{"id":5410,"date":"2025-12-09T00:27:05","date_gmt":"2025-12-09T05:27:05","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=5410"},"modified":"2026-01-12T18:38:38","modified_gmt":"2026-01-12T23:38:38","slug":"cirrhosis-systemic-effects-and-clinical-manifestations","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/cirrhosis-systemic-effects-and-clinical-manifestations\/","title":{"raw":"10p19 Cirrhosis: Systemic Effects and Clinical Manifestations","rendered":"10p19 Cirrhosis: Systemic Effects and Clinical Manifestations"},"content":{"raw":"Cirrhosis: Systemic Effects and Clinical Manifestations<\/strong>\r\n

Pathophysiology and Systemic Manifestations<\/strong><\/h1>\r\n

1.\u00a0 Vascular Changes and Portal Hypertension<\/strong><\/h1>\r\n
    \r\n \t
  • Damage to blood vessels causes\u00a0engorged<\/strong>\u00a0and\u00a0leaky<\/strong>\u00a0vessels.<\/li>\r\n \t
  • Results in\u00a0portal hypertension<\/strong>, leading to:\r\n
      \r\n \t
    • Ascites<\/strong>: Fluid accumulation in the abdominal cavity.<\/li>\r\n \t
    • Edema from\u00a0fluid leakage<\/strong>\u00a0into tissues.<\/li>\r\n \t
    • Splenomegaly<\/strong>\u00a0(enlarged spleen) due to blood congestion.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n

      2.\u00a0 Blood Volume and Kidney Response<\/strong><\/h1>\r\n
        \r\n \t
      • Hypovolemia<\/strong>\u00a0triggers\u00a0renin-angiotensin-aldosterone system (RAAS)<\/strong>:\r\n
          \r\n \t
        • Increased\u00a0aldosterone<\/strong>\u00a0and\u00a0ADH<\/strong>\u00a0retention of water and salt.<\/li>\r\n \t
        • Worsens\u00a0portal hypertension<\/strong>\u00a0and ascites.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
        • Reduced plasma proteins<\/strong>\u00a0(like\u00a0albumin<\/strong>):\r\n
            \r\n \t
          • Causes\u00a0fluid shifts<\/strong>\u00a0into tissues, worsening edema and ascites.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n

            3.\u00a0 Liver Cellular Dysfunction<\/strong><\/h1>\r\n
              \r\n \t
            • Loss of\u00a0hepatocyte<\/strong>\u00a0function:\r\n
                \r\n \t
              • Reduced\u00a0gluconeogenesis<\/strong>.<\/li>\r\n \t
              • Decreased\u00a0bile production<\/strong>\u00a0\u2192 poor fat absorption and deficiency of\u00a0fat-soluble vitamins<\/strong>\u00a0(D, E, K<\/strong>).<\/li>\r\n \t
              • Impaired\u00a0protein synthesis<\/strong>, affecting\u00a0clotting factors<\/strong>, leading to\u00a0bleeding<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n

                4.\u00a0 Bilirubin Metabolism and Jaundice<\/strong><\/h1>\r\n
                  \r\n \t
                • Inability to conjugate bilirubin results in\u00a0hyperbilirubinemia<\/strong>.<\/li>\r\n \t
                • Yellow pigmentation of\u00a0skin<\/strong>\u00a0and\u00a0eyes<\/strong>\u00a0(jaundice<\/strong>).<\/li>\r\n<\/ul>\r\n

                  5.\u00a0 Hepatic Encephalopathy<\/strong><\/h1>\r\n
                    \r\n \t
                  • Failure to detoxify\u00a0ammonia<\/strong>\u00a0and other toxins.<\/li>\r\n \t
                  • Build-up causes:\r\n
                      \r\n \t
                    • Tremors<\/strong>.<\/li>\r\n \t
                    • Confusion<\/strong>.<\/li>\r\n \t
                    • Lethargy<\/strong>.<\/li>\r\n \t
                    • Coma<\/strong>\u00a0and\/or\u00a0death<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n

                      6.\u00a0 Impaired Hormone Metabolism<\/strong><\/h1>\r\n
                        \r\n \t
                      • Estrogen<\/strong> not inactivated properly.\r\n
                          \r\n \t
                        • Causes\u00a0gynecomastia<\/strong>\u00a0in men (breast development).<\/li>\r\n \t
                        • Irregular\u00a0menses<\/strong>\u00a0in women.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                        • Impotence<\/strong>\u00a0in men.<\/li>\r\n<\/ul>\r\n \r\n

