Pancreatitis

The exocrine pancreas is responsible for secretion of ions, including bicarbonate, chloride, sodium, and potassium, which aid in pH balance of the intestinal tract and in the delivery of digestive enzymes. For example, bicarbonate neutralizes gastric acid in the duodenum. The pancreas also secretes several digestive enzymes. Recall that the endocrine cells of the pancreas secrete insulin and other hormones to regulate blood sugar levels. Acute pancreatitis is one of the most common GI causes of hospitalization. Pancreatitis is inflammation of the pancreas, which can disrupt its functioning. Historically thought to be distinct entities, we now understand that acute, acute recurrent, and chronic pancreatitis exist on a continuum, with overlapping features. Of course, not all patients progress along this path, but it's a helpful construction. Key etiologies of Acute Pancreatitis Mnemonic GET SMASHED: Gallstones Ethanol Trauma Steroids Mumps/malignancy Autoimmune Scorpion sting Hyperlipidemia, hypercalcemia, and hyperparathyroidism Endoscopic retrograde cholangiopancreatography Drugs Gallstones and ethanol are responsible for most cases of acute pancreatitis. Key etiologies of Chronic Pancreatitis Memorized by "TIGAR-O": Toxic-metabolic causes (alcohol, nicotine, drugs), Idiopathic Genetic Autoimmune Recurrent acute pancreatitis Obstructive causes Signs and symptoms of pancreatitis include abdominal pain (often described as epigastric pain radiating to the back), with possible nausea and vomiting. Pathogenesis of acute pancreatitis: (1) Triggers, such as alcohol or bile duct obstruction, induce changes in the acinar cells, which leads to premature trypsinogen activation to trypsin; trypsin induces activation of other digestive enzymes. These prematurely activated enzymes damage the acinar cells. (2) Damage to the acinar cells leads to localized damage and inflammation. (3) Activation of the inflammatory response produces systemic issues: Increased capillary permeability, endothelial damage, and microvascular thrombosis, which can lead to multi-organ failure. TWO SUBTYPES: Both characterized by inflammation and fluid accumulation: Interstitial edematous pancreatitis is the most common subtype, and is associated with edema in the pancreas and surrounding tissues (peripancreatic tissues). Necrotizing pancreatitis is associated with tissue death in the pancreas and surrounding tissues; accumulated fluid contains necrotic debris. If fluid accumulation in either subtype lasts longer than 4 weeks, we give the collections special names: Interstitial edematous pancreatitis, it is called an encapsulated pseudocyst. Necrotizing pancreatitis, the necrotic debris and fluid is called "walled-off pancreatic necrosis" (aka, WOPN or WON). Be aware that in either case, the accumulated fluid can become infected. SEVERITY & ORGAN FAILURE: Most cases are mild and self-limited, with only localized inflammation and no complications; these patients recover within a week. Moderately severe cases are characterized by transient organ failure (failure lasts less than 48 hours). Approximately 20% of acute pancreatitis cases are severe, with persistent organ failure; this is associated with high mortality. DIAGNOSIS: 2 of the 3 Revised Atlanta Criteria:

• Abdominal pain consistent with acute pancreatitis
• Serum amylase and/or lipase higher than 3 times upper limit of normal
• Cross-sectional imaging consistent with acute pancreatitis.

Imaging rules out other conditions. To diagnose acute pancreatitis, we look for gland edema, peripancreatic fat stranding, and peripancreatic fluid collection; lack of contrast enhancement in parenchyma indicates the necrotizing subtype. TREATMENT:

• Fluid resuscitation (intravascular volume depletion is common and can contribute to organ failure)
• Nutritional support.
• Addressing the underlying cause (for example, via cholecystectomy or alcohol cessation) is important for avoiding recurrent acute pancreatitis.

Patients with recurrent acute pancreatitis experience a reduced quality of life and are more likely to develop chronic pancreatitis. "Recurrent" is defined as 2 or more episodes of acute pancreatitis 3 or more months apart. This occurs in 10-30% of patients with acute pancreatitis, especially when the trigger of acute pancreatitis is not resolved. Like acute pancreatitis, chronic pancreatitis manifests locally and systemically. LOCAL EFFECTS: Chronic inflammation leads to pancreatic fibrosis, atrophy, and cell death, with ductal strictures and distortions, and calcifications. SYSTEMIC EFFECTS: As a result of pancreatic injury, exocrine and endocrine insufficiency can occur, leading to systemic effects such as: maldigestion, steatorrhea, weight loss, fat-soluble vitamin deficiencies, and hyperglycemia. DIAGNOSIS: We diagnose chronic pancreatitis with CT scan, where we look for the ductal changes and calcifications illustrated above. TREATMENT: Options include pain management, endoscopy, surgical resection, and drainage.