COPD ppt.pptx

respiratory medicine

1. CHRONIC OBSTRUCTIVE PULMONARY DISEASE Dr. INDHUJA I YEAR M.D.,GEN.MEDICINE

2. OVERVIEW DEFINITION RISK FACTORS PATHOPHYSIOLOGY CLINICAL PRESENTATION History Physical findings Lab findings DIAGNOSIS DIFFERENTIAL DIAGNOSIS COMPLICATIONS EXACERBATION OF COPD TREATMENT Pharmacological therapy Non pharmacological therapy

3. DEFINITION Disease state characterized by airflow limitation that is not fully reversible.

4. RISK FACTORS

5. 1. CIGARETTE SMOKING Pack years dose response relation increases with advancing age. < 50 yrs: males > females >50 yrs: equal incidence. Only 15% variability in FEV Additional environmental and genetic factors.

6. Natural history : Severity of COPD depends on: - Intensity - Timing of exposure during growth. - Baseline lung function. Affects both large airways (cough & sputum), small airways & alveoli (physiological).

7. 2. PRIMARY RESPONSIVENESS: DUTCH hypothesis: Asthma and COPD are variations of same disease modulated by environmental and genetic factors. BRITISH hypothesis: Asthma and COPD are fundamentally different. Genetic predisposing factor: ADAM 33 & MMP12 (both asthma & COPD). Increased airway responsiveness = decreased pulmonary function.

8. 3. RESPIRATORY INFECTION : Needs to be proved. 4. OCCUPATIONAL EXPOSURE : Coaling, gold mining, cotton textile dust. Less important than the effect of smoking. 5.AMBIENT AIR POLLUTION: Biomass combustion 6. PASSIVE SMOKING: In utero smoking- reduced postnatal pulmonary functions. Exposure of children to maternal smoking – reduced lung growth.

9. 7 . GENETIC: Severe alpha 1 antitrypsin deficiency. M allele - Normal levels. S allele - Reduced Z allele - Severely reduced. Null allele – Absent enzyme levels. Most common form : piZZ & piZZ/null forms Homozygous piZZ + smoking = early onset copd. LAB: Immunologic levels of enzyme in serum Accompanying asthma & male gender worsens prognosis.

10. Rx : Alpha 1 AT augmentation. Heterozygous PiMZ : intermediate levels of enzyme. Others : Familial aggregation of airflow obstruction within families of COPD pts. Minor allele SNP of MMP12 : reduced expression of MMP12 - asthma & adult smoker. COPD loci : near HHIP gene on chr. 21 chr. 15 ( near NAD receptor)

11. PATHOPHYSIOLOGY

12. AIRFLOW OBSTRUCTION : Most typical finding : persistent reduction in forced expiratory flow rates . Increased residual volume, Residual Volume/TLC , V/P mismatch. Chronically reduced FEV1/FVC with no major improvement on inhaled bronchodilators. Differentiate from asthma Reduced max. expiratory flow rate Early - @ FRC. Advanced – entire breath

13. HYPERINFLATION: Air trapping- increased residual volume & residual volume / TLC Late progressive hyperinflation : increased TLC Flattened diaphragm. GAS EXCHANGE : Normal Pao2 – till FEV1 <50% of predicted Increased Paco2 Chronic hypoxemia Pao2<55 FEV1 < 25% Pulmonary hypertension Cor pulmonale/RVH

14. EMPHYSEMA PANACINAR : Non uniform ventilation and VP mismatch - Acini - Alpha 1 antitrypsin deficiency CENTRIACINAR : - Smoking - Respiratory bronchioles(focal) - Upper lobes & superior segments of lower lobes.

15. PARASEPTAL: -Distal acinus near pleura - Spontaneous pneumothorax. IRREGULAR : -Any type of involvement. SPECIAL VARIETIES : COMPENSATORY : -In response to damage occurring in same or opposite lungs. MEDIASTINAL : -Escape of air rapidly into mediastinum following rupture of overdistended alveoli. -Seen in severe bronchial asthma,rupture of oesophagus , emphysematous bullae rupture.

