As per davidson and macleod and crashcourse

1. Chronic Obstructive Pulmonary
Diseases
COPD
DR MARWAN MAJEED IBRAHIM
ABHS INTERNAL MEDICINE
FICM PULMONARY MEDICINE
MRCP PULMONARY MEDICINE

2. Chronic obstructive pulmonary disease (COPD) is defined as a
preventable and treatable disease characterized by persistent
airflow limitation (usually non-reversible) that
progressive and associated with an enhanced
is usually
chronic
to noxious
inflammatory response in the airways and the lung
particles or gases.
chronic bronchitis (coug h and
Related diagnoses include
sputum for at least 3 consecutive months in each of 2
cons ecutive years) and emphysema (abnormal permanent
enlargement of the airspaces distal to the terminal
bronchioles, accompanied by destruction of their walls and
without obvious fibrosis).

4. Pathophysiology
The presence of airflow limitation combined with premature
airway closure leads to gas trapping and hyperinflation, adversely
affecting pulmonary and chest wall compliance. Pulmonary
hyperinflation also results, which flattens the diaphragmatic
muscles and leads to an increasingly horizontal alignment of the
muscles at a
intercostal muscles,
mechanical disadvantage. The
placing the respiratory
work of breathing is therefore
markedly increased.
Emphysema may be classified by the pattern of the enlarged
airspaces: centriacinar, panacinar and paraseptal. Bullae form in some
individuals. This results in impaired gas exchange and respiratory
failure.
barrel chest
bullae -> can lead to pneumothorax

6. Clinical features
• COPD should be suspected in any patient over the age of 40 years
who presents with symptoms of chronic bronchitis and/or
breathlessness.
• Cough and associated sputum production
symptoms, and are often referred to as
are usually the first
a ‘smoker’s cough’.
Haemoptysis may complicate exacerbations of COPD but should not
without thorough investigation i.e ca
be attributed to COPD
bronchus.
• Breathlessness is common.

7. Physical signs
are non-specific, correlate poorly with lung function, and are seldom
obvious until the disease is advanced. Breath sounds are typically
quiet; crackles may accompany infection but, if persistent, raise the
possibility of bronchiectasis. Finger clubbing is not a feature of COPD
and should trigger further investigation for lung cancer or fibrosis.
Right heart failure may develop in patients with advanced COPD,
particularly if there is coexisting sleep apnoea or thromboembolic
disease (‘cor pulmonale’).

8. • Fatigue, anorexia and weight loss may point to the development of
lung cancer or tuberculosis, but are common in patients with severe
COPD and the body mass index (BMI) is of prognostic significance.
• Prolonged expiratory time >5s, with pursed lipbreathing.
• Two classical phenotypes have been described: ‘pink puffers’ and
‘blue bloaters’. The former are typically thin and breathless, and
maintain a normal PaCO2 until the late stage of disease. The latter
develop (or tolerate) hypercapnia earlier and may develop oedema
and secondary polycythaemia. In practice, these phenotypes often
overlap.

9. Investigations
• CXR chest X-ray is essential to identify alternative diagnoses such
as cardiac failure, other complications of smoking such as lung
cancer, and the presence ofbullae.
• CBC blood count is useful to exclude anaemia or document
polycythaemia, and in younger patients with predominantly basal
emphysema α1-antitrypsin should be assayed.
• Electrolytes
• Echocardiography for cor pulmonale

10. • Pulmonary function test , The diagnosis requires objective
demonstration of airflow obstruction by spirometry and is
established when the post-bronchodilator FEV1/FVC is < 70%. The
severity of COPD may be defined in relation to the post-
volumes provides an assessment of
bronchodilator FEV1
• Measurement of lung
hyperinflation.
• Exercise tests provide an objective assessment of exercise
tolerance and provide a baseline on which to judge the response to
bronchodilator therapy or rehabilitation programs; they may also be
valuable when assessing prognosis

12. • HRCT is likely to play an increasing role in the assessment of COPD,
as it allows the detection, characterisation and quantification of
emphysema
• Arterial blood g a s analysis for possible type ll respiratory
failure.

