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GIR Test 2 > B5.025 Liver Disorders I > Flashcards

B5.025 Liver Disorders I Flashcards

1
Q

primary diseases affecting the bile duct

A 
PBC
PSC 
stones/ obstruction
abscess
congenital hepatic fibrosis/ polycystic liver disease
drug induced liver injury
cholangiocarcinoma
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2
Q

describe a normal bile duct on histo

A

single layer of cuboidal epithelial cells

“string of pearls”

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3
Q

lab values that evaluate hepatocyte integrity

A

AST/ALT

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4
Q

lab values that evaluate biliary excretory function

A

serum bilirubin

plasma membrane proteins (alk phos, GGT)

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5
Q

lab values that evaluate hepatocyte function

A

serum albumin
PT/INR
serum ammonia

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6
Q

lab findings in obstructive liver disease pattern

A

increased alk phos, bilirubin GGT

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7
Q

lab findings in acute hepatitis pattern

A

increased AST and ALT

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8
Q

lab findings associated with cirrhosis pattern

A

decreased albumin, decreased platelets, prolonged PT

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9
Q

what is cholestasis

A

impaired bile formation and bile flow

accumulation of bile pigment in hepatic parenchyma

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10
Q

causes of cholestasis

A

extrahepatic obstruction of biliary tract
intrahepatic obstruction of biliary tract
defects in bile secretion

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11
Q

etiologies of obstruction/obliteration of the bile ducts

A 
cholelithiasis
cholangitis
PBC
PSC
postsurgical strictures
parasitic infection
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12
Q

etiologies of compression of bile ducts outside the liver

A

pancreatic cancer
pancreatitis
extrahepatic biliary cancers

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13
Q

appearance of bile plugs on histo

A

canalicular reddish inclusions

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14
Q

other histo findings with cholestasis

A

small bile ducts form all around main bile duct outside of portal triad to try to compensate backed up flow
bile is chemotactic for neutrophils, so inflammatory infiltrates

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15
Q

canals of hering

A

lead from intrahepatic bile ductile to canaliculi

lined by cells that can differentiate into duct cells or hepatocytes

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16
Q

function of stellate cells

A

in case of inflammation, function as myofibroblasts and secrete type 1 and 3 collagen creating fibrosis

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17
Q

alkaline phosphatase

A

present in bile duct epithelium and canalicular membrane of hepatocytes
released due to detergent action of retained bile salts on hepatocyte membrances

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18
Q

signs and symptoms of cholestasis

A

jaundice
pruritis
skin xanthomas (accumulation of cholesterol)

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19
Q

what is PBC?

A 
chronic bile duct destructive disease
autoimmune disease
aberrant expression of MHC class II molecules on bile duct epithelial cells and autoreactive T cells around ducts
AMA is increased
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20
Q

features of AMA in PBC

A

directed against M2 family of mitochondrial antigens–most frequent is E2 part of pyruvate dehydrogenase

21
Q

clinical presentation of PBC

A

90% female
peak 40-50 yo
elevated GGT and alk phos, minimal bili elevation at first, minimal AST/ALT elevation

22
Q

histopath findings with PBC

A 
destructive (non-suppurative) cholangitis
florid duct lesions
histo evidence of bile duct damage
granulomas in portal tract
lobules of PBC are nearly normal
23
Q

elaborate on features of histo evidence of bile duct damage

A 
disruption of BM
intraepithelial lymphs and plasma cells
cytoplasmic vacuolization
regenerative hyperplasia
occasional mitoses
24
Q

what is a florid duct lesion

A

aggregation of unusual cells and disrupted membranes

25
Q

what does a damaged duct look like?

