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Systemic Pathology- GI > Gallbladder and Biliary Tract > Flashcards

Gallbladder and Biliary Tract Flashcards

1
Q

T/F:

Gallbladder Wall: mucosa (lined by simple tall columnar, with goblet cell) muscularis, serosa/adventitia, NO SUBMUCOSA

A

True

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2
Q

Name the 3 extra hepatic biliary system

A

Extrahepatic biliary system:

cystic, common hepatic, common bile duct

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3
Q

Congenital anomalies of the Gallbladder

A

Duplication
Agenesis
Multiseptation
Phrygian cap deformity

DAMP

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4
Q

Agenesis of the gallbladder

T/F: usually no cystic duct and has no clinical significance

A

True

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5
Q

It is due to incomplete vacuolization of the developing gallbladder bud or persistent wrinkling of gallbladder wall

A

Multiseptate gallbladder

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6
Q

Multiseptate gallbladder are lined by

A

columnar epithelium

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7
Q

Septa causes what signs and symptoms?

A 
impaired motility, 
stasis of bile flow, 
RUQ pain, 
nausea, 
vomiting
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8
Q

It is the inversion of distal fundus into the body

A

Phyrigian cap deformity

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9
Q

Treatment of correctable (10%) biliary atresia (patent proximal bile duct system)

A

Biliary-enteric anastomosis

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10
Q

Treatment of non-correctable (90%) biliary atresia (no patent portion of extrahepatic bile duct system that communicate with intrahepatic portion)

A

porto-enterostomy/ Kasai procedure (pallative) or liver transplantation (curative)

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11
Q

In biliary atresia, there is an increased deposition of what type of collagen in the basement membrane?

A

Type IV

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12
Q

T/F:

In biliary atresia, there is hyperplasia and hypertrophy of hepatic artery and branches

A

True

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13
Q

It is the dilatation of the CBD (some of intra and extra hepatic BD)

A

Choledochal cyst

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14
Q

T/F:

Choledochal cyst is associated with other hepatobiliary tract abnormality

A

True

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15
Q

T/F:

Choledochal cyst may rupture spontaneously causing acute abdomen

A

True

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16
Q

It is the common cause of obstructive jaundice in children beyond infancy

A

Choledochal cyst

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17
Q

2-8% develop biliary tract carcinoma within:

A. Within wall of cyst

B. Within gallbladder

C. Within bile ducts

D. AOTA

A

D. AOTA

There is lower risk if surgery is done early at age less than 10

Pathogenesis that can cause malignancy in this case is chronic inflammation

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18
Q

Type of choledochal cyst:

Segmental or diffuse fusiform dilation of common bile duct (50-90%)

A

Type 1

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19
Q

Type of choledochal cyst:

Diverticulum of the common bile duct

A

Type 2

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20
Q

Type of choledochal cyst:

Dilatation of intraduodenal common bile duct (choledochocele)

A

Type 3

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21
Q

Type of choledochal cyst:

multiple cyst of extrahepatic bile ducts with (4A) or without (4B) cysts of intrahepatic duct

A

Type 4

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22
Q

Type of choledochal cyst:

one or more cyst of intrahepatic ducts (Caroli’s disease)

A

Type 5

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23
Q

Microscopic appearance depends on age of patient at time of removal

On infant

A

intact epithelium , scanty inflammation

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24
Q

Microscopic appearance depends on age of patient at time of removal

On older children

A

more inflammation, epithelium discontinuous

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25
Q

Microscopic appearance depends on age of patient at time of removal

On adults

A

greater inflammation, destruction of epithelium, chronic cholecystitis, papillomas, adenocarcinomas

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26
Q

Heterotropic tissues are most common in

A

Gastric/ intestinal mucosa

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27
Q

It is a general term referring to stone in the biliary system without specific location

A

Cholelithiasis

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28
Q

It is a medical term for stone in the GB lumen

A

Cholecystolithiasis

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29
Q

It is a stone in the cystic duct

A

Choledocholithiasis

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30
Q

Pathogenesis of cholelithiasis

A

o Bile supersaturation with cholesterol

o Nucleation of cholesterol crystals: occur in the mucus gel of epithelial surface

o Precipitation of cholesterol monohydrate crystals

o Growth to stone-sized aggregates

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31
Q

Accumulation of Mucus gel, bile pigments, cholesterol that can be seen in UTZ prior to stone formation

