1. ASTHMA AND COPD 2015 Dr Dhaher Jameel Salih Al-habbo FRCP London UK
Assistant Professor Department of Medicine.College of Mdicine
University of Mosul

3. CHRONIC OBSTRUCTIVE PULMONARY DISEASE
COPD preventable and treatable lung disease with some extrapulmonary effects
(muscle weakness,↑circulating inflammatory markers, impair water salt and excretion, altered fat metabolism and ↑prevalence of osteoporosis)

4. PATHOPHYSIOLOGY OF COPD
Collapse of intrathoracic airways during expiration
Increase V/Q mismach↑dead space volume
Flattening of the diaphragm and ↑horizontal alignment of intercostal muscles please the respiratory muscles at a mechanical disadvantage with ↑ work of breathing..

5. PATHOPHYSIOLOGY OF COPD
Emphysema can be divided according to the pattern of enlarged air space
Emphysema is usually centriacinar involving respiratory bronchioles, alveolar ducts and centrally located alveoli.
Panacinar and paraseptal emphysema with blebs or giant bullae.

6. PATHOPHYSIOLOGY OF COPD
Occurs in Cigarette smokers years after starting .
Affects 10-15% of smokers
"Sputum, spasm, and swelling“.
Chronic excessive mucus secretion .
Hypertrophy of mucus-secreting glands .
Smooth muscle hyperplasia.
Bronchial Hyperresponsivenes
Occurs in 50% of COPD patients

7. CLINICAL FEATURES(Chronic bronchitis)
Any patient who coughed up sputum on most days of at least 3 consecutive months for more than 2 successive years.
This inflammation eventually leads to scarring of the lining of the bronchial tubes.
Chronic bronchitis affects people of all ages, but is higher in those over 45 years old.
Incidence of chronic bronchitis in Females are increased by more than twice in comparison to males

8. CLINICAL FEATURES(Emphysema)
pathological process of permanent destructive enlargement of the airspaces distal to the terminal bronchioles.
Begins with the destruction of air sacs (alveoli) in the lungs where oxygen from the air is exchanged for carbon dioxide in the blood. Damage to the air sacs is irreversible and results in permanent "holes" in the tissues of the lower lungs. 

9. CLINICAL FEATURES
Enquiry should be made as about the presence of oedema and morning headaches which may suggest hypercapnia.
Breath sounds are typically quiet; crackles may accompany infection or bronchiactasis.
Leg oedema usually due to failure of salt and water excretion due to hypoxic and hypercapnic kidney.
Right heart seldom “fails” in COPD

10. Clinical examination
Clinical examination of the chest in mild to moderate disease might be normal.
Variable numbers of inspiratory and expiratory low to medial pitched ronchi are audible in most patients.
Crackles(cripitations)which may disappear after coughing may be audible over the lower zones.

11. CLINICAL FEATURES
Ronchi, especially on forced expiration. A reduction in the length of the trachea palpable above the sternal notch. Trachea descent during inspiration (Tracheal Tug). Contraction of sternomastoid and scalene muscles on inspiration

12. CLINICAL FEATURES
Excavation of the suprasternal and supraclavicular fossae during inspiration, together with indrawing of the costal margins and intercostal spaces.
Increased antero-posterior diameter of the chest relative to the lateral diameter; loss of cardiac dullness.
Loss of weight common (often stimulates unnecessary investigation).

13. CLINICAL FEATURES
Pursed lip breathing-physiological response to decrease air trapping. Flapping tremor and bounding pulse (due to hypercapnia). Peripheral oedema which may indicate corpulmonale. Raised JVP, right ventricular heave, loud pulmonary second sound, tricuspid regurgitation

14. CLINICAL FEATURES
Pink puffers; Thin and breathless and maintain a normal PaCO2 until the late stage of disease
Blue bloaters; They tolerate hypercapnia earlier and may develop oedema and secondarypolycythaemia

17. INVESTIGATIONS OF COPD
Chest x-ray;To Look for lung cancer,bullae.
Complete blood count to document polysthaemia and to exclude anaemia.
For young with basal emphysema α1- antiproteinaseassay.
Lung function test to document obstructive ventilatory defect with partial response to bronchdilatores

20. Wayne McLaren…Former Marlboro Man
Age 30…a robust
young man
Age 51…riding
into the sunset

21. Laboratory study 1-Markedly reduced arterial pO2
Arterial Blood Gas (ABG):
1-Markedly reduced arterial pO2
2-Elevated arterial pCO2 (40-50) mmHg
B-Pulmonary Function Tests:
Residual Volume increased .
FEV1 decreased ,FEV1/FVC decreased .
FEF (mid-flows) decreased
Diffusion capacity (DLCO) near normal

22. MANAGEMENT OF COPD A-Smoking cessation. B-Bronchodilators.
C-Corticosteroids.
D-Pulmonary rehabilitation.
E-Oxygen therapy.
F-Surgical intervention.
G-Other measures.
H-Palliative care.

23. MANAGEMENT OF COPD

24. MANAGEMENT OF COPD E-Oxygen therapy
Arterial blood gases in clinically stable patients on optimal medical therapy on at least two occasion 3 weeks apart:
PaO2<7.3kPa(55mmHg) irrespective of PaCO2 and FEV1<1.5l.
PaO kPa(55-60mmHg)plus pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia.
Patient stopped smoking
Use at least 15hours/day at 2-4L/min to achieve a PaO2>8kPa(60mmHg) with out unacceptable rise in PaCO2

25. Treatments for Alpha1 antitrypsin deficiency-related (AAT) emphysema
Treatments for AAT deficiency emphysema including AAT replacement therapy (a life- long process) and gene therapy are currently being evaluated. 
It is hoped that a clinical trial on gene therapy will take place within the decade.

26. Vaccination in COPD
Although there is little evidence of a direct benefit of vaccination in patients with COPD, It is recommend that;
Pneumococcal vaccination and annual influenza vaccination should be offered to all patients with COPD in an attempt to reduce both disease-specific mortality and mortality from all causes.