This document provides information on various diseases of the lungs including atelectasis, bronchiectasis, emphysema, bronchial asthma, adenocarcinoma lung, pulmonary edema, and bronchopneumonia. For each condition, it discusses etiology, pathogenesis, diagnosis, clinical manifestation, morphology, and management. It also includes histopathology slides illustrating various lung pathologies such as alveolar collapse, inflammatory changes, fibrotic changes, and remodelling of airways in asthma.

1. Diseases of Lungs Patho-B Lab

2. NEW SLIDES Atelectasis with congestion Bronchiectasis Emphysema Bronchial Asthma Adenocarcinoma Lung Pulmonary edema Bronchopneumoniae

3. OLD SLIDES Lobar Pneumoniae Viral Pneumoniae Lung Abscess Tumor Emboli- Lung Chronic Pulmonary Congestion TB Lungs

4. Atelectasis, known as Lung Collapse, is loss of lung volume caused by inadequate expansion of air spaces.

5. Types of Atelectasis Compression Atelectasis- Usually associated with accumulation of fluids/blood/air with in the pleural cavity which mechanically collapse the adjacent lung.. Frequently occurs with pleural effusions caused most commonly by Conjustive Heart Failure. Reversible ResorptionAtelectasis- Occurs when an obstruction prevents the air from reaching distal airways. Most common cause of resorptionatelectasis is obstruction of bronchus by a mucopurulent plug. Reversible Contraction Atelectasis- Occurs when either local or generalized fibrotic changes in the lung/pleura hamper expansion and increase elastic recoil during expiration. Irreversible

6. Diagnosis:- Radiological examination ----X-ray Clinical Manifestation Dyspnea Productive Cough ***Significant adventitious sounds on Auscultation,dullness on percussion Treatment :- Treating the underlying cause. Bacteriological and Mycological examination of sputum( To treat the underlying cause if infectious in nature with relative intervention) Preventive measures for aspiration in childrens, post op surgical patients decreases the risk of Atelectasis Complication:- May worsen bronchial Asthma,Bronchiectasis.

7. LPO Hallmark Alveolar Collapse

8. LPO Hallmark Alveolar Collapse

9. LPO Hallmark Alveolar Collapse

10. Hallmark Alveolar Collapse LPO

11. **Congestion **Anthracosis **Alveolar collapse HPO Congestion Here can give A clue of the Patient sufferering From compressive Type of Atelectasis

12. Bronchiectasis is the permanent (abnormal) dilation of bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue, associated with chronic necrotizing infections. 2 Processes involved in Pathogenesis Obstruction Chronic persistent infection

13. Diagnosis:- Sputum culture – May reveal Pseudomonas aeruginosa, fungi such as Aspergillus and various Mycobacteria Radiological Examination – X-ray findings not significant unless very gross... CT scan is much more sensitive for Bronchiectasis Clinical Manifestation Chronic productive cough(Foul smelling) Fever,Malaise, aand increased cough and sputum volume. Haemoptysis(can be slight of massive) Halitosis is a common feature Clubbing of fingers may develop Management In patients with airflow obstruction, bronchodilators to enhance airway patency. Physiotherapy – to keep the dilated bronchi empty of secretions Antibiotic therapy(Ciprofloxacin, ceftizimide 12 hourly 25—750 mg IV infusion)

14. Normal Bronchus

15. Normal Bronchioles

16. LPO Dilated Bronchiole with secretion within

17. LPO Dilated Bronchiole with secretion within

18. HPO Inflammatory changes in the wall of the bronchiole.. Necrotized smooth muscles and supporting tissue due to inflammation

19. LPO Bronchioles

20. Dilated Bronchi LPO

21. Secretions within The bronchi due to Accumulation of Pus in dilated bronchi LPO

22. Prominent Fibrotic change and Inflammatory change In entire slide

23. Inflammatory and fibrotic Changes found in the Surrounding lung tissue

24. Bronchiectatic cavity Filled with secretions , Lined by normal epithelium With some granulation tissue HPO

25. HPO Inflammatory Changes in the Bronchial wall

26. ** Inflammatory changes **Fibrotic changes **Anthracosis LPO

27. ** Inflammatory changes **Fibrotic changes HPO

28. ** Inflammatory changes **Fibrotic changes LPO

29. Characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of wall without obvious fibrosis Most common cause – Smoking (Nicotine) 2 Pathogenic Mechanisms are Excess cellular proteases with low antiprotease activity Excess of oxygen species

30. Types of Emphysema Centriacinar(Centrilobar) Emphysema Involves central of proximal acinisparring the distal alveoli. Panacinar(Panlobar) Emphysema Uniform enlargement of the acinifrom the level of respiratory bronchiole to terminal alveoli. Distal acinar(Panseptal) Emphysema Proximal part of acini is normal but distal part is involved Irregular Emphysema Irregular involved acini, almost invariably associated with scarring. Most common form of Emphysema

