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Respiratory pathology 1

Respiratory pathology 1

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Respiratory pathology 1

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  1. Respiratory pathology 1

  2. Lobar pneumoniaFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 An entire lobe is involved. Fig. 17.1. In classical type, lobar pneumonia develops in four stages: (1) congestion (serous alveolitis); (2) red hepatization (fibrinous alveolitis); (3) gray hepatization (leucocytic alveolitis); (4) resolution.

  3. Lobar pneumonia stage I (congestion) From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 17.2. Serous alveolitis:(a) parieto-alveolar capillaries are congested; (b) intra-alveolar serous exudate (intense eosinophilicmaterial,rich in proteins,which contains red blood cells and bacteria).

  4. Lobar pneumonia stage II (Red Hepatization) and III (Red Hepatization)From: Stevens A. J Lowe J. Pathology. Mosby 1995From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 17.3.Red Hepatization stage (II) andFibrinous alveolitis: (a) parieto-alveolar capillaries are intensely congested; (b) intra- alveolar fibrinous exudate, as afibrin network, containing erythrocytes, neutrophiles and infectious agents; fibrinous exudate passes through Kohn pores from an alveolus to another (Mallory stain).

  5. Fig. 17.4.Leucocytic alveolitis: (a) parieto-alveolar capillary network is still congested; (b) alveolar lumen contains a suppurative exudate composed of neutrophils-PMNs and macrophages-Mfs.

  6. PulmonarycarnificationFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 17.5.

  7. Fig. 17.6 Fig. 17.5-6. Microscopy: It is a complication of fibrinous alveolitis stage resulting by connective organization of the alveolar fibrinous exudate. The alveolar lumen is occupied by a fibro-vascular granulation tissue (connective vascular tissue of neoformation). (Simionescu staining)

  8. PulmonaryabscessFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 17.7. Pulmonary abscess:(1) the cavity: contains a suppurative material and air content (in case of communication with air conducts); (2) wall: (a) acute abscess – the wall has irregular borders reprezented by suppurative necrotic lung parenchyma; (b) chronic abscess - the wall is a pyogenic membrane that becomes fibrotic by connective organization.

  9. BronchiectasisFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 17.8. Multiple chystic lesions of varying sizes that extend to the pleura, and contain muco-purulent exudates. Affected bronchial walls are dilated and fibrotic, from where iradiates fibrous bands within parenchimal lung.

  10. BronchopneumoniaFrom: Stevens A. J Lowe J. Pathology. Mosby 1995From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 17.9.

  11. Fig. 17.10 Fig. 17.9-10. Microscopy: (1) acute purulent bronchiolitis (purulent exudate in the bronchial lumen and wall; the bronchiolar epithelium is altered and exfoliated into the lumen); (2) peribronchiolar acute exudative alveolitis:(a) leucocytic exudate; (b) fibrino-leucocytic exudate; (c) sero-fibrinous exudate.Between nodular foci of bronchopneumonia the lung tissue is normal.

  12. Bronchopneumonia of aspirationFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 17.11

  13. Fig. 17.12 It appears at newbornes with premature respiration during passage through mother borne channel by aspiration of amniotic fluid (amniotic cells, epidermal descuamated cells, vernix caseosa – fat, lanugo – hair, etc). Microscopy (HE): (a) Alveolar channels and alveolar spaces contain hematoxilinic structures resembling with dry leaves (components of amniotic fluid) and serous exudate with few neutrophils; (b) Congestion of capillaries into alveolar walls.

  14. Pulmonary emphysema From: Stevens A. J Lowe J. Pathology. Mosby 1995From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 17.13 Microscopically, in PE, the lesions interest entire lung acinus or lobule: (1) central acinus (BR); (2) peripheral lung acinus: (a) alveolar channel and (b) alveolar sac.

  15. Fig. 17.14 Fig. 17.3-4.Microscopy: (1) distention of air spaces (alveolar thin walls) and (2) destruction of alveolar walls with fusion of adjacent alveolar lumens and formation of large air spaces. (3) Capillaries of alveolar walls are compressed and reduced in number (pulmonary hypertension).