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

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.

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.

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.

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.

The three main tests used in considering a diagnosis of EPI are Fecal elastase test, fecal fat test, and a direct pancreatic function test. The latter being a limitedly used test that assesses exocrine function in the pancreas by inserting a tube into the small intestine to collect pancreatic secretions.

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.

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.

The pancreas is composed of two sections: the smaller endocrine portion, which is responsible for producing hormones such as insulin, somatostatin, and glucagon, and the larger, exocrine portion, which produces enzymes needed for the digestion of food. Acinar cells make up 82% of the total pancreas; these cells are responsible for the production of the digestive enzymes.

Among the causes of chronic pancreatitis are the following:

The relationship between etiologic factors, genetic predisposition, and the pace of disease progression requires further clarification, though recent research indicates smoking may be a high-risk factor to develop chronic pancreatitis. In a small group of patients chronic pancreatitis has been shown to be hereditary. Almost all patients with cystic fibrosis have established chronic pancreatitis, usually from birth. Cystic fibrosis gene mutations have also been identified in patients with chronic pancreatitis but in whom there were no other manifestations of cystic fibrosis. Obstruction of the pancreatic duct because of either a benign or malignant process may result in chronic pancreatitis.

The most common symptoms of pancreatitis are severe upper abdominal or left upper quadrant burning pain radiating to the back, nausea, and vomiting that is worse with eating. The physical examination will vary depending on severity and presence of internal bleeding. Blood pressure may be elevated by pain or decreased by dehydration or bleeding. Heart and respiratory rates are often elevated. The abdomen is usually tender but to a lesser degree than the pain itself. As is common in abdominal disease, bowel sounds may be reduced from reflex bowel paralysis. Fever or jaundice may be present. Chronic pancreatitis can lead to diabetes or pancreatic cancer. Unexplained weight loss may occur from a lack of pancreatic enzymes hindering digestion.

Autoimmune pancreatitis (AIP) is an increasingly recognized type of chronic pancreatitis that can be difficult to distinguish from pancreatic carcinoma but which responds to treatment with corticosteroids, particularly prednisone. There are two categories of AIP: Type 1 and Type 2, each with distinct clinical profiles.

Type 1 AIP is now regarded as a manifestation of IgG4-related disease, and those affected have tended to be older and to have a high relapse rate. Type 1 is associated with pancreatitis, Sjogren syndrome, Primary sclerosing cholangitis and Inflammatory bowel disease. Patients with Type 2 AIP do not experience relapse, tend to be younger and not associated with systemic disease. AIP occurring in association with an autoimmune disorder has been referred to as "secondary" or "syndromic" AIP. AIP does not affect long-term survival.

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.

Early complications include shock, infection, systemic inflammatory response syndrome, low blood calcium, high blood glucose, and dehydration. Blood loss, dehydration, and fluid leaking into the abdominal cavity (ascites) can lead to kidney failure. Respiratory complications are often severe. Pleural effusion is usually present. Shallow breathing from pain can lead to lung collapse. Pancreatic enzymes may attack the lungs, causing inflammation. Severe inflammation can lead to intra-abdominal hypertension and abdominal compartment syndrome, further impairing renal and respiratory function and potentially requiring management with an open abdomen to relieve the pressure.

Late complications include recurrent pancreatitis and the development of pancreatic pseudocysts—collections of pancreatic secretions that have been walled off by scar tissue. These may cause pain, become infected, rupture and bleed, block the bile duct and cause jaundice, or migrate around the abdomen. Acute necrotizing pancreatitis can lead to a pancreatic abscess, a collection of pus caused by necrosis, liquefaction, and infection. This happens in approximately 3% of cases, or almost 60% of cases involving more than two pseudocysts and gas in the pancreas.

AIP is relatively uncommon and is characterized by the following features:

1. Scleral Icterus (yellow eyes), jaundice (yellow skin) which is usually painless, usually without acute attacks of pancreatitis.

