Lecture 28. common repratory pathological condirtion part 3


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Lecture 28. common repratory pathological condirtion part 3

  1. 1. RESPIRATORY PATHOLOGYCongenital abnormalitiesAtelectasisAcute Pulmonary Injury (eg:pulmonary oedema)Pulmonary InfectionsObstructive Pulmonary Disease (COPD)Restrictive (Infiltrative) Pulmonary DiseaseVascular Pulmonary DiseasesTumors
  3. 3. LEARNING OUTCOMESAt the end of this lecture student will be able to• Define actelectasis• Compare resorption actelectasis, compression actelectasis andcontraction actelectasis in regards predisposing factors,etiologyand morphology• Define bronchiectasis• Discuss the predisposing conditions ,pathogenesis,gross&microscopic morphology ,clinical course and prognosis ofbronchiectasis• Discuss the etiology, pathogenesis, basic morphology andpulmonary reaction and complications of occupational lungsdiseases (pneumoconiosis- anthracosis, silicosis, asbetosis)
  4. 4. BRONCHIECTASISpermanent dilation of bronchi and bronchiolesand is secondary to cycles of obstruction andinfectionIrreversible Dilation of Bronchi andbronchiolesCaused by Destruction of Bronchial WallMuscle and Elastic Elements
  6. 6. BRONCHIECTASISAssociated with chronic necrotizinginfectionA characteristic symptom complexdominated byCoughexpectoration of copious amounts ofpurulent sputum
  7. 7. ETIOLOGY & PATHOGENESISPredisposing conditionsObstruction & infection are the majorinfluencesObstruction is caused byTumorsInhaled foreign bodiesMucous plugs in asthmalymph node enlargementUnder these conditions, the bronchiectasis is localized to the obstructed lungsegment
  8. 8. Post infectious conditions includingNecrotizing pneumoniaCaused byBacteria ( Mycobacterium tuberculosis,Staphylococcus aureus, Haemophilus influenzae,Pseudomonas )viruses ( adenovirus, influenza virus, HIV )fungi ( Aspergillus )
  9. 9. Congenital or hereditary conditionsCystic fibrosis (genetic defect, abnormal viscid mucussecretion → obstruction organ passages)Intralobar pulmonary sequestrations presenceof a discrete mass of lung tissue without normal connection to the airway systemImmunodeficiency statesPrimary ciliary dyskinesiaKartagener syndrome (bronchiectasis, sinusitis, andsitus inversus or partial lateralizing abnormality )
  10. 10. Other conditions :rheumatoid arthritisSLEinflammatory bowel diseasepost transplantation ( chronic lung rejection &chronic graft-versus-host disease after bone marrowtransplantation)
  11. 11. MORPHOLOGYGrossSite :Obstructive bronchiectasis is localized to a singlesegment of the lungsNonobstructive bronchiectasis may be localizedor generalized
  12. 12. Size :Airways are dilated up to 4 times normalsize → sufficiently dilated that they can befollowed directly out to the pleural surfacesShape : cylindrical fusiform saccularBronchial lumens : filled with thickmucopurulent secretion
  13. 13. BronchiectasisThe resected upper lobeshows widely dilated bronchi,with thickening of thebronchial walls and collapseand fibrosis of the pulmonaryparenchyma
  14. 14. BronchiectasisCross-section of lung demonstrating dilated bronchi extending almost to the pleur
  15. 15. Histology vary with activity & chronicity of the diseaseIn the full blown active case,intense acute & chronic inflammatory exudatesdesquamation of lining epithelium &extensive areas of necrotizing ulcerationpseudostratification of columnar cellssquamous metaplasia of remaining epitheliumabscess formationchronic case – fibrosis of bronchial andbronchiolar walls → total or subtotal obliterationof lumen
  16. 16. CLINICAL FEATURESDue to accumulation of pus in dilated bronchi &bronchiolesChronic cough with production of copiousamount of purulent sputumsevere, persistent, worse in morning, induced by change inposture, may be paroxysmalPurulent sputum (foul-smelling) – copious amountOn standing → 3 layered sputum1st – frothy layer2nd – clear mucous layer3rd – suppurated & necrotic debris, RBC
  17. 17. Chronic cough withproduction of copiousamount of purulent sputumsevere, persistent, worse in morning,induced by change in posture, may beparoxysmalPurulent sputum (foul-smelling) – copious amountOn standing → 3 layeredsputum1st – frothy layer2nd – clear mucous layer3rd – suppurated & necroticdebris, RBCCLINICAL FEATURESDue to accumulation of pus in dilated bronchi &bronchioles
  18. 18. CLINICAL FEATURESdue to inflammatory response of the lungparenchyma & pleuraFever → febrile episodesChest pain due to pleuritisHaemoptysis or sometimes bloody sputum causedby rupture of thin walled vessels situated in wall ofdilated bronchiolesOther respiratory symptomsDyspnoea, orthopnoea, cyanosis,clubbing of fingers & toes.
