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PH-GI26

Chronic pancreatitis

How repeated injury from alcohol, smoking, genes, duct blockage or autoimmunity turns the pancreas into scar and stone, why the pain persists, and why digestion and glucose control fail only once most of the gland is lost.

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  • 6 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Describe the acini, ducts and islets of the pancreas and how duct cells keep pancreatic juice flowing.
  • Explain how alcohol, smoking, genetic variants, duct obstruction and autoimmunity lead from repeated injury to fibrosis, using the sentinel acute pancreatitis event model.
  • Explain how protein plugs, calcified stones and duct strictures form, and why the pain has duct, inflammatory and nerve components.
  • Relate exocrine failure to steatorrhoea and fat-soluble vitamin loss, and islet loss to type 3c diabetes with a tendency to hypoglycaemia.
  • Compare acute and chronic pancreatitis, recognise the classic appearances and tests, and explain how enzyme replacement, duct drainage, glucocorticoids and insulin act on the mechanism.

What it is

Chronic pancreatitis is long-lasting inflammation of the pancreas that permanently replaces its tissue with fibrosis, narrows and blocks its ducts, often with calcified stones, and in time causes loss of its exocrine (digestive) and endocrine (hormone) function. Unlike acute pancreatitis, the damage does not resolve. Alcohol and smoking are the main causes; genetic, obstructive and autoimmune forms reach the same end.

5 types to tell apart
Toxic–metabolic (alcohol and smoking)
About half of cases; often follows repeated acute attacks; calcification and duct stones are common.
Genetic (hereditary)
Variants of PRSS1, SPINK1, CTRC or CFTR that let trypsin build up in the gland or thicken its juice; often begins in childhood or youth.
Obstructive
A stricture, tumour or stone blocks the main duct (pancreas divisum is a possible cause); damage lies upstream of the block, usually without stones.
Autoimmune pancreatitis
Type 1 is part of IgG4-related disease; type 2 is a duct-destructive form. Both often present as a swollen gland with painless jaundice and respond to glucocorticoids.
Tropical and idiopathic
Tropical pancreatitis affects children and young adults in regions such as India, Indonesia and Nigeria, with large duct stones; in many people no cause is found.

Normal function

Acini, ducts and islets, with a large reserve

Most of the is exocrine. Acinar cells make the digestive enzymes, kept inactive until they reach the duodenum (see acute pancreatitis). Duct cells add a watery, bicarbonate-rich fluid, secreted through the chloride channel CFTR, which flushes the enzymes down the to the and neutralises stomach acid in the duodenum. Secretin drives the fluid and bicarbonate; cholecystokinin (CCK), released by the duodenum when food arrives, drives the enzymes.

The gland has a large reserve: digestion stays normal until enzyme output falls to about a tenth of normal. Lying quietly around the acini are pancreatic stellate cells, which store vitamin A and can turn into collagen-making cells when the gland is injured.

Scattered through the acinar tissue, the islets of Langerhans make up only a small fraction of the gland. Beta cells make insulin, alpha cells glucagon, delta cells somatostatin and PP cells pancreatic polypeptide.

Point to it on the model