Pathology of Respiratory System Disorders


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Basic level for allied health students. Prepared specifically for Physician assistant course.

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Pathology of Respiratory System Disorders

  1. 1. MX1002-PAS-Wk7-RSThe only place wheresuccess comes beforework is in a dictionary…!Vidal Sassoon
  2. 2. MX1002-PAS-Wk7-RSPathophysiologyRespiratory SystemDr. Venkatesh M. Shashidhar.Associate Professor & Head of Pathology
  3. 3. PAS-Respiratory PathophysiologyIntroduction to Resp. Sys:• 10,000L/day of air – filtered, moistened,warmed, O2/Co2. exchanged.!• Full capacity 6L. (500ml at rest)• Sinusitis, pharyngitis, laryngitis…* URI• Pneumonia: Inflammation of lung * LRI• Chronic: COPD, Fibrosis – Smoking.• Commonest internal Cancer.• Respiratory tract inflammations -commonest in medical practice.• Enormous morbidity & mortality.• Important medical learning. Doctors daily bread….!
  4. 4. PAS-Respiratory PathophysiologyNormal Lung
  5. 5. PAS-Respiratory PathophysiologyRespiration – Respiratory system:5
  6. 6. PAS-Respiratory PathophysiologyRespiration – Respiratory system:6
  7. 7. Normal Lung
  8. 8. PAS-Respiratory PathophysiologyAlveolar Gas Exchange:8Co2O2
  9. 9. PAS-Respiratory PathophysiologyLung Function testing:9Expiration0 ------- Volume ---------------6LInspiration
  10. 10. PAS-Respiratory PathophysiologyLung Function Testing:• Total Lung Capacity (TLC) 6L male/4.7L fem.• Tidal Volume (TV) – 500 / 390ml• Forced Vital Capacity (FVC) 4.8L / 3.7L• Forced Expiratory Volume in 1 Sec - FEV1• FEV1/FVC (FEV1%) - 75–80% normal.1. In Obstructive diseases (COPD) FEV1 low& FVC high. So FEV1/FVC is low (<80%).2. In Restrictive diseases (fibrosis) the FEV1and FVC are both low proportionally and theFEV1/FVC value normal or high. Volume (%FYC)
  11. 11. MX1002-PAS-Wk7-RSFirst step to make yourdreams come trueis to wake up!— Paul Valery
  12. 12. PAS-Respiratory PathophysiologyPneumonia: Infection of lung (LRT)• Inflammation of alveoli• Etiology: pathogens vs defence.• Types: Bacterial, viral, fungal, other.• Clinical: Lobar / Broncho pneumonia.• Symptoms: Fever, cough, dyspnoea.• Complications: Spread  septicemia,abscess, scarring.
  13. 13. PAS-Respiratory PathophysiologyPneumonia Types:Etiologic Types:• Infective– Viral– Bacterial– Fungal– Tuberculosis• Non Infective– Toxins– chemical– AspirationMorphologic types:• Lobar• Broncho• InterstitialDuration:• Acute• ChronicClinical:• Primary / secondary.
  14. 14. 1. Congestion 2.Red HepatisationNormal 4. Resolution 3. Grey HepatizationPathogenesis of Pneumonia
  15. 15. PAS-Respiratory PathophysiologyPneumonia:
  16. 16. PAS-Respiratory PathophysiologyLobar Pneumonia - Primaryin healthy people in community. Gram Positive Cocci, wholelobe unilateral. heals without scar. Rare complications.
  17. 17. PAS-Respiratory PathophysiologyBronchopneumonia - Secondaryin Sick patients, Gram Negative bacilli, bilateral,basal. More complications, heals by scarring.
  18. 18. PAS-Respiratory PathophysiologyBroncho-pneumonia – Lobar-pneumonia• Extremes of age.• Secondary, in sick.• Both genders.• Klebsiella, E.coli• Patchy, basal, bilateral.• Around Small Bronchi• Not limited by anatomicboundaries.• Usually bilateral.• Middle age – 20-50• Primary in a healthy adult.• males common.• 95% pneumococcus• Entire lobe consolidation• Diffuse• Limited by anatomicboundaries.• Usually unilateral
  19. 19. PAS-Respiratory PathophysiologyTuberculosis:• Mycobacterium tuberculosis (typical)• Primary & Secondary,• Chronic, Hypersensitivity to bacteria,• Caseating Granuloma + Fibrosis.• debilitating, weight loss.• Upperlobe, cavity + fibrosing.• Systemic spread, miliary spread.• Tuberculin Test – hypersensitivity.
