This document provides information about COPD (chronic obstructive pulmonary disease). It defines COPD as a condition characterized by airway obstruction that does not change over several months and is not fully reversible. It notes that COPD is caused by both genetic and environmental factors, especially cigarette smoking. The document discusses symptoms, signs, diagnostic tests, and management strategies for COPD including smoking cessation, bronchodilators, inhaled corticosteroids, oxygen therapy, and management of exacerbations.

1. Name: Noorbhaiwala Mudreka
Roll no. 94
Batch: 2019-20
Department of Medicine
ZMCH-DAHOD

2.  COPD is a heterogeneous condition embracing
several overlapping pathological processes
including chronic bronchitis, chronic
bronchiolitis (small
airway disease) and emphysema.
 Many patients also exhibit a systemic component
characterised by impaired nutrition, weight loss
and skeletalmuscle dysfunction.
 COPD is defined by the presence of airways
obstruction, which does not change markedly
over several months and, unlike asthma, is not
fully reversible.

3.  COPD should be suspected in any patient
over the age of 40 yrs who has persistent
cough and sputum production and/or
breathlessness.

5.  Chronic bronchitis is defi ned as cough and
sputum on most days for >3consecutive mths for
>2 successive yrs.
 The level of breathlessness should
be quantified for future reference
 In advanced disease there may be oedema or
morning headaches (hypercapnia).
 Physical signs are non-specifi c, but may help to
indicatethe severity of disease.

6.  ‘Pink puffers’ are thin and breathless, and
maintain a normal PaCO2.
 ‘Blue bloaters’ develop hypercapnia,
oedema and secondary polycythaemia.

7.  Genetic predisposition :
l. a-1 Antitrypsin gene
2. MMP 12 gene
3. a-nicotine ACh receptor
4. Hedge Hog interactivity
protein gene
Environmentalfactors
1. Age: Ageingitselfisa risk
factorforCOPD.
2. Gender: In past prevalence was more
in men than women. But due to increase
in smoking in women prevalence rates
are now approaching equality.
3. Lung growth and development
a. Any factor that affects lung growth
during Gestation and childhood has
potential for increasing individual
risk for COPD.
b. Factors in early life termed“
Childhood
Disadvantage Factors" were as
important as heavy smoking is in
predicting in early adult life.

8.  4. Exposure to Particles
a. Cigarette smoke
b. Other types of tobacco
c. Passive exposure to smoke –
also known as environmental
tobacco smoke.
d. Smoking during pregnancy
affects fetus by affecting lung
growth and development
ofimmune system.
e. Occupational exposures,
including organic and inorganic
dust and chemical agents and
fumes are appreciated risk
factors.
f. Wood, Animal during, crop
residues
and coal, typically burned in open
fires or poorly functioning stoves
or
heating in poorly ventilated
dwelling
- important risk factor.
g. Outdoorairpollution - inurban
areas.
Roleisunclear,but is smallcompared
to smoking. Air pollution from
fossil
fuel combustion is associated with
decrement in lung function.

9.  A. General condition: Patient may be emaciated,
cyanosed and edematous (blue bloater). JVP
may show giant a-waves.
C. Heart
1. Apex beat may not be visible or palpable.
2. Right ventricular heave may be present.
3. Heart sounds may be diminished. Second sound may be
loud. Gallop rhythm may be present. In marked
emphysema, RV heave may not be visible or felt because
the hyperinflated lung may cover it. In
such cases, epigastric pulsations may be the only evidence
of RV enlargement
4. Functionaltricuspidregurgitationmurmur
may be present.
5. Hyperkinetic state with warm limbs and
Waterhammer pulse may be present

10.  CXR reveals hyperinfl ation and occasionally
demonstrates large bullae or other complications
of smoking (lung cancer).
 FBC may demonstrate polycythaemia.
 α1 antitrypsin level should be checked in
younger patients
with a basal distribution of emphysema.
 Spirometry reveals FEV1 <80% predicted value
and FEV1/FVC (forced vital capacity) <70%.
 Severity of disease is defi ned according to
percentage predicted FEV1: mild disease 50–80%,
moderate 30–49%, severe <30%.

