Liver

Question 1

Diseases of hepatocytes Include:

Answer 1

“Heavy Feathers Drown Mallards”

• viral/automminue hepatitis
• nonalcoholic/alcoholic fatty liver disease
• drug toxicity
• metabolic/storage diseases

Question 2

Diseases of the biliary system Include:

Answer 2

“All Owls Attend Demon Training”

• autoimmune biliary diseases (primary sclerosing cholangitis and primary biliary cirrhosis)
• obstruction
• atresia
• drug-induced injury
• transplant rejection/GVHD

Question 3

Diseases of the vasculature Include:

Answer 3

• transplant rejection, GVHD
• systemic vasculitides

Question 4

Answer 4

Portal Inflammation: Inflammatory cells within the portal tract.

• viral hepatitis and autoimmune disorders, the infiltrate is predominantly mononuclear.
• Eosinophils suggest a drug reaction,
• plasma cells are often seen in autoimmune hepatitis.

Question 5

Inflammation, usually lymphocytic, occurring in the limiting plate and damaging the hepatocytes along that boundary.

Answer 5

Interface activity

Question 6

Inflammation, often accompanied by hepatocyte necrosis, farther out from the portal tracts.

Answer 6

Lobular inflammation

Question 7

One way in which hepatocytes become injured and die. The cell swells and the cytoplasm becomes feathery and pale to clear.

Answer 7

Vacuolar degeneration (balloon cell change, or ballooning degeneration)

Question 8

Another way in which hepatocytes die. These cells are similar to dyskeratotic cells in the skin; they are bright pink and shriveled up, with pyknotic nuclei.

Answer 8

Acidophilic bodies

Question 9

A general term indicating too much collagen.

Answer 9

Fibrosis

Question 10

Fat (triglycerides) in the hepatocytes.

Answer 10

Steatosis

• 5–33% of hepatocytes is mild steatosis
• 33–66% of hepatocytes is moderate steatosis
• > 66% of hepatocytes is marked or severe steatosis

Question 11

Answer 11

Steatohepatitis: Steatosis with inflammation (usually lobular) and/or hepatocyte injury

Question 12

Answer 12

Mallory’s hyaline (Mallory bodies): Irregular wormlike pink blobs of condensed cytoskeleton in the cytoplasm, especially within balloon cells; associated with steatohepatitis and alcoholic disease in particular.

Question 13

Markedly enlarged mitochondria that look like red blood cells entrapped in the hepatocyte cytoplasm.

Answer 13

Megamitochondria

Question 14

Abnormal iron deposits detected with either H&E or iron stain, predominantly within macrophages (Kupffer cells).

Answer 14

Iron accumulation:

Question 15

The backup of bile in the liver, visible as yellow globs or chunks in hepatocyte cytoplasm, bile canaliculi, or (less commonly) bile duct lumina.

Answer 15

Cholestasis

Question 16

An increase in the number of bile duct profiles/ ductules in each portal tract beyond the typical one or two per tract.

Answer 16

Bile duct proliferation (ductular reaction)

Question 17

Loss of bile ducts, which is an indicator of chronic damage to the biliary system

Answer 17

Ductopenia, if bile ducts are present in fewer than 80% of the portal tracts. A CK7 immunostain can help with bile duct identification.

Question 18

Damage to the endothelium of the portal or central veins by inflammatory cells. The endothelial cells tend to round up and become more prominent.

Answer 18

Venulitis (endotheliitis), usually an indication of rejection or GVHD.

Question 19

Hematopoietic precursors (megakaryocytes are the most distinctive) in the liver sinuses. It is generally an indication of bone marrow disease, but is physiologic in fetuses and infants.

Answer 19

Extramedullary hematopoiesis

Question 20

ID, timeline & features

Answer 20

Acute rejection usually occurs 5–30 days after transplant, but can be longer. Changes include the following:

– Mixed portal tract inflammation, including lymphocytes, neutrophils, and eosinophils

– Venulitis

– Bile duct inflammation and damage

Question 21

Chronic rejection timeline

Answer 21

Chronic rejection usually occurs after more than 1 year.

Question 22

Answer 22

Hepatic Adenoma

• clinical: noncirrhotic livers of adult women taking OCPs
• histology: circumscribed, partially encapsulated masses of uniform, bland-looking hepatocytes with no central veins or bile ducts; The cells may be pale due to steatosis or glycogen or discolored with entrapped bile. When visualized with the reticulin stain, the hepatocyte plates are still only one to two cells thick (every cell touches reticulin).
• Molecular Groups (4):
  
  • steatotic adenomas (mutated HNF1α)
  • inflammatory (telangiectatic) adenomas
  • β-catenin-activated adenomas
  • “none-of-the-above” adenomas.

Question 23

Answer 23

Bile duct adenoma

• <1 cm and subcapsular, with a well-circumscribed tangle of small simple tubules, with or without inflammation and fibrosis
• may produce mucin but not bile

Question 24

Answer 24

Cholangiocarcinoma

• A primary malignancy of the bile ducts that appears as a nondescript adenocarcinoma infiltrating the liver
• mucin is common, as is an intense desmoplastic response

Question 25

Answer 25

Question 26

Answer 26

Question 27

Answer 27