Loss of Pancreatic enzymes leads to maldigestions and malabsorption which may lead to:

- steatorrhea

- weight loss

- fatigue

- flatulence and abdominal distention (bacterial fermentation of unabsorbed food)

- edema (hypoalbuminemia)

- anemia (Vitamin B12, iron, folate deficiency)

- bleeding disorders (Vitamin K malabsorption)

- Metabolic bone disease (Vitamin D deficiency)

- neurologic manifestation

- hypocalcemia

In animals, signs of EPI are not present until 85 to 90 percent of the pancreas is unable to secrete its enzymes. In dogs, symptoms include weight loss, poor hair coat, flatulence, increased appetite, coprophagia, and diarrhea. Feces are often yellow-gray in color with an oily texture. There are many concurrent diseases that mimic EPI and severe pancreatitis is one that if allowed to continue unabated can lead to EPI.

Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent. Diarrhea, weight loss, flatulence, abdominal bloating, abdominal cramps, and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients with steatorrhea and generalized malabsorption above the normal with 150–200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as coeliac disease. In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed bile acids both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with primary or secondary disaccharidase deficiency. Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer and Crohn disease, but it is absent in many patients with coeliac disease or postgastrectomy malabsorption.

Pancreatitis is inflammation of the pancreas. There are two forms of pancreatitis, which are different in causes and symptoms, and require different treatment:

- Acute pancreatitis is a rapid-onset inflammation of the pancreas, most frequently caused by alcoholism or gallstones.

- Chronic pancreatitis is a long-standing inflammation of the pancreas.

Substantial numbers of patients with intestinal malabsorption present initially with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract. For example, there is increasing epidemiologic evidence that more patients with coeliac disease present with anemia and osteopenia in the absence of significant classic gastrointestinal symptoms. Microcytic, macrocytic, or dimorphic anemia may reflect impaired iron, folate, or vitamin B12 absorption. Purpura, subconjunctival hemorrhage, or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption. Osteopenia is common, especially in the presence of steatorrhea. Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium may all contribute. If calcium deficiency is prolonged, secondary hyperparathyroidism may develop. Prolonged malnutrition may induce amenorrhea, infertility, and impotence. Edema and even ascites may reflect hypoproteinemia associated with protein losing enteropathy caused by lymphatic obstruction or extensive mucosal inflammation. Dermatitis and peripheral neuropathy may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids.

The pancreas is central in the pathophysiology of both major types of diabetes mellitus. In type 1 diabetes mellitus, there is direct damage to the endocrine pancreas that results in insufficient insulin synthesis and secretion. Type 2 diabetes mellitus, which begins with insulin resistance, is characterized by the ultimate failure of pancreatic β cells to match insulin production with insulin demand.

The clinical signs can vary from mild gastrointestinal upset to death, with most dogs presenting with common gastrointestinal signs of upset, such as vomiting, anorexia, painful abdomen, hunched posture, diarrhea, fever, dehydration, and lack of energy, with vomiting being the most common symptom. These signs are not specific just for pancreatitis and may be associated with other gastrointestinal diseases and conditions.

Acute pancreatitis can trigger a build-up of fluid, particularly in abdominal and thoracic (chest) areas, acute renal failure, and cause inflammation in arteries and veins. The inflammation triggers the body's clotting factors, possibly depleting them to the point of spontaneous bleeding. It is this form which can be fatal in animals and in humans.

Chronic pancreatitis can be present even though there are no clinical signs of the disease.

Pancreatitis can result in exocrine pancreatic insufficiency, if the organ's acinar cells are permanently damaged; the pancreatic enzymes then need replacement with pancrelipase or similar products. The damage can also extend into the endocrine portion of the pancreas, resulting in diabetes mellitus. Whether the diabetes is transient (temporary) or permanent depends on the severity of the damage to the endocrine pancreas beta cells.