                          Clinical Signs & Symptoms (Summary Table)<\/strong><\/h1>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n
                          Early Signs and Symptoms:<\/strong><\/td>\r\n<\/td>\r\n<\/tr>\r\n
                          Fatigue and weakness<\/td>\r\nHepatocytes have reduced ability to perform gluconeogenesis<\/strong> (contributing to less blood glucose).\r\n\r\nHepatocyte death is accompanied by inflammation,<\/strong> which can stimulate mental and physical fatigue.\r\n\r\nHepatocytes are less able to convert protein break-down product, ammonia (toxic) to urea for excretion by the kidneys.\u00a0 Ammonia<\/strong> impairs brain function.<\/td>\r\n<\/tr>\r\n
                          Nausea, vomiting, anorexia, and diarrhea<\/td>\r\nToxins (e.g., ammonia) can stimulate emetic center.\r\n\r\nAscites creates pressure on stomach, which can stimulate nausea<\/td>\r\n<\/tr>\r\n
                          Weight loss, malabsorption<\/td>\r\nHepatocytes have reduced ability to produce bile,<\/strong> decreasing the ability to emulsify dietary fats<\/strong>, and therefore reducing the ability to absorb dietary fats and fat-soluble vitamins<\/strong> (including vitamin K<\/strong> which is required for the production of clotting factors).<\/td>\r\n<\/tr>\r\n
                          Anemia<\/td>\r\nRBC production is reduced due to toxins (e.g., ammonia) and malabsorption of vitamin B12<\/sub> and ability to store iron (the liver is the primary storage site for iron).<\/td>\r\n<\/tr>\r\n
                          Pruritis (itchy skin)<\/td>\r\nDue to liver damage resulting in impaired flow of bile into gall bladder.\u00a0 \u00a0Bile salts accumulate in blood which irritates sensory nerves in the skin.<\/td>\r\n<\/tr>\r\n
                          Spider angiomas (nevi)\r\n\r\nGynecomastia, Irregular menses\r\n\r\nTesticular atrophy,\u00a0Reduced libido<\/td>\r\nDue to the liver unable to breakdown estrogen which accumulates, giving rise to vasodilation and angiogenesis.\r\n\r\nDue to increased estrogen stimulating growth breast tissue and disrupting uterine cycle.\r\n\r\nDue to decreased testosterone<\/td>\r\n<\/tr>\r\n
                          Pain under ribs on right side<\/td>\r\nDue to stretching of liver capsule during inflammation<\/td>\r\n<\/tr>\r\n
                          Later Signs and Symptoms:<\/strong><\/td>\r\n<\/td>\r\n<\/tr>\r\n
                          Jaundice<\/td>\r\nDue to reduced conjugation of bilirubin by hepatocytes, leading to hyperbilirubinemia<\/td>\r\n<\/tr>\r\n
                          Dark urine\r\n\r\nPale stools<\/td>\r\nDue to hyperbilirubinemia\r\n\r\nDue to less bile production<\/td>\r\n<\/tr>\r\n
                          Easy bruising and bleeding (e.g., nose bleeds)<\/td>\r\nDue to reduced production of clotting factors by hepatocytes.<\/td>\r\n<\/tr>\r\n
                          Ascites<\/td>\r\nDue to liver fibrosis pinching off blood flow to the liver, resulting in the engorgement of the portal vein, leading to portal hypertension and leakage of fluid from the portal vein into the peritoneal cavity.<\/td>\r\n<\/tr>\r\n
                          Edema of intestinal wall<\/td>\r\nDue to portal vein hypertension. Congestion in intestinal wall can impair digestion and absorption.<\/td>\r\n<\/tr>\r\n
                          General edema and ascites<\/td>\r\nDue to reduced blood flow to kidneys (due to leakage of fluid into peritoneum, ascites), stimulating kidneys to secrete renin and activate aldosterone and ADH, which increase water and salt reabsorption, increasing blood volume.\r\n\r\nDue to hepatocytes reduce ability to produce plasma proteins including albumin, which are required for transport of nutrients as well as ensuring osmotic pressure within blood vessels.\u00a0 Without plasma proteins (solute), blood vessels are more leaky.\r\n\r\nBlocked lymphatics<\/td>\r\n<\/tr>\r\n
                          Esophageal varices (enlarged veins)<\/td>\r\nEsophageal veins become engorged as liver fibrosis pinches off blood flow into the liver, causing blood to back up into the esophageal veins, which become engorged.<\/td>\r\n<\/tr>\r\n
                          Vomiting blood (hematemesis), black tarry stools (melena)<\/td>\r\nDue to bleeding from esophageal or gastric varices (enlarged veins), as the esophageal\/gastric blood vessels become thin and fragile and are susceptible to tears as food passes through the esophagus\/stomach.\u00a0 Rectal varices can also occur.<\/td>\r\n<\/tr>\r\n
                          Splenomegaly and\r\n\r\nLeukopenia, Thrombocytopenia<\/td>\r\nDue to portal vein hypertension, blood backs up into spleen causing damage and trapping and possible destruction of WBCs and platelets within spleen.\u00a0 \u00a0The spleen normally stores 1\/3rd of the body's platelets.\u00a0 Congestion in spleen can also increase hemolysis.\r\n\r\nIncreased risk of infection<\/td>\r\n<\/tr>\r\n
                          Hepatic encephalopathy (confusion, memory loss, forgetfulness, personality changes, irritability, disinterest in personal care)<\/td>\r\nDue to hepatocytes unable to degrade and clear toxins (e.g., ammonia, the natural break-down product of proteins) from the body.<\/td>\r\n<\/tr>\r\n
                          Cerebral edema, kidney failure<\/td>\r\nDue to altered blood chemistry (abnormal electrolytes, increased ammonia, reduced nutrients).<\/td>\r\n<\/tr>\r\n
                          Dyspnea\r\n\r\nFast heart rate<\/td>\r\nUpward pressure from ascites on diaphragm\r\n\r\nActivation of the sympathetic response due to poor blood flow and reduced blood oxygenation.<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n

