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① ACUTE PANCREATITIS

Characterized by reversible pancreatic parenchymal injury and inflammation

o Has many causes: toxic exposures (alcohol), pancreatic duct obstruction (biliary calculi), inherited genetic defects, vascular injury, infections.
Results from inappropriate release and activation of pancreatic enzymes that destroy pancreatic tissue and elicit and inflammatory reaction.

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I
This section of the tissue from pancreas showing necrotic acini (blue
arrow) and necrotic adipose tissue (black) having cloudy appearance
surrounded by inflammatory reaction. [Doc Menor]
This slide can be an acute necrotizing hepatitis.
Appearance of chalky-white color of these fat cells – associated with
Fat Necrosis
Fat Necrosis – triggered by lipase activity -> Saponification, a process
in which fatty acids combine with calcium to form insoluble calcium
soaps that impart a granular blue microscopic appearance to surviving
fat cells.

Sometimes we would also see areas of hemorrhage. Presence of tissue destruction of the pancreatic parenchyma.
Sometimes, it would be liquefactive due to the presence of the
inflammation. Liquefactive would mean loss of outlines.

In this area, there is the presence of fibrocellular mass. In some areas, there would be the presence of coagulative necrosis.
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② ISLET SCLEROSIS

Islets of Langerhans associated with fibrosis. (encircled black) Presence of tissue destruction of the pancreatic parenchyma.
Fibrosis can be due to the presence of inflammation like what happens Sometimes, it would be liquefactive due to the presence of the
in DM type 1 – there is beta cell destruction. inflammation. Liquefactive would mean loss of outlines.
In the case of beta-amyloid type 2 – there would be amyloid
deposition.
To differentiate the two, use Congo red stain.
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⑦ CYSTIC FIBROSIS
Caused by mutations in the CFTR gene that encodes an apical chloride channel.
Loss of CFTR leads to abnormal secretions that promote protein plugging, duct obstruction, and the development of pancreatitis.

What we have here are the presence of hyper concentrated viscid Closer view of the dilated ducts.
secretions. fibrosis M
-
tse pancreas - parenchyma → replaced by dense
There would be atrophy of acinar structures.
several dilated ducts fry mvws)
Notice that the islets of Langerhans are very distinct because of the
fibrosis and the lack of acinar structures surrounding them. Exocrine pancreas → atrophied & fibrotic
Dilated ducts filled with mucus.
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④ ADENOCARCINOMA OF THE PANCREAS

One of the most aggressive of the solid cancers.
Believed to arise from noninvasive precursor lesions referred to as pancreatic intraepithelial neoplasia (panIN).
Epithelial cells in PanIN show dramatic telomere shortening – may accumulate chromosomal abnormalities to invasive carcinoma.
KRAS gene (chromosome 12p) – most frequently altered oncogene.

Encircled is the islet of Langerhans. Presence of glands.

In normal pancreatic tissue, the islet should be surrounded by T des parenchyma → infiltrated by proliferation
mop labia of of malignant
pancreatic structures. glands ( irregularity shaped fund glands)
In this slide, it is instead surrounded by glands.

The glands have pleomorphism, dark chromatin pattern. Presence of signet ring pattern.
Notice columnar cells – these are the gland associated with carcinoma.
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