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Acute pancreatitis

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

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  1. Acute pancreatitis

  2. 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.

  3. Etiology • 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

  4. 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.

  5. Pathopysiology • 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

  6. **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).

  7. 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.

  8. 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).

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