  20. 20. MX1002-PAS-Wk7-RS“Whether you think that youcan or that you cant,you are right…!”– Henry Ford
  21. 21. MX1002-PAS-Wk7-RSChronic Lung disorders:Obstructive & Restrictive
  22. 22. PAS-Respiratory PathophysiologyRestrictive vs Obstructive• Interstitial fibrosis• Stiff hard lung• Increased tissue• Normal FEV1:FVC ratio• Normal PEFR.• Types:– Fibrosis,– Pneumoconiosis• Obstruction to air flow.• Soft lung• Loss of tissue.• Low FEV1:VC ratio• Low PEFR.• Types:–COPD–Asthma
  23. 23. PAS-Respiratory PathophysiologyRestrictive - Obstructive
  24. 24. PAS-Respiratory Pathophysiology• Irreversible, fibrotic pulmonarydisease due to the inhalationof large amounts of silica dustover time.• Road, civil & mining workers.• Toxic  Inflam  fibrosis.• dyspnea, fatigue, weight loss,fever, and pleuritic pain.• Multiple small, fibrotic Nodulesbilateral + emphysema.• Restrictive pattern of PFT.• TB association common.Silicosis: Restrictive COPDFine nodular shadows
  25. 25. PAS-Respiratory Pathophysiology• Beaded protein coveredneedle like microscopic .Asbestos bodies• Within alveoli & sputum.• Dyspnoea, dry cough• Diffuse fibrosis: Honey comblung  Pulmonary failure.• Mesothelioma – pleuralcancer.Asbestosis: Restrictive
  26. 26. MX1002-PAS-Wk7-RSPathology ofChronic ObstructivePulmonary Diseases (COPD)Dr. Venkatesh M. ShashidharAssociate Professor of Pathology
  27. 27. PAS-Respiratory PathophysiologyObstructive Airway Disease:• Localized: Foreign body, aspiration, tumor..• Diffuse – Distal airway diseases– Transient reversible spasm - Asthma– Chronic irreversible permanent – COPD.
  28. 28. PAS-Respiratory PathophysiologyAsthma Clinical Pathology:Chronic hypersensitivity inflammatorydisease of bronchi  excess mucousand spasmodic occlusion.Causes• Allergic: allergens, infection• non-allergic:neurogenic,psychogenicSigns and symptoms• dyspnea, wheezing, catching for air.• cough – viscous thick sputum• Tachycardia & chest pain
  29. 29. BronchialInflammationTRIGGERSAllergens, Exercise,Cold Air, SO2 ParticulatesAirwayHyperresponsivenessGenetic*INDUCERSAllergens,Chemical sensitisers,Air pollutants, Virus infectionsAirflow Limitation
  30. 30. PAS-Respiratory PathophysiologyChronic Obstr. Pulm Disease: COPD• Chronic, irreversible airway obstruction withdestruction of bronchi & alveoli.• Clinical: Chronic bronchitis, Emphysema orCOPD (combined).• Smoking / pollution – commonest cause• 15% smokers develop COPD.• Finally leads to lung failure or Cancer.
  31. 31. PAS-Respiratory PathophysiologySmoking – Pathogenesis• Increase in– Alveolar marcrophages– CD8 Lymphocytes– Neutrophils– Proteases.• Tissue irritation / destruction• Airway damage- Bronchitis• Alveoli damage- Emphysema.Emphysema Bronchitis
  32. 32. PAS-Respiratory PathophysiologySmoking effects: FEV 1 & Age
  33. 33. PAS-Respiratory PathophysiologyPathogenesis – Smoke - Lung Dis.CancerInflam COPDIrritation  Inflammation  Mucous  Infections  destr. COPD  Cancer
  34. 34. PAS-Respiratory PathophysiologyNormal - COPD
  35. 35. PAS-Respiratory PathophysiologyCombined  COPD (common)
  36. 36. PAS-Respiratory PathophysiologyLung Normal & in Smokers:
  37. 37. PAS-Respiratory PathophysiologySmokers lung – COPD Bronchitis
  38. 38. PAS-Respiratory PathophysiologyEmphysema
  39. 39. PAS-Respiratory PathophysiologyEmphysema:Pink Puffer:• Lean/weight loss• Forward stooping• Barrel chest• Flat diaphragm• Hyperlucent Lung
  40. 40. PAS-Respiratory PathophysiologyComplications of COPD:1. Cor Pulmonale – Heart failure.2. Acute Exacerbations.3. Recurrent pneumonia.4. End-stage lung disease.5. Polycythemia – hypoxia.6. Bronchiectasis.7. Lung Cancer.