                          Conclusion<\/strong><\/h1>\r\n
                            \r\n \t
                          • Cirrhosis<\/strong> causes widespread organ dysfunction due to fibrosis,<\/strong> vascular changes<\/strong>, and cellular impairment<\/strong>.<\/li>\r\n \t
                          • Symptoms develop gradually but can be life-threatening if untreated.<\/li>\r\n \t
                          • Management involves addressing symptoms, preventing complications, and possibly liver transplantation.<\/li>\r\n<\/ul>","rendered":"

                            Cirrhosis: Systemic Effects and Clinical Manifestations<\/strong><\/p>\n

                            Pathophysiology and Systemic Manifestations<\/strong><\/h1>\n

                            1.\u00a0 Vascular Changes and Portal Hypertension<\/strong><\/h1>\n
                              \n
                            • Damage to blood vessels causes\u00a0engorged<\/strong>\u00a0and\u00a0leaky<\/strong>\u00a0vessels.<\/li>\n
                            • Results in\u00a0portal hypertension<\/strong>, leading to:\n
                                \n
                              • Ascites<\/strong>: Fluid accumulation in the abdominal cavity.<\/li>\n
                              • Edema from\u00a0fluid leakage<\/strong>\u00a0into tissues.<\/li>\n
                              • Splenomegaly<\/strong>\u00a0(enlarged spleen) due to blood congestion.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                2.\u00a0 Blood Volume and Kidney Response<\/strong><\/h1>\n
                                  \n
                                • Hypovolemia<\/strong>\u00a0triggers\u00a0renin-angiotensin-aldosterone system (RAAS)<\/strong>:\n
                                    \n
                                  • Increased\u00a0aldosterone<\/strong>\u00a0and\u00a0ADH<\/strong>\u00a0retention of water and salt.<\/li>\n
                                  • Worsens\u00a0portal hypertension<\/strong>\u00a0and ascites.<\/li>\n<\/ul>\n<\/li>\n
                                  • Reduced plasma proteins<\/strong>\u00a0(like\u00a0albumin<\/strong>):\n
                                      \n
                                    • Causes\u00a0fluid shifts<\/strong>\u00a0into tissues, worsening edema and ascites.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                      3.\u00a0 Liver Cellular Dysfunction<\/strong><\/h1>\n
                                        \n
                                      • Loss of\u00a0hepatocyte<\/strong>\u00a0function:\n
                                          \n
                                        • Reduced\u00a0gluconeogenesis<\/strong>.<\/li>\n
                                        • Decreased\u00a0bile production<\/strong>\u00a0\u2192 poor fat absorption and deficiency of\u00a0fat-soluble vitamins<\/strong>\u00a0(D, E, K<\/strong>).<\/li>\n
                                        • Impaired\u00a0protein synthesis<\/strong>, affecting\u00a0clotting factors<\/strong>, leading to\u00a0bleeding<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                          4.\u00a0 Bilirubin Metabolism and Jaundice<\/strong><\/h1>\n
                                            \n
                                          • Inability to conjugate bilirubin results in\u00a0hyperbilirubinemia<\/strong>.<\/li>\n
                                          • Yellow pigmentation of\u00a0skin<\/strong>\u00a0and\u00a0eyes<\/strong>\u00a0(jaundice<\/strong>).<\/li>\n<\/ul>\n

