Pathoma Exocrine pancreas, gallbladder, liver

Question 1

acute pancreatitis pathophysiology

Answer 1

autodigestion of pancreas by its own enzymes to pre-activation of enzymes by trypsin.

Question 2

types of nectosis in pancreatitis

Answer 2

• liquefactive necrosis of the pancreas itself

- fat necrosis of the peripancreatic fat

Question 3

alcoholic pancreatitis pathophysiology

Answer 3

• alcohol causes contraction of the sphincter of oddi

Question 4

Common causes of acute pancreatitis and other causes of acute pancreatitis

Answer 4

common: alcohol and gallstones
other:
- scorpion bite
- hypercalcemia, hypelipidemia
- drugs
- mumps
- rupture of posterior duodenal ulcer
- trauma

Question 5

clinical features of pancreatitis

Answer 5

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

Question 6

clinical features of chronic pancreatitis

Answer 6

epigastric pain radiating to the back 
pancreatic insufficiency 
fat soluble vitamin deficiency
secondary diabetes
dystrophic calcification of the pancreas 
increased risk of pancreatic carcinoma

Question 7

pancreatic carcinoma
cell of origin
major risk factors
clinical presentation

Answer 7

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

Question 8

Rokitansky-Aschoff sinuses

Answer 8

–> hallmark of chronic cholecystitis, gall bladder mucus pouches into the smooth muscle of the gallbladder wall.

Question 9

gallbladder carcinoma

Answer 9

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.

Question 10

Gilbert syndrome

Answer 10

autosomal recessive MILD DECREASE in UGT conjugating activity. Increase in unconjugated bilirubin. Jaundice during stress or severe infection, otherwise not clinically significant.

Question 11

Crigler-Najar

Answer 11

ABSENCE of UGT, increased unconjugated bilirubin. kernicterus, often fatal.

Question 12

Dubin-Johnson

Answer 12

autosomal recessive deficiency of bilirubin canalicular transport protein. increased in CB. Black liver. not clinically significant.

Question 13

Rotor syndrome

Answer 13

similar to dubin johnson, but does not have liver discoloration.

Question 14

HEV infection in pregnancy

Answer 14

• can lead to fulminant hepatitis (liver failure with massive liver necrosis)

Question 15

Hep B chart page 120

Answer 15

page 120

Question 16

Hep D

co-infection vs super infection

Answer 16

Hep is dependent on Hep B for infection.

infection at the same time (coinfection) is less severe than super infection.

Question 17

Cirrhosis mediated by which cell?

Answer 17

the stellate cell which is beneath the endothelium and lines the sinusoids.
–> secretes TGF-beta

Question 18

Mallory bodies

Answer 18

DAMAGED INTERMEDIATE FILAMENTS in the hepatocytes seen with alcoholic hepatitis
–>swollen hepatocytes with mallory bodies.

Question 19

Hemochromatosis pathophysiology

Answer 19

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.

Question 20

hemochromatosis treatment

Answer 20

phlebotomy

Question 21

Reye syndrome

Answer 21

fulminant liver failure and encephalopathy in a child with viral illness taking aspirin.

Question 22

Reye syndrome presentation

Answer 22

–> hypoglycemia, elevated liver enzymes, nauseau/vomiting. can progress to coma and death.

Question 23

Hepatic adenoma

Answer 23

• -> related to orla contraceptive use. resolves with discontinuing the medication.
• -> benign tumor, risk of rupture though.

Question 24

how do aflatoxins lead to hepatocellular carcinoma?

Answer 24

–> induce p53 mutations.

Question 25

serum tumor marker for hepatocellular carcinoma

Answer 25

alpha fetoprotein