Pathology Flashcards
covering of the liver
- Glisson’s capsule
- thin layer of connective tissue
production of coagulation factor 8
- endothelial lining
what ducts join to form the common bile duct
- cystic duct and common hepatic duct
major site of production of RBCs in fetuses
- liver
falciform ligament
- separates right and left lobes
blood supply to the liver
- portal vein (70-80%)
- hepatic artery (20-30%), comes from celiac artery
porta hepatis
- exit port of the common hepatic duct
- entry port of the hepatic artery and exit port of portal vein
blood and bile flow
- opposite directions
shape and function of liver lobule
- hexagonal
- blood flow and synthetic function
shape and function of portal lobule
- triangular
- bile synthesis and excretion
shape and function of hepatic acinus
- diamond shaped
- blood flow and disease
zones of hepatic acinus
- zone 1 is best oxygenated but first to see toxins
- zone 3 is least oxygenated and last to see toxins
definition of portal lobule
- the area from which bile flows to one branch of the bile duct
function of hepatocytes
- absorption
- secretion
- production of bile
- storage of excess carbohydrate as glycogen
function of Kupffer cells
- filtration of the portal blood through phagocytosis of old RBCs and bacteria
- secrete growth factors
function of Ito or stellate cells
- store vitamin A
- synthesize hepatic growth factor
- produce extracellular matrix
- formation of fibrosis during cirrhosis
5 responses of the liver to injurious events
- degeneration and intracellular accumulation
- necrosis and apoptosis
- inflammation
- regeneration
- fibrosis
centrilobular necrosis
- characteristic of ischemic injury
midzonal and periportal necrosis
- eclampsia and autoimmune hepatitis
councilman bodies
- fragmented nuclei of apoptotic cells
structure of gallbladder
- lacks a muscularis mucosa and submucosa
spiral valves of Heister
- folds coalesce in the neck of the gallbladder and extend into the cystic duct
focal or spotty necrosis
- limited to scattered cells within hepatic lobules
interface hepatitis
- limited to the interface between the periportal parenchyma and inflamed portal tracts
bridging necrosis
- more severe inflammatory injury involving contiguous hepatocytes
- may span adjacent lobules in portal-to-portal, portal-to-central, or central-to-central fashion
submassive necrosis
- involving entire lobules
massive necrosis
- involving most of the liver parenchyma
regeneration
- when hepatocellular necrosis occurs and connective tissue framework remains intact, almost perfect restitution of liver structure can occur
fibrosis
- generally irreversible hepatic damage
apoptosis
- cells condense and fragment are phagocytized by histiocytes
- NO inflammatory reaction
- apoptotic cells are called councilman bodies
causes of microvesicular fat in the liver
- Reyes syndrome
- fatty liver of pregnancy
- tetracycline or valproic acid toxicity
- nucleoside analogues in HIV
processes of hepatic inflammation
- inflammatory cell infiltration with lymphocytes, monocytes, neutrophils, eosinophils and plasma cells
- Kupffer cell hyperplasia
- binucleate cells (regeneration)
- de-glycogenation
PE findings of cirrhosis
- spider angiomata, palmar erythema, nail changes, clubbing, hypertrophic osteoarthropathy
- Dupurtrens contracture, gynecomastia
- testicular atrophy, ascites, hepatgomegaly, caput medusa, fetor hepaticus, asterixis
lab studies during cirrhosis
- AST higher than ALT
- globulins increased
- alkaline phosphatase increased
hep A lab values
- serum IgM - acute phase
- serum IgG - immunity, persists for life
- high serum bilirubin levels
extrahepatic involvement of hep A
- arthritis, oliguria, urticaria, vasculitis
- rare
high viral DNA, HBsAg+, HBeAg+
- highest probability to develop cirrhosis and HCC
low viral DNA, HBsAg +, HBeAg - and Anti HE +
- does not produce cirrhosis but may generate HCC
essential cryoglobulinemia
- seen with HCV
- purpura, arthralgia, and weakness
immune complex disease associated with HBV
- polyarteritis nodosa
- glomerulonephritis
porphyria cutanea tarda
- associated with HCV
- blisters usually on the hands
macrovesicular alcoholic steatosis
- presence of large fat droplets in hepatocytes
- nuclei are in peripheral location
- 65% of chronic heavy drinkers develop this type
- perivenular central zone is initially involved
- best method to demonstrate fat is osmium tetroxide
