Obstructive lung disease

Obstructive lung disease-asthma-copd

1. Obstructive Pulmonary Disease-
Bronchiectasis/ COPD/ Asthma
By: Darayus P.Gazder (DPG)

2. Bronchiectasis
It is characterized by chronic permanent dilation and
destruction of bronchi due to destructive changes in
elastic and muscular layers of bronchial walls that
may be diffuse or localized resulting in impairment of
drainage of bronchial secretions. Accumulation of
secretions leads to infection
In Pakistan pulmonary TB is the major cause!!

3. Etiology
Congenital
1.Cystic fibrosis
2.Immotile cilia syndrome
3.Kartagener’s syndrome
Acquired: Children
1.Pneumonia
2.Pulmonary Tb
3.Inhaled FB
Acquired adults
1.Pneumonia
2.Pulmonary Tb
3.Bronchial Tumours

4. Bronchiectasis: Clinical
Clinical:
Cough (90 %): Chronic productive cough,There is also
halitosis
Daily sputum production (76%): Sputum is purulent,
more in the mornings
Dyspnea (72%)
Hemoptysis (56%): Slight, massive or recurrent
On Examination:
Weight loss, anorexia, clubbing of fingers/
Auscultation: Coarse crepitation's will be heard over
the affected areas, commonly at lung bases

5. Investigations:
Sputum: C/S:
May reveal S.Aureus, Pseudomonas Aeruginosa, Aspergillus
AFB:
Mycobacterium tuberculosis
Assessment of ciliary function:
It’s the time taken for a small pellet of saccharin placed in the
anterior chamber of the nose to reach the pharynx when the
patient can taste it, it should not exceed 20 minutes.
Electron microscopy:
To check cilia
X-ray Chest:
May be normal or may show dilated bronchi with thickened
bronchial walls and sometimes multiple cysts containing fluid.

6. h
White Arrow: Thin-walled, cystic
structures in right lower lobe
Yellow arrow: Air fluid levels

7. High resolution CT scan
High sensitivity and specificity
Train track sign:
the bronchial wall is thickened and visible; the bronchi
lose the trend of narrowing from proximal to distal
end
Diamond ring sign:
Dilated bronchi appear as ring structures.

9. Bronchoscopy
Evaluating the airways for lesions
Assessing the cause of hemoptysis
Localizing the source of hemoptysis

10. Treatment
Medical management:
1.Bronchodilators
2.Postural drainage
3.Antibiotic therapy: Depending on C/S
Surgical Management
1.When its unilateral, confined to a lobe or segment
and patient is not responding to treatment, surgical
resection is required

11. COPD
It’s a disease characterized by presence of air flow
obstruction due to chronic bronchitis or emphysema.
Chronic bronchitis: Clinical disorder characterized by
productive cough on most of the days for atleast 3
consecutive months for more that 2 successive years.
Emphysema: Abnormal and permanent dilation of air
spaces lying beyond the terminal bronchioles
accompanied by destruction of their walls

12. Risk Factors
Cigarettes (80 to 90% of cases in the US).
Possible exposure to secondhand smoke
Environmental factors such as respiratory
infections
Industrial exposures
Air pollution
Genetic predisposition (e.g. alpha-1
antitrypsin deficiency)

13. releaserelease
Inflammatory Process in COPD
NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001 (Updated 2003).
Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000;343:269-280.
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NeutrophilsNeutrophilsNeutrophilsNeutrophils
Macrophages inMacrophages in
respiratoryrespiratory
tracttract
Macrophages inMacrophages in
respiratoryrespiratory
tracttract
ProteasesProteases ProteasesProteases stimulatestimulate stimulatestimulate
releaserelease
Parenchymal Parenchymal
DestructionDestruction

14. Features of COPD

15. COPD
Diagnostic tests
Clinical Features
Physical examination
Sample of sputum
Chest x-ray
High-resolution CT (HRCT scan)
Pulmonary function test (spirometery)
Pulse oximeter

16. Clinical Features
Cough: Repeated attacks of productive cough, especially
during winter and later it becomes constant. There is
tightness in the chest especially in the morning
Expectoration: Sputum is little, mucoid and tenacious.
Purulent sputum is indicative of infection.
Dyspnea: Noted in heavy exertion, condition progresses it
occurs with mild activity and at rest.

