respiratory medicine

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.