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Hepatocellular carcinoma



Gastrointestinal system


Peritoneum and peritoneal cavity
Upper gastrointestinal tract disorders
Lower gastrointestinal tract disorders
Liver, gallbladder and pancreas disorders
Gastrointestinal system pathology review

Hepatocellular carcinoma


0 / 8 complete


0 / 1 complete
High Yield Notes
18 pages

Hepatocellular carcinoma

8 flashcards

USMLE® Step 1 style questions USMLE

1 questions

A 67-year-old man comes to the clinic due to worsening fatigue and abdominal distension. The patient has lost 11 pounds in the last 2 months with minimal change in appetite. Past medical history is notable for chronic liver disease due to hepatitis B infection that was diagnosed 15 years ago. His most recent colonoscopy 1 year ago showed no abnormalities. His temperature is 37.0°C (98.6°F), pulse is 85/min, and blood pressure is 154/89 mm Hg. Physical examination reveals temporal wasting and scleral icterus. Palmar erythema and multiple spider angiomas are present. The abdomen is distended with shifting dullness to percussion. There is 2+ pitting edema of the lower extremities. Ultrasound shows a single homogenous liver mass with irregular borders. Which of the following best describes the tumor marker that is likely elevated in this patient?

External References

Content Reviewers:

Rishi Desai, MD, MPH


Tanner Marshall, MS

As opposed to benign hepatic tumors, malignant hepatic tumors are cancerous, very severe, and are actually now the third leading cause of cancer deaths worldwide.

With these malignant liver cells or hepatocytes, just like malignant cells in other cancers, they develop some mutation that causes them to replicate at way higher rates and form these masses of cells that continue to grow and potentially spread to other tissues.

This would be a primary hepatic tumor, since it starts in the liver. It’s totally possible, though, for liver tumor to develop as a metastasis from another primary cancer, in which case it would not be hepatocellular carcinoma, but a carcinoma from somewhere else, and this is actually more common than primary liver tumors themselves.

The most common sources of the tumor cells that got to the liver but started somewhere else are the colon, pancreas, lung and breast.

What exactly causes the mutation in the hepatocyte though?

Well the mechanism isn’t fully understood and can probably be caused by a lot of different things, most importantly though, things that put the liver in a constant cycle of damage and repair are the biggest culprits.

If the liver cells are constantly being forced to repair, this raises the chances of genetic mistakes or mutations, potentially leading to carcinogenesis or development of cancer cells.

Examples might be any disease that leads to cirrhosis and scarring of the liver tissue, which can include alcoholic hepatitis and cirrhosis, hereditary hemochromatosis, primary biliary cirrhosis, alpha-1 antitrypsin deficiency, and others.

The most common risk factor, the ones that have been linked the most with hepatocellular carcinoma are the hepatitis B and hepatitis C viruses, both of which can become chronic or long-lasting.

In this case, these cells are at greater risk because of the constant state of infection and immune cell attack, leading to constant damage and repair.

HBV is particularly problematic because of how the virus replicates; the HBV virus is a DNA virus that integrates into the hepatocyte’s DNA, which, although not completely understood, is thought to either directly disrupt regulation of cell growth and replication, leading to carcinoma, or alternatively cause some indirect effect that later leads to unchecked cell growth and replication.

One interesting risk factor, is exposure to aflatoxins.

Aflatoxins are highly toxic chemicals produced by certain aspergillus molds that can be found in certain foods when they start to decay, like grains, peanuts, and vegetables.

As foods that have this type of mold are eaten, aflatoxins are also eaten, and then they’re absorbed in the small intestine and sent to the liver for metabolizing.

The most potent type of aflatoxin thought to be involved in carcinogenesis is aflatoxin B1, and when it gets to the liver, it’s metabolized to aflatoxin B1 8,9 epoxide.

And now this guy can bind right to DNA, called a DNA adduct.

This interaction leads to mutations in the p53 tumor suppressor gene, which usually when it’s functioning right, stops the formation of tumors, so if it becomes mutated and dysfunctional, tumor formation and carcinogenesis might follow.

Because most patients with hepatocellular carcinoma also have cirrhosis, the hepatocellular carcinoma can be hard to spot.