Most of the symptoms of BLS are non specific but nevertheless warrant the utmost attention. These include:

- Loss of appetite

- Nausea

- Flatulence

- Diarrhea

- Fullness after a meal

- Fatty stools (steatorrhea)

- Unintentional weight loss

- Generalised weakness

As a result of the concomitant vitamin and mineral deficiencies that occur as a result of the malabsorption associated with BLS patients with advanced cases should be investigated for:

- Vitamin B12 deficiency

- Folate deficiency

- Iron deficiency

- Vitamin E deficiency

Signs and symptoms of pancreatic pseudocyst include abdominal discomfort and indigestion.

Patients with Zollinger–Ellison syndrome may experience abdominal pain and diarrhea. The diagnosis is also suspected in patients who have severe ulceration of the stomach and small bowel, especially if they fail to respond to treatment.

- Chronic diarrhea, including steatorrhea (fatty stools)

- Pain in the esophagus, especially between and after meals at night

- Nausea

- Wheezing

- Vomiting blood

- Malnourishment

- Loss of appetite

Gastrinomas may occur as single tumors or as multiple small tumors. About one-half to two-thirds of single gastrinomas are malignant tumors that most commonly spread to the liver and to lymph nodes near the pancreas and small bowel.

Nearly 25 percent of patients with gastrinomas have multiple tumors as part of a condition called multiple endocrine neoplasia type 1 (MEN 1). MEN I patients have tumors in their pituitary gland and parathyroid glands, in addition to tumors of the pancreas.

Steatorrhea (or steatorrhoea) is the presence of excess fat in feces. Stools may be bulky and difficult to flush, have a pale and oily appearance and can be especially foul-smelling. An oily anal leakage or some level of fecal incontinence may occur. There is increased fat excretion, which can be measured by determining the fecal fat level. The definition of how much fecal fat constitutes steatorrhea has not been standardized.

A pancreatic fistula is an abnormal communication between the pancreas and other organs due to leakage of pancreatic secretions from damaged pancreatic ducts. An "external" pancreatic fistula is one that communicates with the skin, and is also known as a pancreaticocutaneous fistula, whereas an internal pancreatic fistula communicates with other internal organs or spaces. Pancreatic fistulas can be caused by pancreatic disease, trauma, or surgery.

Canine pancreatitis is inflammation of the pancreas that can occur in two very different forms. Acute pancreatitis is sudden while chronic pancreatitis is characterized by recurring or persistent form of pancreatic inflammation. Cases of both can be considered mild or severe.

HP is characterised by attacks of epigastric pain, which are often associated with nausea and vomiting. Symptoms may start shortly after birth but onset varies periodically, with some patients not exhibiting symptoms until adulthood. There is usually progression to chronic pancreatitis with endocrine and exocrine failure and a mortally increased risk of pancreatic cancer. Lifetime risk of cancer has been variously calculated as 35–54% to the age of 75 years and screening for early pancreatic cancer is being offered to HP sufferers on a scientific basis. Some patients may choose to have their pancreas surgically removed to prevent pancreatic cancer from developing in the future.

The epidemiology of HP follows a similar pattern to alcohol-associated chronic pancreatitis, but there are important differences. For example, HP typically has an earlier age of pancreatitis onset; although malabsorption and diabetes mellitus occur at a later stage in the disease progression.

In the months following birth, signs and symptoms will appear. Some symptoms will manifest gradually during childhood.

- Failure to gain weight

- Failure to thrive

- Diarrhea

- Foul-smelling feces, steatorrhea

- Impaired nervous system functions

- Decreased reflexes, hyporeflexia

Complication of pancreatic pseudocyst include infection, hemorrhage, obstruction and rupture. For obstruction, it can cause compression in the GI tract from the stomach to colon, compression in urinary system, biliary system, and arteriovenous system.

Zollinger–Ellison syndrome (ZES) is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea.

The syndrome is caused by a gastrinoma, a neuroendocrine tumor that secretes a hormone called gastrin. The tumor causes excessive production of gastric acid, which leads to the growth of gastric mucosa and proliferation of parietal and ECL cells.

