COPD - Chronic Obstructive Pulmonary Disease |medico X| Pathology

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1. COPD CHRONIC OBSTRUCTIVE PULMONARY DISEASE

2. OBSTRUCTIVE LUNGS DISEASE Emphysema Chronic bronchitis Asthma Bronchiectasis

3. Emphysema & chronic bronchitis are often clinically grouped together and referred to as chronic obstruction pulmonary disease COPD since majority of patients have features of both almost certainly because they show a major trigger - cigarette smokers In addition small airway disease a variant of chronic bronchitis is now known to contribute to obstruction of both in emphysema & chronic bronchitis while asthma is distinguished from chronic bronchitis and emphysema by the presence of reversible Broncho spasm. Some patient with otherwise typical asthma also a reversible component it is clinically common to label such person as having COPD/Asthma

4. COPD is a major public health problem . It is the 5 th leading cause of morbidity and mortality as world wide. There is clear cut association between heavy cigarette smoking and emphysema , and women and African American are susceptible than other groups . About 40 – 50% of heavy smokers developed COPD conversely 80 % COPD is due to smoking . Other risk factors include environmental and occupational pollutants, airway hyper responsiveness and genetic polymorphism

5. Emphysema Emphysema is characterized by irreversible enlargement of the airspaces distal to the terminal bronchiole , accompanied by destruction of their walls without obvious fibrosis. Based on the segments of the respiratory units that are involved Emphysema is classified into four major types Emphysema is classified according to its anatomical distribution within the lobule ( lobule is a cluster of acini , the terminal respiratory units ) Centriacinar Pancinar Paraseptal Irregular

6. Centriacinar ( Centrilobular Emphysema ) Most common clinically seen Emphysema. Central/proxial parts of the acini , formed by respiratory bronchides are affected. Distal Alveoli are spared Both emphysematous and normal airspaces exist within the same acinus and lobule. Upper lobes of the lungs are affected (particularly the apical segments) Occurs predominantly in Heavy Smokers

7. Panacinar (Panlobular) Emphysema Acini are uniformly enlarged from the level of Respiratory bronchiole to the terminal blind alveoli “PAN” refers to entire acinus . Lower zones (base of the lung ) and anterior margins of the lung are involved. Associated with – α 1 – antitrypsin deficiency.

8. Distal Acinar ( Paraseptal ) Emphysema Distal part is predominantly involved . Proximal portion of acinus is normal . More severe in the upper half of the lungs . Characteristic findings – Multiple, continuous, enlarged airspaces from less than 0.5 cm to more than 2.0 cm in diameter . Associated with Spontaneous PNEUMOTHORAX . Irregular Emphysema – Acinus are irregularly involved . Most common Micro scopic emphysema .

9. Pathogenesis 1 ) Inflamatory mediators and Leukocytes Leukotriene B 4 IL 8 , TNF are increased Released by Epithelial Cells and macrophages Attract inflamatory cells Amplify inflamatory process Induce structural charges (growth factors)

10. 2 ) Protease – Antiprotease Imbalance – Protease – Break down Connective tissue components . Antiprotease – Have protective function . Deficiency of protective Antiprotease leads to Emphysema 3 ) Oxidative stress – Substances in tobacco Smoke produce oxidants Tissue damage and inflammation Inactive NF2Gene (NF2Gene protect cells from oxidant damage , Encodes for a transcription factor that serve as a sensor for oxidants ) 4 ) Infection – Bacterial and viral infections may exacerbate the associated Inflammation .