11.  Lung volumes using helium dilution or body
plethysmography quantify any hyperinfl ation.
 Carbon monoxide transfer factor is low in
emphysema.
 Exercise tests provide an objective assessment
of exercise tolerance.
 Pulse oximetry may prompt referral for a
domiciliary oxygen assessment if <93%.
 CT is likely to play an increasing role in the
assessment of COPD as it allows the
detection,characterisation and quantification of
emphysema.

14.  Pessimism is unjustified, as it is usually
possible to improve breathlessness,
reduce the frequency and severity of
exacerbations, and improve health
status and prognosis.

15.  Smoking cessation: Offer help to stop smoking at every
opportunity. Combine pharmacotherapy with appropriate support
as part of a programme. It is the only intervention proven to
decelerate the decline in FEV1
 Bronchodilators: Short-acting bronchodilators for mild disease
(β2-agonist or anticholinergic). Longer-acting bronchodilators are
more appropriate for patients with moderate to severe disease.
From the wide range available, select a device which the patient
can use effectively. Significant improvements in breathlessness
may be reported despite minimal changes in FEV1, probably
reflecting reduced hyperinflation. Theophylline preparations
improve breathlessness, but use is limited by side-effects. Oral
bronchodilators may be contemplated in patients who cannot use
inhaled devices efficiently.

16. Inhaled corticosteroids:
 Reduce the frequency and severity of exacerbations;
they are recommended in patients with moderate to
severe disease
 (FEV1 <50%) who report >2 exacerbations requiring
antibiotics or oral steroids/yr. Regular use leads to a
small improvement in FEV1 but no change in the rate
of decline of lung function. ICS/LABA combinations
produce further improvements in breathlessness and
exacerbation rate.
 Oral corticosteroids are useful during exacerbations,
but maintenance therapy contributes to osteoporosis
and impaired muscle function and should be
avoided.

17.  Oxygen therapy: Long-term domiciliary oxygen therapy
(LTOT) improves survival, prevents progression of
pulmonary hypertension,decreases the incidence of
secondary polycythaemia and improves neuropsychological
health. A minimum of 15 hrs/day is recommended, to keep
PaO2 >8 kPa (60 mmHg) or SaO2 >90%. Ambulatory oxygen
therapy should be considered in patients who desaturate
on exercise and show objective improvement in exercise
capacity and/or dyspnoea with oxygen. Short-burst oxygen
therapy is widely prescribed but is expensive and of
unproven benefit.
 Surgical intervention: In highly selected patients, lung
volume reduction surgery (removing non-functioning
emphysematous lung tissue) reduces hyperinflation and
decreases work of breathing. Bullectomy is occasionally
performed to remove large bullae that compress
surrounding lung tissue.

18.  These are characterised by an increase in
symptoms and deterioration in lung function.
They are more common in severe disease and
may be caused by bacteria, viruses or a
change in air quality. Respiratory failure
and/or fluid retention may be present. Many
patients can be managed at home with the
use of increased bronchodilator therapy, a
short course of oral corticosteroids and, if
appropriate, antibiotics. Cyanosis, peripheral
oedema or altered conscious level should
prompt hospital referral.

19.  Oxygen therapy: High concentrations of oxygen may
cause respiratory depression and worsening acidosis
(p. 280). Controlled oxygen at 24% or 28% should be
used, aiming for PaO2 >8 kPa (60 mmHg) (or an SaO2
>90%) without worsening acidosis.
 Bronchodilators: Nebulised short-acting β2-agonists
and anticholinergics are used. If concern exists
regarding oxygen sensitivity, nebulisers may be driven
by compressed air.
 Corticosteroids: Oral prednisolone (usually 30 mg for
5–10 days)
reduces symptoms and improves lung function.
Prophylaxis against osteoporosis should be considered
if frequent courses are needed.

20.  Antibiotic therapy: Recommended for an increase in
sputum purulence,sputum volume or breathlessness.
An aminopenicillin or a macrolide shouldbe used. Co-
amoxiclav is only required in regions where β-
lactamaseproducing organisms are known to be
common.
 Non-invasive ventilation (NIV): If patients have
persistent tachypnoea and a respiratory acidosis (H+
≥ 45/pH < 7.35), NIV is associated with reduced
requirements for mechanical ventilation and
reductions in mortality. Consider mechanical
ventilation where there is a reversible cause for
deterioration (e.g. pneumonia), or if there is no prior
history of respiratory
failure.

21. Thank you ….