenicline's mechanism of action. (A) Nicotine from cigarettes stimulates the production of high levels of dopamine in terminal synapse in the nucleus accumbens. (B) No nicotine present, which induces a state of nicotine withdrawal. (C) Varenicline blocks the nicotine-receptor sites and partially agonizes the receptors, stimulating moderate levels of dopamine in the terminal synapse in the nucleus accumbens.
  • Doses & Administrations: AVIAN FLU & INFLUENZA:ADULT DOSE:MILD CASES : 75 mg bid x 5 daysSEVERE CASE: 150 mg bid x 7-10 daysPROPHYLAXIS: 75 mg QD x 7-10 days for avian flu and up to 6weeks for influenzaAdverse Effects: Nausea, vomiting, insomnia, bronchitis
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  • Has no direct effect on lung function or gas exchange. Optimizes other body systems so that the impact of poor lung function is minimized.
  • Replacement therapy consists of giving a concentrated form of AAT that is derived from human plasma. It raises the AAT level in the bloodstream. Once you start replacement therapy, however, you must undergo treatment for life. This is because if you stop, your lungs will return to their previous level of dysfunction and the neutrophil elastase will again start to destroy your lung tissue.
  • An episode of coughing soon after inhalation of the drug was observed in about a quarter of clinical trial participants during at least 20% of visits to study clinics. According to the labeling, the cough generally occurred within 15 seconds after inhaling 75 µg of indacaterol, lasted no more than 15 seconds, and was not associated with bronchospasm, COPD exacerbation or deterioriation, or reduced drug efficacy
  • Chronic Obstructive Pulmonary Disease (Copd)

    1. 1. Chronic Obstructive Pulmonary Disease (COPD) Nadia Ghulam Hussain & Nida Fatima Trainee Pharmacists AKUH, Karachi
    2. 2. Contents• Definition• Epidemiology• Risk factors• Pathophysiology• Diagnosis• Management• Devices• References
    3. 3. COPD• Also known as COLD (Chronic Obstructive Lung Disease ) COAD (Chronic Obstructive Airway Disease) Smoker’s lung CAL (Chronic Airflow Limitation) CORD (Chronic Obstructive Respiratory Disease)
    4. 4. DefinitionChronic obstructive pulmonary disease(COPD) is a preventable and treatable diseasecharacterized by airflow limitation that isprogressive, not fully reversible andassociated with an abnormal inflammatoryresponse of the lungs.
    5. 5. Chronic Bronchitis• Chronic bronchitis is a chronic inflammatory condition in the lungs• It causes a cough that often brings up mucus, as well as shortness of breath,wheezing, and chest tightness
    6. 6. Emphysema• In emphysema, there is over-inflation of the air sacs (alveoli) in the lungs, causing a decrease in lung function, and often, breathlessness. It involves destruction of the lungs.
    7. 7. Epidemiology• More common in older people, especially those >65 years.• Fifth leading cause of death and disability worldwide.• Death rates for males and females are roughly equivalent.• COPD mortality has also increased compared with heart and cerebrovascular disease over the same period.
    8. 8. Risk Factors Exposures Host FactorsEnvironmental tobacco Genetic predisposition smoke (AAT deficiency)Occupational dusts and Airway chemicals hyperresponsiveness Air pollution Impaired lung growth
    9. 9. Risk Factors• Exposures: – Cigarette smoking (tobacco exposure) accounts for 85% to 90% of cases of COPD. – Air pollution and occupational exposures result in inflammation and cell injury which leads to COPD.
    10. 10. Host Factors• Host factor refers to the traits of an individual person that affect susceptibility to disease. – AAT deficiency accounts for less than 1% of COPD cases. – Airway hyperresponsiveness due to various inhaled particles may cause an accelerated decline in lung function. – Impaired lung growth due to low birth weight, prematurity at birth, or childhood illnesses.
