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207 Cards in this Set
- Front
- Back
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dual blood supply of the liver
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hepatic artery from celiac
portal vein from GI |
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contents of each portal tract
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portal vein
hepatic artery bile duct |
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differentiate blood flow vs. bile flow liver
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blood flow - from portal tracts through sinusoids to the central vein
bile flow - opposite direction through bile canaliculi |
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3 zones of the liver
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zone 1 - immediately around the portal tract
zone 2 - midway zone 3 - immediately around the central vein |
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most metabolically active zone in the liver
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zone 3 - but gets blood last
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lymphocytes present exclusively in the portal tracts
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portal hepatitis
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lymphocytes in the hepatic parenchyma and do not involve the portal tract
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lobular hepatitis
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lymphocytes seen in both portal tracts and zone 1
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periportal/interface hepatitis
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associated with chronic active hepatitis and could end up in cirrhosis
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periportal/interface hepatitis
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differentiate cholestatic hepatitis and pure cholestasis
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pure cholestasis has no inflammation present
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differentiate fatty change and steatohepatitis
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steatohepatitis has inflammation present
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associations with steatohepatitis
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EtOH
DM Obesity Medications |
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Causes of zonal necrosis
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zone 3 - circulatory failure, drug reactions
zone 2 - yellow fever zone 1 - eclampsia |
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cause of focal nonzonal necrosis
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anemic infarcts
viral infections (hepatitis or herpes) |
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define cirrhosis
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extensive fibrosis
separated hepatic parenchyma into variable size nodules disrupted normal flow of blood leading to ascites and varices |
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type of focal necrosis in which dead hepatocyte is identifiable as shrunken, eosinophilic round body with variable nucleus, usually not accompanied by inflammation
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acidophil bodies
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intracytoplasmic inclusions of cytokeratin intermediate filaments that are PAS negative
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mallory bodies
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associated with mallory bodies
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alcoholic liver disease
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granules in the cytoplasm of hepatocytes that stain strongly with PAS stain
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alpha-1-antitrypsin globules
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associated with ground glass cells
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HbsAg of hepatitis B
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most common liver finding in newborns with any insult
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giant cells - hepatocytes with multiple nuclei scattered throughout the lobule
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nutmeg liver
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seen in persistent congestive heart failure, causes dilation of central vein and centrilobular atrophy
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benign tumor of hepatocytes occur exclusively in women of reproductive age
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hepatic adenoma
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hepatic tumor with no lobular pattern present (no portal tracts or central veins present)
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hepatic adenoma
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hepatic tumor with characteristic central scar and tortuous bile ducts and larger vessels
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focal nodular hyperplasia
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Kasabach-Meritt Syndrome
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hemangioma with thrombocytopenia that can cause DIC and bleed
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most common hepatic malignancy
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metastatic from somewhere else
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most common sites metastates to the liver
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GI system
breast lung |
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most common visceral malignant tumor in males worldwide - however relatively uncommon in US and Europe
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hepatocellular carcinoma
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Associated with Hepatocellular carcinoma
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Hep B and C
Afflatoxin (aspergillus) alcohol iron overload |
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associated with producing a-FP
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hepatocellular carcinoma
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malignant hepatic tumor found in younger people with better prognosis
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fibrolamellar hepatocellular carcinoma
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causes of cholangiocarcinoma
