respiratory disease

2. INTRODUCTION
 Chronic obstructive pulmonary disease (COPD) is
defined as a disease state characterized by airflow
limitation that is not fully reversible .
 COPD includes
 emphysema, an anatomically defined condition
characterized by destruction and enlargement of
the lung alveoli;
 chronic bronchitis, a clinically defined condition
with chronic cough and phlegm; and
 small airways disease, a condition in which
small bronchioles are narrowed.

3. GOLD Definitions
• The Global Initiative for Chronic Obstructive Lung
Disease (GOLD) defines COPD as follows :
• “Chronic obstructive pulmonary disease (COPD), a
common preventable and treatable disease, is
characterized by airflow limitation that is usually
progressive and associated with an enhanced chronic
inflammatory response in the airways and the lung to
noxious particles or gases. Exacerbations and
comorbidities contribute to the overall severity in
individual patients."

4. Chronic bronchitis
• Chronic bronchitis is defined as a chronic
productive cough for three months in each
of two successive years in a patient in
whom other causes of chronic cough (eg,
bronchiectasis) have been excluded .
• It may precede or follow development of
airflow limitation.

5. Emphysema
• Emphysema is defined by abnormal and
permanent enlargement of the airspaces distal
to the terminal bronchioles that is accompanied
by destruction of the airspace walls, without
obvious fibrosis (ie, there is no fibrosis visible
to the naked eye)

6. Risk factors

7. 1.Cigarette smoking
• cigarette smoking- major risk factor for mortality
from chronic bronchitis and emphysema.
• FEV1 decreases in a dose- response relationship to the
intensity of cigarette smoking, which is typically
expressed as pack-years .
• But only 15% of the variability in FEV1 is explained
by pack-years.
• This finding suggests that additional environmental
and/or genetic factors contribute to the impact of
smoking on the development of airflow obstruction.

8. • 2. Airway Responsiveness and COPD
• Many patients with COPD also share feature of
airway hyperresponsiveness (tendency for
increased bronchoconstriction in response to a
variety of exogenous stimuli, including
methacholine and histamine, which is one of the
defining features of asthma )
• 3. Respiratory Infections
– respiratory infections are important causes of
exacerbations of COPD, the association of both
adult and childhood respiratory infections to the
development and progression of COPD remains
to be proven.

9. Cont..
4.Occupational exposures -occupational
exposures, including coal mining, gold mining,
and cotton textile dust, have been suggested as
risk factors for chronic airflow obstruction.
5. Ambient air pollution-Prolonged exposure to
smoke produced by biomass combustion—a
common mode of cooking in some countries—
also appears to be a significant risk factor for
COPD among women in those countries.

10. • 6. Passive, or Second-Hand, Smoking Exposure
• 7. Genetic Considerations- alpha 1
ANTITRYPSIN DEFICIENCY-In a small percentage of
people, emphysema results from low levels of a protein
called alpha-1-antitrypsin (AAt), which protects the
elastic structures in lungs from the destructive effects of
certain enzymes.
 A lack of AAt can lead to progressive lung damage that
eventually results in emphysema.
 AAt deficiency is a hereditary condition that occurs
when patient inherits two defective genes, one from
each parent.

11. PATHOPHYSIOLOGY
• Persistent reduction in forced expiratory flow rates is the
most typical finding in COPD.
• Increases in the residual volume and the residual
volume/total lung capacity ratio, nonuniform distribution
of ventilation, and ventilation-perfusion mismatching
also occur. 3 main processes are-
1.Airflow Obstruction- chronically reduced ratio of FEV1/FVC.
2.Hyperinflation-"air trapping" (increased residual volume and
increased ratio of residual volume to total lung capacity)
3.Defect in Gas Exchange-PaO2 usually remains near normal
until the FEV1 is decreased to ~50% of predicted,
• Decrease in PaCO2 is not expected until the FEV1 is <25% of
predicted

13. Pathology of emphysema
• Centriacinar emphysema,
– the type most frequently associated with cigarette smoking,
is characterized by enlarged air spaces found (initially) in
association with respiratory bronchioles.
– usually most prominent in the upper lobes and superior
segments of lower lobes and is often quite focal.
• Panacinar emphysema
– refers to abnormally large air spaces evenly
distributed within and across acinar units.
– Panacinar emphysema is usually observed in
patients with alpha 1AT deficiency, which has a
predilection for the lower lobes.

14. CLINICAL PRESENTATION
• Three most common symptoms in COPD are
– cough,
– sputum production, and
– exertional dyspnea.
• Many patients have such symptoms for months or
years before seeking medical attention.
• Although the development of airflow obstruction is a
gradual process, many patients date the onset of their
disease to an acute illness or exacerbation.
• A careful history, however, usually reveals the
presence of symptoms prior to the acute
exacerbation.

15. Physical Findings
• In the early stages of COPD, patients usually have an
entirely normal physical examination.
• Current smokers may have signs of active smoking,
including an odor of smoke or nicotine staining of
fingernails.
• In patients with more severe disease, a prolonged
expiratory phase and expiratory wheezing is present.
• In addition, signs of hyperinflation include a barrel
chest and enlarged lung volumes with poor
diaphragmatic excursion as assessed by percussion.

