Pancreatitis

Pancreatitis Classification and external resources
ICD-10	K85, K86.0-K86.1
ICD-9	577.0-577.1
OMIM	167800
DiseasesDB	24092
eMedicine	emerg/354
MeSH	D010195

Pancreatitis is an inflammation of the pancreas, an important organ for digestion and control of circulating levels of glucose. Acute pancreatitis involves a sudden inflammation of the pancreas, while chronic pancreatitis is a long-standing, slowly progressing inflammation of the pancreas.

Overview

The pancreas is a glandular organ found in vertebrates near the stomach and small intestine. It is one of the few organs that has both an exocrine and an endocrine function. The pancreas' exocrine function involves the secretion of digestive enzymes (trypsin, lipase, chymotrypsin, etc.0 and bicarbonate into the small intestine, to which it is linked by pancreatic duct. Its endocrine function involves the regulation of blood sugar levels by secreting the hormones insulin, glucagon, and somatostatin directly into the blood. Another hormone, vasoactive intestinal peptide (VIP) affects gastrointestinal functioning (Carson-DeWitt 2002).

When the pancreas is damaged in some way, the digestive enzymes may begin to digest the pancreatic tissue (autodigestion), resulting in inflammation. Inflammation is a localized protective response of a body's living tissue to injury, infection, irritation, or allergy and is characterized by the following quintet: redness (rubor), heat (calor), swelling (tumor), pain (dolor), and dysfunction of the organs involved (functio laesa).

Types

There are two basic forms of pancreatitis, which are different in causes and symptoms, and require different treatment.

Acute pancreatitis occurs when there is a sudden inflammation of the pancreas. If treated, most patients recover fully and in about ninety percent of the cases the symptoms disappear within a week after treatment (Carson-DeWitt 2002). Most cases are self-correcting once the damaging agentis eliminated and then there is no re-occurance (Smith 2008). Death occurs in less than five percent of cases and generally because of complications, such as infection or extensive tissue destruction and hemorrhage (Smith 2008).

'Chronic pancreatitis occurs when the disease becomes self-perpetuating and either results in periodic or sporadic attacks similar to the acute form or is persistent and causes few symptoms while much of the pancreas is destroyed (Smith 2008; Carson-DeWitt 2002). As many as fifty percent of cases of chronic pancreatitis are fatal and the pnacreas is permanently impaired, with damage to the tissue (Smith 2008; Carson-DeWitt 2002).

The basic mechanism of pancreatitis is that some cause results in many of the extremely potent enzymes produced by the pancreas, which normally become active only after they are passed into the duodenum, become prematurely activated so they begin their digestive functions within the pancreas. That is, the pancreas begins to digest itself. This causes a cycle of inflammation, including swelling and loss of function, and digestion of the blood vessels within the pancreas leads to bleeding. The leaky, erorded blood vessels also allow activated enzymes to gain access to the bloodstream and circulate throughout the body (Carson-DeWitt 2002).

Causes

There are a number of causes of pancreatitis, with the most common being gallbladder disease (biliary tract disease) and alcoholism (Smith 2008; Carson-DeWitt 2002). The exact biochemical processes responsible for pancreatitis are not known, and though a variety of damaging agents have been identified, as many as 30 percent of cases lack a clear cut cause (known as idiopathic pancreatitis) (Smith 2008). However, for those cases in which the cause is detectable, over eighty percent of all cases of hospitalization for acute and chronic pancreatitits in Europe and the United States are tied to these two diseases (Carson-DeWitt 2002).

The most common cause of acute pancreatitis is gallstones in the common bile duct. Such obstructions can back up the bile into the pancreatic duct and trigger pancreatititis. This seldom leads to chronic pancreatititis because the obstruction can be cleared by surgeons. Alcohol is the most common toxic agent and while heavy drinkers rarely develop acute pancreatitits, a long history of steady drinking is the most common cause of chronic pancreatitis by far (Smith 2008).

Less common causes of pancreatitis include traumatic injury (especially damage by the steering wheel or set belt during an automobile accident); damage during abdominal surgery or endoscopic procedures in the small intestine; viral infections (eg., mumps), hypertriglyceridemia (but not hypercholesterolemia, and only when triglyceride values exceed 1500 mg/dl (16 mmol/L)); hypercalcemia (high blood levels of calcium); viral infection (e.g. mumps), vasculitis (in other words, inflammation of the small blood vessels within the pancreas); and autoimmune pancreatitis. Pregnancy can also cause pancreatitis, but in some cases the development of pancreatitis is probably just a reflection of the hypertriglyceridemia that often occurs in pregnant women. Pancreas divisum, a common congenital malformation of the pancreas may underlie some cases of recurrent pancreatitis. Drugs (such as estrogens, tetracycline, sulfonamides), etc.) cause about five percent of all diagnosed cases of pancreatitis (Carson-DeWitt 2002).