A

Biliary sludge

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32
Q

Basic constituent of bile stone

A

o Cholesterol

o Calcium bilirubinate

o Calcium carbonate

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33
Q

T/F:

PURE GALLSTONE (10%)

o Only one of the above substrates

o Little or no inflammation if cystic duct not obstructed

A

True

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34
Q

Type of stone that is single, spheroidal, roughly nodular, translucent bluish white and most common in multiparous women

A

Cholesterol stones

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35
Q

T/F:

No correlation between cholesterol stone occurrence and level of blood cholesterol

A

True

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36
Q

T/F:

Cholesterol stones: women are twice at risk as much as men

A

True. Because there is hypersecretion of biliary cholesterol

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37
Q

T/F:

D19H variant: absorb less, synthesize more cholesterol (encoded by ABCG5 and ABCG2)

A

True.

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38
Q

Type of gallstone that is characterized by multiple, small, brown to black, faceted, 2-5mm in diameter, associated with cirrhosis, hemolytic disorders, artificial heart valves

A

Calcium bilirubinate stones

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39
Q

Type of gallstone that is characterized by amorphous, Grayish white, Powdery when broken

A

Calcium carbonate stones

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40
Q

Type of gallstones:

Various combinations of 3 basic constituents

Multiple. faceted, laminated (seen when broken)

Chronic cholecystitis: almost always preset

A

Mixed gallstones

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41
Q

Type of gallstone:

Large and single

Either: pure nucleus with mixed shell or reverse

Barrel stones: usually 2 in number, large, faceted on one side

A

Combined gallstones

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42
Q

Gallstones are formed where

A

Lumen of the gallbladder.

May go into cystic ducts or other extrahepatic ducts. They are NOT formed here, only transported

Choledocholithiasis: almost always secondary to cholecystolithiasis

43
Q

cystic dilation of GB

A

Hydrops

44
Q

An edema and compression common hepatic duct due to a travelling stone

A

Mirizzi syndrome

45
Q

Linear yellow streaks in the prominences of the ridges surrounded by congested mucosa with reddish discolorations in between due to congestion is called

A

Strawberry gallbladder

46
Q

Accumulated cholesterol in the lamina propria may grow and protrude into the lumen as a polypoid mass is called

A

Cholesterol polyps

47
Q

Collections of lipid-laden foamy cells (macrophages) in the mucosal tips or in the lamina propria

Lipid laden macrophages are beneath the epithelium of the mucosa of the gallbladder

Inflammation: usually not significant, unless with stones in the cystic duct

A

Cholesterolosis

48
Q

A gallbladder disease with the following most common manifestations:

RUQ pain, nausea and vomiting

A

Acute cholecystitis

49
Q

primary complication of gallstones; MC reason for “E” (emergency) cholecystectomy

A

Acute calculous cholecystitis

50
Q

T/F:

In acute cholecystitis, thre is presence of edema, congestion, hyperemia, extravasation of RBCs

Widespread fibroblastic proliferation

PMNs: usually none, except when there is CBD obstruction by a stone

Epithelium: marked reactive (proliferative) changes of mucosal epithelium

should not be interpreted as dysplastic change

A

True.

51
Q

T/F:
It is not infectious; rather it is Chemical or ischemic

Nearly always related to stone impacted in cystic duct

Impaction: changes in the concentration and composition of bile, interference with venous supply of GB via obstruction of venous supply of GB via obstruction of venous channels around the cystic duct

A

True.

52
Q

Chemical agents contributory to acute cholecystitis

A

trypsin (pancreatic juice), unconjugated bile salts, lysolecithin: leak through wall of GB to cause bile peritonitis

53
Q

No stone involved

More common in children

May follow systemic infections typhoid fever, CMV, HIV)

(Strep septicaemia,

To histologically differentiates this, look for:

Greater degree of bi le infiltration of GB wall
More necrosis of muscle layer

A

Acute acalculous cholecystitis

54
Q

MOST IMPORTANT RISK FACTOR IN CHRONIC CHOLECYSTITIS:

A

Presence of gallstone

55
Q

Aggregates of foamy histiocytes in lamina propria covered by intact epithelium

Morphologic variation of cholesterolosis

No malignant potential

A

Cholesterol polyp

56
Q

Patterns of growth of adenoma

A

Tubular

Tubulovillous (tubulopapillary)

Villous (papillary)

57
Q

T/F:

Some degree of atypia often present (especially of the villous type)

A

True.

