Gallbladder, Extrahepatic Bile Ducts, and Pancreas Flashcards
Gallstones
Pebble-like accretions that form in the gallbladder
2 types
Cholesterol stones
pigment stones
Gallstones are assoc w/
gallbladder inflammation (cholecystitis) causes 9 out of 10 cases of acute cholecystitis
also a major cause of pancreas inflammation (pancreatitis)
causes 4 out of 10 cases of acute pancreatitis
rate of switch for asymptomatic to symptomatic gallstones
2% per year
only 20% with gallstones have sx…. but longer you have them, more likely to get sx
Cholesterol stones %, RFs
80% Ethnicity: U.S.; North Europe; Native Americans - Advancing age - Female sex hormones Female gender Oral contraceptives Pregnancy - Obesity - Rapid weight loss
Pigment stones %, RFs
20%
- Ethnicity: Asian; rural
- Chronic hemolytic syndromes
- Biliary infection
- Ileal disease
Gallstone ileus
gallstones can pass from gb to small intestine thru bile duct or from fistulization to small bowel.
Preferential impaction in ileum
Crystal formation
Cholesterol supersaturation in the bile. Subsequent crystallization. Bile can hold a certain amount of cholesterol, but over a certain amount there isn’t enough room.
Crystallization promotoed by gallbladder hypomotility and excessive mucus
growth: 2mm/year
Cholesterol supersaturation due to increased cholesterol output into bile, but not related to dietary intake. Minority of cases due to decreased bile acid synthesis (genetic component.)
cholecystitis
Inflammation of the gallbladder
acute vs chronic
calculous (gallstones) vs acalculous
Acute cholecystits
90% due to gallstone obstruction of the neck / cystic duct
Less common causes: trauma major surgery severe burns postpartum
Sx
Pain (ruq), fever, leukocytosis
Acute calculous cholecystitis
Gallstone lodges in cystic duct
- mucosal irritation occurs (likely from other gallstones), damage occurs, protective mucus layer disrupted
- enzymes in the mucosa are released that hydrolyze phospholipids.
- accumulation of toxic products in lumen.
- inflamm and injury to wall
- obstruction leads to distension of wall of gallbladder
- distension–> ischemia (microvascular ischemia)–> more inflammation
Histology of acute cholecystitis
inflamm destruc of mucosa
- erosion
- lymphocytes
- neutrophils
- can see microscopic gallstones
Chronic cholecystitis
-Histopathologic term for inflammation and fibrosis of the gallbladder with poor correlation to clinical symptoms
-Pathogenesis is not well established but …
95% are associated with gallstones
Vague sx like food intolerance may occur
?Cause (not great evidence for any of these):
- recurrent attacks of mild acute cholecystitis
- repetitive mucosal trauma from gallstones
- genetics of bile composition or inflammatory response
Gross appearance chronic cholecystitis
- gallstones
- firm thickened gallbladder wall (white/fibrotic)
- surface trabeculations (likely due to fibrosis)
histology of chronic cholecystitis
fibrosis of wall
mononuclear cell infiltrate in mucosa
-thickening of muscular layer
-mucosal herniations/sinuses (herniate thru muscular layer by glandular eptihelium)
carcinoma of gallbladder
rare – 0.5% of cancers
poor survival – 1% alive at 5 years
(because often found @ high grade)
major risk factors:
- gallstones (70% have stones)
- chronic infection
almost all are adenocarcinomas (>90%)
histology of gallbladder cancer
- gland formation (infiltrate of gland forming neoplasm)
- atypical cytology, atypical enlarged nuclei, vary in size/shape
- atypical mitotic figures
Choledocholithiasis
Stones (choledocholiths) within biliary tree
Major cause of ascending cholangitis (usually gram negative, from normal intestinal flora migrating into bile ducts)
90% of choledocholiths were choleliths
small number arise primarily within bile ducts
Choledochal cyst
Congenital dilatation of the common bile duct
(can be hepatic or intrahepatic duct or cystic duct)
