Irregular atrophy and obliteration of pancreatic acini and ducts
Retention of normal lobular pancreatic architecture
– Lobular architecture aids histologic distinction from pancreatic adenocarcinoma
• Pancreatic duct alterations related to fibrosis and destruction
Duct epithelium may show atrophy, reactive, or hyperplastic changes
Squamous, mucinous, or pyloric metaplasia
• Islets of Langerhans usually preserved, may show pseudohyperplasia
Fibrosis and Chronic Inflammation The main features of chronic pancreatitis are fibrosis and chronic inflammation. Note the marked loss of acinar parenchyma. Residual islet cells and ductules are visible within the rounded contour of the lobule.
Preserved Lobular Architecture In chronic pancreatitis, the normal lobular architecture is typically retained, and the rounded configuration of the lobule is apparent at low power. Note the fibrosis and loss of acinar parenchyma. Rare islets are still visible .
Atrophic Lobule With Acinar Loss Atrophic lobules in chronic pancreatitis are characterized by lobular arrangements of small ducts , fibrous tissue, and residual islet cells . No residual acini are seen.
Islet Cell Pseudohyperplasia Islet cell pseudohyperplasia, or proliferation and formation of cords and small clusters, is a common finding in chronic pancreatitis. Note the surrounding marked fibrosis and chronic inflammation. There is essentially no residual acinar parenchyma.
TERMINOLOGY
Abbreviations
• Chronic pancreatitis (CP)
Definitions
• Progressive inflammatory disorder of pancreas resulting in scarring, gland destruction, and functional impairment
ETIOLOGY/PATHOGENESIS
Alcohol
• By far most common cause of CP in developed countries
Anatomic
• Duct obstruction
Stones or tumors involving head of pancreas lead to proximal duct dilatation, gland atrophy, and scarring
• Paraduodenal or “groove” pancreatitis
Metabolic
• Hypercalcemia
• Hyperlipidemia
Hereditary
• Autosomal dominant form
• Several associated gene mutations described
Trypsinogen gene ( PRSS1 ) accounts for 60-80% of hereditary CP cases