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Schistosoma
primary sclerosing cholangitis (associated with ulcerative colitis) |
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associated with jaundice and elevated direct bilirubin
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biliary obstruction
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gallstone ileus
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gall stone that is blocking ileocecal valve
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two general types of gallstones
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cholesterol
bilirubin pigment |
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associated with gallstones in a thickened contracted gallbladder
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chronic cholecystitis
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risk factor for bilirubin pigment stones
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chronic hemolysis: sickle cells anemia, thalassemia
any cause for unconjugated hyperbilirubinemia (breakdown of hemoglobin - heme is turned in unconjungated bilirubin) |
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gallbaldder adenocarcinoma
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poor prognosis
usually incurable |
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acute cholecystitis
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most associated with stones
inflammation of the gallbladder with neutrophils and lymphocytes bacterial infection and perforation are complications |
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3 signs that point toward illness relating to an intrahepatic process
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dark urine
light colored stools scleral icterus |
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LFTs (7)
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total protein
AST ALT ALP direct bilirubin albumin total bilirubin |
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two broad categories of hepatic disease
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cell necrosis - viral or alcoholic hepatitis
cholestasis - drugs, tumor, gallstones |
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indicates liver cell necrosis
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elevated ALT and AST
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indicates cholestasis
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elevated ALP
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elevation of this is more specific for liver disease
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ALT
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differentiate timeline of elevated AST and ALT between acute viral hepatitis and acute ischemic injury
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acute viral hepatitis - peak in 7 to 14 days
acute ischemic injury - levels increase abruptly |
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medications that can cause increased AST and ALT
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acetaminophen
NSAIDs antibiotics |
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indicates chronic liver disease rather than acute
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decreased albumin
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indicates acute liver disease
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increased PT time - decreased factors II, VII, and X
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factors associated with PT
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II, VII, and X
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where is ALP and GGT found
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biliary ductule cells
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differentiate sensitivity and specificity of ALP and GGT
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ALP - sensitive but no specific
GGT - both sensitive and specific |
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two false positive elevations of ALP
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third trimester of pregnancy
intestinal ALP increases in blood groups O and B after eating a fatty meal |
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increased ALP is seen without increase in GGT
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bone origin
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increased total protein with decreased albumin indicates what
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autoimmune disease
multiple myeloma (paraproteinemia) |
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what is the direct fraction of total bilirubin normally
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less than 20% of total normally
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two main functions of bile
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1. excretion of endogenous lipids
2. intestinal absorption of dietary lipids |
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bilirubin is a small part of bile (0.3%) with no known function
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**
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Can you find unconjucated bilirubin in the urine
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No, must be bound to albumin, not water soluble
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what conjucates bilirubin
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UDP-glucuronyltransferase
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what two diseases cause more increased unconjucated bilirubin to conjucated
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hemolytic anemia
Gilbert's disease |
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why does energy deprivation cause increased direct bilirubin
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because secretion of conjucated bilirubin into the bile is an active process - it's the first thing lost
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most common form of intrahepatic cholestasis
cause |
canalicular cholestasis
steroid hormones, acute viral or alcoholic hepatitis |
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associated with striking elevations of ALP with little or no increase in bilirubin
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space occupying lesions intrahepatically
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two examples of extrahepatic cholestasis
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carcinoma of bile ducts
