Pathology Ch. 18: The Biliary Tract

Front 1

Most common aberrant location of the gallbladder

Back 1

Partial or complete embedding within the liver

Front 2

Over 95% of biliary disease is attributable to

Back 2

Cholelithiasis

Front 3

Most common congenital anomaly of the gallbladder

Back 3

Folded fundus, creating a phrygian cap

Front 4

stones comprised of bilirubin calcium salts

Back 4

pigment stones

Front 5

Gallstones composed of crystalline cholesterol monohydrate

Back 5

Cholesterol stones:
90% of all stones

Front 6

Risk factors for pigment gallstones

Back 6

Asian ethnicity
Chronic hemolytic syndromes
Biliary infection
GI disorders

Front 7

Arise in the setting of bacterial infections of the biliary tree and parasitic infections

Back 7

pigment stones

Front 8

How does estrogen influence the formation of cholesterol stones?

Back 8

Increases the expression of hepatic lipoprotein receptors and stimulates hepatic HMG-CoA reductase activity, enhancing both cholesterol uptake and synthesis. This leads to more stones.

Front 9

How does Clofibrate lead to cholesterol stones?

Back 9

Increases hepatic HMG-CoA reductase and decreases conversion of cholesterol to bile acids by inhibiting cholesterol-7-a-hydroxylase activity.

Front 10

Hepatocyte proteins that transport biliary lipids, and confer an increased risk of cholesterol gallstones

Back 10

ATP-Binding Cassette Transporters:
ABCG5
ABG2

Front 11

Genetic variant that encodes the ATP-binding Cassette transporters, and may cause increased cholesterol stones.
What may be the txmt?

Back 11

D19H:
Encoded by ABCG5 and ABG2.
Individuals with the D19H variant synthesize more and absorb less cholesterol. Thus, HMG-CoA reductase inhibitors may decrease the risk.

Front 12

Four conditions required for cholesterol stone formation

Back 12

1. The bile mus be superstaurated with choesterol.
2. Hypomobility of the gallbladder.
3. Increased nucleation of cholesterol.
4. Hypersecretion of mucus in the gallbladder traps the nucleated crystals, leading to their aggregation..

Front 13

How do cholesterol stones form?

Back 13

When cholesterol concentrations exceed the solubulizing capacity of bile, cholesterol can no longer remain dispersed and nucleates into solid cholesterol monohydrate crystals.

Front 14

84 y/o pt with a mechanical mitral valve prosthesis presents with severe, colicky RUQ pn. Ultrasound shows numerous gallstones. What type are they? Why does this occur?

Back 14

Pigment stones:
In individuals with conditions that may cause intravascular hemolysis, increased unconjugated bilirubin forms insoluble calcium salts that combine with other materials to form stones.

Front 15

What properties of gallstones may make it easy diagnose via CT-scan? What may make it difficult?

Back 15

Stones containing calcium carbonate are easily identifiable. Thus, most pigment stones and 10-20% of cholesterol stones are easily identifiable.
Stones comprised mostly of cholesterol are radioluscent.

Front 16

How do infections of the biliary tract with organism such as E coli, Ascaris lumbricoides, or liver flukes, lead to development of pigment stones?

Back 16

Organisms cause release of B-glucuronidases, which hydrolyze bilirubin conjugates, and increase levels of unconjugated bilirubin calcium salts.

Front 17

Acute calculous cholecystitis is precipated almost 90% of the time by obstruction where?

Back 17

In the neck or cystic duct

Front 18

One of the most common indications for abdominal surgery

Back 18

Cholecystitis

Front 19

Acute calculous cholecystitis with symptomatic gallstones develops in what subset of pts?

Back 19

Diabetics

Front 20

Acute acalculous cholecystitis is thought to result from? Why?

Back 20

Ischemia of the cystic artery due to lack of collateral circulation.
Inflammation and edema of the wall compromising blood flow, galbladder stasis, accumulation of microcrystals of cholesterol, viscous bile, increased gallbladder mucus causing cystic duct obstruction.

Front 21

Risk factors for acalculous cholecystitis

Back 21

1. Sepsis with hypotension and multisystem organ failure
2. immunosuppression
3. major trauma and burns
4. diabetes mellitus
5. infections

Front 22

Puss filled luminal exudate of the galbladder

Back 22

empyema

Front 23

Luminal appearance of the gallbladder in acute cholecystitis

Back 23

Filled with large amounts of fibrin, pus, and hemorrhage from subserosal layer

Front 24

During acute cholcystitis, what causes the gallbladder to appear bright red, blotchy violaceous to green-black discoloration

Back 24

Subserosal hemorrhages

Front 25

Severe cases of cholecystitis in which the organ becomes green-black and contains multiple perforations. What type usuallly develops this?

Back 25

Gangrenous cholecystitis:
As a result of either a delay in diagnosis or disease itself, it is much higher in acalculous.

Front 26

In acute cholecystitis, what is the appearance of the serosal layer?

Back 26

It is covered by fibrin, and in severe cases, by a suppurative, coagulated exudate.