17. Examination:
Inspection: Patient has dyspnea/ Accessory muscles
are used/ Pursing of lips/ Indrawing of supraclavicular
fossae and intercostal spaces during inspiration/
Chest becomes barrel shaped
Palpation: Apex beat not palpable/ Chest expansion
becomes decreased
Percussion: Hyper-resonant
Auscultation: Breath sounds decreased/ Coarse
crepitation's at lung bases during inspiration and
expiration

18. COPD Patients—Not Necessarily
the Stereotype
Stereotypical pictures of COPD patients
31
Blue BloaterBlue BloaterPink PufferPink Puffer

20. Reduced expiratory flow rate, destruction of alveoli, and short
exhalation time lead to…
Low, Flattened DiaphragmLow, Flattened Diaphragm Increased A-P DiameterIncreased A-P Diameter
Air TrappingAir Trapping
Hyperinflation

21. More sensitive than a chest-Xray

22. Sputum C/S: It may reveal streptococcal pneumonia,
HI, Moraxella catarrhalis
Alpha 1-Antitrypsin: 2-4g/L
CBC: Hemoglobin level and PCV can be elevated as
a result of persistent hypoxaemia

23. Diagnosis of COPD
Role of Spirometry
•Expiratory airflow limitation is the hallmark physiologic Expiratory airflow limitation is the hallmark physiologic
change of COPDchange of COPD
•FEVFEV
11, FVC, FEV, FVC, FEV
11/FVC all decrease /FVC all decrease
•Spirometry is “the gold standard”—most reproducible, Spirometry is “the gold standard”—most reproducible,
standardized, objective way of measuring airflow limitationstandardized, objective way of measuring airflow limitation

25. GOLD Stages of COPD
NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001 (Updated 2003).

27. Asthma
Asthma is a chronic lung-disease that inflames and
narrows the airways (tubes that bring air into and out
of an individual’s lungs).
Asthma is the most common chronic disease among
children.
Extrinsic (70%) is due to IgE and Th2 mediated
responses to environmental antigens
Intrinsic (30%) is Triggered by non immune stimuli:
Aspirin, stress, exercise, viral infections

28. What substances trigger asthma?
Type of Substance Examples
Air pollutants, including dusts,
smoke, mists & fumes
Diesel exhaust; tobacco smoke;
mineral, rock, coal, & wood dusts;
gases; fumes & vapors from aerosol
agents, chemicals, cleaning materials,
solvents, paints, welding & from heating
& cooling metals quickly
Pollens, mites & molds Trees, flowers, weeds, hay, plants
Animal dander Birds, cats, dogs
Medications Aspirin, anti-inflammatory drugs
Foods Egg, wheat, nuts

30. Mediators
Leukotrienes C4, D4, E4:
Prolonged bronchoconstriction, increased mucin secretion
Acetylcholine:
Stimulation of muscaranic receptors, Inc. Muscle contraction
Histamine:
Causes bronchospasm
Prostaglandin D2:
Elicits Bronchoconstriction
Eosinophils:
Late phase reaction starts 4-8hrs later and persists for 12-
24hrs, it produces leukotrienes, and its toxic to airways

33. Symptoms
Common symptoms of asthma include:
Coughing
Wheezing
Tightness in the chest
Shortness of breath

34. Diagnosis
History :
Periodic attacks / Family history / Seasonal / Early morning
On Examination:
Mild attack:
1.Slight tachycardia/ tachypnea
2.Mild diffuse wheezing
Moderate attack:
1.Use of accessory muscles, retraction of Intercostal muscles
2.Decreased breath sounds, loud wheezing
Severe attack:
1.Fatigue, cyanosis
2.Inaudible breath sounds ( Silent chest)
3.Inability to maintain lying position

35. Investigations
Chest X-ray:
Hyper inflated lungs
Blood tests:
Eosinophils and IgE are usually increased
Skin prick test:
Should be performed in all cases of asthma to help
identify allergic causes