choledocolithiasis |
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where is the majority of urobilinogens and unconjucated bilirubin excreted
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feces (<90%)
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what causes increase urobilinogen in the urine without increased bilirubin
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hemolytic anemia
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what is more common, increased unconjugated bilirubin or increased conjugated
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increased conjugated is more common
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what causes increased levels of unconjugated
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problems early on in the process of bilirubin metabolism: hemolysis, RHF, conjugation abnormalities (Gilbert's syndrome, Crigler-Najjar syndrome)
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what does parenchymal liver disease (necrotic or cholestatic) do to bilirubin
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causes increased conjugated levels via decreased secretion or stopping biliary flow
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differentiate acute viral hepatitis and acute alcoholic hepatitis
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both have increased AST and ALT with little increase in ALP, however the AST/ALT ratio is < 1 in viral hepatitis while it's > 2 in acute alcoholic hepatitis
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Diseases associated with increased ALP
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diffuse or focal intrahepatic cholestasis
extrahepatic obstruction |
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what is the AST/ALT ratio seen in cholestatic diseases
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AST/ALT = 1
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how would you distinguish NASH (nonalcoholic steatohepatitis) from acute viral hepatitis since both have increased AST and ALT with a ratio of AST/ALT < 1
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acute viral hepatitis have much higher levels of AST and ALT than NASH
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ALP predominance over ALT and AST accompanied by normal bilirubin points to what disease
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focal intrahepatic disease
*if accompanied by increased total and direct bilirubin, this means extrahepatic obstruction or diffuse intrahepatic cholestasis |
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what is the total bilirubin levels in hemolysis
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< 6 mg/dL
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what ratio of direct/total bilirubin points to hemolysis or Gilbert's disease
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< 15%
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differentiate causes of increased total bilirubin above and below 25 mg/dL
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> 25 mg/dL = cell necrosis
< 25 mg/dL = cholestasis |
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what are good indicators for the severity of liver disease
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albumin levels
PT level |
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differentiate ability of albumin and PT to predict whether liver disease is chronic or acute
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acute = PT
chronic = albumin |
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what do markedly elevated levels of AST and ALT (greater than 100 times normal) indicate
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toxic or ischemic hepatitis
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the higher the ratio of ALT/ALP more likely indicates what
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acute hepatic necrosis
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what does a proof equal
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1/2 of the percentage of alcohol
200 proof = 100% |
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relevant amounts of alcohol comparing beer, wine, and liquor
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12 oz. of beer
6 oz. of wine 1 oz. in liquor |
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what makes an alcoholic drink smell
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cogeners
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medicinal purpose of ethanol
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acute methanol poisoning
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Effects of alcohol:
GI CNS Liver Pancreas Cardiovascular Endocrine |
GI - irritant, superficial ulcerations
CNS - depressant Liver - cellular dysfunction (increased levels of GGT) Pancreas - acute and chronic pancreatitis Cardiovascular - congestive cardiomyopathy, can increase HDL levels Endocrine - testicular atrophy |
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tumors associated with ethanol
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malignant tumors of the oropharynx
hepatocellular carcinoma associated with cirrhosis |
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Too small, too short, too smooth
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fetal alcohol syndrome:
microcephaly, short palpebral fissures, maxillary hypoplasia, short nose, smooth philtrum and upper lip |
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three liver abnormalities associated with alcohol
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fatty liver
alcoholic hepatitis cirrhosis |
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other causes of fatty liver (steatosis)
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obesity
diabetes kwashiorkor (protein deficiency) prolonged steroid usage |
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does fatty liver change clear is drinking is stopped
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Yes, usually clears totally in weeks to months
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when is alcoholic hepatitis
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frequently after drinking binge
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Histology seen in alcoholic hepatitis
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centrilobular hepatocellular necrosis
ballooning degeneration of hepatocytes mallory bodies collagen deposition |
