Pancreatic Atrophy, Exocrine

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AKA Pancreatic Acinar Athropy (PAA)


Pancreatic atrophy (Image sourced from Bristol Biomed Image Archive with permission)
  • Degeneration of acinar cells ccurs as a sequel to
    • Starvation - loss of zymogen granules
    • Maldigestion
    • Obstruction of the pancreatic ducts by
      • Neoplasm
      • Chronic inflammation and associated fibrosis
      • Foreign bodies (parasites, pancreoliths
    • Specific nutritional deficiencies include: essential amino acids, zinc, copper, selenium

Clinical signs

  • By the time clinical signs of exocrine pancreatic insufficiency (EPI) appear, the pancreas is usually almost totally destroyed
  • Chronic diarrhoea with steatorrhoea and undigested muscle fibres. Large quantities of pale faeces are passed (due to dilution of bile pigment and the presence of undigested fats). The faeces have a characteristic rancid or cheesy odour.
  • Loss of condition despite marked increase in appetite

Macroscopic appearance

  • The pancreas is extremely thin and almost lace-like
  • Primarily acinar tissue affected; the ducts and Islets of Langerhans are relatively normal

Microscopic appearance

  • In these cases the parenchyma is replaced by atypical parenchyma and adipose tissue
  • Irregular, shrunken acini composed of cells with little cytoplasm
  • Some cases show a few areas of apparently normal glandular tissue or foci of cellular infiltraton which have been interpreted as suggesting degenerative changes

Aetiology

  • The underlying cause is not known, possibly due to nutritional imbalances
  • Chronic pancreatitis is a rare cause of EPI
  • Possible hereditary EPI in GSDs and rough coated collies

Diagnosis

  • Low serum trypsin-like immunoreactivity is an early, preclinical diagnostic test for EPI



Extra information for Exocrine Pancreatic Atrophy

Exocrine pancreatic atrophy in GSDs and rough coated collies: an end result of lymphocytic pancreatitis. Wiberg ME et al. Vet Path (1999) 36 530-41

  • Histological changes in EPI dogs
  • Histological changes in the subclinical pancreas (ie; just TLI):
  • Patchy areas of normal and abnormal exocrine parenchyma
  • Consistently a marked lymphoid infiltrate (lesser numbers of plasma cells seen, occasional eosinophils), starting in the border zone with gradual loss of the pancreatic parenchyma
  • Mainly CD3+ T cells, with fewer CD3+ lymphocytes.
  • Some lymphoid follicles (mainly B cells) scattered throughout.
  • No associated increase in fibrous connective tissue
  • Some intra-acinar lymphocytes seen
  • As tissue destruction continued, ductal structures became more obvious
  • Apoptosis seen in the acini often in normal looking acini.
  • Ultrastructure
    • Degenerative changes in acinar cells – dilation of rER, swelling of mitochondria, nuclear pyknosis, aptotitic bodies
  • Histology of clinical EPI:
    • Totally atrophied exocrine pancreas
    • Some dogs had areas of normal acinar structures
    • Little inflammation in the border zone
    • Most of the remaining exocrine pancreas was disorganized, prominent ducts, increased amounts of adipose tissue.
    • Slight increase in fibrous tissue compared to subclinical phase, but replacement with fat was more prominent than fibrosis.
    • No ductular epithelial hyperplasia evident
  • Ultrastructure
    • Often no remaining acinar cells
  • Suggests and immune-mediated destruction - ?hereditary
  • Islet cells usually well preserved in the atrophied pancreas.