  19. 19. COMPLICATIONSLung abscess- the necrosis destroys the bronchial orbronchiolar wallsPneumonia – infection spread to whole lung parenchymaBacteremia, septicemia with metastaticabscess formation e.g. brain abscess, meningitisEmphysema – secondary to obstructionSecondary amyloidosisperibronchiolar fibrosis in chronic widespreaddisease → increase pressure in pulmonary circulation → Corpulmonale and cardiac failure
  23. 23. Chronic Diffuse Interstitial(Restrictive) DiseasesChronic interstitial diseases areheterogeneous group of disorderscharacterized predominantly byinflammation and fibrosis of thepulmonary connective tissue, principallythe most peripheral and delicate interstitium inthe alveolar walls
  24. 24. PNEUMOCONIOSISPneumoconioses arepulmonary diseases caused by mineraldust inhalation in workplaceThe specific types of pneumoconioses arenamed by the substance inhaled(e.g., silicosis, asbestosis, anthracosis)
  25. 25. PNEUMOCONIOSISMineral Dust-Induced Lung DiseaseCoal dust Simple coal workers pneumoconiosis:macules and nodulesComplicated coal workers pneumoconiosis:PMFCoal miningSilica Silicosis Sandblasting,quarrying, mining,stone cutting,foundry work,ceramicsAsbestos Asbestosis pleural effusions, pleural plaques, ordiffuse fibrosis; mesothelioma; carcinoma of thelung and larynxMining, milling,and fabrication ofores andmaterials;installation andremoval ofinsulation
  26. 26. PathogenesisThe reaction of the lung to mineral dustsdepends onsize, shape, solubility, and reactivity of theparticlesPNEUMOCONIOSIS
  27. 27. PathogenesisThe development of a pneumoconiosis depends on(1) the amount of dust retained in the lung andairways(2) the size, shape, and buoyancy of the particles(3) solubility and physiochemical reactivity(4) the possible additional effects of other irritants(e.g., concomitant tobacco smoking)PNEUMOCONIOSIS
  28. 28. Pathogenesis(1)The amount of dust retained in the lungsis determined bydust concentration in surrounding airduration of exposureeffectiveness of clearance mechanismsPNEUMOCONIOSIS
  29. 29. Pathogenesis(2) the size, shape, and buoyancy of theparticlesThe most dangerous particles range from1 to 5 μm in diameter because they may reach theterminal small airways and air sacs and settle intheir liningsPNEUMOCONIOSIS
  30. 30. (3)The solubility and cytotoxicity of particlesmodify the nature of the pulmonary responseSmaller particles tend to cause acute lung injuryLarger particles resist dissolution and so maypersist within the lung parenchyma for years -tend to evoke fibrosing collagenous pneumoconiosesPNEUMOCONIOSIS
  31. 31. PathogenesisThe key factor in the gene-sis ofsymptomatic pneumoconioses is thecapacity of inhaled dusts to stimulatefibrosisThe pulmonary alveolar macrophage is akey cellular element in the initiation andperpetuation of lung injury and fibrosisPNEUMOCONIOSIS
  32. 32. The more reactive particles trigger themacrophagesto release a number of products thatmediate an inflammatory response andinitiate fibroblast proliferation andcollagen depositionPNEUMOCONIOSIS
  33. 33. Pathogenesis(4) the possible additional effects of otherirritants (e.g., concomitant tobaccosmoking)tobacco smoking worsens the effects ofall inhaled mineral dustsPNEUMOCONIOSIS
  34. 34. In simple coal workers’pneumoco-niosismassive amounts of dust areinhaled and engulfed by macrophagesmacrophages pass into the interstitium ofthe lung and aggregate around therespiratory bronchiolesPathogenesis
  35. 35. PathogenesisIn silicosisthe silica particles are toxic tomacrophages,which die and release a fibrogenic factorIn turn,the released silica is again phagocytosedby other macrophagesThe result is a dense fibrotic nodulethe sili-cotic nodule
  36. 36. PathogenesisAsbestosisis characterized bylittle dust and much interstitial fibrosisAsbestos bodies are the classic features
  37. 37. PNEUMOCONIOSISCoal Workers’ Pneumoconiosis Is Due toInhalation of Carbon ParticlesThe spectrum of lung findings in coal workers is wide,varying from(1)asymptomatic anthracosis(2)simple CWP with little to no pulmonarydysfunction(3)complicated CWP(4)progressive massive fibrosis (PMF),
  38. 38. PNEUMOCONIOSISMorphologyAnthracosisAccumulation of carbon particles in thelungs (in the connective tissue along the lymphatics,including the pleural lymphatics, or in organized lymphoidtissue along the bronchi or in the lung hilus)