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where is the collagen deposition seen in alcoholic hepatitis
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perivenular, if severe may lead to portal hypertension without cirrhosis
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other conditions that cause patterns similar to alcoholic hepatitis
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Wilson's disease
diabetes NASH (nonalcoholic steatohepatitis) |
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70% of cirrhosis in the U.S. is caused by what
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alcohol
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what usually precedes cirrhosis
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bouts of alcoholic hepatitis with perivenular fibrosis that resulted from fatty liver
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what causes death in alcoholics with cirrhosis
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hepatic coma - toxins are shunted to the brain instead being metabolized in the liver
GI bleed - esophageal varicies |
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why are women more affected by alcohol than men
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1. less water distribution because increased % body fat
2. less alcohol dehydrogenase found in their stomach |
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what reaction does disulfiram block
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conversion of acetaldehyde to acetyl-CoA
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two different drug interactions associated with ethanol
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1. increases metabolism of other drugs (CYP450 inducers)
2. competitively inhibit the metabolism of other drugs |
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gram% of alcohol that cause:
50% of adults to be intoxicated stupor increased risk of death |
intoxications = 0.15%
stupor = 0.30% death = 0.40% |
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what viral hepatitis have lipid capsules
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HBV
HCV HDV |
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which viral hepatitis has dsDNA
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HBV
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what is the transmission mechanism of HAV and HEV
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fecal-oral route
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why are HAV and HEV no rapidly inactived by bile like HBV, HCV, and HDV
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because they lack a lipid capsule
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viral hepatitis that are associated with chronic hepatitis
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HBV, HCV, and HDV
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which two viral hepatitis' may ultimately lead to the development of hepatocellular carcinoma
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HBV and HCV
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which viral hepatitis is associated with the picronavirus family
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HAV
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how long does it take for viral antibodies to develop against hepatitis
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several weeks
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Lab findings associated with viral hepatitis
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increased ALT
increased total and direct bilirubin small increase in ALP |
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differentiate Anti-viral hepatitis antibodies IgG vs. IgM
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IgM - acute infection
IgG - lifelong immunity |
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what are the different antigens of HBV
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HBsAg
HBcAg HBeAg |
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what are the two circulating forms of HBsAg
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viral particle-bound protein
free noninfectious protein (22 nm spherical and tubular particles) |
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Does detection of HBsAg in serum alone imply infectivity
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No, because HBsAg may exist in blood as free form that are noninfectious
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what are two useful markers for detecting viral replication by HBV
what is the most accurate of the two |
HBeAg
HBcAg - most accurate |
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what are the major vectors for transmission of HBV
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IV drugs
sexual transmission vertical transmission maternal/infant |
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when is maternal transmission to fetus inevitable
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if mother is both HBsAg and HBeAg positive
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what are common extrahepatic features of HBV
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immune complex nephritis
arthritis |
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Do most adults develop chronic HBV and eventually cirrhosis or hepatocellular carcinoma
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No, 5% become chronically infected and < 1% develop cirrhosis/hepatocellular carcinoma
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what causes mortality and necrosis of hepatocytes in person with HBV
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host's immune attack on HBV-infected hepatocytes
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detection of what in the serum indicates presence of eradication of HBV infection
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anti-HBsAg
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what is the most likely caused for immune complex nephritis and arthritis in person with HBV infection
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anti-HBcAg - there is way too much made and does nothing
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serum antigens and antibodies detected in a patient with early acute HBV infection
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positive HBsAg
negative Anti-HBsAg negative Anti-HBcAg |
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serum antigens and antibodies detected in a patient with previous HBV infection
