Pathoma Exocrine pancreas, gallbladder, liver Flashcards
acute pancreatitis pathophysiology
autodigestion of pancreas by its own enzymes to pre-activation of enzymes by trypsin.
types of nectosis in pancreatitis
- liquefactive necrosis of the pancreas itself
- fat necrosis of the peripancreatic fat
alcoholic pancreatitis pathophysiology
- alcohol causes contraction of the sphincter of oddi
Common causes of acute pancreatitis and other causes of acute pancreatitis
common: alcohol and gallstones
other:
- scorpion bite
- hypercalcemia, hypelipidemia
- drugs
- mumps
- rupture of posterior duodenal ulcer
- trauma
clinical features of pancreatitis
epigastric pain radiating to the back
nausea/vomiting
periumbilical/flank hemorrhage
elevation of serum lipase and amylase
–> lipase more specific, could also be from the salivary gland
hypocalcemia
–> calcium taken up as part of fat necrosis, saponification
clinical features of chronic pancreatitis
epigastric pain radiating to the back pancreatic insufficiency fat soluble vitamin deficiency secondary diabetes dystrophic calcification of the pancreas increased risk of pancreatic carcinoma
pancreatic carcinoma
cell of origin
major risk factors
clinical presentation
adenomcarcinoma arising from the pancreatic ducts.
major risk factors - smoking and chronic pancreatitis
obstructive jaundice and pale stools
palpable gall bladder
double duct sign on imaging
CAN PRESENT WITH SECONDARY DIABETES if the tumor is in the body or tail due to destruction of pancreatic islet cells.
additionally signs/symptoms
- migratory thrombophlebitis
- CA19-9 is the serum tumor marker
Rokitansky-Aschoff sinuses
–> hallmark of chronic cholecystitis, gall bladder mucus pouches into the smooth muscle of the gallbladder wall.
gallbladder carcinoma
risk factor is gallstones, long standing. especially with porcelain gallbladder.
This malignancy arises from epithelium of the gallbladder wall.
–> classically presents as acute cholecystitis in elderly women.
Gilbert syndrome
autosomal recessive MILD DECREASE in UGT conjugating activity. Increase in unconjugated bilirubin. Jaundice during stress or severe infection, otherwise not clinically significant.
Crigler-Najar
ABSENCE of UGT, increased unconjugated bilirubin. kernicterus, often fatal.
Dubin-Johnson
autosomal recessive deficiency of bilirubin canalicular transport protein. increased in CB. Black liver. not clinically significant.
Rotor syndrome
similar to dubin johnson, but does not have liver discoloration.
HEV infection in pregnancy
- can lead to fulminant hepatitis (liver failure with massive liver necrosis)
Hep B chart page 120
page 120
Hep D
co-infection vs super infection
Hep is dependent on Hep B for infection.
infection at the same time (coinfection) is less severe than super infection.
Cirrhosis mediated by which cell?
the stellate cell which is beneath the endothelium and lines the sinusoids.
–> secretes TGF-beta
Mallory bodies
DAMAGED INTERMEDIATE FILAMENTS in the hepatocytes seen with alcoholic hepatitis
–>swollen hepatocytes with mallory bodies.
Hemochromatosis pathophysiology
Enterocyte will take up almost all of iron that is in the gut, but monitors blood level and will only dump iron in to the blood when it is a required, the key regulatory step in the human body for iron. We do not really have a way to get rid of iron.
- -> in this disorder, this regulation is lost.
- -> in primary hemochromatosis there is mutation in HFE gene, C282Y.
–> damage is caused by excess iron in the tissue generating free radicals.
- prussian blue stain will stain the iron blue in liver cells distinguishes the brown in the cells from lipofuscin.
hemochromatosis treatment
phlebotomy
Reye syndrome
fulminant liver failure and encephalopathy in a child with viral illness taking aspirin.
Reye syndrome presentation
–> hypoglycemia, elevated liver enzymes, nauseau/vomiting. can progress to coma and death.
Hepatic adenoma
- -> related to orla contraceptive use. resolves with discontinuing the medication.
- -> benign tumor, risk of rupture though.
how do aflatoxins lead to hepatocellular carcinoma?
–> induce p53 mutations.