  39. 39. Coal Workers’ PneumoconiosisMorphologySimple CWP is characterized bycoal macules (1 to 2 mm in diameter, consists ofcarbon-laden macrophages)larger coal nodules (contains small amounts of adelicate network of collagenlocated primarily adjacent to respiratorybronchioles
  40. 40. Complicated CWP (progressive massive fibrosis)is characterized by multipleintensely blackened scars larger than 2 cm,sometimes up to 10 cm in greatest diameterOccur on background of simple CWP bycoalescence of coal nodules and generallyrequires many years to developCoal Workers’ Pneumoconiosis
  41. 41. MicroscopicallyThe lesions consist of dense collagen andpigmentThe center of the lesion is often necrotic,most likely due to local ischemiaCoal Workers’ Pneumoconiosis
  42. 42. Clinical CourseSimple CWP-minor impairment of lung functionComplicated CWP-cause significant respiratory impairmentCaplan syndrome was first described as rheumatoid nod-ules (Caplan nodules) in the lungs of coal minerswith rheumatoid arthritisCoal Workers’ Pneumoconiosis
  43. 43. Silicosis Is Caused by Inhalationof Silicon Dioxide (crystalline Silica)Silica occurs in bothcrystalline and amorphous formscrystalline forms (including quartz,crystobalite, and tridymite) are much morefibrogenic
  44. 44. After inhalation, the particles interact withepithelial cells and macrophagesCausingactivation and release of mediatorsIL-1, TNF, fibronectin, lipid mediators, oxygen-derived free radicals, and fibrogenic cytokinesPathogenesis
  45. 45. SilicosisSIMPLE NODULAR SILICOSISmost common form of silicosisoccur in any worker with long-termexposure to silicasilicotic nodules less than 1 cm indiameter (usually 2 to 4 mm)
  46. 46. Morphologyslowly progressing, nodular, fibrosingpneumoconiosisSilicotic nodules are characterized grossly in theirearly stages bytiny, barely palpable, discrete, pale-to-blackened(if coal dust is also present) nodules in theupper zones of the lungs
  47. 47. Silicotic nodulescharacteristic whorled appearance, withconcentrically arranged hyalinized collagen.At theperiphery are aggregates of mononuclearcells,mostly lymphocytes and fibroblasts.
  48. 48. As the disease progresses, the individualnodules may coalesce intohard, collagenous scars, with eventualprogression to PMFThe intervening lung parenchyma may becompressed or overexpanded, and ahoneycomb pattern may developSilicosis
  49. 49. Fibrotic lesions may also occur in the hilarlymph nodes and pleuraThin sheets of calcification occur in thelymph nodes and are seen radiographicallyas eggshell calcification
  50. 50. Advanced silicosis(transected lung).Scarring has contractedthe upper lobe into asmall dark mass (arrow).Note the dense pleuralthickening
  51. 51. Clinical CourseSimple silico-sisdoes not usually lead to significantrespiratory dysfunctionPro-gressive massive fibrosisdyspnea on exertion and later at restSilicosis is associated with an increasedsusceptibility to tuberculosis
  52. 52. Asbestos-Related DiseasesAsbestos(Greek, “unquenchable”)includes a group of fibrous silicateminerals that occur as thin fibersAsbestos is a family of crystalline hydratedsilicates that form fibers
  53. 53. 2 forms of asbestos2 forms of asbestosa)serpentine (i.e., curly and flexible)b) amphibole (i.e., straight, stiff andbrittle)Asbestosis
  54. 54. AsbestosisAsbestosCausing fibrosis by interacting with lungmacrophagesalso functions as both a tumor initiatorand a promoter
  55. 55. MorphologyAsbestosis is marked by diffuse pulmonaryinterstitial fibrosisCharacterized bythe presence of asbestos bodieswhich are seen as golden brown, fusiform orbeaded rods with a translucent centercoated with an iron-containing proteinaceousmaterialAsbestosis
  56. 56. Asbestos body
  57. 57. Asbestos bodiesThese ferruginous bodies are golden brown and beaded,with a central, colorless, nonbirefringent core fiber
  58. 58. Pleural plaque. The dome of thediaphragm is coveredby a smooth, pearly white, nodular plaqueAsbestos-related pleural plaquesLarge, discrete fibrocalcific plaques are seenon the pleural surface of the diaphragm
  59. 59. Which of the following inhaled pollutants is most likely toproduce extensive pulmonary fibrosis?(A) Silica(B) Tobacco smoke(C) Ozone(D) Wood dust(E) Carbon monoxide(A) Silica crystals incite a fibrogenic response afteringestion by macrophages. The greater the exposure andthe longer the time of exposure, the greater is the lunginjury.