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Negative HBsAg
positive Anti-HBsAg positive Anti-HBcAg |
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serum antigens and antibodies detected in a patient with a vaccine against HBV
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Negative HBsAg
Positive Anti-HBsAg Negative Anti-HBcAg |
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when would a patient have no serum antigen and antibody for HBsAg, but show Anti-HBcAg
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during the window phase when anti-HBsAg and HBsAg are in 1:1 ratio with each other
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what is the most common vector for HCV
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blood transfusion associated
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what are the hallmarks of an HCV infection
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persistent, chronic hepatitis infection
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do the majority of patients with chronic hepatitis from HCV infection get cirrhosis and/or hepatocellular carcinoma
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No, 80% have chronic hepatitis while 20% get cirrhosis and hepatocellular carcinoma
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Therapy for HCV
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a-IFN effective in less than one-half of infected patients - NO VACCINE available
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most common HCV
what is it associated with |
genotype 1
associated with a lower response to antiviral therapy |
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which hepatitis virus depends on HBV as a helper for propagation
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HDV
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differentiate coinfection and superinfection of HDV
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coinfection - simultaneous exposure of HBV and HDV (patient has not been previously infected with HBV)
superinfection - chronically infected with HBV then is infected with HDV |
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what infections is associated with increased likelihood of fulminant hepatitis
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coinfection of HBV and HDV
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what should be expected when a patient with chronic HBV infection has acute exacerbation
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suspect superinfection with HDV
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more likely associated with fulminant liver failure than just hospitalization with jaundice
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xenobiotic-infduced liver toxicity
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where are cytochrome P450 enzymes in greatest concentrations
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central vein (centrilobular hepatocyte)
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two broad classes of xenobiotic-induced liver disease
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intrinsic
idiosyncratic |
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differentiate intrinsic vs. idiosyncratic xenobiotic-induced liver disease
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intrinsic (phase I bioactivates - cytochrom P450) is predictable, dose-dependent and has zonal necrosis
idiosyncratic (immune reaction) - diffuse necrosis, inflammation with signs of hypersensitivity |
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Are most xenobiotic-induced liver injury reversible
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Yes, must recognize and remove offending agent
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drug associated with zonal necrosis
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acetaminophen
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drugs associated with toxic hepatitis via hapten formation
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INH
phenytoin sulfonamides |
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drugs associated with microvesicular and macrovesicular steatosis
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micro - aspirin
macro - ethanol |
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why does aspirin cause microvascular steatosis
|
cause deficient B-oxidation of fatty acids
*leads to hyperammonemia via inhibition of ureagenesis |
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drug associated with canlicular cholestasis
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steroid hormones
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why does ethanol cause macrovesicular steatosis
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increased TG synthesis with decreased exit from liver
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what leads to hyperammonemia via inhibition of ureagenesis
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aspirin due inhibition of B-oxidation of fatty acids
decreased ATP for ureagenesis |
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two mechanisms of cholestasis
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1. actual damage to bile canaliculi
2. change in fluidity and Na/K ATPase via steroid hormones |
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cirrhosis associated with autoimmune T-cell mediated disease of intrahepatic bile ducts
|
primary biliary cirrhosis
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when does secondary biliary cirrhosis occur
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secondary to longstanding extrahepatic bile duct obstruction
|
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laboratory findings in primary biliary cirrhosis
|
elevated ALP and GGT with minimally elevated ALT and AST
|
|
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antimitochondrial antibodies
|
primary biliary cirrhosis
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what are the antibodies against in primary biliary cirrhosis
|
E2 antibodies to mitochondrial pyruvate dehydrogenase
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what is a chronic inflammatory and fibrosing disorder that involves both extrahepatic and intrahepatic biliary ductal system
|
primary sclerosing cholangitis
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what is strongly associated with primary sclerosing cholangitis
|
coexistent inflammatory bowl disease (specifically chronic ulcerative colitis)
