COPD by Vineela N.


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COPD by Vineela N.

  2. 2. *Definition *Types of COPD *Epidemiology *Etiology *Signs and Symptoms *Pathophysiology *Diagnosis *Precautions *Treatment or Management Contents of the seminar:
  3. 3. Definition COPD: Chronic Obstructive Pulmonary Disease (COPD) can be defined as a disease characterized by progressive airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
  4. 4. Types of COPD: Chronic Bhronchitis Emphysema
  5. 5. Chronic Bhronchitis: It is associated with chronic or recurrent excess mucus secretion into the bronchial tree with cough that occurs on most days for at least 3 months of the year for at least 2 consecutive years when other causes of cough have been excluded.
  6. 6. Chronic Bronchitis
  7. 7. Emphysema: Emphysema is defined as abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls, but without obvious fibrosis.
  8. 8. Epidemiology of COPD o Chronic Obstructive Pulmonary Disease (COPD) kills more than 3 million people every year, making it the 4th largest cause of death in the world. o It has been estimated that by the year 2030, COPD will become the third biggest cause of death. o According to the World Health Organisation, COPD kills more people than HIV-AIDS, Malaria and Tuberculosis all put together in the South East Asian region.
  9. 9. Etiology of COPD COPD might be caused from a rare genetic disorder known as alpha 1 antitrypsin deficiency, which results in the missing protein alpha 1 antitrypsin.
  10. 10. Signs and Symptoms of COPD:  Chronic cough with sputum  Cyanosis of mucosal membranes  Barrel chest  Increased resting respiratory rate  Use of accessory respiratory muscles severe  Shallow breathing  Pursing of the lips during expiration  Worsening dyspnea  Chest tightness  Malaise Exacerbation  Fatigue  Decreased exercise tolerance
  11. 11. Pathophysiology of COPD There are 2 different mechanisms in the pathogenesis of COPD • Activation of WBC’s. • Activation of Oxidative stress.
  12. 12. Etiologic factors like tobacco smoke, noxious gases,etc activates neutrophils, macrophages and CD8+ lymphocytes causes release of chemical mediators like TNFα, IL-8, LTB4 leads to destructive changes in the airways, Pulmonary vasculature and lung parenchyma Activation of WBC’s:
  13. 13. Activation of oxidative stress: Here an imbalance between aggressive and protective defense system in lungs Increased oxidants generated by cigarette smoke reacts and damages various proteins and lipids Leading to cell and tissue damage Oxidants also promote inflammation directly and inhibits anti-protease activity Leads to protease-antiprotease imbalance
  14. 14. • Antiprotease has protective activity • Antiprotease inhibits several protease enzymes like neutrophil elastase • Protease enzymes like elastase attacks elastin of alveolar walls and causes its damage. • Hereditary deficiency of AAT causes increased risk of premature emphysema • In emphysema from cigarette smoking, there will be increased protease activity and decreased anti-protease activity. • Activated inflammatory cells releases some proteases like cathepsins and metalloproteinase(MMPs). • An inflammatory exudate is present in airways increases the number and size of goblet cells. • Mucus secretion will increase, thickening of smooth muscles and connective tissue in airways and decreases ciliary motility.
  15. 15. • Parenchymal changes affects the gas-exchanging units of lungs. • Smoking causes centrilobular emphysema. • AAT deficiency causes panlobular emphysema.
  16. 16. Diagnosis  By patients symptoms and history of exposure to risk factors like tobacco smoke and occupational exposures.  Pulmonary Function Tests (Spirometry) • In COPD, FEV1 and FVC will decrease. • FEV1/FVC ratio to less than 70% • An improvement in FEV1 of less than 12% after inhalation of a rapid-acting bronchodilator is an evidence of irreversible airflow obstruction.  Arterial Blood Gases(ABG) • Until the FEV1 is less than 1L, there wont be significant changes in arterial blood gases. • When FEV1<1, then hypoxemia and hypercapnia occurs. • In severe COPD, there will be low arterial oxygen tension(Pao2=45- 60mmHg) and high arterial carbondioxide tension(Paco2=50-60mmHg)
  17. 17.  Chest X-ray Abnormal chest X-ray findings are usually not seen until COPD is severe. In this case, the X-ray may show: • Flattening of the diaphragm, the large muscle that separates the lungs and heart from the abdominal cavity. • Increased size of the chest, as measured from front to back. • A long narrow heart. • Abnormal air collections within the lung (focal bullae). A normal chest X-ray does not mean you do not have COPD. It may be most useful for ruling out other conditions that might be causing your breathing problems, such as lung cancer, heart failure, pneumonia, or tuberculosis.