14. Manag ement
• 1-Reducing exposure to noxious
sustained smoking in mild to moderate
particles and gases ,
COPD is
cessation
accompanied by a reduced compared to
persistent smokers, and cessation remains
decline in FEV1
the only strategy
that impacts favorably on the natural history of COPD.
• 2-Smoking stopping s t r a t e g i e s , n i c o t i n e replacement
therapies, Bupropion, Varenicline.

15. • 3- Bronchodilators Bronchodilator therapy is central to the
management of breathlessness. Short-acting bronchodilators may
be used for patients with mild disease but longer-acting
bronchodilators are usually more appropriate for those
with moderate to severe disease.
• Beta agonist: Salbutamol , salmeterol and formtoterol.
• Antimuscarinic: Ipratropium and tiotropium.
• 4- Combined inhaled glucocorticoids and bronchodilators ,
improves lung function, reduces the frequency and severity of
exacerbations and improves quality of life.Long acting
antimuscarinics (LAMAs) should be used with caution in patients
with significant heart disease or a history of urinary retention.

16. during
• 5- Oral g lucocorticoids Oral glucocorticoids are useful
exacerbations (prednisone 20 mg twice daily for 5 days).
• 6- Pulmonary rehabilitation
• 7- Oxygen therapy Long-term domiciliary oxygen therapy
(LTOT) improves survival in selected patients with COPD
complicated by severe hypoxaemia (arterial PaO2 < 7.3 kPa (55
mmHg). It is most conveniently provided by an oxygen
concentrator and patients should be instructed to use oxygen for a
minimum of 15 hours/ day; greater benefits are seen in those
who use it for more than 20 hours/day. The aim of therapy is to
increase the PaO2 to at least 8 kPa (60 mmHg) or SaO2 to at least
90%.

18. • 8- Surg ical intervention Bullectomy may be considered when
tissue. Patients
large bullae compress surrounding normal lung
with predominantly upper lobe emphysema, preserved
transfer and
benefit from
no evidence
lung volume reduction surgery (LVRS), in
gas
of pulmonary hypertension may
which
peripheral emphysematous lung tissue is resected with the aim
of reducing hyperinflation and decreasing the work of
breathing.

19. selective phosphodiesterase 4
• 9-PDE4
inhibitor
Inhibitors The
roflumilast
exacerbation frequency
has been demonstrated to
in patients with severe COPD,
(PDE4)
reduce
chronic
bronchitis, and a prior history of exacerbations; its effects on airflow
obstruction and symptoms are modest.
• 10- Theophylline.
• Patients with COPD should be offered an annual influenza
vaccination and, a s appropriate, pneumococcal
vaccination.

21. 2024 UPDATE

23. 2024 UPDATE

25. 2024 UPDATE

26. Prognosis

28. Acute exacerbations of COPD
• Acute exacerbations of COPD are characterised by an increase
in symptoms and deterioration in lung function and health
status. They become more frequent as the disease progresses
and are usually triggered
air quality. They may be
respiratory failure and/or
accompanied by
fluid retention
the development
and represent
by bacteria, viruses or a change in
of
an
important cause of death.
• The presence of cyanosis, peripheral oedema or an alteration
in consciousness should prompt referral to hospital.

29. • Oxyg en therapy :high concentrations of oxygen may cause
respiratory depression and worsening acidosis . Controlled
oxyg en at 24% or 28 % should be use d with the aim of
maintaining a PaO2 of more than 8 kPa (60 mmHg) (or
an SaO2 of more than 9 0 % ) without worsening acidosis.
• Bronchodilators Nebulised short-acting β2-agonists combined
agent (e.g. salbutamol and ipratropium)
with an anticholinergic
should be administered.

30. • Glucocorticoids Oral prednisolone reduces symptoms and
improves lung function. Doses of 30 mg for 10 days are currently
recommended but shorter courses (40 mg for 5 days) may be
acceptable. Prophylaxis against osteoporosis should be considered
in patients who receive repeated courses of glucocorticoids.
• Antibiotic therapy such as an aminopenicillin, a tetracycline or a
macrolide or respiratory fluroquinolons.

31. • Non-invasive ventilation in patients with respiratory failure,
defined as Paco2 > 45 mmHg or mechanical ventilation
indicated for patients w ith severe respiratory distres s
despite initial therapy, life-threatening hypoxemia, severe
hypercarbia and/or acidosis, markedly impaired mental
status, respiratory arrest, hemodynamic instability.