Diseases of lungs

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Diseases of lungs

  1. 1. Diseases of Lungs<br />Patho-B Lab<br />
  2. 2. NEW SLIDES<br />Atelectasis with congestion<br />Bronchiectasis<br />Emphysema<br />Bronchial Asthma<br />Adenocarcinoma Lung<br />Pulmonary edema<br />Bronchopneumoniae<br />
  3. 3. OLD SLIDES<br />Lobar Pneumoniae<br />Viral Pneumoniae<br />Lung Abscess<br />Tumor Emboli- Lung<br />Chronic Pulmonary Congestion<br />TB Lungs<br />
  4. 4. Atelectasis, known as Lung Collapse, is loss of lung volume caused by inadequate expansion of air spaces.<br />
  5. 5. Types of Atelectasis<br />Compression Atelectasis- Usually associated with accumulation of fluids/blood/air with in the pleural cavity which mechanically collapse the adjacent lung..<br />Frequently occurs with pleural effusions caused most commonly by Conjustive Heart Failure.<br />Reversible<br />ResorptionAtelectasis- Occurs when an obstruction prevents the air from reaching distal airways.<br />Most common cause of resorptionatelectasis is obstruction of bronchus by a mucopurulent plug.<br />Reversible<br />Contraction Atelectasis- Occurs when either local or generalized fibrotic changes in the lung/pleura hamper expansion and increase elastic recoil during expiration.<br />Irreversible<br />
  6. 6. Diagnosis:- <br />Radiological examination ----X-ray <br />Clinical Manifestation<br />Dyspnea<br />Productive Cough<br />***Significant adventitious sounds on Auscultation,dullness on percussion<br />Treatment :- Treating the underlying cause.<br />Bacteriological and Mycological examination of sputum( To treat the underlying cause if infectious in nature with relative intervention)<br />Preventive measures for aspiration in childrens, post op surgical patients decreases the risk of Atelectasis<br />Complication:- May worsen bronchial Asthma,Bronchiectasis.<br />
  7. 7. LPO<br />Hallmark<br />Alveolar Collapse<br />
  8. 8. LPO<br />Hallmark<br />Alveolar Collapse<br />
  9. 9. LPO<br />Hallmark<br />Alveolar Collapse<br />
  10. 10. Hallmark<br />Alveolar Collapse<br />LPO<br />
  11. 11. **Congestion<br />**Anthracosis<br />**Alveolar collapse<br />HPO<br />Congestion <br />Here can give <br />A clue of the <br />Patient sufferering<br />From compressive<br />Type of Atelectasis<br />
  12. 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.<br />2 Processes involved in Pathogenesis<br />Obstruction<br />Chronic persistent infection<br />
  13. 13. Diagnosis:-<br />Sputum culture – May reveal Pseudomonas aeruginosa, fungi such as Aspergillus and various Mycobacteria<br />Radiological Examination – X-ray findings not significant unless very gross... CT scan is much more sensitive for Bronchiectasis<br />Clinical Manifestation <br />Chronic productive cough(Foul smelling)<br />Fever,Malaise, aand increased cough and sputum volume.<br />Haemoptysis(can be slight of massive)<br />Halitosis is a common feature<br />Clubbing of fingers may develop <br />Management<br />In patients with airflow obstruction, bronchodilators to enhance airway patency.<br />Physiotherapy – to keep the dilated bronchi empty of secretions<br />Antibiotic therapy(Ciprofloxacin, ceftizimide 12 hourly 25—750 mg IV infusion)<br />
  14. 14. Normal Bronchus<br />
  15. 15. Normal Bronchioles<br />
  16. 16. LPO<br />Dilated Bronchiole<br />with secretion within<br />
  17. 17. LPO<br />Dilated Bronchiole<br />with secretion within<br />
  18. 18. HPO<br />Inflammatory changes in the wall of the bronchiole..<br />Necrotized smooth muscles and supporting tissue due to inflammation<br />
  19. 19. LPO<br />Bronchioles<br />
  20. 20. Dilated Bronchi <br />LPO<br />
  21. 21. Secretions within <br />The bronchi due to<br />Accumulation of <br />Pus in dilated <br />bronchi<br />LPO<br />
  22. 22. Prominent<br />Fibrotic change and <br />Inflammatory change<br />In entire slide<br />
  23. 23. Inflammatory and fibrotic <br />Changes found in the <br />Surrounding lung tissue<br />
  24. 24. Bronchiectatic cavity <br />Filled with secretions ,<br />Lined by normal epithelium<br />With some granulation tissue<br />HPO<br />
  25. 25. HPO<br />Inflammatory <br />Changes in the<br />Bronchial wall<br />
  26. 26. ** Inflammatory changes<br />**Fibrotic changes<br />**Anthracosis<br />LPO<br />
  27. 27. ** Inflammatory changes<br />**Fibrotic changes<br />HPO<br />
  28. 28. ** Inflammatory changes<br />**Fibrotic changes<br />LPO<br />
  29. 29. Characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of wall without obvious fibrosis<br />Most common cause – Smoking (Nicotine)<br />2 Pathogenic Mechanisms are<br />Excess cellular proteases with low antiprotease activity<br />Excess of oxygen species<br />
