This document provides an overview of chronic obstructive pulmonary disease (COPD), including its definition, risk factors, pathophysiology, clinical presentation, diagnosis, complications, and treatment. COPD is characterized by persistent airflow limitation that is usually progressive. The major risk factor is cigarette smoking. Clinical features include cough, sputum production, and exertional dyspnea. Diagnosis is confirmed by spirometry showing reduced FEV1/FVC ratio. Treatment involves smoking cessation, bronchodilators, inhaled corticosteroids, pulmonary rehabilitation, oxygen therapy, and management of exacerbations with bronchodilators and antibiotics.

1. 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).

8. 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.

9. 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.

10. 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.

11. 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)

12. PATHOPHYSIOLOGY

13. 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

14. 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

15. 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.

16. 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.

17. 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.

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

19. CLINICAL
PRESENTATION

20. 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.

21. 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

22.  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.

23. LABORATORY FINDINGS

24. 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

25. GOLD CRITERIA FOR
COPD SEVERITY

26. BODE INDEX
VARIABLE 0 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

27. RADIOLOGY

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

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

30. 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)

31. 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

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

33. 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

35. EXACERBATIONS OF COPD

36.  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.

37. COMPLICATIONS
Pneumothorax
Respiratory failure
Cor pulmonale
Polycythemia

38. TREATMENT

39. STABLE PHASE
Smoking cessation
Oxygen therapy
Lung volume reduction
surgery

41. PHARMACOTHERAPY

42. 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.

43. 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

44. 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.

45. 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

46. 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

47. 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

48. NON PHARMACOLOGIC
THERAPY

49. 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

50. 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

52. 4 . LUNG
TRANSPLANTAION :
 2nd leading indication – COPD
Severe disability despite maximal
medical treatment
Free of comorbid conditions

53. 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%

54. 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

55. 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.

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