Resumed Understanding Complicated Digestive System: Acute Pancreatitis, Exocrine Pancreatitis, Pancreatitis, The Ageing Pancreas

  Provided to you by: Atlas of Veterinary Clinical Anatomy














Overtime the Pancreas Inflames Easily ?

In dogs, the pancreas can become more easily inflamed over time because several long-term changes and repeated stresses slowly lower its tolerance. Here are the main reasons:

 Repeated low-grade inflammation

Even mild, subclinical pancreatitis (no obvious symptoms) can cause: 
  • Microscopic scarring
  • Altered enzyme regulation
This makes the pancreas more reactive to future triggers. (Think of it like a sunburn that never fully heals—each new exposure hurts faster)

Symptoms of subclinical pancreatitis: 

(These signs are usually mild, vague, or intermittent)

Digestive & appetite changes

  • Nausea signs (grass eating, lip licking, swallowing, )
  • Mild, short-lived diarrhea or softer stools
  • Occasional skipped meals or reduced interest in food
  • Gassiness or bloating
  • Occasional vomiting (infrequent, not severe)

Behavior & comfort
  • Subtle abdominal sensitivity (may avoid being picked up)
  • Mild lethargy or “off” days
  • Being quieter than normal
  • Less enthusiasm for walks or play
  • Sitting or lying down more often

Body & metabolic clues
  • Weight fluctuation despite similar intake
  • Difficulty maintaining body condition
  • Increased sensitivity to dietary fat or new foods
  • Mild or intermittent elevation in canine pancreatic lipase (cPLI)
  • Borderline increases in liver enzymes
  • Lab findings (often how it’s discovered)
  • Changes may come and go
  • Mild dehydration during episodes
Why subclinical pancreatitis matters

Each mild episode can cause microscopic damage. Over time, this lowers the pancreas’s tolerance

Can progress to:
  • Recurrent pancreatitis
  • Chronic pancreatitis
  • Diabetes or digestive enzyme insufficiency (EPI)
This explains why dogs may “suddenly” get pancreatitis later—when the pancreas has actually been struggling quietly for a long time.

 Changes in fat metabolism

As dogs age or develop metabolic issues:
  • Fat digestion becomes less efficient
  • Blood triglycerides may rise
The pancreas must work harder to release enzymes → higher inflammation risk. High-fat meals are a common trigger because they sharply increase pancreatic enzyme secretion.

 Oxidative stress accumulation

Over time, dogs experience:
  • Increased oxidative stress
  • Reduced antioxidant defenses
Pancreatic cells are particularly sensitive to this imbalance. This is why chronic disease, aging, and poor recovery periods increase risk.

 Hormonal & endocrine influences

Conditions that develop over time can sensitize the pancreas:
  • Diabetes mellitus
  • Cushing’s disease
  • Hypothyroidism
These alter lipid metabolism and inflammatory signaling.

Medication exposure

Long-term or repeated use of certain medications can increase susceptibility:

  • Corticosteroids
  • Some anticonvulsants
  • Potassium bromide
Not all dogs are affected—but repeated exposure can lower the pancreas’s threshold.

 Dietary pattern changes

  • Over time, dogs may experience:
  • Repeated diet changes
  • Exposure to table scraps or high-fat treats
  • Inconsistent feeding routines
These repeated “insults” increase pancreatic sensitivity.

Why it feels like “it inflames more easily now”?

Once the pancreas has been inflamed before:

  • Enzyme activation becomes easier
  • Protective mechanisms are weakened
  • Inflammation can be triggered by smaller dietary or metabolic changes
So what once caused no issue may later cause a flare.

Summery: 

Pancreatitis in dogs often becomes easier to trigger over time because of:

Cumulative inflammation
Metabolic and hormonal changes
Oxidative stress
Reduced recovery capacity

This is why consistent low-fat diets, routine feeding, and being attentive to adapting to their needs (listening to how their body responds to a treat or food, eliminating triggers even if its your "bonding treat") becomes more important as dogs get older or after their first episode.

Resources

Intestinal permeability (“leaky gut”) & inflammation

Bischoff, S. C., Barbara, G., Buurman, W., Ockhuizen, T., Schulzke, J. D., Serino, M., … Wells, J. M. (2014).
Intestinal permeability—A new target for disease prevention and therapy. BMC Gastroenterology, 14, 189. https://doi.org/10.1186/s12876-014-0189-7

Camilleri, M. (2019).
Leaky gut: Mechanisms, measurement, and clinical implications. Gut, 68(8), 1516–1526. https://doi.org/10.1136/gutjnl-2019-318427

Turner, J. R. (2009).
Intestinal mucosal barrier function in health and disease. Nature Reviews Immunology, 9(11), 799–809. https://doi.org/10.1038/nri2653

Canine pancreatitis & chronic pancreatic inflammation

Steiner, J. M. (2012).
Diagnosis of pancreatitis. Veterinary Clinics of North America: Small Animal Practice, 42(6), 1187–1203. https://doi.org/10.1016/j.cvsm.2012.08.005

Watson, P. (2015).
Pancreatitis in dogs and cats: Definitions, epidemiology, and pathophysiology. Journal of Small Animal Practice, 56(1), 3–12. https://doi.org/10.1111/jsap.12293

Xenoulis, P. G., & Steiner, J. M. (2010).
Canine pancreatitis. Veterinary Clinics of North America: Small Animal Practice, 40(3), 475–498. https://doi.org/10.1016/j.cvsm.2010.02.001

Gut–pancreas axis & microbiome

Petrov, M. S., & Shanbhag, S. (2018).
Gut microbiota and pancreatitis: A review of the literature. World Journal of Gastroenterology, 24(18), 1885–1898. https://doi.org/10.3748/wjg.v24.i18.1885

Suchodolski, J. S. (2016).
Diagnosis and interpretation of intestinal dysbiosis in dogs and cats. Veterinary Journal, 215, 30–37. https://doi.org/10.1016/j.tvjl.2016.02.017

Diet, inflammation, and intestinal barrier (veterinary context)

Hall, E. J., & German, A. J. (2010).
Diseases of the small intestine. In S. J. Ettinger & E. C. Feldman (Eds.), Textbook of Veterinary Internal Medicine (7th ed.). Elsevier.

German, A. J., Hall, E. J., & Day, M. J. (2003).
Chronic intestinal inflammation and intestinal disease in dogs. Journal of Veterinary Internal Medicine, 17(1), 8–20. https://doi.org/10.1111/j.1939-1676.2003.tb01321.x


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