pancreatic Flashcards
basolateral cells of panc have R for
CCK
NT- GRP, Vip, ACH
ductules
large volume secretions that bring pH close to normal in order to
- inactivate pepsin
- increase solubility of fatty and bile acids
- block mucosal damage
- optimize pancraetic ad BB enzyeme fx
regulators of acinus
endo: CCK, secretin
neuroendocrine: Ach, Grp, vip, subs p
regulators of duct
scretin
ach
pathway of food
food–>i cells–> cck–>acinus–>digestive enzymes
duodenal acidity pathway
–>S cells–>secretin–>duct–>HCO3- and water
CCK mech
no receptors in acinus
stimulate vagal afferents–> basal ganglia–>vagal efferents–>pancreatic paraS gang–>ach, vip, grp–>acinar cells–>ezyme–>digest food
secretin mceh
h+ secretion–>direct and indirect effects on acinar cells–>HCO3- ad h20
enterokiase
on duo enterocytes
claeves trypsinogen–>trypsin
acidic pH inhibits trypsin
lack of inh genes
pancreatitis
grey turnre sign
ecchymoisis on 1/both flanks
cullen sign
ecchymoisis periumilical region
serum ca in panc
increase lipase–>desroy fat–>sequeser ca
atlanta criteria
abdominal distention consistent w/ acute pancreatitis
increase amylase/lipase >3x normal
+ changes on CT
gallstones do not lead o
chronic pancreatitis
hereditary ways to get pancreatitis
trypsinogen mutations that make it more resistant to deactivation
def of antitrypsin
cystic fibrosis
familial hypertriglyc
early complications of pancreatitis
massive volume losses secondary to third spacing
SiRS
metabolic abnormalities
peripancreatic necrosis
late complications of pancreatiti
pseudocysts & abscesses
mortality <1 week
secondary to sirs or multiorgan failure
mortality >1 week
pancreatic sepsis or multiorgan failure
tx mild pancreatitis
iv hydration
rest
remove offending agent
tx severe
supportive
ERCP for stones, but risk factor fo acute panc
typse of mild pancreatitis
interstitial or edematous pancreatitis
types of severe pancreatitis
necrotizing or hemorrhagic pancreatitis