  60. 60. • A 63-year-old male worked for 20 years in the sand-blasting business, and he used no respiratory precautionsduring that time. He now has increasing dyspnea withoutfever, cough, or chest pain. Which of the followinginflammatory cell types is most crucial to the developmentof his underlying disease?•(A) Plasma cell•(B) Mast cell•(C) Eosinophil•(D) Macrophage•(E) Natural killer (NK) cell
  61. 61. The correct answer is (D)Silica is a major component of sand, which contains themineral quartz. The small silica crystals are inhaled, andtheir buoyancy allows them to be carried to alveoli. Therethey are ingested by macrophages, which then secretecytokines that recruit other inflammatory cells andpromote fibrogenesis.Plasma cells secrete immunoglobulins, which are not a majorcomponent of this process.Mast cells and eosinophils are prominent in type I hypersensitivityresponse.NK lymphocytes are more likely to be a prominent component ofinflammatory processes directed against infectious agents.
  62. 62. A 75-year-old male experienced increasing dyspnoea. Themicroscopic appearance of the lung is shown here. This ismost characteristic for(A) Anthracosis(B) Berylliosis(C) Silicosis(D) Calcinosis(E) Asbestosis
  63. 63. The answer is (E)The ferruginous bodies shown here are long, thin crystals of asbestosthat have become encrusted with iron and calcium. The inflammatoryreaction incited by these crystals promotes fibrogenesis and resultantpneumoconiosis.Berylliosis is marked by noncaseating granulomas.Anthracosis is a benign process seen in all city dwellers as a consequence ofinhaled carbonaceous dust.Silica crystals are not covered by iron and tend to result in formation offibrous nodules (i.e., silicotic nodules).Calcium deposition may occur along alveolar walls with a high serum calcium(i.e., metastatic calcification).
  64. 64. Which of the following morphologic changes can beseen in advanced cases of both obstructive and restrictivelung disease?(A) Marked medial thickening of pulmonary arterioles(B) Destruction of elastic tissue in the alveolar walls(C) Fibrosis of the alveolar walls(D) Hemorrhage in the alveolar lumen(E) Hyaline membranes lining the airspacesThe correct answer is (A)Changes of pulmonary hypertension are characteristic for restrictive andobstructive lung diseases. This explains, for example, the occurrence of corpulmonale and right-sided CHF in persons with chronic obstructive pulmonarydisease or with pneumoconiosis
  65. 65. Atelectasis (Collapse)AtelectasisNeonatal atelectasisincomplete expansion of the lungsAcquired atelectasiscollapse of previously inflated lungproducing areas of relatively airlesspulmonary parenchyma
  66. 66. Acquired atelectasis may be dividedinto Resorption (or obstruction) Compression Contraction atelectasisATELETASIS (Collapse)
  67. 67. Resorption atelectasisis the consequence ofcomplete obstruction of an airway leads toresorption of the oxygen trapped in thedependent alveoliwithout impairment of blood flow through theaffected alveolar wallslung volume is diminishedthe mediastinum shifts toward the atelectatic lungATELETASIS (Collapse)
  68. 68. Airway obstruction is caused by excessive secretions (e.g., mucus plugs) orexudates within smaller bronchi (bronchialasthma, chronic bronchitis, bronchiectasis) postoperative states aspiration of foreign bodies bronchial neoplasms (rarely)ATELETASIS (Collapse)
  69. 69. Compression atelectasisresults wheneverpleural cavity is partially or completely filled byfluid exudate, tumor, blood, or air (pneumothorax)or with tension pneumothorax, when air pressureimpinges on and threatens the function of thelung and mediastinum, especially the majorvesselsmediastinum shifts away from the affected lungATELETASIS (Collapse)
  70. 70. Compression atelectasis
  71. 71. Contraction atelectasisoccurs whenlocal or generalized fibrotic changes in thelung or pleura prevent full expansionATELETASIS (Collapse)
  72. 72. reduces oxygenationpredisposes to infectioncollapsed lung parenchyma can be re-expanded (reversible disorder)except that caused by contractionATELETASIS (Collapse)
  73. 73. ANY QUESTIONS?