16. CHRONIC BRONCHITIS : Cough & sputum occur on most days for at least 3 consecutive months for at least 2 successive years. PINK PUFFERS: Thin, breathlessness , normal PaCO2 till late stages. BLUE BLOATERS: Early hypercapnoea, oedema, secondary polycythemia.

17. PATHOGENESIS Elastase – antielastase hypothesis Inflammation & extra cellular matrix proteolysis Cell death Ineffective repair

18. CLINICAL PRESENTATION

19. HISTORY Most common symptoms are: -Cough : Nocturnal, productive, prolonged, paroxysmal -Sputum production : Early morning, mucoid -Exertional dyspnoea Symptoms are seen mainly prior to acute exacerbation.

20. PHYSICAL EXAMINATION Early stages- normal Evidence of smoking - nicotine stained nails, odour Increased expiratory phase/ expiratory wheeze Signs of hyperinflation : barrel chest(1:1) lung volumes, poor diaphragmatic excursion, acc. Muscles of respiration used, cyanosis, sits in tripod fashion

21. Advanced : Systemic wasting, significant wt loss, bitemporal wasting, diffuse loss of adipose tiisue, Hoovers sign, high Reid index. Cor pulmonale Clubbing is not associated with COPD.

22. LABORATORY FINDINGS

23. Hallmark : airflow obstruction Reduced FEV1(<80%) & reduced FEV1/FVC(<70%) Increased TLC, FRC, Residual volume. Emphysema : Reduced DLCo2 ABG & oximetry : symptoms of exacerabation Increased hematocrit & signs of RVH – chronic hypoxemia

24. GOLD CRITERIA FOR COPD SEVERITY

25. BODE INDEX VARIABLE 1 2 3 FEV1 >=65 50-64 36-49 <=35 DISTANCE WALKED IN 6 MIN (m) >=350 250-349 150-249 <=149 MMRC DYSPNOEA SCALE 0-1 2 3 4 BODY MASS INDEX >21 <=21

26. RADIOLOGY

27. Chest XRAY -Bullae -Paucity of parenchymal markings -Hyperlucency -Tubular heart -Low flat diaphragm

28. CT : Quantification of emphysema Sensitive in detecting bullae. Definitive test. Used in surgical therapy

29. ECG IN COPD Chou’s ECG criteria for COPD P-pulmonale P wave axis ≥ +80° QRS amplitude less than 5 mm in all limb leads QRS axis > +90° QRS amplitude less than 5 mm in V5, V6 S1-S2-S3 pattern with R/S <1  in lead I, II, III Atrial arrhythmias (especially Multifocal Atrial Tachycardia or MAT)

30. Schamroth’s Sign Criteria for COPD:  Isoelectric P wave in lead I Very small QRS complex of less than 1.5 mm total deflection T wave of less than 0.5 mm in lead I

31. OTHERS Alpha 1 antitrypsin measurement – recent advancement When reduced , determine type of protease inhibitor. Isoelectric focusing of serum is done. Molecular genotypes of DNA

32. DIFFERENTIAL DIAGNOSIS ASTHMA : Early age of onset, presence of atopy, lack of smoking history, variability of symptoms over time, highly reversible airflow obstruction, worm like sputum with casts. BRONCHIECTASIS : Fetid sputum, differentiate by CT. BRONCHIOLITIS OBLITERANS

33. EXACERBATIONS OF COPD

34. Episodes of severe dyspnoea and cough with change in amount and character of sputum . Increased ratio of diameter of pulmonary artery to aorta on chest ct - increased r/o COPD. Cause : infections. Bacterial – S.pneumoniae, H.influenza, M.catarrhalis, Viral Assess severity of preexisting disease & recent exacerbation.

35. COMPLICATIONS Pneumothorax Respiratory failure Cor pulmonale Polycythemia

36. TREATMENT

37. STABLE PHASE Smoking cessation Oxygen therapy Lung volume reduction surgery

38. PHARMACOTHERAPY

39. Smoking cessation : Bupropion Nicotine replacement Rx Varenicline – nicotinic acid receptor agonist- antagonist Recomm : For all adult non pregnant smokers considering quitting , in the absence of any contraindication, pharmacotherapy is advised.

