Pancreatitis Flashcards
function of acinar cells
the exocrine functions. secretes bicarbonate and electrolyes and water + proenzymes.
endocrine pancreatic function
insulin, glucagon, somatostatin, pancreatic polypeptides, amylin
why does the pancreas no digest itself?
enzymes are synthesized as inactive zymogens. enterokinase (converts to active form) are restircuted to the small intestine usually.
compare and contrat acute and chronic pancreatitis.
chronic pancreatitis is atrophic and acute is often a biochemical explosion that is typically self-limited and often not as atrophic.
outline the mechanism of acute pancreatitis
- an insult to pancreas occurs
- results in early zymogen actiavgtion, geenration of inflammatory mediators like CYTOKINE STORM
- cytokine storm decreases blood flow and can cause ischemia, inflammation, multiorgan failuyre.
- Neurogenic stimulation occurs as well, causing pain, necrosis, and apoptosis.
main causes of acute pancreatitis
alcohol and gallstones.
how does alcohol affect the pancreas.
etOH is toxic to acinar cells. Causes CCK release and subsequent aceinar cells become sensitized to CCK, causing zymogen activation and cytokine geneartion. There is also abnormal blood flow which causes sphincter of Oddi Spasm
toxic metabolites from alcohol also causes oxidative stress.
How do Gallstones cause pancreatitis?
women have more gallstones because of estrogen, low Fe, and Fe is needed for bile acid conjugation. these gall stones leave the cystic duct and then GC migrates down to pancreatic suct, causing swelling of biliary pancreas.
ALT also rises first to cause AP.
iatrogenic causes of acute pancreatitis
ERCP. That’s why you shouldn’t do it unless necessary (Gallstone blockage in DILATED extrahepatic bile duct)
structural cause of acute pancreatitis
pancreatic divism– the two lobes don’t fuse.
If you don’t drink, smoke or have elevated pancreatic enzymes or have elevated liver enzymes (gallstones) but you still have acute pancreatitis, you can consider ERCP to MINOR DUCT to reduce recurrent Acute pancreatitsi.
how do patients with acute pancreatitis present?
diagnostic criteria for acute pancreatitis
bedside assessment of severity of acute pancreatitis
imaging modalities in acute pancreatitis
CT, MRCP or ERCP (not recommended cause can cause pancreatitis), EUS
basic treatment options for AP
localized and systemic complications from AP
localized: pancreatic pseudocytst, necrosis, ascites and third spacing, pancreatic hemorrahge, splenic vein thrombosis
systemic: pulmonary edema, renal failure, hypcalcemia, hyperglycemia, multiorgan failure and SIRS
T/F: pancreatic pseudocysts can occur when onset of acute pancreatitis is happening
false. Occurs late >4 weeks after diseasse onset. this is due to ductal disruption. Not lined by epithelium.
hallmarks of chronic pancreatitis
chronic abdominal pain, pancreatic insufficiency– less enzymes, shrunken.
pancreatic calcification.
this is not due to a cytokine storm.
Is pain worse at the beginning of chronic pancreatitis or after 15 years of onset?
pain is prevalent at the beginning, but as one ages, pain subsides even though the physilogical symptoms are worsening – ex higher rates of calcification, malabsorption and diabetes.
main causes of chronic pancreatitis.
A person comes in with obstructive jaundice, abdominal pain, a high serum igG/igG4 and upon CT scan, a sausage like pancreas is seen. What could be happening? How would you treat?
autoimmune chronic pancreatitis. treat with steroids (retuximap)
how to differentiate between pancreatic cancer and autoimmune pancreatitis on the CT scan
no dilation of pacnreatic ducts = autoimmune pacnreatitsi
dilation of the pancreatic ducts + mass visualization = cancer.
autoimmune pancreatitis can present with a mass as well, but it is not cancerous unless the ducts are dilated.
change in stool in someone with chronic pancreatitis
steattorhea is seen in 90% of pancreatic patients.
what type of abdominal pain is mostly associated with pancreatitis
epigastric pain radiating front to back.
why is steattorhea a symptom of chornic pancreatitis
- decreased concentratino of lipase
- decreased duodenal pH (inactivation of pacnreatic lipase pH<4.5, there is a precipitation of bile salts.
the acidity of duodenal pH is because acinar cells in the pancreas are affected, causing less bicarbonate nutralization.
what tests can we order in CP?
- tests of pancreatic structure/diagnotic imaging/ CT
- tests of pancreatic function: fecal fat, blood glucose (diabetes r/o), fecale elastase.
treating chronic pancreatitis
treat the cuase. must stop drinking alcohol. Also treat the complications of chornic pancreatitis. manage exocrine insufficeincy with diet and exogenous enzumes. Modify fat intake, and REPLACE THE FAT SOLUBLE VITAMINS, B12 AND CALCIUM.
treat pain with narcotics or neuromodulators (TCAs)
Why might malnutrition occur in someone with CP
because there is decreased FAT absorption and breakdown since lipase is decreased (it’s increasd in acute pancreatitis). without fat absorption, fat soluble nutrients will be less likely absorbed. therefore, you can see defieicnies in vitamins ADEK
intervention strategies for chronic pancreatitis
EUS guided celiac plexus block
ERCP with pancreatic duct stenting (if you see strictures, stones etc).
pancreaticojejunoostomy.
symptoms that chronic pancreatitis is turning into pancreatic cancer.
Overall:
