The pancreas has both endocrine and exocrine functions. The endocrine pancreas consists of the islets of Langerhans and is
particularly important to carbohydrate metabolism. Diseases of the endocrine pancreas include diabetes mellitus and hormone-producing
tumors such insulinomas and glucagonomas. The exocrine pancreas consists of the acinar and ductular cells. The exocrine
pancreas produces enzymes, zymogens and other products that aid in the digestion of food. Diseases of the exocrine pancreas
include pancreatitis, exocrine pancreatic insufficiency and carcinomas.
Pancreatitis is thought to be due to the premature activation of zymogens within the pancreas. Zymogens are synthesized as
inactive enzymes to prevent cell membrane damage within the pancreas. These zymogens are activated in the duodenum. Pancreatitis
is the result of fusion of lysosomal enzymes with zymogen granules in the acinar cells. As a result, autodigestion of the
pancreas occurs, inflammatory cells are recruited, free radicals produced, and inflammatory mediators are produced. As a
result further damage and additional inflammation occurs. There are several mechanisms in place that help prevent premature
activation of the granules, pancreatitis and systemic inflammation. These include storage of zymogens in granules, co-secretion
of pancreatic secretory trypsin inhibitor (PSTI), secretion into the duodenum as inactive zymogens, the pancreatic duct, the
sphincter of Oddi, and circulating protease inhibitors.
Acute and chronic forms of pancreatitis have been described in dogs and cats. In acute pancreatitis inflammation is present
but fibrosis and atrophy are absent. With chronic pancreatitis fibrosis and pancreatic atrophy are present. Both forms may
have neutrophilic and lymphocytic inflammatory cell infiltrates, edema and necrosis.
Most cases of pancreatitis are idiopathic. There are several conditions which have been associated with the development of
pancreatitis including dietary indiscretion, inflammatory bowel disease, biliary disease, hyperlipidemia, certain drugs, hypercalcemia,
zinc toxicosis, organophosphate poisoning, obesity, hyperadrenocorticism, hypothyroidism, diabetic ketoacidosis, trauma, ischemia,
Babesia canis, Toxoplasma gondii, and flukes. In the Miniature Schnauzer mutations in the SPINK 1 gene, which encodes for PSTI, have been identified. The
significance of this is unknown but PSTI is a trypsin inhibitor cosecreted with trypsinogen that is thought to help deter
premature activation of the zymogens.
There is no age or sex predisposition. All breeds can be affected but there is an increased incidence in Miniature Schnauzers,
Shetland Sheepdogs, Yorkshire terriers, poodles, Bichon frises, maltese, shih tzus, Samoyeds and many others.
The clinical presentation is variable but animals with acute pancreatitis tend to have more severe signs than those with chronic
pancreatitis. In dogs anorexia, vomiting, lethargy, and abdominal pain are common. Fever and diarrhea are not as common.
Most cats have very non-specific signs including anorexia and lethargy. Less common are weight loss, icterus, fever, hypothermia,
abdominal pain, and diarrhea. In dogs and cats signs of systemic inflammation such a dyspnea and cardiac arrhythmias as well
as circulatory shock may be present.
Bloodwork may reveal a relative polycythemia, anemia, neutrophilia with a left shift, thrombocytopenia, elevated liver enzymes,
azotemia, decreased albumin, and hypocalcemia on the CBC and biochemical profile.
Tests used historically to diagnose pancreatitis are serum amylase and lipase, trypsinlike immunoreactivity and pancreatic
lipase immunoreactivity. Amylase and lipase lack sensitivity and specificity in dogs and cats for detecting pancreatitis.
Trypsinlike immunoreactivity is a sensitive test for the diagnosis of exocrine pancreatic insufficiency but not for pancreatitis
in the dog and cat. Pancreatic lipase immunoreactivity is the most sensitive and specific test for diagnosing pancreatitis
in the dog and cat. IDEXX Laboratories has developed a commercial Spec cPL for dogs, a SNAP cPL for dogs, and SNAP fPL for
cats making testing more readily available. The SNAP tests only read as positive or negative whereas the PLI and Spec cPL
provide actual values.
Radiographs are not preferred but may be valuable in eliminating other causes of clinical signs. Classic radiographic changes
seen in the dog, but not the cat, include decreased abdominal detail, cranial abdominal mass effect, widening of the juncture
between the pylorus and duodenum, displacement of the stomach, and ileus. Abdominal ultrasound is preferred. The pancreas
may be surrounded by fluid, enlarged, heterogenous, hypoechoic, or contain fluid-filled structures. A hypoechoic pancreas
with hyperechoic peripancreatic fat is suggestive of pancreatic necrosis. A heterogenous pancreas is more suggestive of fibrosis
seen with chronic pancreatitis. Unfortunately for cats ultrasonographic changes of the pancreas are not as reliable indicators
of pancreatitis. Ultrasound has the additional advantage of the ability to sample the pancreas and visualize other abdominal
structures. Pancreatic cytology is done with needle aspirates. Pancreatic aspirates may be helpful in cases of acute pancreatitis
by identifying pancreatic necrosis. Aspirates are also useful in diagnosing pancreatic neoplasia. Cross-sectional imaging
has not been studied extensively in dogs and cats for the diagnosis of pancreatitis.
Histologic examination of the pancreas is considered the gold standard for diagnosis. It is possible to miss significant
lesions with biopsy and lesions consistent with pancreatitis are found in animals with no clinical signs. This again emphasizes
the importance of performing diagnostic tests in animals with clinical signs. Unfortunately there is concern that in obtaining
biopsies a patient will be at risk for developing more severe pancreatitis. Biopsies can be taken surgically or laparoscopically.