The more mundane, but far more common causes of pancreatitis, as mentioned above, must always be considered first. However, the known porphyrinogenicity of many drugs, hormones, alcohol, chemicals, and the association of porphyrias with autoimmune disorders and gallstones do not exclude the diagnosis of heme disorders when these explanations are used. A primary medical disorder, including an underlying undetected inborn error in metabolism, supersedes a secondary medical complication or explanation.

Autoimmune disorders, lipid disorders, gallstones, drug reactions, and pancreatitis itself are not primary medical disorders.

A useful mnemonic for remembering the causes of acute pancreatitis is (I get smashed):

• Idiopathic
• Gallstones
• Ethanol
• Trauma
• Steroids
• Mumps
• Autoimmune causes
• Scorpion venom
• Hyperlipidaemias
• ERCP (Endoscopic retrograde cholangiopancreatography, resulting in injuries)
• Drugs (such as Azathioprine)

Porphyrias

Acute hepatic porphyrias, including acute intermittent porphyria, hereditary coproporphyria, and variegate porphyria, are genetic disorders that can be linked to both acute and chronic pancreatitis. Acute pancreatitis has also occurred with erythropoietic protoporphyria.

Conditions that can lead to gut dysmotility predispose patients to pancreatitis. This includes the inherited neurovisceral porphyrias and related metabolic disorders. Alcohol, hormones, and many drugs including statins are known porphyrinogenic agents. Physicians should be on alert concerning underlying porphyrias in patients presenting with pancreatitis and should investigate and eliminate any drugs that may be activating the disorders.

Still, notwithstanding their potential role in pancreatitis, the porphyrias (as a group or individually) are considered to be rare disorders. However, since there are no systematic studies to determine the actual incidence of latent dominantly-inherited porphyrias in the world population, and there is DNA or enzyme evidence of high rates of latency of classic textbook symptoms in families where porphyrias have been detected, and since the technology is not developed to detect all latent porphyrias, the diagnosis of underlying inborn errors of metabolism impacting heme should not be routinely eliminated in pancreatitis.

Medications

Many medications have been reported to cause pancreatitis. Some of the more common ones include the AIDS drugs DDI and pentamidine, diuretics such as furosemide and hydrochlorothiazide, the chemotherapeutic agents L-asparaginase and azathioprine, and estrogen (birth control pills). Just as is the case with pregnancy-associated pancreatitis, estrogen may lead to the disorder because of its effect of raising blood triglyceride levels.

Genetics

Hereditary pancreatitis may be due to a genetic abnormality that renders trypsinogen active within the pancreas, which in turn leads to digestion of the pancreas from the inside.

Pancreatic diseases are notoriously complex disorders resulting from the interaction of multiple genetic, environmental, and metabolic factors.

Three candidates for genetic testing are currently under investigation:

• Trypsinogen mutations (Trypsin 1)
• Cystic Fibrosis Transmembrane Conductance Regulator Gene (CFTR) mutations
• SPINK1, which codes for PSTI - a specific trypsin inhibitor (Whitcomb 2006).

Symptoms and signs

Severe upper abdominal pain, with radiation through to the back, is the hallmark of pancreatitis. This pain is usually very intense and steady. Relief of pain by sitting up and bending forward is typical. Breathing may be shallow as deep breathing causes more pain (Carson-DeWitt 20020.

Other prominent symptoms are nausea and vomiting (emesis). There may be a slight fever and in severely ill patients there may be shock. The blood pressure may be high (when pain is prominent) or low (if internal bleeding or dehydration has occurred). Typically, both the heart and respiratory rates are elevated. Abdominal tenderness is usually found but may be less severe than expected given the patient's degree of abdominal pain. Bowel sounds may be reduced as a reflection of the reflex bowel paralysis (i.e. ileus) that may accompany any abdominal catastrophe.

Findings on the physical exam will vary according to the severity of the pancreatitis, and whether or not it is associated with significant internal bleeding.

Diagnosis

The diagnostic criteria for pancreatitis are "two of the following three features: 1) abdominal pain characteristic of acute pancreatitis, 2) serum amylase and/or lipase greater than or equal to 3 times the upper limit of normal, and 3) characteristic findings of acute pancreatitis on a CT scan" (Banks and Freeman 2006).

An early diagnosis can be made by observing high levels of pancreatic enzymes in the blood (amylase and lipase). Often one, or both, are elevated in cases of pancreatitis. Two practice guidelines state:

{{quote|It is usually not necessary to measure both serum amylase and lipase. Serum lipase may be preferable because it remains normal in some nonpancreatic conditions that increase serum amylase including macroamylasemia, parotitis, and some carcinomas. In general, serum lipase is thought to be more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis" (Banks and Freeman 2006).

Insert the text of the quote here, without quotation marks.

• Smith, R. 2008. Pancreatitis. Pages 2060-2062 in A. Chang, et al., Magill's Medical Guide, Volume IV, Neuralgia, neuritis, and neuropahty—Smallpox, 4th revised edition. Pasadena, Calif: Salem Press. ISBN 9781587653841 (set). ISBN 9781587653889 (volume).

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