Clinical Presentation Of COPD

2. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
By :
Hammad Ahmad
4rth Proff

3. INTRODUCTION TO COPD
• The World Health Organization (WHO) defines chronic obstructive pulmonary disease (COPD)
as: 'a lung disease characterized by chronic obstruction of lung airflow that interferes with normal
breathing and is not fully reversible'. The airflow obstruction in COPD is due to damage to the
lung structure and destruction of lung tissue (emphysema). This is normally due to smoking, but
recurrent infection also contributes to the process. COPD is also frequently associated with, and
may contribute towards, numerous co-existing diseases such as heart disease, osteoporosis and
diabetes, which influence morbidity and mortality.

4. SYMPTOMS
• Common symptoms of COPD include: chronic cough, sputum production and
shortness of breath. People with COPD are at increased risk of chest infections,
some of which will be severe enough to require hospitalisation.

5. PATHOPHYSIOLOGY OF COPD
• Chronic inflammatory changes lead to destructive changes and chronic airflow
limitation. The most common cause is exposure to tobacco smoke.
• Inhalation of noxious particles and gases activates neutrophils, macrophages and
CD8+ lymphocytes, which release chemical mediators , including tumor necrosis
factor alpha ,interleukin-8, and leukotriene B4. Inflammatory cells and mediators
lead to widespread destructive changes in airways , pulmonary vasculature and
lung parenchyma.

6. CONTINUE…
• Oxidative stress and imbalance between aggressive and protective defense systems
in the lungs (proteases and antiproteases) may also occur. Oxidants generated by
cigarette smoke react with and damage proteins and lipids, contributing to tissue
damage. Oxidants also promote inflammation and exacerbate protease–
antiprotease imbalance by inhibiting antiprotease activity.
• The protective antiprotease α1-antitrypsin (AAT) inhibits protease enzymes,
including neutrophil elastase. In presence of unopposed AAT activity, elastase
attacks elastin, a major component of alveolar walls. Hereditary AAT deficiency
increases risk for premature emphysema. In emphysema from cigarette smoking,
imbalance is associated with increased protease activity or reduced antiprotease
activity.

7. CONTINUE…
• Inflammatory exudate in airways leads to increased number and size of goblet cells
and mucus glands. Mucus secretion increases and ciliary motility is impaired. There
is thickening of the smooth muscles and connective tissues in airways. Chronic
inflammation leads to scarring and fibrosis. Diffuse airway narrowing occurs and is
more prominent in small peripheral airways.
• Smoking-related COPD usually results in centrilobular emphysema that primarily
affects respiratory bronchioles. Panlobular emphysema is seem in AAT deficiency
and extends to the alveolar ducts and sacs.

8. CONTINUE…
• Vascular changes include thickening of pulmonary vessels that may lead to
endothelial dysfunction of pulmonary arteries. Later, structural changes
increase pulmonary pressures, especially during exercise. In severe COPD,
secondary pulmonary hypertension leads to right-sided heart failure (cor
pulmonale).

10. CLINICAL PRESENTATION
• Initial symptoms include chronic cough and sputum production; patients may have
symptoms for several years before dyspnea develops.
• Physical examination is normal in most patients in milder stages. When airflow
limitation becomes severe, patients may have cyanosis of mucosal membranes,
development of a “barrel chest” due to hyperinflation of the lungs, increased resting
respiratory rate, shallow breathing, pursing of lips during expiration, and use
of accessory respiratory muscles.

11. CONT…
• Patients experiencing COPD exacerbation may have worsening dyspnea,
increased sputum volume, or increased sputum purulence. Other features of
exacerbation include chest tightness, increased need for bronchodilators, malaise,
fatigue, and decreased exercise tolerance.

12. DIAGNOSIS
• Diagnosis is based in part on patient symptoms and history of exposure to risk
factors such as tobacco smoke and occupational substances. • Classification of
disease severity is based on assessment of airflow limitation by spirometry,
measurement of symptom severity, and assessment of exacerbation frequency.
Symptom severity is assessed by the COPD Assessment Test (CAT) or the modified
Medical Research Council (mMRC) scale. Patients are first classified
according to severity of airflow obstruction (Grades 1–4) and then placed
into a Group (A, B, C, or D) based on the impact of symptoms and risk for
future exacerbations.

13. TREATMENT
• Goal of Treatment:
Prevent or minimize disease progression, relieve symptoms,
improve exercise tolerance, improve health status, prevent and treat exacerbations,
prevent and treat complications, and reduce morbidity and mortality.

14. NONPHARMACOLOGICAL THERAPY
• Smoking cessation is the only intervention proven to affect long-term decline in
FEV1 and slow COPD progression. Pulmonary rehabilitation programs include
exercise training, breathing exercises, optimal medical treatment, psychosocial
support, and health education. Administer vaccinations as appropriate (eg,
pneumococcal vaccine, annual influenza vaccine). Once patients are stabilized as out
patients and pharmacotherapy is optimized, institute long-term oxygen therapy if
either (1) resting Pao2 less than 55 mm Hg or SaO2 less than 88% with or without
hypercapnia, or (2) resting Pao2 55 to 60 mm Hg or SaO2 less than 88% with
evidence of right-sided heart failure, polycythemia, or pulmonary hypertension. The
goal is to raise PaO2 above 60 mm Hg.

15. PHARMACOLOGICAL
TREATMENT