Pathophysiology
Summary
Focal nodular hyperplasia (FNH) is the most prevalent benign, non-vascular liver mass. FNH manifests as a solitary area of hepatocyte proliferation, forming a nodular star pattern around a large central artery. These nodules are composed of hepatocytes, bile ductules, arterioles, and portal venules. Contrast imaging reveals a ‘spoke wheel’ vascular pattern. FNH primarily occurs in women of reproductive age, as its growth is influenced by estrogen, particularly during pregnancy or with the use of OCPs.
Hepatic hemangiomas are the most common benign liver mass overall. These vascular liver tumors contain ‘cavernous’ areas of cystic dilation, and show dilated vascular spaces filled with RBCs. Hepatic hemangiomas are prone to hemorrhage, manifesting as acute RUQ pain. Importantly, attempting to biopsy these masses may result in profuse bleeding.
Hepatic adenomas are benign liver masses comprised of large hepatocytes filled with glycogen or fat. These tumors can be large—resulting in massive hemorrhaging and even hypovolemic shock when ruptured. Anabolic androgens and type 1 & type 3 glycogen storage diseases are associated with the development and growth of hepatic adenomas. Unlike FNH, hepatic adenomas lack bile ducts, and contain a small risk of transforming into HCC.
Hepatocellular carcinoma (HCC) stands as the predominant form of primary liver cancer. While cirrhosis is its most frequent antecedent, HCC can also arise in the context of AFLD, NAFLD, hereditary hemochromatosis, & autoimmune liver diseases. Viral hepatitis, (primarily Hep B) remains the most common cause of HCC globally. Exposure to aflatoxin produced by Aspergillus, as well as environmental toxins like azo dyes can also lead to HCC. On histological analysis, well-differentiated HCC tumors contain bile-containing pseudo-canaliculi, whereas poorly differentiated tumors contain giant cells. HCC commonly presents with acute liver decompensation, and can also cause Budd-Chiari syndrome due to hepatic vein occlusion. Serum alpha-fetoprotein (AFP) is used as a tumor marker.
The malignant neoplasm angiosarcoma affects hepatic vascular endothelial cells and is also prone to rupture and massive hemorrhage. Risk factors include exposure to arsenic, vaporized polyvinyl chloride (PVC), & Thorotrast (radioactive thorium dioxide). Angiosarcomas typically express CD31.
Lastly, it's important to note that most liver malignancies are actually metastases, often stemming from primary cancers in the colon or lungs.
Lesson Outline
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FAQs
Focal Nodular Hyperplasia (FNH) stands out as the most prevalent benign, non-vascular liver mass. It typically manifests as a unique nodular region of hepatocyte proliferation, forming a distinct star pattern. A prominent feature of FNH is its large central artery, which, when viewed through contrast imaging, exhibits a "spoke wheel" vascular pattern. This liver mass also comprises bile ductules, arterioles, and portal venules, further distinguishing it.
Estrogen plays a pivotal role in promoting the growth of both FNH and hepatic adenomas. This hormonal influence explains why these liver conditions are more prevalent in women of reproductive age, especially during pregnancy or among those on oral contraceptives (OCPs). In each of these scenarios, estrogen levels are notably elevated, driving the growth of these liver masses.
Hepatic hemangiomas are recognized as the predominant benign liver mass and are characterized by their vascular nature, specifically their ‘cavernous' dilated cystic regions. On a histological level, these hemangiomas reveal dilated cystic spaces brimming with red blood cells, each lined by a singular endothelial layer. This unique structure is devoid of smooth muscle and can result in hemorrhage, often manifesting as acute pain in the right upper quadrant (RUQ). Diagnostic procedures like fine needle aspiration or biopsy can trigger extensive bleeding.
Hepatocellular carcinoma (HCC) is the most prevalent primary liver cancer and is attributed to a myriad of factors. Cirrhosis emerges as the predominant etiology, stemming from conditions like alcoholic liver disease, non-alcoholic fatty liver disease, hereditary hemochromatosis-induced iron overload, autoimmune liver diseases, or α-1 antitrypsin deficiency. Chronic infections from hepatitis B and C often culminate in HCC, typically following a progression to cirrhosis. Moreover, environmental exposures, such as to aflatoxin produced by the Aspergillus fungus or prolonged contact with azo dyes, have been linked to HCC development.
Hepatic adenomas are benign liver masses that can attain considerable sizes, reaching up to 30 cm. Their fragile nature poses a significant risk of rupture, which can lead to extensive hemorrhaging, manifesting as acute pain in the right upper quadrant (RUQ) and hypovolemic shock in severe cases. Furthermore, there's hepatic adenomas are at risk evolving into hepatocellular carcinoma (HCC). Substances such as anabolic androgens and conditions such as type 1 and type 3 glycogen storage diseases can induce the formation of these adenomas.
