Pancreas and Hepatobiliary Diseases Flashcards Preview

Block 7 - GI > Pancreas and Hepatobiliary Diseases > Flashcards

Flashcards in Pancreas and Hepatobiliary Diseases Deck (39)
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What is the duodenal mucosal response to food and acid?

S cells release secretin - stimulates biliary and pancreatic duct epithelium to secret bicarb and water
I cells cause release of CCK - enzyme secretion from pancreatic acinar cells and stimulates gallbladder contraction, relaxes sphincter of oddi


What are risk factors for pigment gallstones?

excess bilirubin --> black stones
bacterial contamination of bile - bacteria chemically alter bile --> soft brown stones


What is the pathophysiology of the development of acute pancreatitis?

inciting factor induces premature enzyme activation, immune system activation, oxidative stress, and ischemia-reperfusion injury that drive local manifestations (edema, necrosis, sequestration of fluid)


What is the pathophysiology of chronic pancreatitis?

irreparable damage to liver from number of sources
mutations that create super trypsin resistant to cleavage and inactivation
CFTR mutations impair ductal bicarb secretion


What drives the progression to pancreatic adenocarcinoma?

Over expression of growth factors (EGF, TGF-alpha)
activation of oncogenes (K ras)
inactivation of tumor suppressors (p53, p16)
paracrine effects of islet cell hormones (IGF)
overexpression of TGF beta drives fibrosis


What is the progression of lesions in pancreatic cancer?

precursor lesions within duct called PanINs
then angiogenesis, neural invasion, metasatic spread


What are exceptions to the no surgery for asymptomatic cholelithiasis rule?

sickle cell
extreme remote assignments (space, pilots)
liver transplant recipients (gallbladder removed)


What is the pathophysiology of biliary colic?

episodic abdominal pain caused by gallbladder attempting to contract in presence of obstructed cystic duct


What investigations should be used with biliary colic?

sonogram demonstrating cholelithiasis
absence of cholelithiasis --> CCK HIDA


What results from a CCK HIDA indicate a biliary source of symptoms of biliary colic?

diminished gallbladder EF and pain with CCK infusion


What is the pathophysiology of acute cholecystitis?

gallbladder wall is inflamed
usually caused by stasis of bile due to gallstone obstructing cystic dugt
sometimes ischemia (PAN) or inf cause


What are the clinical features of acute cholecystitis?

RUQ sharply localized pain, tenderness over gallbladder, fever, Murphy's sign


What investigations are used to evaluate acute cholecystitis?

leukocytosis, sonogram shows cholelithiasis if that's the cause, thickened gallbladder wall or pericholecystic fluid collection on sonogram
HIDA scan if still doubt - if dye concentrates in gallbladder, NOT acute cholecystitis


What is the pathophysiology of ascending cholangitis?

stagnant bile proximal to obstructed common bile duct becomes infected with bacteria (usually GNR)


What are the clinical features of ascending cholangitis?

fever, jaundice, RUQ pain = Charcot's triad
septic appearance (hypotensive)


What is Reynold's Pentad?

constellation of symptoms seen in ascending cholangitis = delirious, febrile, septic appearing (hypotensive), elderly, jaundice and tenderness in RUQ


What investigations are done in ascending cholangitis?

leukocytosis, elevations in all liver enzymes, elevated bilirubin, schistocytes and left shift, positive blood cultures
sonogram MAY show dilated common duct


What is the treatment of ascending cholangitis?

antibiotics (quinolones), repletion of fluids, urgent dcompression of duct by ECRP to remove stone or PTC


What is the treatment for acute cholecystitis?

cholecystectomy, antibiotics in toxic patients or in those with complication


What are the most common risk factors for acute pancreatitis?

choledocholithiasis (middle aged women and elderly patients)


What are the clinical features of acute pancreatitis?

sharp epigastric pain radiating to interscapular, subsequent nausea and emesis, maybe fever, volume depletion (orthostasis), decreased bowel sounds


Why are antibiotics usually not indicated in acute pancreatitis?

infection does not occur earlier than 5-7 days after symptom onset, no antibiotics before this time


What is a possible complication of acute pancreatitis and what does it cause?

retroperitoneal hemorrhage
Cullen sign - ecchymoses around umbilicus
Grey-turner sign - eccyhmoses in flanks or loins


What lab investigations are seen with acute pancreatitis?

elevated pancreatic enzymes (amylase, lipase)
leukocytosis, plain ab films may show focal or diffuse ileus, elevated hematocrit IF SEVERE


What is the best imaging modality for the pancreas?

ab CT with IV and oral contrast


What is the leading cause of mortality 2-3 weeks after symptom onset of acute pancreatitis?

infection of necrotic pancreas


When should multi-phasic CT be used in patients with acute pancreatitis?

diagnosis in doubt
deteriorate or fail to improve
>50 YO and unclear etiology (r/o cancer)
evidence of ongoing biliary obstruction


If the gallbladder is still present, what additional imaging test must be done to work up acute pancreatitis?

sonogram - need to look for gallstones
if choledocholithiasis --> ERCP


What determines severity of an episode of acute pancreatitis?

scoring systems up to 48 hrs from symptom onset
dev of local complications, systemic complications, need for surgery, death
patients not meeting criteria w/i 24-48 hrs not likely to be severe course (majority)


What is the usual treatment of acute pancreatitis?

fasting, IV volume repletion*, narcotic analgesics (demerol > morphine), antiemetics, nasogastric tube if symptomatic ileus, monitor urine output and oxygenation, daily CBC, metabolic panel, liver panel, Ca and Mg testing


When should antibiotics be used in the treatment of acute pancreatitis?

only in necrotic pancreas, hematocrit >40


When should nutritional support be provided in the treatment of acute pancreatitis?

predicted to follow severe course
failure to improve after 48-72 hours
manifestations of severity


When and why should ERCP be used in the treatment of acute pancreatitis?

if gallstones and patient worsens or fails to improve - reduces risk of cholangitis without worsening pancreatitis
quinolone antibiotics and time to those improving to try and pass stones


What are risk factors for pancreatic carcinoma?

chronic pancreatitis
hereditary pancreatitis
hereditary pancreatic cancer


What is the relationship between diabetes and pancreatic carcinoma?

glucose intolerance can be a manifestation of cancer, but not a large percentage of diabetics get cancer


What is the most common marker checked in patients suspected of having pancreatic cancer?

CA 19-9, marker for adenocarcinoma
levels >250 in presence of mass and absence of pancreatitis usually diagnostic


What is the diagnostic modality of choice in otherwise normal pancreas to work up pancreatic cancer?

EUS - also when CT equivocal, or tissue diagnosis required prior to therapy
CT biopsies when EUS not available
MRI/MRCP depends, but superior to CT in detecting peritoneal metastases


What is the surgical procedure performed for resectable pancreatic carcinoma?

Whipple (or variant that spares the stomach)


What are palliative procedures performed in pancreatic carcinoma?

decompress bile obstruction (ERCP)
relief of duodenal obstruction (gastrojejunostomy)
can also give Gemcitabine to prolong survival