1. Chronic obstructive pulmonary disease

2. DEFINITION
It is a disease state characterized by air flow limitation that is not fully reversible.
COPD is a general term that covers a variety of other disease, including:
Chronic bronchitis
Emphysema 

3. Risk factors The risk factors associated with the development of COPD can be divided into host factors and environmental factors and combination of these risks leads to expression of the disease. Risk factors for development of COPD
AAT (alpha1 - antitrypsin) is a plasma protein that protects cells, especially those in the lung, from destruction by elastase released by neutrophils.
Environmental exposures
Host factors
Cigarette smoking and environmental tobacco smoke
Genetic predisposition (AAT deficiency)
Occupational dusts and chemicals
Airway hyperresponsiveness
Air pollution
Impaired lung growth

4. Etiology and pathogenesis
Smoking is the most important risk factor in the development of COPD, it causes tissue destruction &impaired repair mechanism .Not all smokers go on to develop COPD ,but a genetic factors can modified each individual's risk ,as well as the age when starting to smoke &total pack/years smoked contribute to the problem .
Occupational exposure to chemical, fumes, irritants, dust & gases cause also inflammatory response in the lungs (airways, parenchyma & pulmonary vasculature).

5. The observation that α1-antitrypsin-deficient individuals are at increased risk of developing emphysema has led to an imbalance between proteinases and antiproteinases leads to lung destruction.
Oxidative stress also contributes to the development of COPD by damaging various proteins and lipids, leading to cell and tissue damage. It also decreases the activity of antiproteinases.

6. Inflammation here is different from that of asthma; the inflammatory cells that predominate differ between the two conditions, with neutrophils playing a major role in COPD and eosinophils and mast cells in asthma. Mediators of inflammation also differ with LTB4, IL-8, and TNF-α predominating in COPD, compared with LTD4, IL-4, and IL-5 among the numerous mediators modulating inflammation in asthma.
Pathological changes of COPD are widespread , affecting large and small airways, lung parenchyma and the pulmonary vasculature. An inflammatory exudate is present that leads to mucous hyper secretion, ciliary's dysfunction, airflow limitation and hyperinflation , gas exchange abnormalities, pulmonary hypertension.

7. In sever COPD, secondary pulmonary hypertension leads to the development of right-sided heart failure or cor pulmonale.
Another important systemic consequence of COPD is a loss of skeletal muscle mass and general decline in the overall health status.

8. Pathophysiology of COPD

9. Chronic bronchitis
It is a condition with chronic or recurrent excessive mucus secretion into bronchial tree with cough that is present on most days for at least 3 months of the year during at least 2 consecutive years. 

10. Clinical features of chronic bronchitis
Chronic productive cough, excess mucus production and a degree bronchospasm, resulting in wheezing & dyspnea.
Hypoxia & hypercapnia (high level of CO2 in tissue) are also common, that is why patient referred to as a" blue bloater ', i.e. cyanosed.

11. Emphysema
It’s a permanent changes in the anatomy of the lung with enlargement &destruction of the alveoli, respiratory bronchioles, alveolar duct & alveolar sac result in loss of available gas exchange surface , impaired gas exchange &impaired ventilation.
Secondly it loses elastic recoil in the small airways.

12. Clinical features of emphysema
A patient with emphysema will experience increasing dyspnea even at rest , there is minimal cough &the sputum produced is scanty &mucoid.
The patient will breath rapidly (tachypnea).
Emphysema patients are termed ''pink-puffers'' because they maintain adequate oxygenation through an increased work of breathing .

14. Investigation of COPD
Lung function tests by using Spirometer, to measure lung volume .Main measurement made is the forced expiratory volume .
Additional investigations at the diagnosis of COPD are: Chest x-ray, pulse oximetry, full blood count (to identify anemia or polycythemia), alpha 1 antitrypsin (in case of no or minimal smoking or presence of family history). ECG (to assess cardiac status if features of cor- pulmonale) & sputum culture (to identify organisms if sputum is persistently present &purulent).

15. Aim of treatment Treatment 1-Prevent disease progress.
2-Relive symptoms.
3- Improve exercise tolerance.
4- Improve health status.
5-Prevent &treat complication (hypoxemia& infection).
6- prevent and treat exacerbations.
7- Reduce mortality.

16. Bronchodilators
Used to reverse airflow limitation.
Short acting bronchodilators
B2 agonist
Among bronchodilators there are Inhaled B2 adrenoceptor agonists. It should be tried initially ,they produce rapid relief and have a low incidence of SE .
The effects short acting B2 agonists last for 4 h and they should be used as required for symptom relief.

17. Anticholinergic drugs
Ipratropium bromide is the primary anticholinergic agent used in COPD, given as mitered dose inhaler (MDI) & as a solution for nebulization. Onset of action 15 minutes, with a maximum bronchodilator effect in hr & a duration of action 4-6 hr.

18. If patients remain symptomatic despite a short acting bronchodilators then maintenance therapy is recommended, with:
FEV1 is greater than or equal to 50% predicted: long acting B2 agonist or long acting anticholinergic.
FEV1 is less than 50% predicted: a combination of either long acting B2 agonist and inhaled corticosteroid or long acting B2 and long acting anticholinergic.

19. If the patients remain shortness of breath, or has exacerbation, then triple therapy should be considered ( inhaled corticosteroid and long acting B2 in a combination inhaler together with a long acting anticholinergic).

20. Long acting bronchodilators
Long acting bronchodilators include long acting B2 agonist and long acting anticholinergic.
1- long acting B2 agonist/ e.g. Salmeterol & Formoterol used twice daily.
2- long acting anticholinergic agent / e.g. Tiotropium has 24hr duration .

21. Methylxanthin
The use of theophylline should considered after a trial of short acting with long acting bronchodilators.
Whenever it is tried in managing COPD ,a trial of several weeks should be carried & if an improvement obtained, then theophylline can be continued as a maintenance therapy.

22. Corticosteroids
Patient with COPD shows a poor response to corticosteroid.
The long term benefits of inhaled corticosteroids in COPD have only seen in patients with moderate to severe disease, it causes a reduction in the number of exacerbation &a slowing of the decline in health status, but not effect in improving lung function and result in an increased risk of pneumonia.
Some patients with advanced disease may require maintenance oral therapy, in such case a lowest possible dose should be used and the patient regularly assessed for the development of osteoporosis.

23. Mucolytic
It may be benefit in stable COPD, if there is a chronic productive cough (with sputum).Benefit must be assessed for a reduction in the frequency of cough &for sputum production.

24. Antibiotics and immunization
Antibiotic therapy is vital if a patient develops purulent sputum.
A single dose of pneumococcal vaccine and annual influenza vaccinations should be offered to those with chronic airflow obstruction.

25. Supplement oxygen therapy
It is necessary to improve hypoxia &prevent secondary organ damage. 

26. Finally we can say treatment of COPD require stop of smoking, physiotherapy , artificial ventilation, hydration & drainage (to remove excessive mucous).

27. Treatment of Cor-pulmomale
Treatment is symptomatic &involves managing the underlying airways obstruction, hypoxemia& pulmonary edema that developed.
Peripheral edema managed by using thiazide or loop diuretic. Oxygen is used to treat hypoxemia.