36. Spirometry
>12% AND 200 ML REVERSIBILTY

37. Step 1: Mild intermittent asthma
Step 5: Continuous or frequent
use of oral steroids
Step 4: Persistent poor control
Step 3: Add-on therapy
Step 2: Regular preventer therapy
Management
•Learning to recognize one’s own triggers and taking steps
to avoid them./Avoid aggravating factors:
•Stepwise management of asthma in adults

38. Step 1: Mild intermittent asthma
Inhaled short acting ß
2
agonist as required
Stepwise management of asthma in adults

39. Step 2: Regular preventer therapy

Inhaled steroids should be prescribed for patients:
With exacerbation of asthma in the last 2 years
Using inhaled beta
2
agonists three times a week or more
Symptomatic three times a week or more
Waking one night a week or more
Start patients at inhaled steroid dose appropriate to disease severity (e.g.
adults: 400 micrograms per day; beclomethasone), higher doses in smokers
are required
Use lowest dose at which effective control of asthma is maintained
AE: Oropharyngeal candidiasis/ Dec bone growth
In children on inhaled steroids with decreased consciousness, check blood glucose
levels urgently and consider IM hydrocortisone

In adults doubling the dose of inhaled steroids at the time of exacerbation is of unproven
value
Inhaled steroids are the most effective preventer drug for adults and
children for achieving overall treatment goals

40. Stepwise management of asthma in adults
Step 3: Add-on therapies
1. Check inhaler technique
2. Add inhaled long-acting ß
2
agonist (LABA) ex: Salmetrol (12hrs)
3. Assess control of asthma:
•Good response to LABA – continue LABA
•Benefit from LABA but control still inadequate – continue LABA and
increase inhaled steroid dose to 800 micrograms/day * (if not already on
this dose)
•NO response to LABA – stop LABA and increase inhaled steroid to
800 micrograms/day *. If control still inadequate, institute trial of other
therapies
(e.g. leukotriene receptor antagonist or SR theophylline)
Step 1: Mild intermittent asthma
Step 2: Regular preventer therapy
Start at dose of inhaled
steroid appropriate to
severity of disease.

41. Stepwise management of asthma in adults
Step 3: Add-on therapies
1. Check inhaler technique
2. Add inhaled long-acting ß
2
agonist (LABA) ex: Salmetrol (12hrs)
3. Assess control of asthma:
•Good response to LABA – continue LABA
•Benefit from LABA but control still inadequate – continue LABA and
increase inhaled steroid dose to 800 micrograms/day * (if not already on
this dose)
•NO response to LABA – stop LABA and increase inhaled steroid to
800 micrograms/day *. If control still inadequate, institute trial of other
therapies
(e.g. leukotriene receptor antagonist or SR theophylline)
Step 1: Mild intermittent asthma
Step 2: Regular preventer therapy
Start at dose of inhaled
steroid appropriate to
severity of disease.

43. Step 4: Persistent poor control
Consider trials of:
•increasing inhaled steroid up to 2000mcg/day *
•Addition of oral therapy(e.g. leukotriene
receptor antagonist, SR theophylline, ß
2
agonist
tablet)
Step 1: Mild intermittent asthma
Step 3: Add-on therapy
Step 2: Regular preventer therapy
Start at dose of inhaled
steroid appropriate to
severity of disease.
Stepwise management of asthma in adults

44. Step 5: Continuous or frequent use of oral steroids
Use daily steroid tablet in lowest dose providing adequate control
Maintain high dose inhaled steroid at 2000mcg/day *
Consider other treatments to minimise the use of steroid tablets
AE: When use is >3months or receiving more than 3-4 courses
Step 1: Mild intermittent asthma
Step 3: Add-on therapy
Step 2: Regular preventer therapy
Start at dose of inhaled
steroid appropriate to
severity of disease.
Step 4: Persistent poor control
Stepwise management of asthma in adults

45. Step-down therapy
Once asthma control is established, the dose of
C/S should be titrated to the lowest dose at which
control is maintained.
Decreasing the dose by 25-50% every 3 months
is a reasonable strategy

46. THANK-YOU