  30. 30. Types of Emphysema<br />Centriacinar(Centrilobar) Emphysema<br />Involves central of proximal acinisparring the distal alveoli.<br />Panacinar(Panlobar) Emphysema<br />Uniform enlargement of the acinifrom the level of respiratory bronchiole to terminal alveoli.<br />Distal acinar(Panseptal) Emphysema<br />Proximal part of acini is normal but distal part is involved<br />Irregular Emphysema<br />Irregular involved acini, almost invariably associated with scarring.<br />Most common form of Emphysema<br />
  31. 31. Diagnosis<br />Alpha1-antiprotease assay<br />CT is more sensitive that X-ray for Emphysema<br />Clinical Manifestation<br />Dyspnea is usually the first symptom(Progressive)<br />Cough and Wheezing in patient with underlying Chronic bronchitis or Chronic asthmatic bronchitis.<br />Weight loss<br />Barrel Chest<br />Management<br />Smoking cessation<br />Oxygen Therapy<br />Pulmonary rehabilitation<br />Mucolytic therapy<br />
  32. 32. Thinning <br />And destruction of <br />Alveolar walls<br />LPO<br />
  33. 33. LPO<br />Thinning <br />And destruction of <br />Alveolar walls<br />
  34. 34. Thinning <br />And destruction of <br />Alveolar walls<br />LPO<br />
  35. 35. Thinning <br />And destruction of <br />Alveolar walls<br />LPO<br />
  36. 36. Characterized by chronic airway inflammation and increased airway hyper-responsiveness<br />Funtionally characterized by the presence of airflow obstruction which is variable over the short periods of time or is reversible with treatment<br />
  37. 37. Types of Asthma<br />Atopic/Extrinsic Asthma – Most common type<br />+ve Family History common<br />+ve Allergy causing Attacks (Rhinitis, urticaria, eczema)<br />Elevated Ig-E serum levels<br />Non Atopic/ Intrinsic /Acquired Asthma– Non immune in nature<br />+ve Family history uncommon<br />No associated Allergy<br />Ig-E serum levels are normal<br />Drug Induced Asthma<br />Drug like Aspirin provoke asthma<br />Patient with Aspirin sensitivity present with Recurrent Rhinitis,Bronchospasm,urticaria<br />Occupational Asthma<br />Stimulated by fumes(plastics,resins), organic and chemical dusts(wood,cotton)<br />Attacks usually develop after repeated exposure to the inciting agents<br />
  38. 38. Triad of Reversible airway obstruction<br />Chronic inflammation with eosinophils<br />Bronchial smooth muscle cell hypertrophy<br />Hyperreactivity<br />
  39. 39. Significant Morphology in Asthma<br />Macroscopic<br />Occlusion of the bronchi and bronchioles by thick, tenacious Mucous plugs.<br />Microscopic<br />Mucous plug contain whorls of shed epithelium(Curschmann spirals)<br />Numerous eosinophils and Charcot leyden crystals(collections of crystals made of eosinophil proteins) are also present<br />
  40. 40. Diagnosis<br />Diagnosis is made on the basis of compatible clinical history combined with the demonstration of the airflow obstruction<br />Pulmonary function tests<br />Measurement of allergic status( Elevated sputum or peripheral blood eosinophil count )<br />Airway inflammation assessment<br />Clinical Manifestation<br />Typically symptoms includes recurrent episodes of wheezing, chest tightness, breathlessness and cough<br />Management<br />Avoiding aggravating factors <br />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)<br />Long acting beta2 agonist(salmeterol,formoterol) if patient remains poorly controlled<br />Low/high dose steroid therapy depending on the severity of symptoms<br />
  41. 41. **Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrate in walls<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />LPO<br />
  42. 42. **Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrate in walls<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />LPO<br />
  43. 43. **Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrate in walls<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />LPO<br />
  44. 44. **Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrate in walls<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />LPO<br />
  45. 45. **Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrate in walls<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />LPO<br />
  46. 46. **Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrates in wall<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />LPO<br />
  47. 47. HPO<br />**Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrates in wall<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />
  48. 48. **Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrates in wall<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />HPO<br />
