Gallbladder, Extrahepatic Bile Ducts, and Pancreas Flashcards

1
Q

Gallstones

A

Pebble-like accretions that form in the gallbladder

2 types
Cholesterol stones
pigment stones

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2
Q

Gallstones are assoc w/

A
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

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3
Q

rate of switch for asymptomatic to symptomatic gallstones

A

2% per year

only 20% with gallstones have sx…. but longer you have them, more likely to get sx

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4
Q

Cholesterol stones %, RFs

A
80%
Ethnicity: U.S.; North Europe; Native Americans
- Advancing age
- Female sex hormones
	Female gender
	Oral contraceptives
	Pregnancy
- Obesity
- Rapid weight loss
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5
Q

Pigment stones %, RFs

A

20%

  • Ethnicity: Asian; rural
  • Chronic hemolytic syndromes
  • Biliary infection
  • Ileal disease
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6
Q

Gallstone ileus

A

gallstones can pass from gb to small intestine thru bile duct or from fistulization to small bowel.
Preferential impaction in ileum

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7
Q

Crystal formation

A

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.)

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8
Q

cholecystitis

A

Inflammation of the gallbladder

acute vs chronic
calculous (gallstones) vs acalculous

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9
Q

Acute cholecystits

A

90% due to gallstone obstruction of the neck / cystic duct

Less common causes:
trauma
major surgery
severe burns
postpartum

Sx
Pain (ruq), fever, leukocytosis

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10
Q

Acute calculous cholecystitis

A

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
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11
Q

Histology of acute cholecystitis

A

inflamm destruc of mucosa

  • erosion
  • lymphocytes
  • neutrophils
  • can see microscopic gallstones
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12
Q

Chronic cholecystitis

A

-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):

  1. recurrent attacks of mild acute cholecystitis
  2. repetitive mucosal trauma from gallstones
  3. genetics of bile composition or inflammatory response
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13
Q

Gross appearance chronic cholecystitis

A
  • gallstones
  • firm thickened gallbladder wall (white/fibrotic)
  • surface trabeculations (likely due to fibrosis)
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14
Q

histology of chronic cholecystitis

A

fibrosis of wall
mononuclear cell infiltrate in mucosa
-thickening of muscular layer
-mucosal herniations/sinuses (herniate thru muscular layer by glandular eptihelium)

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15
Q

carcinoma of gallbladder

A

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%)

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16
Q

histology of gallbladder cancer

A
  • gland formation (infiltrate of gland forming neoplasm)
  • atypical cytology, atypical enlarged nuclei, vary in size/shape
  • atypical mitotic figures
17
Q

Choledocholithiasis

A

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

18
Q

Choledochal cyst

A

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)
19
Q

Bile duct carcinoma

A

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
20
Q

Pancreatitis

A

Inflammation of the pancreas
acute or chronic

Sequelae:
Pseudocysts
Abscesses
Pancreatic insufficiency
Secondary diabetes (pancreas can't perform hormonal functions)
21
Q

Causes of acute pancreatitis

A

gallstones 45%
alcohol 35%
other 20% (drugs, toxins, etc)

elevated lipase
abdominal pain radiating to back

22
Q

acute pancreatitis due to gallstones

A
  • 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
23
Q

alcohol causing acute pancreatitis

A

? 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

24
Q

Acute pancreatitis gross

A
  • hemorrhagic necrosis
  • yellow areas: autodigested areas of fat tissue (lipase secreted by pancreas)

Pancreatic pseudocysts
-no epithelial lining

25
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
26
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)
27
Chronic pancreatitis (gross)
- fibrous tissue - atrophy - presence of stones due to stasis of secretions
28
Chronic panc (histology)
atrophy fibrosis of parenchyma fibrosis surrounding ducts
29
Pancreatic Neoplasia
``` ductal adenocarcinoma (95%) endocrine neoplasms (2%) ```
30
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 ```
31
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%
32
PEN gross findings
round, well demarcated, fleshy tumor (amorphous, fibrotic if ductal adenocarcinoma) don't usually cause ductal obstruction
33
PEN histology
typical endcrine appearance ribbon-like growth pattern morphologically: regular round nuclei