    11. 11. Pathophysiology of COPD1. Airway inflammation2. Structural changes3. Mucociliary dysfunction- Chronic inflammatory cascade for COPD
    12. 12. Diagnosis1. Clinical presentation: – History – Physical examination2. Diagnostic testing: – Pulmonary function testing – Laboratories – Imaging
    13. 13. Clinical Presentation Physical History Examination - Cyanosis of mucosal- Symptoms: Cough, membranesdyspnea, sputum, - Barrel chestwheezing - Increased resting- Smoking history, respiratory rateenvironmental and - Shallow breathingoccupational risk - Pursed lips duringfactors expiration - Use of accessory respiratory muscles
    14. 14. Diagnostic Testing• Pulmonary function testing or Spirometry – Comprehensive assessment of lung volumes and capacities – Performed in all patients suspected of COPD – FEV1 defines the severity of expiratory airflow obstruction and is a predictor of mortality• Bronchodilator reversibility: – A large increase in post- bronchodilator FEV1 supports the diagnosis of asthma
    15. 15. Diagnostic Testing• Laboratories: – ABG Monitoring: • Done for patients with severe COPD, respiratory failure or a severe exacerbation – ATT levels (1.5 - 3.5 gram / liter): • Measured in young patients who develop COPD and have a strong family history. • A serum value <15–20% of the normal limits is highly suggestive of α1-antitrypsin deficiency.
    16. 16. Diagnostic Testing• Imaging: – Chest radiographs • Not sensitive for the diagnosis of COPD • Helpful in excluding other diseases (pneumonia, cancer, congestive heart failure, pleural effusion & pneumothorax) – Chest CT • For patients with severe COPD for lung volume reduction surgery (LVRS) & lung transplantation.
    17. 17. COPD Management• Goals of COPD Management: – To relieve symptoms – To improve quality of life – To decrease the frequency & severity of acute attacks – To slow the progression of disease – To prolong survival
    18. 18. COPD ManagementNonpharmacologic Pharmacologic Treatment Treatment Smoking cessation Corticosteroids Immunization Bronchodilators Long term oxygen AAT Replacement therapy therapy Pulmonary rehabilitation
    19. 19. Smoking Cessation• Only proven intervention to affect long term decline in FEV1 & slow the progression of COPD – Nicotine replacement therapy • Transdermal patch • Chewing gum • Inhaler • Nasal spray • Lozenges – Non-nicotine pharmacotherapy • Bupropion • Varenicline
    20. 20. Smoking Cessation Product Side effects/PrecautionsNicotine replacement therapy Headache, insomnia, nightmares, nausea, dizziness, blurred visionBupropion Headache, insomnia, nausea, dizziness, xerostomia, hypertension, seizure. Avoid monoamine oxidase inhibitorsVarenicline Nausea, vomiting, headache, insomnia, abnormal dreams Worsening of underlying psychiatric illness
    21. 21. Immunization• Influenza vaccination – Reduces the incidence of influenza-related acute respiratory illness in COPD patients – Patients with serious allergy to eggs should not be given this vaccine. – Brand available: Fluarix® – An oral antiinfluenza agent (Oseltamivir) can be given to such patients but its less effective and causes more side effects. – Available brand: Tamiflu®
    22. 22. Immunization• Polyvalent pnuemococcal vaccine – Recommended for all COPD patients • 65 years and older • Less than 65 years only if the FEV1 is less than 40% predicted. – Dosage: 0.5ml IM – Available brand: Pneumovax® (0.5ml pre-filled syringes)
    23. 23. Long-term Oxygen Therapy• Should be started if – Resting PaO2 is less than 55 mm Hg – Evidence of right-sided heart failure, polycythemia, or impaired neuropsychiatric function with a PaO2 of less than 60 mm Hg
    24. 24. Pulmonary Rehabilitation• Improves symptoms and quality of life• Reduces frequency of exacerbations• Components include: – Exercise training – Nutritional counselling – Psychosocial support
    25. 25. Pharmacologic Treatment 2-agonists Long-acting Anticholinergics MethylxanthinesBronchodilators 2-agonists Short-acting Anticholinergics
    26. 26. Short-acting 2-agonists • Stimulate adenyl cyclase to increase the formation of cAMP MOA which causes bronchodilation. • Improve mucociliary clearanceDuration of action • 4 to 6 hours Selective 2- • Albuterol (Ventolin®), agonists levalbuterol, pirbuterolLess selective 2- • Metaproterenol, isoetharine, agonists isoproterenol, epinephrine