11. Clinical Features Dyspnea Weight loss History of smoking Pursed lip breathing Flat diaphram Barrel shaped chest Impaired Expiratory Airflow- measured through Spirometery Patients are known as PINK PUFFERS . Death occurs due to –. Coronary artery disease Respiratory failure Right sided heart failure Massive collapse of lung Treatment Smoking cessation Oxygen therapy Long term bronchodilators with inhaled corticosteroids Lung Transplantation Physical therapy

12. Other forms of Emphysema Compensatory Hyperinflation – Hyper expansion of residual lung Parenchyma following surgical removal of a diseased lung/lobe. Obstructive overinflation - Lung expands because air is trapped within it. example- congenital lobar overinflation in infants Overinflation Bullous Emphysema- Large subpleural blebs/bullae (spaces greater than 1 cm in diameter in distended slate. Interstitial Emphysema – Entrance of air into the connective tissue Stroma of the lung , mediastinum/subcutaneous tissue Because collaterals bring in air behind the Obstruction. (Collateral consist of PORES OF KOHN and Canals of lambert) Because of Obstructive agent

13. ASTHMA Usually caused by an Immunological reaction which is marked by episodic Bronchoconstriction due to Increased airway sensitivity to a variety of stimuli Inflammation of the bronchial walls Increased mucus secretion Asthma is a Chronic disorder of the Airway(Reversible COPD)

14. CLASSIFICATION OF ASTHMA ATOPIC/EXTRINSIC NON ATOPIC/INTRINSIC

15. ATOPIC ASTHMA The most common type of asthma classic example of IgE mediated (type 1) hypersensitivity reaction family history present (commonly) Trigger environmental allergens dust,pollen,animal dander and food Skin test is positive in atopic asthma

16. NON-ATOPIC ASTHMA Not allergens sensitization Family history less common Skin test usually negative Triggering events Respiratory infection due to viruses (rhinovirus, parainfluenza virus) Inhaled air pollutants – smoke O3 NO2 etc. Nasal polyps and chronic bronchitis are commonly present in non atopic asthma

17. OTHER ASTHMA Drug induced asthma Aspirin sensitive asthma aspirin drug inhibits cyclooxygenase pathway of arachidonic acid metabolism produce leukotrienes bronchoconstriction asthma

18. Occupational asthma Triggering agents fumes(epoxy resins, plastic ) organic and chemical dusts (wood cotton platinum ) Gases (Toluene

19. Environmental factors Industrialise environments contains - polluants SO2 , O3 , NO2 etc. Microbial antigens -virus infection Allergic factor - dust , pollen etc. Hygiene hypothesis The idea that microbial exposure during early development reduces the later incidence of allergic diseases .

20. Pathogenesis

21. Acute immediate response Increased IgE in serum bind with mast cells mast cell degranulation release mediators like - Histamine - bronchoconstriction leukotrienes –prolong bronchoconstriction increased vascular permeability increased mucus secretion prostaglandins -bronchoconstriction Vasodilation platelets activating factors chemical facto9rs

22. MORPHOLOGICAL FEATURES Gross features- Lungs are over distended due to over inflation cut surface shows- occlusion of bronchi and bronchioles by mucus plugs Microscopic features - Churchman' s spirals Charcot Leyden crystals Bronchial wall shows - thickened basement membrane submucosal edema inflammatory infiltrates hypertrophy of submucosal glands and smooth muscle

23. Clinical features A classis acute asthma attack lasts up to several hours Cardinal symptoms- chest tightness, dyspnea, wheezing, cough ( with or without sputum production ). 2. status asthmatics when attack occurs continuously it may result in more serious condition

24. BRONCHIECTASIS Bronchiectasis is a disorder in which destruction of smooth muscles and elastic tissue by chronic necrotizing infections leads to permanent dilation of bronchi and bronchioles. Most characteristic clinical manifestation Persistent cough with expectoration of copious amounts of foul smelling, purulent sputum

25. These 2 Mechanism are seen in Hereditary & Congenital factor Obstruction As secondary complication Inflammatory destructive process of bronchial wall Endobronchial obstruction Infections by two mechanism ETIOPATHOGENESIS

26. These 2 Mechanism are seen in Hereditary & Congenital Factors Congenital bronchiectasis Cystic fibrosis Primary immunodeficienies Kartageners syndrome Atopic bronchial asthma

27. (B) OBSTRUCTION due to Foreign bodies Endobronchial tumors Compression by enlarged hilar lymph node Healed Tuberculosis (C) As Secondary Complication Necrotizing pneumonia 2) Tuberculosis

28. Morphological Features Grossly : - Lung may be involved diffusely or segmentally. Bilateral involvement of lower lobes; left lower lobe is more often involved. Pleura – fibrotic & thickened & adhere with chest wall. Lung parenchyma – fibrotic & reduce.