A

irregular epithelial cells , no string of pearls appearance

fibrosis

26
Q

treatment of PBC

A

oral UDCA
slow progression
mechanism is uncertain, but is presumably related to ability of UDCA to enter bile acid pool and alter composition of bile

27
Q

features of PSC

A

involvement of extrahepatic and intrahepatic biliary tree
M:F = 2:1, 20-40 yrs
70-80% of pts also have ulcerative colitis
p-ANCA in 80%

28
Q

appearance of p-ANCA on fluorescent microscopy

A

illumination around multi-lobed neutrophil nuceli

29
Q

evidence of immunologically mediated injury in PSC

A

T cells in periductal stroma
presence of circulating autoAb (p-ANCA)
association with HLA-B8 and other MHC antigens

30
Q

discuss the linkage between PSC and UC

A

T cells activated in damaged mucosa of patients with UC migrate to liver and recognize a cross reacting bile duct antigen

31
Q

findings in PSC

A

increased GGT and alk phos
mild increase in AST/ALT and bilirubin
beaded areas of bile ducts on ERCP
progressive concentric periductal fibrosis “onion skin”

32
Q

histopath findings in PSC

A

fibrous cholangitis
adjacent mixed inflammatory infiltrate
lesions are focal, patchy (can lead to a negative biopsy)
can have ductopenia without ductal scars

33
Q

clinical sequelae of PSC

A

acute bouts of ascending cholangitis
persistent alk phos elevation
25% develop cholelithiasis
lifetime risk of cholangiocarcinoma =20%

34
Q

possible etiologies of large duct obstruction

A

gallstones
malignancy of biliary tree or head of pancreas
stricture from previous surgery
kids: biliary atresia, CF, choledochal cysts, insufficient bile ducts

35
Q

ascending cholangitis

A

secondary bacterial infections
enteric organisms (enterococci, E.coli)
suppurative cholangitis
fever, chills, ab pain, jaundice

36
Q

histo features of large duct obstruction

A

distention of upstream bile ducts leading to bile duct dilatation
ductular proliferation at portal-parenchymal interface (canals of Hering)
periductular neutrophils
bile infarcts and bile lakes

37
Q

what is cholestasis of sepsis

A

direct effects of intrahepatic bacterial infection
ischemia relating to hypotension caused by sepsis
circulating microbial products inhibit biliary secretions

38
Q

most well known drugs with liver toxicity

A 
antibiotics
psychotropics
anticonvulsants
oral contraceptives
anti-inflammatories
39
Q

features of predominantly cytolytic acute injury

A

spotty necrosis
submassive necrosis
massive necrosis
(APAP, psychotropics, herbal meds, cocaine, carbon tetrachloride)

40
Q

features of predominantly cholestatic acute injury

A 
intrahepatic cholestasis (mostly in centrilobular hepatocytes, formation of canalicular plugs)
anabolic or contraceptive steroid use
41
Q

what are choledochal cysts

A

congenital dilatation of common bile duct
most present in kids <10yrs with jaundice and ab pain
F:M = 3-4:1
increased risk of stones, strictures, stenosis, obstructive biliary complications, bile duct carcinoma

42
Q

what are fibropolycystic diseases

A

congenital malformations of biliary tree:
von meyenburg complexes-small bile duct hamartomas
polycystic liver disease
caroli disease
congenital hepatic fibrosis

43
Q

what do von meyenburg complexes look like on histo

A

branching profiles from bile ducts

lots of fibrosis

44
Q

formation of cholesterol stones

A

cholesterol must be made soluble in bile, aggregation with water soluble bile salts which act as detergents
when cholesterol concentration exceeds solubilizing capacity of bile solid crystals of cholesterol form
free cholesterol is toxic to gallbladder

45
Q

formation of pigment stones

A

complex mixture of abnormal insoluble calcium salts and unconjugated bilirubin
form w/ and increase in bilirubin or infection of the biliary tract

46
Q

clinical features of stones

A

majority are asymptomatic
colicky pain
smaller stones cause more pain

47
Q

risk factors for cholangiocarcinoma

A

PSC
congenital fibropolycystic diseases
previous exposure Thorotrast (old biliary tree contrast)
opisthorchis sinesis (liver fluke)

48
Q

features of cholangiocarcinoma

A 
poor prognosis (median survival 6 months)
adenocarcinoma
49
Q

histo features of cholangiocarcinoma

A

pleomorphic- all cells look different

GIR Test 2 (20 decks)

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