  41. 41. PAS-Respiratory PathophysiologyBronchiectasis:• Permanent dilatation ofbronchi with pus.• Cough, copious purulentsputum (pus).• Lower lobes common• Complications -Pneumonia, septicemia,meningitis.• Management – surgicalresection.
  42. 42. MX1002-PAS-Wk7-RS“Get me well so I can get ontelevision and tell people tostop smoking…!”-- Nat King Cole
  43. 43. “Troubles are often the tools by whichnature fashions us for better things”- Henry Ward Beecher
  44. 44. Life’s battles don’t go always to the stronger orfaster man, sooner or later, The man who wins isthe man who thinks he can….!
  45. 45. MX1002-PAS-Wk7-RSPathology ofLung tumors(Lung Cancer)Dr. Venkatesh M. ShashidharA/Prof. & Head of PathologySchool of Medicine45
  46. 46. PAS-Respiratory PathophysiologyLung Cancer Intro:• Most common & fatal cancer (internalmalignancy)• Kills more people than colorectal,breast, and prostate cancers combined.• Significant increase in incidence..(developing countries*)• Now Increasing in females > breastcancer.• 90% of lung cancers are related tosmoking..! (passive smoking in 5%)• Mutagen sensitive genotype : P-450enzyme• Poor prognosis ~ 5% 5y survival *46
  47. 47. PAS-Respiratory PathophysiologyLung Cancer Incidence:47
  48. 48. PAS-Respiratory PathophysiologyLung Cancer & Smoking:• Proportional to duration, amount & quality of smoking &deep inhaling.• 90% are smokers and 10% are non smokers• 20 fold risk if >40cigarettes per day• >100 fold combined with Asbestos, coal, radon, etc.• Atypical cells in sputum in 96.7% of smokers - 0.9% in nonsmokers.• Smoke has several irritants & carcinogens.– Initiators – Benzo[o]pyrenes– Promoters – Phenol derivatives– Radioactive substances – Polonium, C14, K4048
  49. 49. PAS-Respiratory PathophysiologyLung tumors Classification:• Benign tumours – rare (Adenoma, Hamartoma)• Malignant (common):– Bronchogenic Carcinoma: (95%)– Bronchial Carcinoid Tumor (5%)– Other Tumors (<1%)– Metastasis (common)• Tumors of Pleura– Mesothelioma – asbestosis *49
  50. 50. PAS-Respiratory PathophysiologyTypes of Bronchogenic Ca.:• Bronchogenic Carcinoma (95%)– Small cell ca. SCC – 15-20% (oat cell carcinoma)– Non Small cell NSCC– 80%• Squamous cell carcinoma – 20-30%• Adeno carcinoma – 30-40%• Large cell anaplastic carcinoma• Clinical / prognostic classification:SCC - small cell CaEarly spreadSurgery not possible.Responds to chemo50Non-SCCLate spread – localizedStaging & SurgeryDoes not respond to chemo.
  51. 51. PAS-Respiratory PathophysiologyClinical features & complications.• Local:– Obstruction– Effusion– Pneumonia* lipid, other.– Bronchiectasis– Atelectasis– Haemoptysis– COPD (risk)• Systemic:– Cachexia– Paraneoplastic sy– Clubbing– Pulm. Osteoarthropathy.– Bone pain– CNS dysfunction51
  52. 52. PAS-Respiratory PathophysiologyPathogenesis – Smoke - Lung Dis.CancerInflam COPDMultiple mutations in oncogenes  CancerK-RasC-mycp53
  53. 53. PAS-Respiratory Pathophysiology53Lung Ca – AP & Lateral viewHistological Type ? NSCC
  54. 54. PAS-Respiratory PathophysiologySquamous Cell Carcinoma:(CT)54NSCC
  55. 55. PAS-Respiratory PathophysiologySquamous carcinoma:55Origin in main bronchusNSCC
  56. 56. PAS-Respiratory PathophysiologyLungAdenocarcinoma:PeripheralNon smokersFemales56NSCC
  57. 57. PAS-Respiratory PathophysiologySCC Small Cell Ca.Infiltrative pattern aroundmajor bronchi.57SCC
  58. 58. PAS-Respiratory PathophysiologyLung Metastasis(Numerous metastases from a renal cell ca.)58
  59. 59. PAS-Respiratory PathophysiologyTNM: Staging of Lung Ca.59T – Tumor (T1-4)N – Node (N1-3)M – Metastasis (M0-1)Lung Cancer Staging:I - T1 N0 M0II - T1 N1 M0III - Tn N2 M0IV - Any M1Based on Anatomical structure involved.
