Faculty Mentor

Dr. Judd Case

Document Type


Publication Date

Spring 2020




Chronic cirrhosis takes the lives of approximately 41,000 individuals each year in the United States. This disease is a result of either chronic alcohol abuse, fatty liver, genetic disorders, and hepatitis. Liver disease leads to excessive fibro-genic scarring due to cytokine signaling, hepatocyte apoptosis, and replacement of collagen type III by collagen type I. The purpose of this study is to present a systematic review of the available evidence based on histological pathology slides and the literature surrounding Hepatic Cirrhosis. The research investigated is: to assess the role of the hepatocytes when a liver is cirrhotic, pathway of Hepatitis C, how/why fibrosis happens by analyzing cytokine signaling, hepatic cellulite cells (HCS) activation, and to analyze the types of collagen affected. The research conducted was through an analysis of histological slides ranging from normal liver histology to cirrhotic hepatitis C pathology. The pathology slides of exhibited signs of cirrhosis indicated by multiple areas where parallel fields of collagen I fibers cut off nutrients from sinusoids to the surrounding hepatocytes. The fibrous areas are linked to portal tracts and therefore no nutrients can reach the hepatocytes. According to the literature, excessive cytokinin signal production alters fibroblasts to myofibroblasts, which then produce excessive amounts of linear Type I collagen. As a consequence of this fibrous growth, the hepatocytes become smaller, dehydrated cells, whereas, the hepatocytes outside of the fibrous areas look to be enlarged cells compared to normal hepatocytes in non-diseased livers.