Pancreas and Hepatobiliary Diseases Flashcards

1
Q

What is the duodenal mucosal response to food and acid?

A

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

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2
Q

What are risk factors for pigment gallstones?

A

excess bilirubin –> black stones

bacterial contamination of bile - bacteria chemically alter bile –> soft brown stones

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3
Q

What is the pathophysiology of the development of acute pancreatitis?

A

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

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4
Q

What is the pathophysiology of chronic pancreatitis?

A

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

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5
Q

What drives the progression to pancreatic adenocarcinoma?

A

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

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6
Q

What is the progression of lesions in pancreatic cancer?

A

precursor lesions within duct called PanINs

then angiogenesis, neural invasion, metasatic spread

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7
Q

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

A

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

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8
Q

What is the pathophysiology of biliary colic?

A

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

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9
Q

What investigations should be used with biliary colic?

A

sonogram demonstrating cholelithiasis

absence of cholelithiasis –> CCK HIDA

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10
Q

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

A

diminished gallbladder EF and pain with CCK infusion

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11
Q

What is the pathophysiology of acute cholecystitis?

A
gallbladder wall is inflamed
usually caused by stasis of bile due to gallstone obstructing cystic dugt
sometimes ischemia (PAN) or inf cause
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12
Q

What are the clinical features of acute cholecystitis?

A

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

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13
Q

What investigations are used to evaluate acute cholecystitis?

A

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

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14
Q

What is the pathophysiology of ascending cholangitis?

A

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

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15
Q

What are the clinical features of ascending cholangitis?

A
fever, jaundice, RUQ pain = Charcot's triad
septic appearance (hypotensive)
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16
Q

What is Reynold’s Pentad?

A

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

17
Q

What investigations are done in ascending cholangitis?

A

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

18
Q

What is the treatment of ascending cholangitis?

A

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

19
Q

What is the treatment for acute cholecystitis?

A

cholecystectomy, antibiotics in toxic patients or in those with complication

20
Q

What are the most common risk factors for acute pancreatitis?

A

choledocholithiasis (middle aged women and elderly patients)

alcohol

21
Q

What are the clinical features of acute pancreatitis?

A

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

22
Q

Why are antibiotics usually not indicated in acute pancreatitis?

A

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

23
Q

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

A

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

24
Q

What lab investigations are seen with acute pancreatitis?

A

elevated pancreatic enzymes (amylase, lipase)

leukocytosis, plain ab films may show focal or diffuse ileus, elevated hematocrit IF SEVERE

25
Q

What is the best imaging modality for the pancreas?

A

ab CT with IV and oral contrast

26
Q

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

A

infection of necrotic pancreas

27
Q

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

A

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

28
Q

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

A

sonogram - need to look for gallstones

if choledocholithiasis –> ERCP

29
Q

What determines severity of an episode of acute pancreatitis?

A

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)

30
Q

What is the usual treatment of acute pancreatitis?

A

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

31
Q

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

A

only in necrotic pancreas, hematocrit >40

32
Q

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

A

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

33
Q

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

A

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

34
Q

What are risk factors for pancreatic carcinoma?

A

smoking
chronic pancreatitis
hereditary pancreatitis
hereditary pancreatic cancer

35
Q

What is the relationship between diabetes and pancreatic carcinoma?

A

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

36
Q

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

A

CA 19-9, marker for adenocarcinoma

levels >250 in presence of mass and absence of pancreatitis usually diagnostic

37
Q

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

A

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

38
Q

What is the surgical procedure performed for resectable pancreatic carcinoma?

A

Whipple (or variant that spares the stomach)

39
Q

What are palliative procedures performed in pancreatic carcinoma?

A

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