Week 2: Acute and chronic pancreatitis

Question 1

Define acute pancreatitis

Answer 1

• inflammatory chain reaction consequent to premature or persistent trypsin activation
• trypsin converts proenzymes in pancreatic secretions to their active form

Question 2

Diagnosis of acute pancreatitis

Answer 2

• 2 of the 3:
  1. sustained epigastric pain radiation to the back,
  2. amylase or lipase greater than 3x upper limit of normal,
• levels don’t correlate with severity
  3. imaging findings consistent with pancreatitis

Question 3

classification of acute pancreatitis

Answer 3

1. Mild -90%
   - edematous, interstitial pancreatitis
   - minimal systemic dysfunction
   - complications unusual
2. Severe
   - necrosis of pancreatic tissue and peripancreatic fat
   - systemic cytokine storm: Il1, TNF, organ failure
   - complicaitons: pancreatic abscess, pseudocyst
   - high mortality

Question 4

etiology of acute pancreatitis

Answer 4

I Get Smashed: Idiopathic, Gallstones, Etanol, Trauma
Steroids,Mumps/infections/maligancy, Autoimmune, Scorpion stings, Hyperlipidemia/hypercalcemia, Ercp, Drugs
-Hypertriglyceridemia: TGs level are over 1000mg/dL.
-autoimmune: elevated IgG4 levels, responds to steroids
-Genetic: PRSS1 mutation (trypsin that can’t be inactivated) or CFTR mutation
-Hypercalcemia: blocks cleavage and thus inactivation of trypsin->chronically elevated trypsin
-Pancreas divisum: failed fusion of dorsal and ventral ducts in development. inadequate drainage
-Drugs: azathioprine, valproic acid, didanosine, pentamidine. Via HyperTG: thiazides, estrogen Vit A
-Malignancy: if greater than 50, need to rule out ampullarf cancer, pancreas cancer, IPMN (intraducal papillary mutinous neoplasms), MCN (mutinous cystic lesion)

Question 5

Workup of acute pancreatitis

Answer 5

• History: Drinking, crampy pain after fatty meals, high cholesterol, family hx of pancreatitis, abdominal trauma, jaundice, weight loss
• labs: amylase, lipase, AST, ALT, ALK phos, bilirubin, Ca levels, TGs, IgG4
• Imaging: ultrasound for gallstones.

Question 6

Ranson’s Criterion

Answer 6

1. Admission: GA LAW
   -Glucose>200mg/dl
   -age>55 years
   -LDH>350 IU/L
   -AST> 250 IU/L
   -WBC> 16000/mcl
   More than 3 means severe acute pancreatitis
2. at 48 hours: C HOBBS
   -Calcium 4 Meq/L (become acidodic)
   -sequestration of fluids >6L
   This 48 hour score used to predict outcome, patient mortality

Question 7

Treatment of acute pancreatitis

Answer 7

• agressive IV hydration and close monitoring. Prevent necrosis due to hypovolemia and hypo perfusion
• antibiotic Rx not indicated for mild disease
• NPO for 3-5 das then nutrition initiated via per mouth or nano-jejunal tube
• cholecystectomy if gallstone pancreatitis. Indicated in cholangitis or ongoing bile duct obstruction

Question 8

Systemic complications of acute pancreatitis

Answer 8

-ARDS
-DIC
-hypocalcemia from saponification
Treatment is supportive

Question 9

Local complications of acute pancreatitis

Answer 9

1. Pseudocyst
   - collection of peripancreatic juice surrounded by NON epithelialize wall (granulation tissue and fibrous tissue)
   - forms after 4 weeks
   - Rx only if symptomatic
2. Necrosis
   - if pseudocyst infected–> abscess
3. Other complications
   - hemorrhage from erosions into mesenteric vessel
   - thrombosis of mesenteric vessels
   - common bile duct obstruction due to edema
   - progression to chronic pancreatitis

Question 10

Definition of chronic pancreatitis

Answer 10

• most likely results from recurrent episodes of acute pancreatitis
• duct fibrosis due to recurrent or severe pancreas injury
• exocrine dysfunction may lead to malabsorption
• endocrine dysfunction may lead to diabetes
• vast majority of tissue must be destroyed for exocrine and endocrine dysfunction

Question 11

Pancreatic function tests

Answer 11

1. Fecal fat: fat absorption first to become abnormal in chronic pancreatitis
   - patient ingests 100gm of fat daily and fat collection of more than 7 gm signifies malabsorption
2. Fecal pancreatic elastase-1: pancreatic specific protein in stool which is not degraded in the intestines. Decreased stool levels correlate with moderate to severe exocrine dysfuction.
3. Secretin stimulation test: secretin stimulates bicarb secretion from pancreas.
   - Administer IV secretin
   - nasoenteric tube used to measure bicarb volume. NOT USED.

Question 12

Structural evaluation of chronic pancreatitis

Answer 12

1. histologic: fibrosis, inflammatory cells, stones, ductal dilation, loss of exocrine parenchyma
2. Cambridge Criterion: based on ERCP-but don’t due diagnostic ERCP anymore because of contrast agent toxicity
   Mild: prominent pancreatic duct side branches
   Moderate: dilated main pancreatic duct and side branches
   Severe: markedly abnormal main pancreatic duct and side branches
3. CT
4. Endoscopic ultrasound

Question 13

Management of chronic pancreatitis

Answer 13

1. exocrine dysfunction
   - pancreatic enzyme supplementation: 300,000 lipase units each meal
   - low fat diet, medium chain TGs
   - low fiber, antioxidants
2. Endocrine
   - insulin and glucagon production injured. Less strict management guidelines for DM to prevent hypoglycemia
3. Pain management
   - uncoated pancreatic enzymes to destroy CCK releasing hormone, which stimulates pancreatic activity, to rest the pancreas
   - decompression-relate to large duct obstruction
   - nerve block of celiac plexus