1. Chronic obstructive pulmonary disease
Dr.kassim.M.sultan
F.R.C.P

2. Objectives:
Upon completion of this lecture the students will be able to :
Define Chronic obstructive pulmonary disease ( COPD )
Identify its etiological causes
Describe its clinical features
Illustrate ways of diagnosis
Distinguish between COPD and other causes of dyspnea
Manage a straight case of COPD

3. Definition
Chronic slowly progressive disorder,characterised by air flow limitation that is not fully reversible.
It includes the following diseases:
1-chronic bronchitis.
2-emphysema.
3-chronic bronchiolitis(narrowing of small bronchioles).

4. Chronic bronchitis
Chronic cough with expectoration of sputum(phlegm)for 3 months or more,for 2 successiveyears or more.
Other causes of chronic cough like asthma,pulmonarytuberculosis,gastroesophage-al reflux disease&sinusitis should be excluded.

5. Emphysema
Defined pathologically as: permanent(irreversible)destruction of the alveolar wall &enlargement of the terminal air spaces.
Emphysema has 3 radiological patterns:
1- Panacinar emphysema can occur with dilated air spaces evenly distributed across the acinii.
2- Centriacinar or proximal emphysema can occur with dilated air spaces found in association with the respiratory bronchioles.
3- Periacinar or paraseptal emphysema can occur with dilated air spaces at the edge of the acinar unit and abutting a fixed structure, such as the pleura or a vessel.
Chronic bronchitis &emphysema frequently co-exist together.

6. Anatomic varieties of emphysema. A. Centriacinar (centrilobular). B
Anatomic varieties of emphysema. A. Centriacinar (centrilobular). B . Paraseptal (distal acinar). C .Panacinar (panlobular). D. Irregular (scar). The dashed lines mark the edge of the acinus. Only centriacinar and panacinar emphysema are commonly observed in COPD

8. ETIOLOGY
1-cigarette smoking:remains the most important factor,acounts for more than 90% of cases depending on intensity&duration of smoking(number of packs /day multiplied by number of years: pack/year 2-recurrent respiratory infection may accelerate decline in FEV1.e.g:. HIV infection associated with emphysema . 3-Occupation-coal&gold miners,cotton textiles&cadmium(battery industry)

9. Etiology-continue
4-Outdoor and indoor air pollution.E.g those who use wood,animal dung,coal for heating&cooking purposes.
5-Lung growth-insults including childhood infections or maternal smoking may affect growth of lung during childhood.
6-Low birth weight.
7-Low socioeconomic status .
8-Genetic factors:autosomal recessive,α1- antitrypsindeficiency (protease inhibitor) in 1-2%of COPD patients

10. pathology
In chronic bronchitis there is an increase in number of goblet cells&decrease in ciliated cells with adventitial fibrosis&neutrophils infilteration.
In emphysema there is destruction&dilatation of airspaces distal to terminal bronchioles, without obvious fibrosis with subsequent loss of elastic recoil and hyperinflated lungs.

11. Clinical features
The three most common symptoms in COPD are cough(often referred as smoker”s cough), sputum production, and exertional dyspnea.
Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without exclusion of bronchogenic carcinoma.
Exacerebations are defined as an increase in cough amount&colour of sputum&increase dyspnea.

12. Examination
systemic wasting, with significant weight loss, bitemporal wasting, and diffuse loss of subcutaneous adipose tissue seen in advanced emphysema.
Increase respiratory rate,cyanosis,flapping tremor(asterixis)seen in respiratory failure.
Sweating,bounding pulses&morning headache due to CO2 retention.
Raised J.V.P,Rt.ventricular heave,loud P2,tender hepatomegaly&pitting edema due to corpulmonale.

13. examination May be normal in mild-moderate cases.
odor of smoke or tar staining of fingernails.
The three most common symptoms in COPD are cough(often referred as smoker”s cough), sputum production, and exertional dyspnea.
Wheezes,rhonchi,&crackles(cleared by cough).
Barrel chest,decrease in tracheal l;ength above sternal angle,distended neck viens during expiration.
Pursed lip breathing, Use of accessory muscles of respiration.

14. investigations FBC,ESR. Imaging: a-Chest x-ray shows:
1-chronic bronchitis:increase hilar shadowing(linear lines arising from the hila)
2-emphysema:hyper inflated chest,low tented diaphragm,small elongated heart,prominent pulmonary artery,bullae,incraese radiolucency of retrosternal space on lateral CXR.
b-chest CT scan:used to asses the severity of emphysema,locate the anatomical distribution of bullae before surgery&before lung transplant.