  18. 18.  Sputum culture test: A sputum culture is a test to detect and identify bacteria or fungi (plural of fungus) that are infecting the lungs or breathing passages. A sample of sputum is placed in a container with substances that promote the growth of bacteria or fungi. If no bacteria or fungi grow, the culture is negative. If organisms that can cause infection (pathogenic organisms) grow, the culture is positive. • Colour • Odour (smell) • Thickness
  19. 19. Treatment  Pharmcological treatment  Sympathomimetics  Anticholinergics  Combination of sympathomimetics and anticholinergics  Methylxanthines  Corticosteroids
  20. 20.  Sympathomimetics: (ß2 selective agonists) Short acting: albuterol, levalbuterol, bitolterol, pirbuterol, terbutaline Long acting: Formoterol, Salmeterol Mode of action: Stimulates enzyme adenyl cyclase –› increases the formaton of cAMP –› Vasodilation of bronchials. Dose: Levalbuterol: ORAL INHALATION, 1.25 to 2.5 mg every 20 min for 3 doses, then 1.25 to 5 mg every 1-4 hr as needed. Route of administration: Inhalation DI: ß blockers and monoamine oxidase inhibitors. ADR’s: Rash, Diarrhea, Feeling nervous, Tremor, Asthma, Rhinitis, Viral disease, Accidental injury, Fever, Viral disease, Electrocardiogram abnormal, Hypertension, Syncope, Tachycardia, Metabolic acidosis Anaphylaxis, Paradoxical bronchospasm
  21. 21.  Anticholinergics: Short acting: Ipratropium bromide Long acting: Tiotropium bromide Mode of action : Blocks cholinergic receptors present on bronchial smooth muscles –› inhibits acetylcholine action (bronchoconstriction) –› leading to bronchodilation. Dose : Ipratropium bromide: (inhalation solution 0.02%) 500 mcg NEBULIZED 3 to 4 times per day; separate doses by 6 to 8 hours. DI : betel nut and belladonna ADR’s : Abnormal taste in mouth, Bitter, Xerostomia, Bronchitis Nasal mucosa dry, Sinusitis, Death, Myocardial infarction, Anaphylaxis, Immune hypersensitivity reaction, Cerebrovascular accident, Bronchospasm.
  22. 22.  Combination of anticholinergics and sympathomimetics:  Combination of bronchodilators of different MOA will decrease the effective dose and adverse effects.  Combination of short and long ß2 agonists with ipratropium has added symptomatic relief and improved pulmonary function.  A combination of albuterol and ipratropium is used for chronic maintenance of COPD.
  23. 23.  Methylxanthines: • Theophylline and Aminophylline Mode of action: These drugs causes bronchodilation by • Inhibition of Phosophodiesterase • Inhibition of calcium ion influx into smooth muscle • Prostaglandin antagonism • Stimulation of endogenous catecholamines • Adenosine receptor antagonism • Inhibition of release of mediators from mast cells and leukocytes Dose: DI: erythromycin, ciprofloxacin, enoxacin, cimetidine, thiabendazole. ADR’s: dyspepsia, nausea, vomiting, diarrhea, headache, dizziness and tachycardia, arrhythmias and seizures.
  24. 24. • Chronic Theophylline use in COPD improves lung function like vital capacity and FEV1 . • Theophylline is used in patients, who are intolerant inhaled bronchodilators. • If the patient does not achieve the optimal clinical response with ß2 agonists and anticholinergics, then methylxanthines are added to the regimn. • Factors that decrease theophylline clearance (increased serum conc.)are viral/bacterial pneumonia, heart failure, liver dysfunction. • Factors that increase theophylline clearance (decreased serum conc.) are tobacco, marijuana smoking, hyperthyroidism.
  25. 25.  Corticosteroids: Mode of action: • Reduction in capillary permeability to decrease mucus • Inhibition of release of proteolytic enzymes from leukocytes • Inhibition of prostaglandins Dose: DI: ADR’s: hoarseness, sore throat, oral candidiasis, skin bruising, adrenal suppression, osteoporosis and cataract.
  26. 26.  Non-Pharmacological treatment: • Quit smoking • When Working in a hazardous environment, wear a respirator mask, use air filters at work place. • Treating asthma effectively • Avoid exposure to cold climate. • Drink plenty of fluids. drink at least 6 to 8 eight-ounce glasses of non-caffeinated beverages, fresh fruits, vegetables, meat, poultry, seafood,etc.. each day to keep mucus thin and easier to cough up. • Avoid overeating and foods that cause gas or bloating