  60. 60. PAS-Respiratory PathophysiologyComplications:60
  61. 61. PAS-Respiratory PathophysiologyCushing’s syndrome in SCC61Paraneoplastic syndrome:• Tumour producing ACTH hormone.• Excess adrenal glucocorticoids.• Central obesity, diabetes etc..
  62. 62. PAS-Respiratory PathophysiologyMesothelioma:• Tumor of Pleural covering.• Asbestosis – risk factor.• Poor prognosis• 50% mortality in first year.62
  63. 63. Bernie BantonAsbestosis victim died Aug 2007.Had Asbestosis, asbestos-related pleuraldisease (ARPD),stomach cancer & Peritoneal mesothelioma.He became the face of the fight to getcompensation for affected workers and wonhis final victory less than a week before hisdeath..!.Mr Banton was awarded Order of Australia.“until they put me in the box, Ill be out there fighting…!".-- Bernie Banton, in his speech to ABC.Commitment always wins….!
  64. 64. PAS-Respiratory PathophysiologyClinical Case 1:A 28y Indonesian student presents with weight loss over a four-month period and the recent onset of fever and chills at night.Had several courses of antibiotics from his GP withoutimprovement. Admission chest x-ray revealed an irregular opacityof the right apical lobe of lung with pleural effusion. Clinicalexamination revealed cervical and axillary lymphadenopathy.What is the likely problem? Chronic, infection, of origin? Epidemiology.What further tests? Bacterial culture, biopsy, PCR.What is the prognosis? resistant, imm, risk factors.64Tuberculosis
  65. 65. PAS-Respiratory PathophysiologyClinical Case 2:• An 18y student from Tully, presented with wheezing anddifficulty in breathing. These attacks occurredintermittently since childhood worse during winter. An x-ray of the chest was normal, but lung function testsduring attack demonstrated a markedly decreasedFEV1, which improved significantly after he inhaledbronchodilator. The patient was prescribedbronchodilator & steroid inhalers which some relief, butthe patient continued to experience episodes ofbreathlessness in the coming years.• What is the likely problem? Chronic, recurrent, seasonal• Why many attacks ? hypersensitivity/allergy.• What is the prognosis? Nature, preventive only.65Asthma
  66. 66. PAS-Respiratory PathophysiologyClinical Case 3:• A 41y man was brought to emergency with high fever, shaking chills,coughing up rusty sputum. On history, hed been fine the day beforebut that morning he had begun to shake uncontrollably and feltalternately cold then hot and sweaty. His chest hurt on breathing. Onexamination, thin white male who was anxious and mildly cyanotic,tachypnea, fine rales and decreased breath sounds by auscultationover the right lower chest. Temp100.2°F, but his pulse was normal.WBC high, with 70% polys, 18% bands, and 12% lymphocytes.Blood gases hypoxia & respiratory alkalosis. sputum gram-positivediplococci.• What is the problem? Acute infection of lungs – pneum.• What & Why is he cyanotic? Co2 excess. Gas exch.• Fine rales over RLL? Fluid – lobar pneumonia.• Why his WBC count is high? – Acute inflammation.• Gram Positive Diplococci ? – common, Strep. pneumoniae.66Pneumonia
  67. 67. PAS-Respiratory Pathophysiology“A good scare is worth more toa man than good advice."- Edgar Watson Howe - Country Town Sayings (1911)That’s why we haveExams!
  68. 68. PAS-Respiratory PathophysiologyLearning Objectives:• Respiratory anatomy, upper & lower resp. tracts.• Review the process of ventilation & respiration.• Pulmonary function tests (FVC, FEV1, FEV1/VC)• Overview of chest radiograph & imaging.• Respiratory infections - pneumonia and TB.• Overview of obstructive and Restrictivepulmonary disorders, Asthma, COPD, Fibrosis.• Describe respiratory failure and its causes *• Lung cancer, etiology, types and features.68