31. Diagnosis Alpha1-antiprotease assay CT is more sensitive that X-ray for Emphysema Clinical Manifestation Dyspnea is usually the first symptom(Progressive) Cough and Wheezing in patient with underlying Chronic bronchitis or Chronic asthmatic bronchitis. Weight loss Barrel Chest Management Smoking cessation Oxygen Therapy Pulmonary rehabilitation Mucolytic therapy

32. Thinning And destruction of Alveolar walls LPO

33. LPO Thinning And destruction of Alveolar walls

34. Thinning And destruction of Alveolar walls LPO

35. Thinning And destruction of Alveolar walls LPO

36. Characterized by chronic airway inflammation and increased airway hyper-responsiveness Funtionally characterized by the presence of airflow obstruction which is variable over the short periods of time or is reversible with treatment

37. Types of Asthma Atopic/Extrinsic Asthma – Most common type +ve Family History common +ve Allergy causing Attacks (Rhinitis, urticaria, eczema) Elevated Ig-E serum levels Non Atopic/ Intrinsic /Acquired Asthma– Non immune in nature +ve Family history uncommon No associated Allergy Ig-E serum levels are normal Drug Induced Asthma Drug like Aspirin provoke asthma Patient with Aspirin sensitivity present with Recurrent Rhinitis,Bronchospasm,urticaria Occupational Asthma Stimulated by fumes(plastics,resins), organic and chemical dusts(wood,cotton) Attacks usually develop after repeated exposure to the inciting agents

38. Triad of Reversible airway obstruction Chronic inflammation with eosinophils Bronchial smooth muscle cell hypertrophy Hyperreactivity

39. Significant Morphology in Asthma Macroscopic Occlusion of the bronchi and bronchioles by thick, tenacious Mucous plugs. Microscopic Mucous plug contain whorls of shed epithelium(Curschmann spirals) Numerous eosinophils and Charcot leyden crystals(collections of crystals made of eosinophil proteins) are also present

40. Diagnosis Diagnosis is made on the basis of compatible clinical history combined with the demonstration of the airflow obstruction Pulmonary function tests Measurement of allergic status( Elevated sputum or peripheral blood eosinophil count ) Airway inflammation assessment Clinical Manifestation Typically symptoms includes recurrent episodes of wheezing, chest tightness, breathlessness and cough Management Avoiding aggravating factors Short acting inhaled beta2- Agonist (Bronchodilators) – For patients with mild intermittent asthma(Symptoms less than once a week for 3 months and fewer than 2 nocturnal episodes) Long acting beta2 agonist(salmeterol,formoterol) if patient remains poorly controlled Low/high dose steroid therapy depending on the severity of symptoms

41. **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrate in walls -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls LPO

42. **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrate in walls -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls LPO

43. **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrate in walls -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls LPO

44. **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrate in walls -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls LPO

45. **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrate in walls -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls LPO

46. **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrates in wall -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls LPO

47. HPO **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrates in wall -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls

48. **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrates in wall -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls HPO

49. **Airway Remodelling in Asthma** -Thickening of Basement membrane of the bronchial epithelium -Edema and inflammatory infiltrates in wall -Increase in the size of the glands -Hypertrophy of the bronchial muscle walls HPO

50. Classification of Lung tumors for therapeutic purposes Small Cell Lung Carcinomas(SCLC) All small cell lung carcinomas have metastasized by the time they are diagnosed hence they cannot be cured by surgery, Chemotherapy and Radiation is the only treatment for SCLC Non small cell lung Carcinoma(NSCLC)- poor response to chemotherapy and are better treated by surgery. Squamous cell Adenocarcinoma ----- Most common of lung cancer in women and non smoker Large cell carcinoma

51. Most common of lung cancer in women and non smoker Precursor –Atypical adenomatous hyperplasia(AAH) Occur as central lesions but are more peripherally located Many arising in relation to peripheral lung scars (scar carcinomas) Histological types Acinar(Gland forming) Papillary Solid

52. In general all Adenocarcinomasgrow slowly and form smaller masses than other subtypes but they tend to metastasize widely at an early stage. Diagnosis:- Histologic diagnosis Bronchoscopy Bronchial biopsy CT/Ultrasound Clinical Manifestation Cough is common early symptom Haemoptysis Bronchial obstruction Recurrent pneumonia Lassitude and Weight loss- indicated metastatic spread Hoarseness Management Surgical resection for all Non small cell lung carcinoma-NSCLC

53. **Stromal invasion(Bronchial mucosa) **Desmoplasia (growth of fibrous or connective tissue)

54. **Stromal invasion(Bronchial mucosa) **Desmoplasia (growth of fibrous or connective tissue) ** Acinar type Gland forming Adenocarcinoma

55. **Stromal invasion **Desmoplasia (growth of fibrous or connective tissue)

56. **Stromal invasion(Bronchial mucosa) **Desmoplasia (growth of fibrous or connective tissue)

57. **Cytologicatypia **Pleomorphism

58. **Cytologicatypia **Pleomorphism

59. Caused due to accumulation of fluids in lungs Etiology Cardiogenic pulmonary edema Most common clinical problem seen frequently in left ventricular failure. Noncardiogenic pulmonary edema Renal failure Acute Respiratory distress syndrome(ARDS)

60. Signs:- JVP – increased, sweating, cool extremities, dullness and crepitation at base. Chest radiograph:- Cardiomegaly,pleural effusion. ECG- decreased left ventricular function Decreased PaO2 Can lead to Acute severe dyspnea. Management:- Treating the underlying cause Usually the prognosis is poor(with survival 2-3 years) unless Heart-lung transplantation is performed.