16. Cont..
• Patients with severe airflow obstruction
may also use accessory muscles of
respiration, sitting in the characteristic
"tripod" position to facilitate the actions of
the sternocleidomastoid, scalene, and
intercostal muscles.
• Patients may develop cyanosis, visible in
the lips and nail beds.

17. • As the severity of the airway obstruction
increases, physical examination may reveal
– hyperinflation (eg, increased resonance to percussion),
– decreased breath sounds,
– wheezes,
– crackles at the lung bases, and/or
– distant heart sounds .
• Features of severe disease include an increased
anteroposterior diameter of the chest (“barrel-
shaped” chest) and a depressed diaphragm with
limited movement based on chest percussion.

19. • Advanced disease may be accompanied by
– systemic wasting, with significant weight loss,
– bitemporal wasting, and
– diffuse loss of subcutaneous adipose tissue.
• This syndrome has been associated with both inadequate oral
intake and elevated levels of inflammatory cytokines (TNF- ).
• Such wasting is an independent poor prognostic factor in
COPD.
• Some patients with advanced disease have paradoxical inward
movement of the rib cage with inspiration (Hoover's sign), the
result of alteration of the vector of diaphragmatic contraction
on the rib cage as a result of chronic hyperinflation.

20. Cont..
• Signs of overt right heart failure, termed cor
pulmonale, are relatively infrequent since the advent
of supplemental oxygen therapy.
• Clubbing of the digits is not a sign of COPD, and its
presence should alert the clinician to initiate an
investigation for causes of clubbing.
• In this population, the development of lung cancer is
the most likely explanation for newly developed
clubbing.

21. Lab findings
• Assessment for anemia is an important step in the
evaluation of dyspnea.
• Measurement of plasma brain natriuretic peptide
(BNP) or N-terminal pro-BNP (NT-proBNP)
concentrations is useful as a component of the
evaluation of suspected heart failure (HF).
• Among stable COPD patients with normal kidney
function, an elevated serum bicarbonate may
indirectly identify chronic hypercapnia. In the
presence of chronic hypercapnia.

22. Lab cont..
• Testing for alpha-1 antitrypsin (AAT) deficiency
should be obtained in all symptomatic adults with
persistent airflow obstruction on spirometry.
• Especially suggestive subsets include the
– presence of emphysema in a young individual (eg,
age ≤45 years),
– emphysema in a nonsmoker or minimal smoker
– emphysema characterized by predominantly basilar
changes on the chest radiograph, or a
– family history of emphysema

23. Pulmonary function tests
• Pulmonary function tests, particularly
spirometry, are the cornerstone of the
– diagnostic evaluation of patients with
suspected COPD.
– are used to determine the severity of the airflow
limitation,
– assess the response to medications, and
– follow disease progression.

24. PFTS
• Spirometry — When evaluating a patient for possible
COPD, spirometry is performed pre and post
bronchodilator administration to determine whether
airflow limitation is present and whether it is partially
or fully reversible.
• Airflow limitation that is irreversible or only
partially reversible with bronchodilator is the
characteristic physiologic feature of COPD.

25. • PFTS shows airflow obstruction with a reduction in
FEV1 and FEV1/FVC .
• With worsening disease severity, lung volumes may
increase, resulting in
– an increase in total lung capacity,
– functional residual capacity, and
– residual volume.
• In patients with emphysema, the diffusing capacity
(DLCO) may be reduced, reflecting the lung
parenchymal destruction characteristic of the disease.

26. ABG
• The indications for measuring ABGs (eg, arterial oxygen
tension [PaO2], carbon dioxide tension [PaCO2], and acidity
[pH]), which must be considered in the clinical context,
include the following:
• ●Low FEV1 (eg, <50 percent predicted)
• ●Low oxygen saturation by pulse oximetry (eg,SpO2 <92
percent)
• ●Depressed level of consciousness
• ●Acute exacerbation of COPD
• ●Assessment for hypercapnia in at risk patients 30 to 60
minutes after initiation of supplemental oxygen

27. Gold Criteria for COPD Severity

28. CHEST Xray
• Radiographic features suggestive of COPD (usually
seen in advanced disease) include:
• Bullae, defined as radiolucent areas larger than 1 cm
in diameter. They are due to locally severe disease,
and may or may not be accompanied by widespread
emphysema
• When advanced COPD leads to pulmonary
hypertension and cor pulmonale, prominent hilar
vascular shadows and encroachment of the heart
shadow on the retrosternal space may be seen

29. Xray
• Rapidlytapering
vascular shadows,
increased radiolucency
of the lung, a flat
diaphragm, and a long,
narrow heart shadow
• ●A flat diaphragmatic
contour and an increased
retrosternal airspace on
a lateral radiograph).
These findings are due
to hyperinflation.