58
Q

T/F

It is very rare for an adenoma to develop to a gallbladder malignancy

A

True

59
Q

T/F:

Evidence of adenomas

Frequent expression of beta-catenin mutations (rare in Ca)

Lack of mutations in TP53 and P16 (tumor suppressor genes), KRAS (protooncogene) (frequent in cancer)

> 50% cases: (+) estrogen receptors: manifestation of metaplastic change in epithelium (and not neoplastic change)

A

True

60
Q

MC AbN lab Finding in gallbladder malignancy

A

elevated Alkaline Phosphatase level

61
Q

Initial event in the development of GB CA:

A

Inflammation

62
Q

Gross:

Poorly defined area of diffuse thickening and induration of GB wall

More difficult to assess especially if there are recurrent bouts of chronic cholecystitis

A

Diffuse growing/infiltrating (70%)

63
Q

GROSS:

Grows into lumen as an irregular, cauliflower mass

May neck underlying wall

A

Polypoid/exophytic (30%)

64
Q

MC sites of involvement of gallbladder malignancy

A

neck or fundus

65
Q

Well-formed glands with wide lumina lined by one to few rows of highly atypical cuboidal cells

Surrounding stroma: cellular, arranged concentrically

Characteristic: glands are well-differentiated at an architectural level but poorly differentiated at a cytologic level

A

Adenocarcinoma

66
Q

Histochem, IHC, EM or adenocarcinoma

A

Mucin: sialomucin type (normal: sulfomucin/ sulfated mucin)

CK7+ / CK20 (cholangiocarcinoma: CK7+/CK20-)

EMA + (Epithelial Membrane Ag)
CEA + (Carcinoembryonic Ag)

AFP occasionally + (request if considering primary hepatic malignancy)

Electron Microscopy: Pleomorphic microvilli, mucin vacuoles, abundant lysosomes

67
Q

Molecular Genetic Features:

Polymorphisms of:

A

Cyt P450 1A11, DNA repair genes, hormone-rel gene, inflammation genes, insulin sensitivity genes, lipid metabolism pathway genes

68
Q

Molecular Genetic Features:

Accumulation of multiple genetic alterations:

A

Oncogenes, tumor suppressor genes, DNA repair genes

69
Q

Molecular Genetic Features:

TP53 mutations (with overexpressed p53)

A

> 50% of cases; more in high grade tumors

70
Q

Molecular Genetic Features:

KRAS (proto-oncogene) mutations

A

Associated with Ca with anomalous arrangement of pancreaticobiliary duct

71
Q

(Best prognosis)

Predominant or exclusive papillary pattern

A

Papillary carcinoma

72
Q

High grade

Very difficult to diagnose in light microscope

EM: Dense core secretory granules

A

Small cell neuroendocrine carcinoma

73
Q

Adenoacanthoma (well – benign)

Adenosquamous CA (poor – malignant)

A

Squamous metaplasia

74
Q

MC of GB carcinoma

A

Intestinal metaplasia, dysplasia, and CIS Biliary Intraepithelial Neoplasia)

75
Q

T/F:

Spread and metastasis

Great propensity to directly invade liver

Also stomach and duodenum

Metastasis to liver (via portal tract), cystic and pericholedochal LN in lesser omentum, LN behind

the 1 st part of duodenum, aortocaval LN

A

True.

76
Q

T/F:

Frequency of LN involvement:

Dependent on depth of invasion of primary tumor

A

True.

77
Q

GB ➡️CD ➡️CBD ➡️LN posterior to 1 st part of duodenum and pancreatic head

Most common pathway

A

Cholecystoretropancreatic

78
Q

GB ➡️gastrohepatic ligament ➡️celiac nodes

A

Cholecystoceliac

79
Q

GB posterior to pancreas ➡️ aortocaval LN

A

Cholecystomesenteric

80
Q

Prognostic Factor:

most important prognostic determinant

A

Stage

81
Q

Prognostic Factor:

main determinant in early stage disease

A

Surgical margins

82
Q

Prognostic Factor:

most favourable: well-differentiatd papillary adenocarcinoma

A

Grading

83
Q

Prognostic Factor:

DNA content:

A

questionable

84
Q

Prognostic Factor:

KRAS

A

(+) of codon 12 mutations is unfavourable

85
Q

Prognostic Factor:

HER2 oncogene:

A

no correlation

86
Q

Prognostic Factor:

Angiogenesis

A

(+) correlation

87
Q

One of the complications of calculous cholecystitis

Due to stone impaction in the cystic duct

A

Cholangitis

88
Q

Unknown etiology

Rare

Diffuse thickening of the wall
Lumen obstruction ➡️decreased lumen

Dense fibrosis

Sparse mixed inflammatory infiltrate

Intact epithelium

A

Sclerosing cholangitis

89
Q

EARLY STAGES of sclerosing cholangitis

Best seen in the liver biopsy specimens

Fibrous obliterative cholangitis

Replacement of duct segments by fibrous cords of connective tissue

Leads to complete loss of bile ducts

DDX?