                                            5.\u00a0 Hepatic Encephalopathy<\/strong><\/h1>\n
                                              \n
                                            • Failure to detoxify\u00a0ammonia<\/strong>\u00a0and other toxins.<\/li>\n
                                            • Build-up causes:\n
                                                \n
                                              • Tremors<\/strong>.<\/li>\n
                                              • Confusion<\/strong>.<\/li>\n
                                              • Lethargy<\/strong>.<\/li>\n
                                              • Coma<\/strong>\u00a0and\/or\u00a0death<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                                6.\u00a0 Impaired Hormone Metabolism<\/strong><\/h1>\n
                                                  \n
                                                • Estrogen<\/strong> not inactivated properly.\n
                                                    \n
                                                  • Causes\u00a0gynecomastia<\/strong>\u00a0in men (breast development).<\/li>\n
                                                  • Irregular\u00a0menses<\/strong>\u00a0in women.<\/li>\n<\/ul>\n<\/li>\n
                                                  • Impotence<\/strong>\u00a0in men.<\/li>\n<\/ul>\n

                                                     <\/p>\n

                                                    Clinical Signs & Symptoms (Summary Table)<\/strong><\/h1>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
                                                    Early Signs and Symptoms:<\/strong><\/td>\n<\/td>\n<\/tr>\n
                                                    Fatigue and weakness<\/td>\nHepatocytes have reduced ability to perform gluconeogenesis<\/strong> (contributing to less blood glucose).<\/p>\n

                                                    Hepatocyte death is accompanied by inflammation,<\/strong> which can stimulate mental and physical fatigue.<\/p>\n

                                                    Hepatocytes are less able to convert protein break-down product, ammonia (toxic) to urea for excretion by the kidneys.\u00a0 Ammonia<\/strong> impairs brain function.<\/td>\n<\/tr>\n

                                                    Nausea, vomiting, anorexia, and diarrhea<\/td>\nToxins (e.g., ammonia) can stimulate emetic center.<\/p>\n

                                                    Ascites creates pressure on stomach, which can stimulate nausea<\/td>\n<\/tr>\n

                                                    Weight loss, malabsorption<\/td>\nHepatocytes have reduced ability to produce bile,<\/strong> decreasing the ability to emulsify dietary fats<\/strong>, and therefore reducing the ability to absorb dietary fats and fat-soluble vitamins<\/strong> (including vitamin K<\/strong> which is required for the production of clotting factors).<\/td>\n<\/tr>\n
                                                    Anemia<\/td>\nRBC production is reduced due to toxins (e.g., ammonia) and malabsorption of vitamin B12<\/sub> and ability to store iron (the liver is the primary storage site for iron).<\/td>\n<\/tr>\n
                                                    Pruritis (itchy skin)<\/td>\nDue to liver damage resulting in impaired flow of bile into gall bladder.\u00a0 \u00a0Bile salts accumulate in blood which irritates sensory nerves in the skin.<\/td>\n<\/tr>\n
                                                    Spider angiomas (nevi)<\/p>\n

                                                    Gynecomastia, Irregular menses<\/p>\n

                                                    Testicular atrophy,\u00a0Reduced libido<\/td>\n

                                                    		Due to the liver unable to breakdown estrogen which accumulates, giving rise to vasodilation and angiogenesis.<\/p>\n

