{"id":5400,"date":"2025-12-08T23:33:47","date_gmt":"2025-12-09T04:33:47","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=5400"},"modified":"2026-01-12T18:38:38","modified_gmt":"2026-01-12T23:38:38","slug":"liver-disease-cirrhosis-and-its-causes","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/liver-disease-cirrhosis-and-its-causes\/","title":{"raw":"10p18  Liver Disease: Cirrhosis and Its Causes","rendered":"10p18  Liver Disease: Cirrhosis and Its Causes"},"content":{"raw":"<h2><strong>Overview of Cirrhosis<\/strong><\/h2>\r\n<ul>\r\n \t<li><strong>Cirrhosis<\/strong>: Progressive, chronic destruction of the liver, which can take weeks <strong>(acute<\/strong> liver failure) to decades <strong>(chronic<\/strong> liver failure).<\/li>\r\n \t<li>Characterized by\u00a0<strong>extensive fibrosis<\/strong>\u00a0(scarring) leading to\u00a0<strong>shrinkage<\/strong>\u00a0and\u00a0<strong>loss of liver function<\/strong>.<\/li>\r\n \t<li>Death of hepatocytes is accompanied by inflammation.<\/li>\r\n \t<li>Often results from\u00a0<strong>chronic liver injury<\/strong>.<\/li>\r\n \t<li>Cirrhosis increases the risk of developing <strong>hepatocellular carcinoma<\/strong>.<\/li>\r\n<\/ul>\r\n<h1><strong>Causes of Cirrhosis include:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Viruses (e.g., Hepatitis C Virus)<\/li>\r\n \t<li>Drugs, toxins<\/li>\r\n \t<li>Alcoholism<\/li>\r\n<\/ul>\r\n<h1><strong>1.\u00a0 Alcoholic Liver Disease and Stages:<\/strong><\/h1>\r\n<h1>a) Initial stage: <strong>Fatty liver (Steatosis)<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Accumulation of\u00a0<strong>triglycerides<\/strong>\u00a0within hepatocytes.<\/li>\r\n \t<li>Liver enlarges (<strong>hepatomegaly<\/strong>).<\/li>\r\n \t<li>Usually\u00a0<strong>reversible<\/strong>\u00a0with alcohol cessation.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1>b) Next stage: <strong>Alcoholic hepatitis<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Significant inflammation.<\/li>\r\n \t<li>Cell death.<\/li>\r\n \t<li>Usually\u00a0<strong>not reversible<\/strong>.<\/li>\r\n \t<li>Symptoms:\u00a0<strong>Nausea, anorexia, tender liver<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1>c) Final stage: <strong>End-stage Cirrhosis<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Extensive fibrosis and\u00a0<strong>muscle atrophy<\/strong>.<\/li>\r\n \t<li>Loss of function.<\/li>\r\n \t<li><strong>Portal hypertension<\/strong>\u00a0develops.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>2.\u00a0 Viral Hepatitis:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Chronic infections (especially\u00a0<strong>Hepatitis B<\/strong>\u00a0and\u00a0<strong>C<\/strong>).<\/li>\r\n \t<li>Causes tissue destruction, fibrosis, and cirrhosis.<\/li>\r\n \t<li><strong>Post-necrotic cirrhosis<\/strong>: caused by long-term viral or toxic injury.<\/li>\r\n<\/ul>\r\n<h2><strong>3.\u00a0 Other Causes:<\/strong><\/h2>\r\n<ul>\r\n \t<li><strong>Biliary cirrhosis<\/strong>: autoimmune diseases affecting bile ducts.<\/li>\r\n \t<li><strong>Gallstones<\/strong>: cause blockages.<\/li>\r\n \t<li><strong>Cystic fibrosis<\/strong>: excess mucus blocks bile flow.<\/li>\r\n \t<li><strong>Toxins<\/strong>: drug toxicity or environmental toxins.<\/li>\r\n \t<li><strong>Genetic diseases<\/strong>\u00a0affecting nutrient storage.<\/li>\r\n<\/ul>\r\n<h1><strong>Pathophysiology and Macroscopic Changes<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Initial stage:<\/strong>\u00a0Liver enlarges due to inflammation.<\/li>\r\n \t<li><strong>Fibrosis and scarring<\/strong>\u00a0replace healthy tissue.<\/li>\r\n \t<li><strong>Atrophy<\/strong>\u00a0occurs, leading to\u00a0<strong>shrinking liver<\/strong>.<\/li>\r\n \t<li>Blood flow\u00a0<strong>becomes obstructed<\/strong>, causing\u00a0<strong>portal hypertension<\/strong>.<\/li>\r\n \t<li><strong>Bile duct scarring<\/strong>\u00a0causes\u00a0<strong>bile backup<\/strong>\u00a0(<strong>biliary stasis<\/strong>).