  49. 49. **Airway Remodelling in Asthma**<br />-Thickening of Basement membrane <br /> of the bronchial epithelium<br />-Edema and inflammatory <br /> infiltrates in wall<br />-Increase in the size<br /> of the glands<br />-Hypertrophy of the <br /> bronchial muscle walls<br />HPO<br />
  50. 50. Classification of Lung tumors for therapeutic purposes<br />Small Cell Lung Carcinomas(SCLC)<br />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<br />Non small cell lung Carcinoma(NSCLC)- poor response to chemotherapy and are better treated by surgery.<br />Squamous cell<br />Adenocarcinoma ----- Most common of lung cancer in women and non smoker<br />Large cell carcinoma<br />
  51. 51. Most common of lung cancer in women and non smoker<br />Precursor –Atypical adenomatous hyperplasia(AAH)<br />Occur as central lesions but<br /> are more peripherally located<br />Many arising in relation to peripheral lung scars<br /> (scar carcinomas)<br />Histological types<br />Acinar(Gland forming)<br />Papillary<br />Solid <br />
  52. 52. In general all Adenocarcinomasgrow slowly and form smaller masses than other subtypes but they tend to metastasize widely at an early stage.<br />Diagnosis:-<br />Histologic diagnosis<br />Bronchoscopy<br />Bronchial biopsy<br />CT/Ultrasound<br />Clinical Manifestation<br />Cough is common early symptom <br />Haemoptysis<br />Bronchial obstruction<br />Recurrent pneumonia<br />Lassitude and Weight loss- indicated metastatic spread<br />Hoarseness<br />Management<br />Surgical resection for all Non small cell lung carcinoma-NSCLC<br />
  53. 53. **Stromal invasion(Bronchial mucosa)<br />**Desmoplasia<br />(growth of fibrous <br />or connective tissue)<br />
  54. 54. **Stromal invasion(Bronchial mucosa)<br />**Desmoplasia<br />(growth of fibrous <br />or connective tissue)<br />**<br />Acinar type<br />Gland forming<br />Adenocarcinoma<br />
  55. 55. **Stromal invasion<br />**Desmoplasia<br />(growth of fibrous <br />or connective tissue)<br />
  56. 56. **Stromal invasion(Bronchial mucosa)<br />**Desmoplasia<br />(growth of fibrous <br />or connective tissue)<br />
  57. 57. **Cytologicatypia<br />**Pleomorphism<br />
  58. 58. **Cytologicatypia<br />**Pleomorphism<br />
  59. 59. Caused due to accumulation of fluids in lungs<br />Etiology<br />Cardiogenic pulmonary edema<br />Most common clinical problem seen frequently in left ventricular failure.<br />Noncardiogenic pulmonary edema<br />Renal failure<br />Acute Respiratory distress syndrome(ARDS)<br />
  60. 60. Signs:- JVP – increased, sweating, cool extremities, dullness and crepitation at base.<br />Chest radiograph:- Cardiomegaly,pleural effusion.<br />ECG- decreased left ventricular function<br />Decreased PaO2<br />Can lead to Acute severe dyspnea.<br />Management:- <br />Treating the underlying cause<br />Usually the prognosis is poor(with survival 2-3 years) unless Heart-lung transplantation is performed.<br />
  61. 61.
  62. 62.
  63. 63.
  64. 64.
  65. 65. 4 stages of lobar/Broncho Pneumonia<br />Congestion<br />Affected lobe is heavy, red boggy,histologicallyvascular congestion can be seen with scattered neutrophils in the alveoli.<br />Red hepatization<br />Lung shows liver like consistency, the alveolar spaces are packed with neutrophils, red cells and fibrin.<br />Gray hepatization<br />Lung is dry,gray, and firm, because the red cells are lysed while the fibrinosuppurativeexudate persists within the alveoli<br />Resolution<br />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.<br />
  66. 66. Pneumonia<br />Diagnosis<br />Radiological- X-ray(Pleural effusions)<br />Microbiological- sputum direct smear<br />Blood culture +ve for pneumococcal pneumonia<br />Serology-For viral infections,mycoplasma,legionella<br />Clinical Manifestation<br />Typically presents as acute illness<br />Systemic features – fever, shivering, vomiting,anorexia, headache.<br />Pulmonary symptoms-cough(initially dry,painful and later accompanied by expectoration of mucopurulent sputum)<br />Management<br />Rest, cessation of smoking<br />Antibiotic therapy<br />Oxygen to all patients with tachypnea,hypoxemia,acidosis.<br />Analgesic for pleural pain<br />
  67. 67. Pneumonia generally defined as any infection in the lung.<br />Initial infection is in bronchi which gradually extends in adjacent alveoli.<br />Patchy distribution of inflammation implies Bronchopneumonia and is usually involves more than one lobe.<br />
  68. 68. Bronchiolitis<br />
  69. 69. Vascular congestion<br />
  70. 70. Congestion<br />Red Hepatization<br />Gray hepatization<br />
  71. 71.
