1. Digestive pathology 2

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

3. Fig. 22.2
Fig (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 N
Moderate CH
Mild CH
Severe 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 hepatitis From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi
Fig. 22.4
Fig 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 hepatitis From cases of the Pathology Department - U
Moderate chronic hepatitis From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi
Fig. 22.5
Fig (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 (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 cirrhosis From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi
Fig. 22.7
Van Gieson staining

9. Fig. 22.8
Fig 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 cirrhosis From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 22.9

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

12. Hepatocellular carcinoma From: Stevens A. J Lowe J. Pathology
Hepatocellular carcinoma From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig.22.11
Fig (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 Multiple, well defined tumoral nodules replacing hepatic parenchyma.

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

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

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

17. Fig
Fig Marked cellular atypia forming tumoral cords.

18. Cholelithiasis-Cholesterol stones From: Stevens A. J Lowe J. Pathology
Cholelithiasis-Cholesterol stones From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig

19. Cholelithiasis - Pigmented stones
Fig

20. Cystic duct obstruction From: Stevens A. J Lowe J. Pathology
Cystic duct obstruction From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig
Fig 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. Chronic cholecystitis From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig
Fig Large cholecyst with thick fibrous wall and a lumen containing yellow - greenish bile and a large calculus.

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

24. Acute pancreatitis with cytosteatonecrosis From: Stevens A. J Lowe J
Acute pancreatitis with cytosteatonecrosis From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig
Fig 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 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 carcinoma From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig
Fig. 25. Pancreatic carcinoma locations: (a) Head - 60%; (b) Body and tail - 10%; (c) Diffuse - 20%.

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