15. Investigations-continue
E.C.G:low voltage complexes,p- pulmonale,Rt.ventricular hypertrophy.
Pulmonary function test:
1- inhaledB2-agonist reversibility test(no 15%decline in FEV1,used to differentiate COPD from asthma)
2-FEV1 less than 80%predicted indicate mild disease,between 50-80% indicate moderate disease,between 30-50% indicate severe disease,whie less than 30% indicate very severe disease.

16. Investigations-continue
FEV1/FVC less than 70%.
Residual volume increase& total lung capacity leadind to air trapping.
Dlco:co transfer factor is markedly decreased in severe emphysema.
Blood gases:increase in Pco2&decrease in po2

17. Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease. The lungs are hyperinflated with flattening of both hemidiaphragms.

18. COPD/lat.view showing barrel chest due to increase in retrosternal airspace

19. Differential diagnosis&complications
1-asthma:family history of atopy,occur at any age,intermittent symptoms,+ve reversibility test. 2-LVF:cardiomegaly,S3,basal rales,kerly B lines. Complication: 1-respiratory failure. 2-corpulmonale. 3-pneumothorax(ruptured bullae).

20. Treatment Stop smoking. Avoidance of dusty,polluted environment.
Treat infection(the commonest organisms that cause acute exacerebation are streptococci,H.influenzae&moraxella catarrhalis)according to sputum culture&sensitivity by amoxycillin 250 mg 8hourly,or amoxiclav(if B- lactamase resistant)375mg 8hourly for 5-10 days
Pneumococcal vaccine&infleunza immunization.

21. Treatment
Bronchodilators:inhaled short acting B2-agonist in mild COPD,if no response,add inhaled short acting ipratropium bromide,if no benefits add inhaled long acting B2-agonist(salmetrol,formeterol)
Add inhaled long acting anticholinergic(tiotropium),if the above treatment failed
Inhaled longactingCorticosteroid(budesonide,fl- uticasone) indicated when FEV1 decreased to less than 50% or the patient has 2 or more exacerebation in the last year.

22. Treatment
Oral methylxanthines, such as theophyllines, can be used as a maintenance therapy and may improve symptoms.
Mucolytic agents like N-acetyl-cystiene 200mg 8hourly orally used in chronic cough&sputum.
Long-term domiciliary oxygen therapy (LTOT) a minimum of 15 hours/day has been shown to improve survival, prevent progression of pulmonary hypertension, decrease the incidence of secondary polycythaemia, and improve neuropsychological health.

23. Treatment
Pulmonary Rehabilitation: breathing techniques ,education,good nutrition&psycho-social support.
Specific treatment in the form of intravenous alpha1AT augmentation therapy is available for individuals with severe alpha1AT deficiency.
Smoking cessation programs by nicotine replacement therapy(gum,transdermal patches,nasal spray,inhalers)&bupropion(antidpressant)

24. Acute exacerbations of COPD
defined as increase in dyspnea and cough and change in the amount and character of sputum.
They may or may not be accompanied by other signs of illness, including fever, myalgias, and sore throat.

25. Causes
1-infections: Viral respiratory infections are present in approximately one-third of COPD exacerbations(rhinovirus, influenza, coronavirus, and adenovirus)
bacterial in 1/3 of patients(Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis)
2-In a significant minority of instances (20–35%), no specific precipitant can be identified but may be change in air quality.

26. TREATMENT oxygen: 24% or 28% should be used.
- Bronchodilators:increase the doses of inhaler or Nebulised short-acting β2-agonists combined with an anticholinergic agent should be administered.
- Glucocorticoids: Oral prednisolone 30 mg for 10 days are recommended but shorter courses may be acceptable.
Antibiotics.
Mechanical Ventilatory Support:
a-noninvasive positive pressure ventilation when the respiratory rate between 25-35/min,the patient is co- operative &conscious.
b- -invasive mechanical ventilation when the respiratory rate above 35/min,the patient is unco-operative or unconscious.

27. Summary :
*COPD is a chronic progressive disease, related mainly to smoking.
*Patient presented with chronic cough, sputum and dyspnea.
*Hyperinflation and air trapping are recognize features.
*Treated by stopping smoking, O2, Inhaled bronchodilator and steroid in acute exacerbation.

28. Thanks for your listening