Wk5 Liver Path pt2 Flashcards
early EtOH abuse
enlarged, lipid filled liver
How does it look microscopically?
Alcoholic steatosis–fatty liver
large lipid vacuoles
**reverses with abstinence
Alcoholic hepatitis = steatosis + ?
hepatocyte injury and/or inflammation
“steatohepatitis”
Cytokeratin aggregates in hepatocytes:
Associated with?
Mallory bodies
Alcoholic hepatitis
Usually seen surrounding Mallory bodies:
neutrophilic inflammation
Alcoholic hepatitis occurrence
pre-cursor to cirrhosis
steatofibrosis
**perivenular and pericellular
Grossly: fibrosis + nodules
cirrhosis
Liver in early stages of alcoholic cirrhosis
enlarged
fatty
micronudular (less 3 mm)
Liver in late stages of alcoholic cirrhosis:
shrunken
non-fatty
variable nodule size
cholestasis usually present
5 major causes of death from alcoholic liver disease:
- hepatic encephalopathy and coma
- Massive GI tract hemorrhage (esophageal varicies)
- infx
- hepatorenal syndrome
- hepatocellular carcinoma
NAFLD?
Patient profile?
Non-alcoholic fatty liver disease
- metabolic syndrome
- obesity
- DM2
- dyslipidemia
- insulin resistance
autoimmune cholangiopathy
progressive destruction of small and medium sized INTRAhepatic bile ducts
extrahepatic ducts are spared
middle age females
Primary biliary cirrhosis
AMA (antimitochondrial antibodies)
associated with other autoimmune disorders
Primary biliary cirrhosis
fatigue
anicteric pruritis
xanthomas
steatorrhea
vit D malabsorption
Primary biliary cirrhosis
Tx for PBC:
urodeoxycholic acid
liver transplant
Dx of PBC:
liver biopsy
Damage due to prolonged EXTRAhepatic bile duct obstruction
Secondary biliary cirrhosis
progressive
RANDOM
autoimmune
uneven fibroinflammatory
extra/intrahepatic bile ducts
Primary sclerosing cholangitis (PSC)
pANCA
IBD association
Primary sclerosing cholangitis
“beaded” appearance on cholangiogram
PSC
primary sclerosing cholangitis
disorders of excessive iron absorption resulting in accumulation of iron in tissues producing organ injury
hemochromotosis
Inheritance pattern of primary hemochromotosis
autosomal recessive
Liver protein decreased in hemochromotosis
hepcidin –> excessive intestinal iron absorption
Most common genetic mutation in hereditary hemochromotosis
HFE – chromosome 6
C282Y – 80% of cases in adults
**most common in male of northern european descent
low penetrance so not all homozygotes express disease
Causes of secondary hemochromotosis
parenteral Fe overloads (transfusions)
ineffective erythropoesis –> increased Fe absorption
-(B-thalassemis, sideroblastic anemia)
increased oral intake of Fe
Chronic EtOH liver disease
Reread slide 42
distribution of excess Fe
Early pathological finding of primary hemochromotosis:
periPORTAL iron deposits in hepatocytes
Early pathological finding of secondary hemochromotosis (different from primary):
Fe accumulates in Kupffer cells not hepatocytes
Classic triad for hemochromotosis presentation:
- cirrhosis
- diabete
- skin pigmentation
“Bronze diabetes”
**also may see sx in other organ systems (heart, joints, etc.)