Acute pancreatitis
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Acute pancreatitis. Introduction . Acute pancreatitis is the acute inflammation of the pancreas and is characterized by: by upper abdominal pain , vomiting , fever , tachycardia , ​elevated WBC, and elevated serum amylase. Etiology .

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  • Acute pancreatitis is the acute inflammation of the pancreas and is characterized by:

  • by upper abdominal pain,

  • vomiting,

  • fever,

  • tachycardia,

  • ​elevated WBC, and

  • elevated serum amylase.


  • The main two etiologies are alcohol and gallstones

  • Less common etiologies include:

  • infections,

  • ​hyperlipidemia,

  • hypercalcemia.

  • Some drugs may also cause pancreatitis. These include:

  • ​--5-ASA​--Pentamidine

  • ​--Azathioprine/6MP​--Bactrim

  • ​--Metronidazole​--Valproic acid

Clinical presentation
Clinical presentation

  • Epigastric pain,

  • Nausea with or without vomiting.

  • Fever,

  • tachycardia.

  • High WBC and serum amylase.

  • Grey-Turner’s Sign: ecchymoses around the flanks.

  • Cullen’s Sign: ecchymoses around the umbilicus.

  • Both of these signs, as well as hypotension, oliguria, or altered Hct, signify severe pancreatitis.

  • **Fat necrosis and fluid collections are common problems.


  • Alcohol and hypercalcemia cause increased permeability of pancreatic enzymes within the pancreas.

  • Gallstones cause bile reflux and obstructive damage to pancreatic ducts.

  • **Blockade of zymogen granule secretion leads to fusion of zymogens with lysosomeswhich in turn leads to activation of ​enzymes within the pancreas leading to intracellular injury

  • **Spillage of lipase leads to fat necrosis.

  • **Spillage of trypsin leads to elevated WBC, vasodilation, increased capillary permeability, ​destruction of cell membranes and blood vessels.

  • Complications of this destruction include ​ARDS, DIC, and third-space fluid accumulation (leads to hypotension, tachycardia).

Treatment of acute pancreatitis
Treatment of acute pancreatitis.

  • Treatment is mostly palliative.

  • Try to reduce complications and give fluids/nutritional support.

  • Pancreatitis hurts really bad thus patients would need morphine.

  • Pancreatic exocrine suppress: H2 antagonists (Cimetidine) or Somatostatin (Octreotide)

  • Protection from free radicals: Free radical scavengers, xanthineoxidase inhibitors (Allopurinol)

  • Lexipafantis an inhibitor of platelet-activating factor. It does not improve overall mortality ​or sepsis, but does help prevent organ failure and local complications.

Genetic predispositions to pancreatitis
Genetic Predispositions to Pancreatitis

  • This will present in childhood, and may progress to chronic pancreatitis, calcifications, exocrine ​failure, diabetes, or cancer.

  • 1. Cationic Trypsinogen (PRSS1) mutation. This results in a single AA substitution at residue 122 ​which renders trypsin able to resist proteases (“gain of function”). Trypsin becomes unregulated ​and begins autodigestion of the pancreas.

  • 2. CFTR mutation. This is the autosomal recessive mutation that causes cystic fibrosis.

  • 3. SPINK1 mutation. This inhibits trypsin by blocking its active site. SPINK1 mutation isn’t enough ​to cause hereditary pancreatitis on its own, but serves as a disease modifier (lowers the ​threshold for pancreatitis).