<\/li>\r\n<\/ul>\r\n<h1><strong>Complications<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Portal hypertension<\/strong>\u00a0leads to:\r\n<ul>\r\n \t<li><strong>Ascites<\/strong>: Fluid buildup in the abdominal cavity.<\/li>\r\n \t<li><strong>Varices<\/strong>\u00a0(enlarged veins).<\/li>\r\n \t<li>Risk of\u00a0<strong>bleeding and hemorrhage<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Impaired liver functions<\/strong>:\r\n<ul>\r\n \t<li>Decreased\u00a0<strong>gluconeogenesis<\/strong>.<\/li>\r\n \t<li>Reduced\u00a0<strong>protein<\/strong>\u00a0and\u00a0<strong>bile<\/strong>\u00a0production.<\/li>\r\n \t<li><strong>Inability<\/strong>\u00a0to detoxify blood.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Signs and Symptoms of Cirrhosis<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Fatigue, weakness<\/strong>.<\/li>\r\n \t<li><strong>Jaundice<\/strong>: due to bilirubin buildup.<\/li>\r\n \t<li><strong>Ascites<\/strong>: abdominal swelling.<\/li>\r\n \t<li><strong>Edema and varices<\/strong>.<\/li>\r\n \t<li><strong>Impaired glucose regulation<\/strong>:\r\n<ul>\r\n \t<li>Decreased\u00a0<strong>gluconeogenesis<\/strong>.<\/li>\r\n \t<li>Decreased\u00a0<strong>glycogen<\/strong>\u00a0storage.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Reduced bile secretion<\/strong>\u00a0\u2192\u00a0<strong>impaired fat digestion and absorption<\/strong>.<\/li>\r\n \t<li><strong>Bleeding tendencies<\/strong>: due to\u00a0<strong>clotting factor deficiencies<\/strong>.<\/li>\r\n<\/ul>\r\n<h1><strong>Summary<\/strong><\/h1>\r\n<ul>\r\n \t<li>Cirrhosis results from ongoing liver damage, often from alcohol or viral hepatitis.<\/li>\r\n \t<li>Leads to significant\u00a0<strong>fibrosis<\/strong>,\u00a0<strong>vascular changes<\/strong>, and\u00a0<strong>organ failure<\/strong>.<\/li>\r\n \t<li>Early detection and lifestyle modifications are critical to slow progression and prevent complications.<\/li>\r\n<\/ul>","rendered":"<h2><strong>Overview of Cirrhosis<\/strong><\/h2>\n<ul>\n<li><strong>Cirrhosis<\/strong>: Progressive, chronic destruction of the liver, which can take weeks <strong>(acute<\/strong> liver failure) to decades <strong>(chronic<\/strong> liver failure).<\/li>\n<li>Characterized by\u00a0<strong>extensive fibrosis<\/strong>\u00a0(scarring) leading to\u00a0<strong>shrinkage<\/strong>\u00a0and\u00a0<strong>loss of liver function<\/strong>.<\/li>\n<li>Death of hepatocytes is accompanied by inflammation.<\/li>\n<li>Often results from\u00a0<strong>chronic liver injury<\/strong>.<\/li>\n<li>Cirrhosis increases the risk of developing <strong>hepatocellular carcinoma<\/strong>.<\/li>\n<\/ul>\n<h1><strong>Causes of Cirrhosis include:<\/strong><\/h1>\n<ul>\n<li>Viruses (e.g., Hepatitis C Virus)<\/li>\n<li>Drugs, toxins<\/li>\n<li>Alcoholism<\/li>\n<\/ul>\n<h1><strong>1.\u00a0 Alcoholic Liver Disease and Stages:<\/strong><\/h1>\n<h1>a) Initial stage: <strong>Fatty liver (Steatosis)<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Accumulation of\u00a0<strong>triglycerides<\/strong>\u00a0within hepatocytes.<\/li>\n<li>Liver enlarges (<strong>hepatomegaly<\/strong>).<\/li>\n<li>Usually\u00a0<strong>reversible<\/strong>\u00a0with alcohol cessation.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1>b) Next stage: <strong>Alcoholic hepatitis<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Significant inflammation.<\/li>\n<li>Cell death.<\/li>\n<li>Usually\u00a0<strong>not reversible<\/strong>.<\/li>\n<li>Symptoms:\u00a0<strong>Nausea, anorexia, tender liver<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1>c) Final stage: <strong>End-stage Cirrhosis<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Extensive fibrosis and\u00a0<strong>muscle atrophy<\/strong>.<\/li>\n<li>Loss of function.<\/li>\n<li><strong>Portal hypertension<\/strong>\u00a0develops.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>2.