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associated with a beaded appearance of biliary ducts with multiple strictured and normal segments
|
primary sclerosing cholangitis
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what is the genetic background of hemochromatosis
|
associated with HLA-H
autosomal recessive on chromosome 6 |
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differentiate hemochromatosis vs. hemosiderosis
|
hemochromoatosis - idiopathic abnormal regulation of intestinal iron absorption
hemosiderosis - secondary form of iron overload due to too many transfusions |
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places with the highest accumulation of iron in hemochromatosis
|
pancreas and liver - heaviest
myocardium endocrine glands synovial linings |
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heterozygote for hemochromatosis
|
no organ damage, but could have abnormal serum transferrin saturation and ferritin
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effective tests to determine hemochromatosis
|
serum transferrin saturation
ferritin gene identification if elevated |
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inborn error of copper metabolism causing increased store through the body
|
Wilson's disease
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|
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Pathophysiology of Wilson's disease
|
increased body stores of copper due to decreased excretion of copper into bile - accumulates in lysosomes within hepatocytes and spills into other organs over time
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two disease that can see Kayser-Fleischer ring
|
Wilson's disease - most important
May see in primary biliary cirrhosis |
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where is the copper deposition in a Kayser-Fleischer ring
|
Descemet's membrane
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|
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laboratory findings in patient with Wilson's disease
|
serum ceruloplasmin levels blow 20 mg/dL - not diagnostic alone however
|
|
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what does decreased serum ceruloplamin indicate
|
increased copper stores because there is decreased in blood
|
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two diseases associated with a1-antitrypsin deficiency
|
emphysema
neonatal hepatitis |
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what are two phenotypes for a1-antitrypsin deficiency
|
PiMM - most common (normal)
PiZZ - homozygous have highest risk for developing clinical disease |
|
|
hepatitis associated with PAS positive granules that are resistant to diastase
|
a1-antitrypsin deficiency
|
|
|
thrombotic occlusion of major hepatic veins
|
Budd-Chiari syndrome
|
|
|
Who is associated with Budd-Chiari syndrome
|
women taking oral contraceptives
pregnant or recently delivered Factor V Leiden Protein C deficiency |
|
|
nonthrombotic, most likely fibrotic process that obliterates centrilobular veins of the liver
|
veno-occlusive disease
|
|
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causes of veno-occlusive disease
|
plant alkaloids
high dose hepatic radiation |
|
|
Child with acute encephalopathy, fatty infiltration of the liver, who is recovering from viral illness most likely took what medication
|
aspirin
|
|
|
4 causes for NASH (nonalcoholic steatohepatitis)
|
1. hyperlipidemia
2. hypertension 3. CAD 4. DM |
|
|
Can a person with fatty liver because they are obese develop cirrhosis
|
Yes - 15% of patients with fatty liver can progress to cirrhosis, no matter the cause
|
|
|
Pathological findings found in NASH
|
macrovesicular fat
portal and lobular inflammation Mallory's hyaline fibrosis **closely resembles alcoholic liver disease |
|
|
associated with periportal hepatitis due to increased plasmocytes and autoantibodies in the serum
|
autoimmune hepatitis
|
|
|
4 main causes of cirrhosis
|
*alcohol abuse
*chronic hepatitis biliary disease iron overload |
|
|
major source of most of the ECM that accumulate during cirrhosis and cause disruption of normal liver architecture resulting in decreased blood flow
|
stellate cell
|
|
|
normal function of stellate cell
what happens during cirrhosis |
normally - storage site for vitamine A
cirrhosis - transforms to myofibroblast |
|
|
6 major cardinal manifestations of liver failure
|
ascites
encephalopathy portal HTN hepatorenal syndrome hepato-pulmonary syndrome endocrine disturbances |
|
|
most common cause of ascites
|
cirrhosis
|
|
|
differentiate causes for ascites when transudation vs. exudation is found within fluid
|
transudation - cirrhosis, hepatocellular carcinoma, and HF
exudation - peritoneal carcinomas, TB peritonitis |
|
|
serum-ascitic albumin gradient of 11 g/L of greater
|
associated with portal HTN
|
|
|
flapping tremor of the hands associated with hepatic encephalopathy
|
asterixis
|
|
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what is increased in hepatic encephalopathy
|
ammonia concentration
|
|
|
endocrine dysfunctions associated with liver failure
|
abnormal glucose intolerance
increased aldosterone cushingoid features hypogonadism |
|
|
why is AST more elevated than ALT in alcoholic liver disease
|
because alcohol is a mitochondrial toxin , ALT is confined to the cytoplasm unlike AST
|
|
|
two exceptions in which AST is higher than ALT
|
Alcoholic injury
Reye's syndrome |
|
|
what does elevated ALP and GGT indicate
|
problem with bile flow
|
|
|
what breaks down unconjugated to conjugated bilirubin
|
bacterial B-glucuronidases found in the colon
|
|
|
fibrosis seen in portal HTN
|
bridging between centrilobular areas
|
|
|
fibrosis seen in PBC and chronic biliary obstruction
|
fibrosis connecting portal areas - around in a circle
|
|
|
fibrosis seen in alcoholic cirrhosis
|
fibrosis connecting both portal and centrilobular areas
|
|
|
what causes itching in pruritis
|
increased direct bilirubin
|
|
|
patients presents with painless jaundice
|
adenocarcinoma of head of pancreas
|
|
|
dubin johnson syndrome
|
inability to excrete conjugated bilirubin from the liver
|
|
|
associated with councilman bodies and numerous lymphocytes
|
viral hepatitis
*also seen in autoimmune and toxic hepatitis as well |
|
|
where are lymphocytes seen in viral, autoimmune, or toxic hepatitis
|
periportal area
|
|
|
where are lymphocytes seen in PBC
|
portal ducts
|
|
|
associated with neutrophils infiltrating the bile ducts
|
acute bile duct obstruction
|
|
|
differentiate micronodular and macronodular cirrhosis
|
micronodular - alcohol, hemachromatosis (cell death around the portal areas)
macronodular - viral hepatitis, autoimmune, toxic |