  72. 72. Bronchiolitis<br />
  73. 73. Congestion<br />
  74. 74. Congestion<br />Red Hepatization<br />Gray hepatization<br />
  75. 75. Red Hepatization<br />Gray hepatization<br />
  76. 76.
  77. 77. LPO<br />Patchy Inflammation of the <br />Interstitium and Septa<br />Mononuclear infiltrates in alveolar wall<br />
  78. 78. Inflammatory changes <br />only in the interstitium<br />
  79. 79. LPO<br />Edematous walls<br />Mononuclear infiltrates in<br />The alveolar walls<br />
  80. 80.
  81. 81. There is fibrosis in the alveoli <br />Along with purulent exudate<br /> (at the pointer)<br />HPO<br />Congested alveolar wall<br />
  82. 82. Purulent exudate in High power shows presence of neutrophils<br />HPO<br />
  83. 83. Exudates in alveoli<br />
  84. 84. Exudates in alveoli<br />
  85. 85. Bronchopneumonia<br />Bronchopneumonia:- Infection involving bronchi initially and then alveoli<br />Viral pneumonia:- Interstitium involves<br />Bacterial pneumonia:- Alveoli filled with exudates and fluid<br />Viral pneumonia<br />Bacterial pneumonia<br />
  86. 86. Etiology:-Aspiration of Pyogenic organism most common cause of lung abscess <br />Liquefactive type of necrosis.<br />In lung abscess there is localized collection of pus, or a cavity lined by chronic inflammatory tissue.<br />It may also be produced by infection of previously healthy lung tissue with Staph. Aureus,Klebsiella pneumonia.<br />
  87. 87. Diagnosis –<br /> X-ray(segmental opacity with consolidation or collapse)<br />Clinical Manifestation:-<br />High Pyrexia<br />Systemic upset<br />Clubbing(10-14 days)<br />Consolidation on chest examination<br />Pleural rub common<br />Management<br />Oral Amoxicillin 6hourly effective in most of the patients- 2 weeks<br />If Anaerobic – Metronidazole 400mg 8 hourly -2weeks<br />
  88. 88. Complete destruction of lung parenchyma<br />Due to the chronic inflammation<br />
  89. 89. Complete destruction of lung parenchyma<br />Due to the chronic inflammation<br />
  90. 90. Neoplastic cells<br />Within the vessel<br />
  91. 91. Neoplastic cells<br />Within the vessel<br />
  92. 92. Congestion is a passive process resulting from impaired venous return out of the tissue.<br />It may occur systematically, as in cardiac failure or it may be local as in venous obstruction.<br />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.<br />Productive cough associated with dyspnea is usually the first symptom<br />It involves treating the underlying cause usually.<br />
  93. 93. **Thickened & fibrotic septa<br />** Alveolar space contains <br />numerous Hemosiderin laden <br />Macrophages (heart failure cells)<br />
  94. 94. **Thickened & fibrotic septa<br />** Alveolar space contains <br />numerous Hemosiderin laden <br />Macrophages (heart failure cells)<br />
  95. 95. TB-LUNGS<br />Caseative type of necrosis caused by Mycobacterium.<br />M. Tuberculosis Spreads through inhalation of aerosolised droplet nuclei from other infected patients.<br />Characterized by granulomatous inflammation.<br />Diagnosis:- <br />Usually confirmed by direct microscopy and culture of sputum samples. <br />Tuberculin test<br />Fluid examination(pleural fluid)<br />Clinical Manifestation<br />Chronic cough often with haemoptysis<br />Pyrexia <br />Unresolved pneumonia<br />Exudativepleural effusion<br />Weight loss<br />Management<br />Classical 4 drug TB therapy<br />
  96. 96.
  97. 97.
  98. 98.
  99. 99.
  100. 100. Reference<br />Robbins -8th Ed<br />Davidson’s principles and practice of Medicine<br />http://www.virtualmedicalcentre.com/humanatlas1/vmc_white.asp?anid=0004<br />
  101. 101. Thanking to the entire Universe<br />

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