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

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)

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..

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.

PATHOPHYSIOLOGY OF COPD Occurs in Cigarette smokers 10-12 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

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

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. 

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

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.

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

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).

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

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

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

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

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 25-75 (mid-flows) decreased Diffusion capacity (DLCO) near normal

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.

MANAGEMENT OF COPD

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. PaO2 7.3-8 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

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.

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.