29. Types of bronchial dilatations in bronchiectasis

30. Cut section of bronchiectasis

31. Microscopically Bronchial epithelium. may be Normal/Ulcerated/Squamous metaplasia 2) Bronchial wall. Leucocytes infiltration 3) Muco -pus. 4) Mucosal layer damaged.

32. Microscopic features of bronchiectasis

33. Clinical features Chronic cough with foul smelling sputum Hemoptysis Recurrent pneumonia Sinusitis (diffuse bronchiectasis) Late complications (when uncontrolled for years) Clubbing of fingers Amyloidosis (AA type) Metastatic abscesses

34. Chronic bronchitis chronic bronchitis is define clinically as the persistence cough with sputum production for at least 3 months in last 2 consecutive years in absence of any other identifiable cause . common in habitual smokers inhabitants of smog laden cities . chronic bronchitis is one of the spectrum of COPD with emphysema being the other most patients lies somewhere in between having features of both.

35. Chronic Bronchitis for Year accelerate declining in lung function leads to cor pulmonale & heart failure Atypical metaplasia and dysplasia in respiratory epithelium Can transform into cancer OR

36. Etiopathogenesis Two most common etiological factors responsible for majority of cases of chronic bronchitis are cigarette smoking and atmospheric pollution . Other contributory factors are occupational, inflectional ,familial and genetic factors

37. SMOKING Most common identified factor implicated in causation of chronic bronchitis and in emphysema is heavy smoking. Heavy cigarette smokers have 4-10 times higher proneness to develop chronic bronchitis . Prolong cigarette smoking appears to act on lungs in many ways . It impairs ciliary movement. It inhibits the function of alveolar macrophages. It leads to hypertrophy and hyperplasia in mucus secreting glands. It causes considerable obstruction in small airways. It stimulates the vagus and causes bronchoconstriction.

38. ATMOSPHERIC POLLUTION The incidence of chronic bronchitis is higher in industrialized urban area where air is polluted . Some of the atmospheric pollutants which increase the risk of developing chronic bronchitis are Sulphur dioxide nitrogen dioxide particulate dust and toxic fumes OCCUPATION Worker engaged in certain occupation such as in cotton mills Plastic factories etc. are exposed to various organic or inorganic dust which contribute to Disabling chronic bronchitis in such individual.

39. INFECTION Bacterial viral and mycoplasma infection do not initiate chronic bronchitis but usually occur secondary to bronchitis . Cigarette smoke however predispose to infection responsible for acute exacerbation in chronic bronchitis. FMAILIAL AND GENETIC FACTORS There appears to be poorly define familial tendencies and genetic predisposition to developed disabling chronic bronchitis. However it more likely that non smokers family members who remain sin the air pollution of home are significantly exposed to smoke and hence have increased blood level of CO

40. MORPHOLOGIC FEATURES Grossly- the bronchial wall is thickened hyperemic and edematous . Lamina of bronchi and bronchioles may contains mucus plug and exudates. Microscopically There is increased Reid index ; Reid index is ratio between thickness of the submucosal mucus gland ( ie.hypertrophy and hyperplasia) in the cartilage containing large airways to that of the total bronchial wall as measured from the basement membrane to the cartilage . Increase in thickness can be quantitatively assessed by micrometer lens or by morphometry . Bronchial epithelium may show squamous metaplasia and dysplasia There is little chronic inflammatory cells infiltrate Non cartilage containing small airways show goblet cell hyperplasia and intraluminal and peribronchial fibrosis

41. CLINICAL FEATURES Persistent cough with copious expectoration of long duration ; initially beginning in the heavy smokers with ‘morning catarrh’ or ‘throat clearing’ which worsens in winter Recurrent respiratory infection are common Dyspnea is generally not prominent at rest but is more on exertion. Patient are called ‘ blue bloaters’ due cyanosis and edema Features of right heart failure ( cor pulmonale ) are common Chest x-ray show enlarge with prominent vessels.

42. SMOKING KILLS

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