Histopathology - Liver

Question 1

Answer 1

Cholestasis – Core Biopsy

 Normal lobular structure maintained

 Greenish/brown material located between cells in Disse spaces is bile.

 Intracellular accumulation in hepatocytes caused by:

o Impaired metabolism
o Extrahepatic bile obstruction
o Reduced excretion due to severe inflammation

 Cholestasis (stasis of bile flow) is pathological

 Cholestasis in bigger duct = obstruction

 Cholestasis in smaller duct = hepatocyte malfunction (as in this case)

Question 2

Answer 2

Fatty Degeneration

 Dark sections: dense septa of CT

 Lobular structure maintained

 Fibrosis (connective tissue) around portal triad

 Holes are artifacts of fatty degeneration

 In the cytoplasm of some hepatocytes, there is the beginning of fatty degeneration: pushing

nucleus and cytoplasm to the border

 Organs with high fat metabolism can undergo fatty degeneration.

o The other organ is the heart (“tiger heart”)
o If the liver cannot metabolize the fat it receives through the portal vein, the fat will

accumulate in the cytoplasm of the hepatocytes.
o Causes: alcoholism, hypoxia, storage disease, viral infections, obesity, diabetes

 Brown pigment fine granulations in the hepatocytes could be: o Bile – no, usually in ducts

o Lipofuscin – yes
o Hemosiderin – in macrophages, except in hemochromatosis, where it would be in the

hepatocytes

 Frozen section or Sudan black can be used to see fat accumulations

 Fat can be deposited in the hepatic lobules in different patterns:

o Diffuse: vacuoles are evenly spread out within a lobule. Alcoholism produces this pattern, since it reduces fat metabolism in all cells

o Zonular: fat vacuoles appear either peripherally or centrally in the lobules. Stasis causes accumulation in the central zone due to hypoxia there. Acute poisoning (including binge drinking) causes fat to accumulate in the periphery, since there are higher amounts of toxins in the periphery.

 Macroscopic: yellow, soft, enlarged

Question 3

Answer 3

Nutmeg Liver

 Backward RHF causes stasis in viscera
o R.V. fails to pump blood into the lungs (due to pulmonary embolism, pneumonia,

etc.), and pools in IVC. This leads to systemic congestion.  Three phases of liver congestion:

o Dilation of the central veins
o Central zone fatty accumulation and fatty degeneration in the hepatocytes

surrounding the central veins.
Lipids  steatosis hepatis (fatty degeneration). Brown dots surrounded by yellow

o Sinusoids dilate due to increasing pressure, compressing the hepatic cords and causing atrophy of the trabeculae around the central vein. The dying hepatocytes will be replaced by fibrosis (“cardiac cirrhosis”)

 Brown spots are hemosiderin-laden Kupffer cells

 Rhythmicity in RBC cluster

 Lipofuscin is orangy

 Here, RBC increase in sinusoids make trabeculae smaller, hepatocytes lose cytoplasm. The

trabeculae are disorganized in atrophied in these regions.

 Central veins are dilated. Lighter areas on the section are the parenchymal tissue

surrounding the central veins (3rd stage of congestion)

o These areas appear lighter because the dilated sinusoids have lost their blood.

 Around the damaged areas, the hepatocytes show fatty accumulation o karyolysis

 Brown pigments could either be lipofuscin or hemosiderin

Question 4

Answer 4

Chronic Hepatitis

 Needle biopsy

 Chronic hepatitis is mostly caused by

Hepatitis C, which begins as chronic (not

acute) form. Histology does not reveal etiology. For that, we use serology.

 Increased transaminase levels

 Drugs can be used as treatment to kill the virus; they are more efficient the earlier the virus is

recognized

 With low power, note darker areas. In higher power, we see that these occur in the portal

areas due to follicular pattern of lymphocytes

 With higher power, note fatty change (steatosis)

 Border between inflammation and parenchyma is sharp in some areas.

 Characteristic of CPH (Chronic Persistent Hepatitis), which has a benign outcome  In other areas, there is interface between spread of inflammatory cells and parenchyma

 CAH (Chronic Active Hepatitis)

 Together, CPH and CAH have a biphasic pattern. Nowadays, scoring is used to categorize

chronic hepatitis, rather than these terms

 In the parenchyma, stellate myofibroblasts (Ito cells, hard to see) are deposited. These lead to

cirrhosis.

 With highest magnification, one might see apoptotic cells (hard to see)

 Councilman (hyaline) bodies = apoptotic hepatocytes; eosinophilic, surrounded by normal parenchyma

Question 5

Answer 5

Hepatitis B

 Most common form of hepatitis, especially in Asia and Africa

 Vaccine now used, based on surface antigen

 Hepatitis B virus can cause acute, chronic, or acutechronic hepatitis

 Transmission can be vertical from mother to baby

 Child is immune intolerant, and more likely to develop chronic form: cirrhosis and cancer

 Horizontal spread in adults is usually acute

 Needle biopsy

 Portal area has mild inflammation

 Ground-glass (i.e. opaque) cells, swollen, larger cytoplasm

 Derive from the HepBV surface antigen of the Dane particle

 Indicated increased of ER, and is not specific for HepB

 Here, it has not progressed to fibrosis

 Infectious

Question 6

Answer 6

Cirrhosis

 Bottom shows islands of hepatocytes separated by CT septa

 Liver reconstruction within lobules

 Bile duct proliferation (source of the regeneration?)

 Mild inflammation in septa

Question 7

Answer 7

Cirrhosis – picrosirius stain

 Collagen I and III stained to demonstrate reconstruction

 Regardless of etiology, cirrhosis has this etiology

Question 8

Answer 8

Hepatocellular carcinoma

 Hepatocellular carcinoma is a complication of cirrhosis

 Common in Africa and Asia, making it the third most common carcinoma worldwide, and it

is increasing in incidence

 Metastatic tumors in the liver are general 20x more common.

 If the liver is not cirrhotic, it is most likely a metastasis. The exception is HCC in children, who acquire HepB from their mother, which leads to HCC without cirrhosis

 The most common primary liver tumor is hepatocellular carcinoma.

 Factors that increase HCC: HepB, Aflatoxin from Aspergillus

 The capsule is the sharp line in the middle separating the cirrhotic liver below from the

cancer above

 HCC are frequently encapsulated

 The cancer has polygonal cells with large nuclei and pseudoacinar structure

 No portal area seen

 Abnormal arrangement

 Well-differentiated

 If tumor is removed, the cirrhotic liver cannot regenerate, thus transplant is the best option.