Front 27

Pathogenesis of acute calculous cholecystitis

Back 27

The action of mucosal phospholipases hydrolyzes luminal lecithins into toxic lysolecithins. The normally protected glycoprotein mucus layer is disrupted, exposing the mucosal layer to bile salt detergents. Prostaglandins released within the wall contribute to mucosal and mural inflammation. Gallbladder dysmotility results and distention with increased intraluminal pressure compromise blood flow

Front 28

Results from chemical irritation and inflammation of the obstructed gallbladder

Back 28

Acute calculous cholecystitis

Front 29

Gallbladder cultures of individuals with chronic cholecystitis often show?

Back 29

Ecoli and enterococci organisms

Front 30

Extensive dystrophic calcification of the gallbladder wall as a result of chronic cholecystitis. Increased risk of?

Back 30

Porcelain gallbladder:
Increased risk of cancer

Front 31

Rare condition in which the gallbladder has a massively thickened wall, is shrunken, nodular, and chronically inflamed with foci of necrosis and hemorrhage

Back 31

Xanthogranulomatous cholecystitis

Front 32

Condition of gallbladder atrophy, and chronic obstruction, in which it may contain only clear secretions

Back 32

Hydrops of the gallbladder

Front 33

Appearance of the serosa in chronic cholecystitis

Back 33

Smooth and glistening but may dulled by fibrosis. Dense fibrous adhesions may remain as sequlae of acute inflammation. In advanced cases there is marked subserosal fibrosis with mononuclear cell infiltration.

Front 34

Main factor predisposing someone to chronic cholecystitis

Back 34

Supersaturation of the bile, which also leads to stone formation

Front 35

The presence of stones within the bile ducts of the biliary tree. Type of stone most common? Associated with?

Back 35

Choledocholithiasis:
Pigment stones most common
Associated with biliary tract infections.

Front 36

Bacterial infection of the biliary ducts

Back 36

Cholangitis

Front 37

Choledocholithiasis may lead to?

Back 37

1. obstruction
2. pancreatitis
3. cholangitis
4. hepatic abscess
5. secondary biliary cirrhosis
6. acute calculous cholecystitis

Front 38

In cholangitis, where and what type of bacteria most commonly occur?

Back 38

Enter through the sphincter of oddi
The bacteria are usually enteric gram- aerobes such as E coli, Kliebsella, Interococcus, or Enterobacter

Front 39

Pt presents with fever, chills, abd pn, and jaundice. Ct scan shows inflammation of the bile ducts

Back 39

Chlangitis:
with neutrophils within the luminal space.

Front 40

Infection of hepatic biliary radicles

Back 40

ascending cholangitis

Front 41

Does acute cholecystitis usually present with jaundice? What would hyperbilirubinemia suggest?

Back 41

NO! because the common bile duct is most likely still unobstructed!!!
That the common bile duct is obstructed

Front 42

A complete or partial obstruction of the lumen of the extrahepatic biliary tree within the first 3 months of life. Major contributor to? Characterized by?

Back 42

Biliary atresia:
Neonatal cholestasis
Progressive inflammation and fibrosis of intrahepatic or extrahepatic bile ducts.

Front 43

Most frequent cause of death from liver disease in early childhood

Back 43

Biliary obstruction

Front 44

Most common form of biliary atresia. Etiology?

Back 44

Perinatal:
Obliteration of the biliary tree after birth
Unknown

Front 45

Cause of fetal form of biliary atresia

Back 45

Ineffective establishment of laterality of thoracic and abdminal organ developement, including malrotation of abd viscera

Front 46

Biliary atresia is surgically correctable if the inflammation and fibrotic stricture involves the?

Back 46

Common duct or hepatic bile duct.
Obstruction of the bile ducts at or above the porta hepatis.

Front 47

Neoplasms of the gallbladder are derived from

Back 47

Epithelial lining of the biliary tree

Front 48

Hyperplasia of the muscular layer of the gallbladder, containing intramural hyperplastic glands

Back 48

adenomyosis

Front 49

Sessile mucosal projections with a surface stroma infiltrated with chronic inflammatory cells and lipid-laden macrophages

Back 49

inflammatory polyps

Front 50

Most important risk factor for gallbladder carcinoma

Back 50

Gallstones

Front 51

Two patterns of growth in gallbladder carcinoma

Back 51

Infiltrating:
More common and appears as a poorly defined diffuse thickening and induration of the gallbladder wall that may ulcerate into surrounding tissues and form fistulas.
Exophytic:
Irregular cauliflower mass that invades the underlying wall and may become necrotic, hemorrhagic, or ulcerated.

Front 52

Most common sites of involvement in gallbladder CA

Back 52

Fundus and body, while the lateral walls comprise 20%

Front 53

By the time most gallbladder neoplasms have been found, what has occurred?

Back 53

Most have invaded the liver centrifugally, and many have extended to the cystic ductand adjacent bile ducts and portal-hepatic lymph nodes. The peritoneum, GI tract, and lungs are commonly seeded.