- typically present in young (may be in adulthood)
- vary based on location
- present with findings of biliary obstruction (jaundice, etc)
Bile duct carcinoma
very rare
nearly all are adenocarcinoma
look like histology of gallbladder cancer
RFs
- choledochal cyst in older adults (why surgically taken care of if found in kids)
- primary sclerosing cholangitis (inflammatory disease)
- infections (liver flukes)
- ? cholelithiasis
Pancreatitis
Inflammation of the pancreas
acute or chronic
Sequelae: Pseudocysts Abscesses Pancreatic insufficiency Secondary diabetes (pancreas can't perform hormonal functions)
Causes of acute pancreatitis
gallstones 45%
alcohol 35%
other 20% (drugs, toxins, etc)
elevated lipase
abdominal pain radiating to back
acute pancreatitis due to gallstones
- not simply mechanical obstruction due to stone coming thru common bile duct (gallstone can just be nearby, in common bile duct not even obstructing panc duct)
- increased intraductal pressure (panc)
- secretions trapped in panc ducts
- digestive enzymes leak into pancreas and can get activated
- autodigestion, tissue injury, inflamm, edema, ishcemia, distention–> more injury
- vicious circle
alcohol causing acute pancreatitis
? direct toxic effect of alcohol on pancreas leading to injury (not just that though)
- alcohol stimulates secretion of digestive enzymes
- accumulate within pancreatic ducts
- alcohol causes contraction of sphincter of oddi
- secretion + obstruction leads to accumulation of products that leak back into pancreas
- alcohol also causes defective packaging of enzymes
- priming enzymes for inappropriate activation
Another theory:
-acute pancreatitis w/ alcohol is exacerbation of underlying chronic pancreatitis
Acute pancreatitis gross
- hemorrhagic necrosis
- yellow areas: autodigested areas of fat tissue (lipase secreted by pancreas)
Pancreatic pseudocysts
-no epithelial lining
histology of acute pancreatitis
edematous non-necrfotic pancreas
near complete destruction of parenchyma, fibrin and neutrophils infiltrate
Pancreatic pseudocysts
lining is fibrous tissue w/ overlying layer of fibrin
-inflammatory cells in wall
-hemorrhage
chronic pancreatitis
Irreversible parenchymal destruction and fibrosis
Causes:
- most common identifiable cause is alcohol abuse
- long-standing duct obstruction
- hereditary forms of pancreatitis
- large proportion (40%) are idiopathic
Pathophysiology (alcohol):
chronic duct obstruction by secretions
(abnormal pancreatic secretions plug ducts)
direct toxic effects on acinar cells from alcohol
inducing oxidative stress on acinar cells
necrosis-fibrosis
(acinar cell necrosis and replacement by fibrous tissue)
Chronic pancreatitis (gross)
- fibrous tissue
- atrophy
- presence of stones due to stasis of secretions
Chronic panc (histology)
atrophy
fibrosis of parenchyma
fibrosis surrounding ducts
Pancreatic Neoplasia
ductal adenocarcinoma (95%) endocrine neoplasms (2%)
ductal carcinoma
4th leading cause of death in US from cancer
very poor prognosis (5% at 5 years)
- mass forming lesion in pancreas
- characteristically obstructs either panc duct, common bile duct, or both
Histology: gland forming tumor malignant glands infiltrative atypical cells
Pancreatic endocrine neoplasm (PEN)
nonfunctional vs functional
well-diff vs non-diff
most clinically relevant tumors are:
nonfunctional and well-differentiated
Most don’t produce hormones that cause clinical problems
behavior hard to predict based on appearance
functional tumors:
- insulinoma 42% (fainting spells)
- gastrinoma 24% (present w/ PUD; Zollinger Ellison syndrome)
- glucagon 14%
PEN gross findings
round, well demarcated, fleshy tumor (amorphous, fibrotic if ductal adenocarcinoma)
don’t usually cause ductal obstruction
PEN histology
typical endcrine appearance
ribbon-like growth pattern
morphologically: regular round nuclei
