Pancreas Flashcards
What vascularity supplies the pancreas
Celiac axis and SMA
What innervates the pancreas
ANS
What are the pancreas’s Exocrine functions
Amylase: breakdown starch
Lipase: breakdown fat
Protease: breakdown proteins
What stimulates the pancreas to release it’s juices
Gastric acid
CCK
Vagal stimulation
What is in pancreatic “juice”
Electrolytes, bicarbonate, digestive enzymes
It neutralizes gastric acid and provides basic environment for pancreatic enzymes
What is the pancreas’s Endocrine function
Insulin released in response to increased blood glucose (increases permeability of cell membranes to glucose= lower blood glucose)
Glucagon released in response to low blood sugar (causes conversion of glycogen to glucose in the liver= increase blood sugar)
Where is amylase found
secreted from pancreatic *acinar cells, into duodenum to digest starch
Also in saliva, ovaries, skeletal muscle, and gallbladder (sensitive but not specific to pancreatic disease)
How do amylase levels change
Normal: 60-120
Abnormal levels w/in 12 hours of pancreatic injury
Return to normal in 48-72 hours
What causes amylase to leak into circulation
Damage to acinar cells (pancreatitis) or obstruction of pancreatic flow (CA or CBD stones)
What happens to amylase in chronic pancreatitis
Usually not increased in circulation because with chronic, acinar cells are destroyed- so there is no amylase even made!
Where is Lipase found
Secreted by pancreas into duodenum to breakdown TG into fatty acids
More specific but can also be found in renal failure or intestinal infarct
How do Lipase levels change
Normal: 0-160
non-pancreatic elevation: <3 of upper limit normal
Acute pancreatitis: Rise 24-48 hrs post injury
Return to normal in 5-7 days
What is acute pancreatitis
Inflammatory disease w/ autodigestion of pancreas by proteolytic enzymes prematurely activated in pancreas
What causes acute pancreatitis
MC: alcohol and gallstones*** Also blunt trauma, ERCP Hypertriglyceridemia**, hypercalcemia Ischemia, vasculitis mumps, CMV, EBV, HIV, varicella
What toxins can cause acute pancreatitis
Alcohol*
Thiazide diuretics , Estrogen, sulfonamides, Salicylates, Valproic acid, 6-MP, anti-HIV meds, Scorpion venom
How does acute pancreatitis present (oldcarts)
O: acute, after eating meal L: midepigastric radiating to back D: constant C: steady, boring A: lying supine worsens Sx R: sitting and leaning forward makes it better Sx: anorexia, n/v, abdominal distention
Clinically how does acute pancreatitis present
fever, tachy/tachy, +/- hypotension Jaundice 2/2 biliary obstruction Hypoactive/absent bowel sounds Significant midepigastric ttp w/ or w/o guarding/rebound Cullen's sign: periumbilical ecchymosis Grey-turner sign: flank ecchymosis
Lab workup for acute abdominal pain should always include
Amylase and Lipase!!
Diagnostics for acute pancreatitis will show
Elevated: amylase, lipase, WBC, HCT, Creatinine, Glucose (mild), LFT (transient)
Decreased: Calcium, O2 (on ABG)
What LFT’s strongly suggest acute pancreatitis
ALT >150 gallstone pancreatitis
High bilirubin: gallstone pancreatitis
What radiographs get you get to find acute pancreatitis
XR: normal vs ileus
CT: pancreatic edema, calcifications, pseudocysts, necrosis, abscess
MRCP
*Endoscopic US: best test, highest sensitivity
What are XR beneficial for in acute pancreatitis
CXR: R/o pulmonary infiltrates or pleural effusions!
Abd XR is likely to r/o obstruction (stones), ileus (sentinel loop), or perforation
CT abdomen is used for
Diagnosis, showing enlargement of pancreas, blurring of fat planes/fat stranding
ID severity of disease
ID complications (necrosis, pseudocysts, abscess, hemorrhage)
Why are MRI/MRCP better than CT
Lower risk nephrotoxicity
Increased characterization of fluid collections, necrosis, abscess, and pseudocysts
Better view of biliary and pancreatic ducts (good if you can’t see CBD stone on CT/US and you expect biliary pancreatitis)