ZES may occur on its own or as part of an autosomal dominant syndrome called multiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the pancreas, duodenum or abdominal lymph nodes, but ectopic locations (e.g., heart, ovary, gallbladder, liver, and kidney) have also been described.

Marked recent weight loss is a major clinical manifestation, and unresponsiveness of the ascites to diuretics is an additional diagnostic clue.

Chronic pancreatitis is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions. It can present as episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption. It is a disease process characterized by irreversible damage to the pancreas as distinct from reversible changes in acute pancreatitis.

Blind loop syndrome (BLS), commonly referred to in the literature as small intestinal bacterial overgrowth (SIBO) or bacterial overgrowth syndrome (BOS), is a state that occurs when the normal bacterial flora of the small intestine proliferates to numbers that cause significant derangement to the normal physiological processes of digestion and absorption. In some cases of blind loop syndrome, overgrowth of pathogenic non-commensal bacteria has also been noted. It has long been understood that from birth, and throughout life, large amounts of bacteria reside symbiotically within animal gastrointestinal tracts such as the human gastrointestinal tract. The understanding of this gut flora has even led to novel treatments for bowel irregularity that utilize so called "probiotics" or good bacteria that aid in normal digestion.

The problem of BLS arises when the bacterial colonies residing in the upper gastrointestinal tract begin to grow out of control or are altered in their makeup thereby creating a burden on the normal physiological processes occurring in the small intestine. This results in problems inclusive of but not restricted to vitamin B12 deficiency, fat malabsorption and steatorrhea, fat-soluble vitamin deficiencies and intestinal wall injury.

Pancreatic diseases that affect digestion refers to disorders affecting the exocrine pancreas, which is a part of the pancreas involved in digestion.

One of the most common conditions of the exocrine pancreas is acute pancreatitis, which in the majority of cases relates to gallstones that have impacted in the pancreatic part of the biliary tree, or due to acute or chronic alcohol abuse or as a side-effect of ERCP. Other forms of pancreatitis include chronic and hereditary forms. Chronic pancreatitis may predispose to pancreatic cancer and is strongly linked to alcohol use. Other rarer diseases affecting the pancreas may include pancreatic pseudocysts, exocrine pancreatic insufficiency, and pancreatic fistulas.

Pancreatic disease may present with or without symptoms. When symptoms occur, such as in acute pancreatitis, a person may suffer from acute-onset, severe mid-abdominal pain, nausea and vomiting. In severe cases, pancreatitis may lead to rapid blood loss and systemic inflammatory response syndrome. When the pancreas is unable to secrete digestive enzymes, such as with a pancreatic cancer occluding the pancreatic duct, result in jaundice. Pancreatic disease might be investigated using abdominal x-rays, MRCP or ERCP, CT scans, and through blood tests such as measurement of the amylase and lipase enzymes.

Early signs of abnormality include polyhydramnios (an excess of amniotic fluid), low birth weight, and feeding intolerance immediately after birth.

Hereditary pancreatitis (HP) is an inflammation of the pancreas, attributed to genetic causes. It was first described in 1952 by Comfort and Steinberg but it was not until 1996 that Whitcomb "et al" isolated the first responsible mutation in the trypsinogen gene ("PRSS1") on the long arm of chromosome seven ("7q35").

The term "hereditary pancreatitis" is used when a genetic biomarker is identified, and "familial pancreatitis" otherwise.

DIOS is sometimes classified by the degree of obstruction as incomplete or complete DIOS.

Fibrosing colonopathy is a disease that arises in patients with cystic fibrosis treated with enteric coated pancreatic enzyme supplements. The disease is associated with high dose of these supplements. The clinical presentation of fibrosing colonopathy is non-specific. Abdominal pain, distension, vomiting, and constipation are frequent

features and have led initially to confusion with distal intestinal obstruction syndrome. In some instances, the clinical and radiological features were suggestive of Crohn's disease or inflammatory colitis.