microvesicular alcoholic steatosis (foamy steatosis)
- hepatocytes have small fat droplets throughout the cytoplasm
- nuclei are centrally located
- no Mallory bodies are seen
- jaundice and elevation of alkaline phosphatase are seen but no fever or leukocytosis like in alcoholic hepatitis
alcoholic hepatitis
- most useful test is GGT
- necrosis and inflammation is in centrolobular area
- Mallory bodies present
- “chicken wire” fibrosis
alcoholic siderosis
- increased stainable iron
- synergy with hemochromatosis
Aflatoxin B
- mold foods
- causes jaundice, fatty liver, Reyes, HCC, and phlebitis
Amanita phalloides
- mushrooms
- centrolobular and massive necrosis
lead poisoning
- nuclear inclusions
- steatosis and hepatitis
drug induced hepatitis
- indistinguishable from viral hepatitis
- most often causes from oral contraceptives and anabolic steroids
- presence of non-caseating granulomas
autoimmune hepatitis
- female predominance
- absence of viral serologic markers
- elevated serum IgG levels
- high serum levels of autoantibodies (ANA, SMA, LKM)
- rosetting or piecemeal necrosis of hepatocytes
- should have good response to steroids with or without azathioprine
gene associated with hemochromatosis
- HFE gene (C282Y, H63D)
hemochromatosis
- increased intestinal iron absorption causing excessive deposition in tissues
- “bronze diabetes”
screening for hemochromatosis
- ferritin levels >200 in men and >150 in women
- iron saturation >45-60
- hepatic iron index (HII) of 1.9 consistent with disease
treatment of hemochromatosis
- phlebotomy
presentation of alpha 1-antitrypsin deficiency
- accumulated AAT appears as inclusions within hepatocytes that stain positively with PAS reagent but resist digestion by diastase
- PAS (+), diastase (-)
function of AAT
- proteolytic enzyme of elastase
Wilsons disease
- defect of cellular copper export
- Kayser-Fleischer ring
- accumulation of copper in liver, brain and other tissues
lab findings in Wilsons
- decreased serum ceruloplasmin
- elevated 24 hour urinary copper excretion
- elevated quantitative hepatic copper
treatment of Wilsons
- copper chelators
- D-penicillamine
- Budd-Chiara syndrome
- hypercoaguable state
- occlusion of main hepatic veins
- usually a sudden thrombotic accident or slow fibrous occlusion
- dilated sinusoids will have lysed RBCs are difference with passive congestion due to heart failure
- if occlusion is sudden and massive: sudden massive ascites, ab pain, liver failure in a few days
Veno-occlusive disesae of small intrahepatic veins
- concentric occlusion of the affected veins by loose connective tissue
Gilberts
- unconjugated hyperbilirubinemia
- mild deficiency of glucuronyl transferase
- does not cause problems
Crigler Najjar, type 1
- severe deficiency of glucuronyl transferase
- death within 1-2 years with kernicterus
- unconjugated bilirubinemina
Crigler Najjar, type 2
- moderate deficiency of glucuronyl transferase
- normal development but may suffer bilirubin encephalopathy, kernicterus
- unconjugated bilirubinemina
Dubin-Johnson
- no pruritis or elevation of serum alkaline phosphatase, liver is black but normal
- chronic benign jaundice
- conjugated hyperbilirubinemia
Familial Recurrent Intrahepatic Cholestasis of Pregnancy
- occurs during 3rd trimester
- safe for the mother but not the fetus
- premature births and stillbirths due to placental infarcts
- Sometimes the disorder manifests itself only with presence of pruritus without jaundice (Pruritus gravidarum)
pathogenesis of primary biliary cirrhosis
- ongoing immunologic attack on the intralobular bile ducts that eventually leads to cirrhosis and liver failure
- T lymphocyte mediated
- primarily affects women
- Antimitochondrial antibodies (AMA) are normally found
symptoms of PBC
- epithelial damage, granuloma formation
- bile duct atrophy, periductal hepatitis
treatment for PBC
- ursodeoxycholic acid
primary sclerosing cholangitis
- chronic cholestatic disease
- can lead to end stage liver disease
- progressive inflammation, fibrosis and stricturing of the intrahepatic and extrahepatic bile ducts
- beaded appearance
- ANA, SMA, P-ANCA in 75% of patients
associations with PSC
- 90% of patients also have UC
- 70% of patients are men
treatment of PSC
- ursodeoxychoic acid and liver transplant
Klatskin tumor
- Tumor arising from common bile duct between cystic duct and right and left hepatic ducts