A

Biliary atresia

90
Q

Sclerosing cholangitis has INCREASED INCIDENCE in patients with

A

HLA DRW52a antigen

91
Q

Sclerosing cholangitis is ASSOCIATED with:

A

Riedel thyroiditis

Crohn disease

Ulcerative colitis: high frequency of serum anticolon antibodies

92
Q

T/F:

The dysplastic changes can sometimes evolve to cholangiocarcinoma

A

True

93
Q

Most common manifestation of cholangiocarcinoma

A

90%: jaundice (MC manifestation)

Since jaundice is the most common manifestation, a good differential would be your liver disease or liver CA

94
Q

Cholangiocarcinoma has INCREASED INCIDENCE in:

A

Ulcerative colitis

Sclerosing cholangitis

Chronic infections with:
Clonorchis sinensis Vietnam) infection (Japan, Korea, Vietnam)
Opithorchis viveririni infection (Thailand, Laos, Malaysia)

Choledochal cysts, Caroli disease

Thorium dioxide (thorotrast) exposure: radiologic contrast dye used between 1930- 1950

95
Q

T/F

Cholangiocarcinoma can develop in any level of the biliary trees

A

True.

Anatomical divisions:

Upper third: 50-75% (most proximal, nearest the liver)

Middle third: 10 -25 %

Lower third: (distal, nearest the duodenum) 10-20 %

96
Q

Anatomic Classification by Bismuth:

What type?

below the confluence of right and Left hepatic ducts

A

Type 1

97
Q

Anatomic Classification by Bismuth:

What type?

reaching the confluence

A

Type 2

98
Q

Anatomic Classification by Bismuth:

What type?

occluding the common hepatic duct and either the right (IIIA) of left (IIIB) hepatic duct

A

Type 3

99
Q

Anatomic Classification by Bismuth:

What type?

multi-centric, or involving the confluence and both the right and left hepatic ducts

A

Type 4

100
Q

T/F:

Cholangiocarcinoma GROSS FEATURES:

May be Polypoid and superficial

Most are nodular or sclerosing with deeper penetration into the wall

Occasional: multi-centric accompanied by extensive intraepithelial component OR associated with GB carcinoma

Upper third lesions: direct extension to liver is common

Lower third lesions: extension into the pancreas

A

True.

Metastasis to regional lymph node: Frequent

o MC affected: those around lower portion of the hepatoduodenal ligament, superoposterior pacreaticoduodenal group and superior mesenteric artery group.

o AFP always positive for HCC and negative for CCA

101
Q

T/F:

Cholangiocarcinoma MICROSCOPIC FEATURES:

MC: well differentiated, mucin secreting adenocarcinoma

Papillary Surface: more common in distal lesions

A

True.

Heterogeneity of cells within the same gland

Concentric layering neoplastic glands of cellular stroma around

Increase N:C ratio

Prominent nucleoli

Stromal and peri-neural invasion

*The best diagnostic tool is the first one and the last one

102
Q

T/F:

(+) expression of muco-substances and CEA

(+) expression of CDX2 and MUC2: intestinal differentiation

Metaplastic and Dysplastic changes in adjacent epithelium
o this is more common in bile duct CA compared to gall bladder CA

IMMUNOHISTOCHEMISTRY
o Overexpression of p53

o Overexpression of DPC4 tumor suppressor gene implicated in genesis of pancreatic cancer this is more specific for bile duct CA

A

True.

103
Q

a.k.a. Sclerosing carcinoma of the bile ducts

A

ALTEMEIER – KLATSKIN TUMOR

104
Q

It mimics sclerosing cholangitis because of extensive necrosis, the difference is you see here neoplastic glands

Begins at hepatic duct junction

Spreads to long segments of the biliary tree

Long clinical course

Well differentiated microscopic appearance

Extensive fibrosis

DDx?

A

Sclerosing cholangitis

Systemic Pathology- GI (1 decks)

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