Digestive pathology 2

1. Digestive pathology 2

2. Acute viral hepatitisFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 22.1

3. Fig. 22.2 Fig. 22.1-2. (1) Degenerative lesions of hepatocytes (hydropic degeneration, hepatocyte necrosis- citolytic necrosis and apoptotic necrosis); (2) Inflammatory reactions (intralobular mononuclear infiltrate associated to intralobular hepatocyte necrosis, hyperplasia of Kupffer cells along sinusoides and mononuclear inflammatory infiltration into portal tracts); (3) Regenerative lesions of hepatocytes.

4. Chronic hepatitis Moderate CH Severe CH N Mild CH Morphology: depending on severity of the lesion degrees - 3 histological types: (a) mild chronic hepatitis (b) moderate chronic hepatitis (c) severe chronic hepatitis Fig. 22.3

5. Mild chronic hepatitisFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 22.4 Fig. 22.4. Mild chronic hepatitis: (a) Hepatic lobular architecture is preserved; (b) Portal tract area is enlarged by lymphocytic inflammatory infiltrate; (c) Limiting plate of hepatocytes is intact.

6. Moderate chronic hepatitisFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 22.5 • Fig. 22.5. (a) Lobular liver architecture is in course of changing. (b) Portal tract is enlarged and stellated by presence of limpho-plasmocytic inflammatory infiltrate into portal tract and around it. (c) Foci of destruction of limiting plate of hepatocytes by inflammatory infiltrate - interface hepatitis or “piecemeal necrosis“. (d) Rare portal fibrosis.

7. Severe chronic hepatitis Fig. 22.6 Fig. 22.6. (a) Lobular hepatic architecture is restored. (b) Porto-biliary tract is enlarged (infiltrated by inflammatory limpho-plasmocytic cells). (c) Inflammatory cells form inflammatory bridges connecting portal tracts, central veins, and portal tracts with central veins. (d) Portal tract fibrosis.

8. Hepatic cirrhosisFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 22.7 Van Gieson staining

9. Fig. 22.8 Fig. 22.7-8. Liver architecture is destroyed by replacement with regenerative nodules (absence of radiary hepatocyte cords; hepatocytes show degenerative lesions, unicellular necrosis, steatosis, cholestasis; no central vein; if exists, is located to the periphery of the hepatic nodule;) surrounded by fibrous bands (collagen fibers and fibroblasts; chronic inflammatory infiltrate; hyperplastic biliary ducts and vessels;).

10. Hepatic cirrhosisFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 22.9

11. Fig. 22.10 Fig. 22.9-10. Hepatic cirrhosis: Liver structure is completely destroyed and replaced by nodules of regenerated hepatocytes surrounded by bands of fibrosis.

12. Hepatocellular carcinomaFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig.22.11 Fig. 22.11. (1) Nodular tumor (large, solitary, gray, nodular tumor with imprecise limits) or multinodular tumor (ussualy associated with liver cirrhosis); (2) Diffuse tumor (massive tumor with diffuse liver infiltration replacing slowly the liver parenchyma);

13. Hepatic metastases Fig. 22. 16 Fig.22.16. Multiple, well defined tumoral nodules replacing hepatic parenchyma.

14. Hepatocellular carcinomaFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 22.12 Fig. 22.12. Pluristratified cords composed of hepatic atypical cells.

15. Fig. 13 Fig. 13. Tumoral cells resemble with hepatocytes.

16. Hepatocellular carcinomaFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 22.14 Fig. 22.14. Sheats of atypical cells developed on cirrhotic nodules.

17. Fig. 22.15 Fig. 22.15. Marked cellular atypia forming tumoral cords.

18. Cholelithiasis-Cholesterol stonesFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 22.17

19. Cholelithiasis - Pigmented stones Fig. 22.18

20. Cystic duct obstructionFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 22.19 Fig. 22.19. Distention of the gallbladder with watery bile (hydrops) or mucus (mucocele).

21. Cholesterolosis It consists in focal accumulation of cholesterol loaded macrophages (xantic cells) in the stroma of the gallbladder appearing as yellow granularities called achene, contrasting with red background of congested mucosa. It looks like strawberry (strawberry gallbladder). Fig. 22.20

22. Chronic cholecystitisFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 22.21 Fig.22.21. Large cholecyst with thick fibrous wall and a lumen containing yellow - greenish bile and a large calculus.

23. Carcinoma of the gallblader Fig. 22.22 • Fig. 22.22. Ulcero-vegetative carcinoma appears as a prominent and ulcerated tumor in the gallbladder fundus.

24. Acute pancreatitiswith cytosteatonecrosisFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 22.23 Fig. 22.23. Pancreatic parenchyma is edematous and covered by white patches representing areas of necrosis of adipose tissue.

25. From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 24 • Fig. 22.24. Areas of interstitial fat cell necrosis (preserved fat cell shape "cell shadows“, nucleus disappearance, granular eosinophilic cytoplasm by precipitation of fatty acids or a basophifilc granular cytoplasm by formation of calcium salts) surrounded by inflammatory neutrophils.

26. Pancreatic carcinomaFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 22.25 Fig. 25. Pancreatic carcinoma locations: (a) Head - 60%; (b) Body and tail - 10%; (c) Diffuse - 20%.

27. Fig. 22.26 Fig. 22.26. Gray homogenous nodular or diffuse tumor replacing normal pancreatic parenchyma.