Cause of Canine and Feline Pancreatitis: Understanding
It has been reported in several studies that there is an alarming overabundance of Miniature Schnauzers, suggesting that their genetic susceptibility may be akin to that of human patients with hereditary pancreatitis. Other research has noted an increase in the incidence of pancreatitis in breeds such as the Yorkshire Terrier, Cocker Spaniel, Dachshund, Poodle, Sled Dogs, and others.
Dietrelated issues are considered a common risk factor in dogs, essentially because they tend to consume anything and everything they can get their paws on!
High triglyceride levels, highfat diets, and if severe (i.e., serum concentrations of 500 milligrams per deciliter or more), are recognized as risk factors for pancreatitis in dogs, but not in cats.
Some studies have cited high adrenal cortical hormones as a potential risk factor for pancreatitis.
Severe blunt trauma, such as in car accidents or feline highrise syndrome, can also trigger pancreatitis.
Surgeries have been considered another risk factor; however, most postoperative pancreatitis cases are now believed to result from inadequate pancreatic perfusion during anesthesia.
Infectious diseases have been implicated, but the evidence of causation is often weak. In dogs, pancreatitis has been reported in association with parvovirus and coronavirus infections. In feline species, toxoplasmosis and feline infectious peritonitis are considered the most significant.
Many medications are associated with human pancreatitis, but few have been confirmed in dogs and cats. Generally, most medications should be regarded as potential causes of pancreatitis; cholinesterase inhibitors, calcium, potassium bromide, phenobarbital, asparaginase, estrogen, salicylic acid, azathioprine, thiazide diuretics, and vincristine may be among the most critical.
A variety of different injuries can ultimately lead to pancreatitis through a common pathway. The initial stage of pancreatitis involves a reduction in pancreatic juice secretion. This is followed by the colocalization of zymogen granules and lysosomes, leading to trypsinogen activation within the colocalized organelles. Trypsin, in turn, activates more trypsinogen and other zymogens. Prematurely activated digestive enzymes result in local damage to the pancreas' exocrine secretion, accompanied by pancreatitis, edema, hemorrhage, inflammation, necrosis, and peripancreatic fat necrosis. The subsequent inflammatory process leads to an increase in white blood cells and the production of cytokines. Activated enzymes, and more importantly, cytokines circulate in the blood, leading to distant complications such as systemic inflammation, disseminated intravascular coagulation, diffuse lipodystrophy, pancreatic encephalopathy, hypotension, kidney failure, lung failure, myocarditis, and even multiple organ failure.