\u00a0 Viral Hepatitis:<\/strong><\/h1>\n<ul>\n<li>Chronic infections (especially\u00a0<strong>Hepatitis B<\/strong>\u00a0and\u00a0<strong>C<\/strong>).<\/li>\n<li>Causes tissue destruction, fibrosis, and cirrhosis.<\/li>\n<li><strong>Post-necrotic cirrhosis<\/strong>: caused by long-term viral or toxic injury.<\/li>\n<\/ul>\n<h2><strong>3.\u00a0 Other Causes:<\/strong><\/h2>\n<ul>\n<li><strong>Biliary cirrhosis<\/strong>: autoimmune diseases affecting bile ducts.<\/li>\n<li><strong>Gallstones<\/strong>: cause blockages.<\/li>\n<li><strong>Cystic fibrosis<\/strong>: excess mucus blocks bile flow.<\/li>\n<li><strong>Toxins<\/strong>: drug toxicity or environmental toxins.<\/li>\n<li><strong>Genetic diseases<\/strong>\u00a0affecting nutrient storage.<\/li>\n<\/ul>\n<h1><strong>Pathophysiology and Macroscopic Changes<\/strong><\/h1>\n<ul>\n<li><strong>Initial stage:<\/strong>\u00a0Liver enlarges due to inflammation.<\/li>\n<li><strong>Fibrosis and scarring<\/strong>\u00a0replace healthy tissue.<\/li>\n<li><strong>Atrophy<\/strong>\u00a0occurs, leading to\u00a0<strong>shrinking liver<\/strong>.<\/li>\n<li>Blood flow\u00a0<strong>becomes obstructed<\/strong>, causing\u00a0<strong>portal hypertension<\/strong>.<\/li>\n<li><strong>Bile duct scarring<\/strong>\u00a0causes\u00a0<strong>bile backup<\/strong>\u00a0(<strong>biliary stasis<\/strong>).<\/li>\n<\/ul>\n<h1><strong>Complications<\/strong><\/h1>\n<ul>\n<li><strong>Portal hypertension<\/strong>\u00a0leads to:\n<ul>\n<li><strong>Ascites<\/strong>: Fluid buildup in the abdominal cavity.<\/li>\n<li><strong>Varices<\/strong>\u00a0(enlarged veins).<\/li>\n<li>Risk of\u00a0<strong>bleeding and hemorrhage<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Impaired liver functions<\/strong>:\n<ul>\n<li>Decreased\u00a0<strong>gluconeogenesis<\/strong>.<\/li>\n<li>Reduced\u00a0<strong>protein<\/strong>\u00a0and\u00a0<strong>bile<\/strong>\u00a0production.<\/li>\n<li><strong>Inability<\/strong>\u00a0to detoxify blood.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Signs and Symptoms of Cirrhosis<\/strong><\/h1>\n<ul>\n<li><strong>Fatigue, weakness<\/strong>.<\/li>\n<li><strong>Jaundice<\/strong>: due to bilirubin buildup.<\/li>\n<li><strong>Ascites<\/strong>: abdominal swelling.<\/li>\n<li><strong>Edema and varices<\/strong>.<\/li>\n<li><strong>Impaired glucose regulation<\/strong>:\n<ul>\n<li>Decreased\u00a0<strong>gluconeogenesis<\/strong>.<\/li>\n<li>Decreased\u00a0<strong>glycogen<\/strong>\u00a0storage.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Reduced bile secretion<\/strong>\u00a0\u2192\u00a0<strong>impaired fat digestion and absorption<\/strong>.<\/li>\n<li><strong>Bleeding tendencies<\/strong>: due to\u00a0<strong>clotting factor deficiencies<\/strong>.<\/li>\n<\/ul>\n<h1><strong>Summary<\/strong><\/h1>\n<ul>\n<li>Cirrhosis results from ongoing liver damage, often from alcohol or viral hepatitis.<\/li>\n<li>Leads to significant\u00a0<strong>fibrosis<\/strong>,\u00a0<strong>vascular changes<\/strong>, and\u00a0<strong>organ failure<\/strong>.<\/li>\n<li>Early detection and lifestyle modifications are critical to slow progression and prevent complications.<\/li>\n<\/ul>\n","protected":false},"author":1370,"menu_order":21,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-5400","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":67,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5400","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":6,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5400\/revisions"}],"predecessor-version":[{"id":5560,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5400\/revisions\/5560"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/67"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5400\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=5400"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=5400"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=5400"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=5400"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}