30. BODE Index
• APPROXIMATE 4 YEAR SURVIVAL INTERPRETATION
• 0-2 Points: 80%
• 3-4 Points: 67%
• 5-6 Points: 57%
• 7-10 Points: 18%

31. Treatment

32. Anti smoking therapy
• Nicotine replacement therapy– Transdermal
patches, gums, sprays, lozenges, inhalers
• Bupropion ( Anti depressant)
• Nicotinic receptor partial agonist - Varenicline
• Psychosocial approaches – Cognitive behavioral
therapy
VACCINES
Influenza vaccines and Pneumococcal polysaccharide vaccine is
recommended for COPD patients
• 65 years or more
• younger than age 65 with FEV1< 40% predicted

33. Anticholinergic agents
• Ipratropium bromide improves symptoms and
produces acute improvement in FEV1.
• Tiotropium, a long-acting anticholinergic, has been
shown to improve symptoms and reduce
exacerbations.
• Side effects are minor, and a trial of inhaled
anticholinergics is recommended in symptomatic
patients with COPD.

34. Beta agonists
• These provide symptomatic benefit.
• The main side effects are tremor and tachycardia.
• Long- acting inhaled agonists, such as
salmeterol, have benefits comparable to
ipratropium bromide. Their use is more
convenient than short-acting agents.
• The addition of a agonist to inhaled
anticholinergic therapy has been demonstrated to
provide incremental benefit.

35. Glucocorticoids
• A trial of inhaled glucocorticoids should be considered
in patients with frequent exacerbations, defined as two
or more per year, and in patients who demonstrate a
significant amount of acute reversibility in response to
inhaled bronchodilators.
• The chronic use of oral glucocorticoids for treatment
of COPD is not recommended because of an
unfavorable benefit/risk ratio. The chronic use of oral
glucocorticoids is associated with significant side
effects, including osteoporosis, weight gain, cataracts,
glucose intolerance, and increased risk of infection.

36. • Theophylline
• Theophylline produces modest improvements in expiratory
flow rates and vital capacity
• Nausea is a common side effect; tachycardia and tremor
have also been reported.
• Oxygen
• Supplemental O2 is the only pharmacologic therapy
demonstrated to unequivocally decrease mortality rates in
patients with COPD.
• used for patients with resting hypoxemia (resting O2
saturation 88% or <90% with signs of pulmonary
hypertension or right heart failure)

37. Non pharmacological therapies
• Lung volume reduction surgery (LVRS) is
more efficacious than medical therapy among
patients with upper-lobe predominant
emphysema and low exercise capacity.
• LVRS is costly relative to health-care programs
not including surgery.
• In appropriately selected patients with very
severe COPD, lung transplantation has been
shown to improve quality of life and functional
capacity.

38. EXACERBATIONS OF
COPD
• Exacerbations are episodes of increased
dyspnea and cough and change in the amount
and character of sputum. They may or may not
be accompanied by other signs of illness,
including fever, myalgias, and sore throat.

39. Treatment of Exacerbations
• Bronchodilators
• Typically, patients are treated with an inhaled agonist, often
with the addition of an anticholinergic agent.
• initially with nebulized therapy, as such treatment is often
easier to administer in older patients or to those in respiratory
distress.
• The addition of methylxanthines (such as theophylline) to this
regimen can be considered, although convincing proof of its
efficacy is lacking.
• If added, serum levels should be monitored in an attempt to
minimize toxicity.

40. Antibiotics
• Patients with COPD are frequently colonized with
potential respiratory pathogens,
• Bacteria frequently implicated in COPD exacerbations
include Streptococcus pneumoniae, Haemophilus
influenzae, and Moraxella catarrhalis. In addition,
Mycoplasma pneumoniae or Chlamydia pneumoniae
are found in 5–10% of exacerbations.
• The choice of antibiotic should be based on local
patterns of antibiotic susceptibility of the above
pathogens as well as the patient's clinical condition
• .Most practitioners treat patients with moderate or
severe exacerbations with antibiotics,

41. Glucocorticoids
• Among patients admitted to the hospital, the use of
glucocorticoids has been demonstrated to reduce the
length of stay, hasten recovery, and reduce the chance of
subsequent exacerbation or relapse for a period of up to
6 months.
• One study demonstrated that 2 weeks of glucocorticoid
therapy produced benefit indistinguishable from 8 weeks
of therapy.
• The GOLD guidelines recommend 30–40 mg of oral
prednisolone or its equivalent for a period of 10–14
days.

42. Oxygen
• Supplemental O2 should be supplied to
keep arterial saturations 90%. Hypoxemic
respiratory drive plays a small role in
patients with COPD.

43. Mechanical Ventilatory Support
• Initiation of noninvasive positive-pressure
ventilation (NIPPV) in patients with respiratory
failure, defined as PaCO2 >45 mmHg, results in a
significant reduction in mortality rate, need for
intubation, complications of therapy, and hospital
length of stay.
• Invasive (conventional) mechanical ventilation via
an endotracheal tube is indicated for patients with
severe respiratory distress despite initial therapy, life-
threatening hypoxemia, severe hypercarbia and/or
acidosis, markedly impaired mental status, respiratory
arrest, hemodynamic instability, or other complications.

44. Difference b/w asthma and COPD

45. Thank you