2. Relatively mild symptoms, such as minimal weight loss or nausea.

3. Increased serum levels of gamma globulins, immunoglobulin G (IgG) or IgG4.

4. The presence of serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF).

5. Contrast-enhanced CT demonstrates a diffusely enlarged (sausage-shaped) pancreas.

6. Diffuse irregular narrowing of the main pancreatic duct, and stenosis of the intrapancreatic bile duct on endoscopic retrograde cholangiopancreatography (ERCP).

7. Rare pancreatic calcification or cyst formation.

8. Marked responsiveness to treatment with corticosteroids.

Two-thirds of patients present with either obstructive painless jaundice or a "mass" in the head of the pancreas mimicking carcinoma. It is mandatory to rule out carcinoma prior to making a diagnosis of AIP.

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

"Laboratory changes": massive accumulation of chylomicrons in the plasma and corresponding severe hypertriglyceridemia. Typically, the plasma in a fasting blood sample appears creamy (plasma lactescence).

"Clinical symptoms:" The disease often presents in infancy with colicky pain, failure to thrive, and other symptoms and signs of the chylomicronemia syndrome. In women the use of estrogens or first pregnancy are also well known trigger factors for initial manifestation of LPLD. At all ages, the most common clinical manifestation is recurrent abdominal pain and acute pancreatitis. The pain may be epigastric, with radiation to the back, or it may be diffuse, with the appearance of an emergent acute abdomen. Other typical symptoms are eruptive xanthomas (in about 50% of patients), lipemia retinalis and hepatosplenomegaly.

"Complications:" Patients with LPLD are at high risk of acute pancreatitis, which can be life-threatening, and can lead to chronic pancreatic insufficiency and diabetes.

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

An external pancreatic fistula is an abnormal communication between the pancreas (actually pancreatic duct) and the exterior of the body via the abdominal wall.

Loss of bicarbonate-rich pancreatic fluid via a pancreatic fistula can result in a hyperchloraemic or normal anion gap metabolic acidosis. Loss of a small volume of fluid will not cause a problem but an acidosis is common if the volume of pancreatic fluid lost from the body is large.

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

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

Individuals are classified as having a functional gallbladder disorder if the above criteria are met, if the gallbladder is present, and if the testing of liver enzymes, conjugated bilirubin, and pancreatic enzymes (amylase and lipase) are normal.

Functional disorders of the gallbladder, bile duct and pancreas have been defined and classified by the Rome criteria for functional gastrointestinal disorders. The criteria outline three variants of functional disorders of the gallbladder, bile duct and pancreas, termed "functional gallbladder disorder", "functional biliary sphincter of Oddi disorder" and "functional pancreatic sphincter of Oddi disorder". All of the following criteria need to be met for as part of the definition of a functional disorder of the gallbladder:

- the pain must be located in the upper part of the abdomen and/or the right upper quadrant of the abdomen

- episodes of pain must last at least 30 minutes

- the symptoms must be recurrent, and occur at differing intervals

- the pain must incrementally increase to a "steady level"

- the pain must be severe enough the patient's daily activities are affected, or that the patient must attend the emergency department

- the pain must not be relieved by any of bowel movements, change in posture, or antacids; and,

- other structural disorders that could explain the symptoms must be excluded.

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.

Often symptoms will arise that indicate the body is not absorbing or making the lipoproteins that it needs. These symptoms usually appear "en masse", meaning that they happen all together, all the time. These symptoms come as follows:

- Failure to thrive/Failure to grow in infancy

- Steatorrhea/Fatty, pale stools

- Frothy stools

- Foul smelling stools

- Protruding abdomen

- Intellectual disability/developmental delay

- Developmental coordination disorder, evident by age ten

- Muscle weakness

- Slurred speech

- Scoliosis (curvature of the spine)

- Progressive decreased vision

- Balance and coordination problems