40. 2. BRONCHODILATORS : Inhaled route preferred due to reduced side effects. 3 . ANTICHOLINERGICS : Ipratropium bromide – acute improvement of symptoms and FEV1 Tiotropium reduces exacerbation Both do not affect rate of decline of FEV1 Reduced mortality rate in tiotropium treatment but statistically insignificant

41. 4. BETA AGONISTS : Symptomatic benefit S/E : tremor & tachycardia LABA preferred over SA drugs Beta agonist + inhaled anticholinergic Incremental benefit LABA without concomitant inhaled steroids Increased r/o death.

42. 5. INHALED GLUCOCORTICOID : Regular use – doubtful improvement in rate of decline of lung function Increased r/o oropharyngeal candidiasis Reduce exacerbation frequency by 25 % 6 . ORAL GLUCOCORTICOID : Chronic use c/i due to adverse risk/benefit ratio. SIDE EFFECTS Weight gain Osteoporosis, Glucose intolerance Infection

43. 7. THEOPHYLLINE : Modest improvement in expiratory flow rate & VC Slight improvement in O2 & CO2 levels most common side effect- tachycardia, tremor. Therapeutic drug monitoring to reduce toxicity Selective PDE4 inhibitor Roflumilast – reduces exacerbation frequency. 8. ANTIBIOTICS : RCT with azithromycin daily in pts with exacerbation in past 6 months has reduced its frequency

44. 9.SUPPLEMENTAL OXYGEN : Reduced mortality in pts with resting hypoxemia & signs of pulmonary HT/ RV failure Mortality benefit = no. of hours/ day O2 used Used in exertional/ nocturnal hypoxemia. 10. OTHER AGENTS : NAC – mucolytic & anti oxidant IV alpha1 AT augmentation therapy if serum levels < 11 microns PiZ HBV vaccination prior to augmentation therapy

45. NON PHARMACOLOGIC THERAPY

46. 1 .GENERAL MEDICAL CARE : Annual influenza vaccine Polyvalent pneumococcal vaccine Bordetella pertussis vaccine 2 . PULMONARY REHABILITATION : Education & cardiovascular conditioning Reduced rate of hospitalization over 6-12 months

47. 3. LUNG VOLUME REDUCTION SURGERY C/I in significant pleural disease -Pulmonary artery systolic pressure > 45 mmhg - Ccf, FEV1 20 % of predicted -Diffusely distributed emphysema in CT Reduced mortality rates & symptomatic benefit. Prognosis – anatomic distribution of emphysema & post rehab exercise capacity Benefits in upper lobe predominant emphysema & low post rehab exercise capacity

48. 4 . LUNG TRANSPLANTAION : 2 nd leading indication – COPD Severe disability despite maximal medical treatment Free of comorbid conditions

49. TREATMENT OF EXACERBATION 1.Bronchodilators- Inhaled SABA+anticholinergics methylxanthines. 2.Antibiotics – According to susceptibility Moderate to severe infections. 3.Glucocorticoids – 30 -40 mg of oral prednisolone or its equivalent for 10- 14 days reduces relapse upto 6 months S/E : hyperglycemia in DM patients 4. Supplemental O2 till spO2 levels >90%

50. 5 . Mechanical ventilatory support : NIPPV in PaCO2>45 mmhg (respiratory failure ) reduces mortality rates. C/I : CVS instability, impaired mental status, craniofacial deformity, extreme obesity, burns & copious secretions. Invasive ventilation with ET tube – severe resp. distress Sufficient expiratory time in pts with severe airflow obstruction & presence of auto PEEP. Mortality rates : 17 – 30% & 60% in >65 yrs

51. PROGNOSIS Main prognostic factor : Degree of airway obstruction Directly proportional to post bronchodilator FEV. Inversely related to the age of the patient. BODE INDEX : Better predictor of mortality. Other factors : Degree of weight loss pulmonary hypertension .

52. REFERENCES HARRISON’S PRINCIPLES OF INTERNAL MEDICINE 18 th edition. DAVIDSON’S PRINCIPLES & PRACTICE OF MEDICINE 21 st edition GOLDMAN & CECIL MEDICINE 25 th edition.

53. THANK YOU