    27. 27. Short-acting Anticholinergics • Competitively inhibit cholinergic receptors in bronchial smooth muscle, block Ach, with the net MOA effect of reduction in cGMP, which normally constrict bronchial smooth muscle.Duration of • 4 to 6 hours, slower onset of action in comparison to - action agonists • Ipratropium (Atrovent®,Examples Atem®) • Atropine
    28. 28. Long-acting 2-agonists • Same as that of short-acting MOA 2-agonistsDuration • 12 hoursof action • Salmeterol (Serevent®)Examples • Formoterol • Arformoterol
    29. 29. Long-acting Anticholinergics • Same as that of short-acting MOA anticholinergicsDuration • Cause bronchodilation within 30 minutes, which persists for 24 hours,of action allowing once daily dosingExample • Tiotropium
    30. 30. Combination Anticholinergics & 2- agonists• Combining bronchodilators with different MOA allows reduced doses to be administored, reducing side effects.• Albuterol and Ipratropium available as an MDI Combivent®
    31. 31. Methylxanthines • Produce bronchodilation by: MOA • Inhibition of PDE, increasing cAMP levels • Inhibition of calcium ion influx into smooth muscle • Prostaglandin antagonism • Stimulation of endogenous catecholamines • Inhibition of release of mediators from mast cells and leukocytes Therapeutic • 8-12 mcg/mlSerum Levels
    32. 32. Methylxanthines• Minor side effects: – dyspepsia, nausea, vomiting, diarrhea, headache, dizziness, tachycardia• Serious toxic effects: – arrhythmias and seizures• Considered in patients who donot respond well to bronchodilators
    33. 33. Corticosteroids• Mechanism of Action – Reduction in capillary permeability to decrease mucus – Inhibition of release of proteolytic enzymes from leukocytes – Inhibition of prostaglandins• ICS: Beclomethasone (Bekson, Clenil-A, Clenil Forte, Rinoclenil), flunisolide, budesonide, fluticasone, mometasone• Systemic CS: Prednisolone (Deltacortil), Methylprednisolone, Prednisone
    34. 34. Corticosteroids• Inhaled CS – Considered for symptomatic stage III or IV disease who experience repeated exacerbation despite bronchodilator therapy• Systemic CS – Short term use for acute exacerbations – Not used in chronic management because of high risk of toxicity
    35. 35. Combination ICS & Bronchodilators• Effective in reducing the rate of COPD exacerbations• Reduces the number of total inhalations needed, more patient compliance• Available combination: – Beclomethasone with salbutamol (Clenil Compositum®) – Budesonide with formeterol – Fluticasone with salmeterol
    36. 36. AAT Replacement Therapy• Considered for patients with AAT deficiency• Life time treatment• Therapy consists of giving a concentrated form of AAT, derived from human plasma.• The recommended dosing regimen for replacing AAT is 60 mg/kg administered IV once a week.
    37. 37. Indacaterol• Indacaterol is an ultra-long-acting beta- adrenoceptor agonist• Approved by FDA on July 1, 2011• Requires once daily dosing, unlike other long- acting• In clinical trials, the most common adverse events were runny nose, cough, sore throat, headache, and nausea.• Recommended dose is one capsule (75mcg) per day. Overview of Management
    38. 38. Devices used in COPD• Inhalers• Small, handheld devices that deliver a puff of medicine into the airways.• Metered-dose inhalers (MDIs)• Dry powder inhalers (DPIs) or breath activated inhalers• Inhalers with spacer devices
    39. 39. Metered-dose Inhalers• Contains a liquid medication delivered as an aerosol spray.• Quick to use, small, and convenient to carry.• Needs good co- ordination to press the canister, and breathe in fully at the same time
    40. 40. Breath-activated inhalers or DPI• It releases a puff of dry powder instead of a liquid mist• Require less co- ordination than the standard MDI.• Slightly bigger than the standard MDI.• Example: Rotahaler
    41. 41. Inhalers with spacer devices• Spacer devices are used with pressurised MDIs• The spacer between the inhaler and the mouth holds the drug like a reservoir when the inhaler is pressed.
    42. 42. Nebulizers• Nebulisers are machines that turn the liquid medicines into a fine mist, like an aerosol.• Useful in people who are very breathless e.g. In severe attack of COPD• They are not portable
    43. 43. References• BMJ Best Practices• American Thoracic Society COPD guidelines• The Washington’s manual of medical therapeutics• Pharmacotherapy : A pathophysiologic approach, Joseph T. DiPiro• Respiratory care pharmacology, Rau, Joseph