65. 4 stages of lobar/Broncho Pneumonia Congestion Affected lobe is heavy, red boggy,histologicallyvascular congestion can be seen with scattered neutrophils in the alveoli. Red hepatization Lung shows liver like consistency, the alveolar spaces are packed with neutrophils, red cells and fibrin. Gray hepatization Lung is dry,gray, and firm, because the red cells are lysed while the fibrinosuppurativeexudate persists within the alveoli Resolution Follows in umcomplicated cases, as exudates within the alveoli are enzymatically digested to produce granular, semifluid debris that is resorbed, ingested by macrophages, organized by fibroblast growing into it.

66. Pneumonia Diagnosis Radiological- X-ray(Pleural effusions) Microbiological- sputum direct smear Blood culture +ve for pneumococcal pneumonia Serology-For viral infections,mycoplasma,legionella Clinical Manifestation Typically presents as acute illness Systemic features – fever, shivering, vomiting,anorexia, headache. Pulmonary symptoms-cough(initially dry,painful and later accompanied by expectoration of mucopurulent sputum) Management Rest, cessation of smoking Antibiotic therapy Oxygen to all patients with tachypnea,hypoxemia,acidosis. Analgesic for pleural pain

67. Pneumonia generally defined as any infection in the lung. Initial infection is in bronchi which gradually extends in adjacent alveoli. Patchy distribution of inflammation implies Bronchopneumonia and is usually involves more than one lobe.

68. Bronchiolitis

69. Vascular congestion

70. Congestion Red Hepatization Gray hepatization

72. Bronchiolitis

73. Congestion

74. Congestion Red Hepatization Gray hepatization

75. Red Hepatization Gray hepatization

77. LPO Patchy Inflammation of the Interstitium and Septa Mononuclear infiltrates in alveolar wall

78. Inflammatory changes only in the interstitium

79. LPO Edematous walls Mononuclear infiltrates in The alveolar walls

81. There is fibrosis in the alveoli Along with purulent exudate (at the pointer) HPO Congested alveolar wall

82. Purulent exudate in High power shows presence of neutrophils HPO

83. Exudates in alveoli

84. Exudates in alveoli

85. Bronchopneumonia Bronchopneumonia:- Infection involving bronchi initially and then alveoli Viral pneumonia:- Interstitium involves Bacterial pneumonia:- Alveoli filled with exudates and fluid Viral pneumonia Bacterial pneumonia

86. Etiology:-Aspiration of Pyogenic organism most common cause of lung abscess Liquefactive type of necrosis. In lung abscess there is localized collection of pus, or a cavity lined by chronic inflammatory tissue. It may also be produced by infection of previously healthy lung tissue with Staph. Aureus,Klebsiella pneumonia.

87. Diagnosis – X-ray(segmental opacity with consolidation or collapse) Clinical Manifestation:- High Pyrexia Systemic upset Clubbing(10-14 days) Consolidation on chest examination Pleural rub common Management Oral Amoxicillin 6hourly effective in most of the patients- 2 weeks If Anaerobic – Metronidazole 400mg 8 hourly -2weeks

88. Complete destruction of lung parenchyma Due to the chronic inflammation

89. Complete destruction of lung parenchyma Due to the chronic inflammation

90. Neoplastic cells Within the vessel

91. Neoplastic cells Within the vessel

92. Congestion is a passive process resulting from impaired venous return out of the tissue. It may occur systematically, as in cardiac failure or it may be local as in venous obstruction. Chronic Passive congestion is a long standing congestion in which the stasis of poorly oxygenated blood causes chronic hypoxia which in turn leads to the death of the parenchymal tissue. Productive cough associated with dyspnea is usually the first symptom It involves treating the underlying cause usually.

93. **Thickened & fibrotic septa ** Alveolar space contains numerous Hemosiderin laden Macrophages (heart failure cells)

94. **Thickened & fibrotic septa ** Alveolar space contains numerous Hemosiderin laden Macrophages (heart failure cells)

95. TB-LUNGS Caseative type of necrosis caused by Mycobacterium. M. Tuberculosis Spreads through inhalation of aerosolised droplet nuclei from other infected patients. Characterized by granulomatous inflammation. Diagnosis:- Usually confirmed by direct microscopy and culture of sputum samples. Tuberculin test Fluid examination(pleural fluid) Clinical Manifestation Chronic cough often with haemoptysis Pyrexia Unresolved pneumonia Exudativepleural effusion Weight loss Management Classical 4 drug TB therapy

100. Reference Robbins -8th Ed Davidson’s principles and practice of Medicine http://www.virtualmedicalcentre.com/humanatlas1/vmc_white.asp?anid=0004

101. Thanking to the entire Universe