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GI & Liver > Path: biliary tract diseases > Flashcards

Path: biliary tract diseases Flashcards

1
Q

Types of biliary tract diseases

A
  • Extrahepatic (CBD) bile duct obstruction: most common
  • Primary biliary cirrhosis (PBC)
  • Primary sclerosing cholangitis (PSC)
  • Gallbladder: cholelithiasis, acute and chronic cholecystitis
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2
Q

Extrahepatic bile duct obstruction etiologies

A
  • Acute: choledocholithiasis, acute pancreatitis, acute stricture of CBD, masses (CCA, pancreatic CA)
  • Chronic: long term strictures (chronic pancreatitis), extra hepatic biliary atresia (neonates), parasitic infections
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3
Q

Presentation and path of extra hepatic bile duct obstruction 1

A
  • Ab pain (often RUQ/epi)
  • Fever and leukocytosis (cholangitis), Jaundice
  • AST/ALT 100-200 (<300), markedly elevated AP
  • Path: bile duct dilation (should be no space w/in duct) and periductal edema (if acute)
  • If acute cholangitis (bacterial superinfection on CBD obstruction): PMNs w/in the lumen of the duct and invading the the basement membrane, along w/ preductal PMNs
  • Possible to see micro abscesses around portal tracts, cholestasis
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4
Q

Presentation and path of extra hepatic bile duct obstruction 2

A
  • Bile duct infarcts (feathery degeneration) and bile lakes are rare (seen in later stages), but are diagnostic for extra hepatic bile duct obstruction
  • Eventually there can be bile duct proliferation, mallory bodies in periportal hepatocytes (during chronic)
  • There may be fibrosis around portal tracts if chronic obstruction, along w/ a mixed (lymphocyte and PMN) inflammation
  • Periductal fibrosis occurs over months, w/ secondary biliary cirrhosis (all cirrhosis looks the same) occurring over years in adults (6 mo for children)
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5
Q

Rx of extra hepatic bile duct obstruction

A
  • ERCP for obstruction in CBD (i.e. stone, stricture), removal of tumor
  • Antibios for the causative organisms (E Coli, klebsiella)
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6
Q

PBC 1

A
  • Chronic, slowly progressive cholestatic liver disease characterized by non-suppurative (mono inflammation) destruction of bile ducts w/ progression to biliary cirrhosis (and portal HTN)
  • Occurs in middle aged women (30-70)
  • There is insidious onset of pruritus, darkening of skin and eventually jaundice
  • Malabsorption eventually occurs due to lack of bile (ADEK def)
  • ERCP is nl in PBC b/c there is only inflammation of small intrahepatic bile ducts, large bile ducts not affected
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7
Q

PBC 2

A
  • Can also present w/ hepatomegaly, splenomegaly, or ASx
  • Labs: AP generally >3x nl, AST/ALT slightly elevated, bili starts nl but becomes greatly elevated if disease progresses
  • There is selective IgM elevation (high total protein, nl albumin), hypercholesterolemia, INR nl
  • AutoAb: antimito Ab (AMA M2) almost always positive and is diagnostic
  • Strong association w/ other autoimmune d/os e.g. Sjogren syndrome (dry mouth dry eyes, autoimmune)
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8
Q

PBC pathology

A
  • T cells target duct epithelium, unclear how AMA plays a role
  • Early on there is infiltration of lymphocytes thru BM and in btwn epithelial cells (non-suppurative destruction)
  • Biliary fibrosis occurs w/ cholangiocyte proliferation and mild portal fibrosis, granulomas may be seen
  • Can lead to piecemeal necrosis: periportal inflammation and destruction of periportal hepatocytes (looks similar to autoimmune/viral hepatitis)
  • As fibrosis continues there is portal-portal bridging fibrosis w/ decreased bile ducts
  • Biliary cirrhosis develops, may see mallory bodies
  • PBC cirrhosis can transform into HCC
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9
Q

Rx of PBC

A
  • Immunosuppression: steroids, AZP/6MP
  • Cholestyramine to Rx pruritus (prevents reabsorption of bile)
  • Urosdeoxycholic acid (UDCA): can help dissolve gallstones/thin bile
  • Only cure is Tx
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10
Q

PSC 1

A
  • Chronic cholestatic liver disease characterized by diffuse fibrosis obliterative cholangitis and inflammation of both intra and extra hepatic bile ducts
  • Predominantly in young-middle age males (around 40)
  • Variable course but usually progressive to biliary cirrhosis and portal HTN
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11
Q

PSC 2

A
  • Usually associated w/ UC, common to have p-ANCA + (p-ANCA + seen in UC)
  • Some are Asx, but common Sxs include pruritus, jaundice, hepatomegaly, splenomegaly, recurrent bouts of colangitis, eventually to cirrhosis in many pts
  • The predicate fibrosis seen can lead to multiple strictures along the biliary tree
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12
Q

PSC associated diseases

A
  • Strongest association (75%) w/ UC
  • Other autoimmune d/os: sjogren’s, AIH, RA, vasculitis
  • Pathophys: genetic predisposition, possible acute insult to biliary tree (viral/bacterial infection, toxins, ischemia) and may alter bile ducts, marking them as foreign
  • Followed by T cell attack
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13
Q

Lab data for PSC

A
  • AP greatly elevated (>3x nl)
  • Slightly abnormal AST/ALT
  • Elevated bili
  • Positive p-ANCA in 75%
  • AMA NEGATIVE
  • Must do radiographic procedure (ERCP, MRCP) to identify strictures/dilations (beading of bile ducts)
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14
Q

PSC path

A
  • Both large and small ducts show periductal fibrosis w/ surrounding lymphocytic infiltrates (onion skinning)
  • There can be variable stages of duct proliferation
  • Eventually the lumens become obliterated from the huge amounts of fibrosis
  • Progression w/ disease generally correlates to decreased number of ducts, w/ cirrhosis often showing no ducts at all
  • Possible to see mallory bodies
  • Cirrhosis occurs usually 3-5 yrs
  • CCA is a possible complication of PSC
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15
Q

Rx of PSC

A
  • Cholestyramine for pruritus
  • UDCA for gallstone dissolution
  • Immunosuppression
  • ERCP for stenting
  • Tx
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16
Q

Gallbladder 1

A
  • Cholelithiasis: stones often ASx, intermittent pain due to transient impaction in GB neck or CD
  • Sxs of this include: colicky pain, N/V, no fevers/chills
  • Acute cholecystitis: persistent impaction of stone in CD
  • Sx: ab pain + guarding, may have palpable GB, low fever
  • Usually resolves, but complications can occur: jaundice, high fever, leukocytosis, ascending cholangitis, acute pancreatitis, rupture, chronic cholecystitis (ASx or repeated bouts of colic, can lose GB function)
  • Chronic cholecystitis histopath: thick muscle bundles w/ variable chronic inflammation, rokitansky-aschoff sinus formation (glands forming under mucosa, looks like adenoCA but is not)
17
Q

Gallbladder 2

A
  • Rarely chronic cholecystitis can transform into adenoCA (usually only if calcified)
  • Choledocholithiasis: obstructive jaundice (very high bili, AP) from obstruction in CBD usually complicated by infection w/ GN bacteria (E coli, klebsiella)
  • Usually from stones, can also be from pancreatitis, tumors
  • Sx: fever, chills (bacteremia common), RUQ pain, leukocytosis, blood Cx positive
  • If stone is obstructing pancreatic duct outflow, can lead to pancreatitis

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