                                                    Due to increased estrogen stimulating growth breast tissue and disrupting uterine cycle.<\/p>\n

                                                    Due to decreased testosterone<\/td>\n<\/tr>\n

                                                    Pain under ribs on right side<\/td>\nDue to stretching of liver capsule during inflammation<\/td>\n<\/tr>\n
                                                    Later Signs and Symptoms:<\/strong><\/td>\n<\/td>\n<\/tr>\n
                                                    Jaundice<\/td>\nDue to reduced conjugation of bilirubin by hepatocytes, leading to hyperbilirubinemia<\/td>\n<\/tr>\n
                                                    Dark urine<\/p>\n

                                                    Pale stools<\/td>\n

                                                    		Due to hyperbilirubinemia<\/p>\n

                                                    Due to less bile production<\/td>\n<\/tr>\n

                                                    Easy bruising and bleeding (e.g., nose bleeds)<\/td>\nDue to reduced production of clotting factors by hepatocytes.<\/td>\n<\/tr>\n
                                                    Ascites<\/td>\nDue to liver fibrosis pinching off blood flow to the liver, resulting in the engorgement of the portal vein, leading to portal hypertension and leakage of fluid from the portal vein into the peritoneal cavity.<\/td>\n<\/tr>\n
                                                    Edema of intestinal wall<\/td>\nDue to portal vein hypertension. Congestion in intestinal wall can impair digestion and absorption.<\/td>\n<\/tr>\n
                                                    General edema and ascites<\/td>\nDue to reduced blood flow to kidneys (due to leakage of fluid into peritoneum, ascites), stimulating kidneys to secrete renin and activate aldosterone and ADH, which increase water and salt reabsorption, increasing blood volume.<\/p>\n

                                                    Due to hepatocytes reduce ability to produce plasma proteins including albumin, which are required for transport of nutrients as well as ensuring osmotic pressure within blood vessels.\u00a0 Without plasma proteins (solute), blood vessels are more leaky.<\/p>\n

                                                    Blocked lymphatics<\/td>\n<\/tr>\n

                                                    Esophageal varices (enlarged veins)<\/td>\nEsophageal veins become engorged as liver fibrosis pinches off blood flow into the liver, causing blood to back up into the esophageal veins, which become engorged.<\/td>\n<\/tr>\n
                                                    Vomiting blood (hematemesis), black tarry stools (melena)<\/td>\nDue to bleeding from esophageal or gastric varices (enlarged veins), as the esophageal\/gastric blood vessels become thin and fragile and are susceptible to tears as food passes through the esophagus\/stomach.\u00a0 Rectal varices can also occur.<\/td>\n<\/tr>\n
                                                    Splenomegaly and<\/p>\n

                                                    Leukopenia, Thrombocytopenia<\/td>\n

                                                    		Due to portal vein hypertension, blood backs up into spleen causing damage and trapping and possible destruction of WBCs and platelets within spleen.\u00a0 \u00a0The spleen normally stores 1\/3rd of the body’s platelets.\u00a0 Congestion in spleen can also increase hemolysis.<\/p>\n

                                                    Increased risk of infection<\/td>\n<\/tr>\n

                                                    Hepatic encephalopathy (confusion, memory loss, forgetfulness, personality changes, irritability, disinterest in personal care)<\/td>\nDue to hepatocytes unable to degrade and clear toxins (e.g., ammonia, the natural break-down product of proteins) from the body.<\/td>\n<\/tr>\n
                                                    Cerebral edema, kidney failure<\/td>\nDue to altered blood chemistry (abnormal electrolytes, increased ammonia, reduced nutrients).<\/td>\n<\/tr>\n
                                                    Dyspnea<\/p>\n

                                                    Fast heart rate<\/td>\n

                                                    		Upward pressure from ascites on diaphragm<\/p>\n

                                                    Activation of the sympathetic response due to poor blood flow and reduced blood oxygenation.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

                                                    Conclusion<\/strong><\/h1>\n
                                                      \n
                                                    • Cirrhosis<\/strong> causes widespread organ dysfunction due to fibrosis,<\/strong> vascular changes<\/strong>, and cellular impairment<\/strong>.<\/li>\n
                                                    • Symptoms develop gradually but can be life-threatening if untreated.<\/li>\n
                                                    • Management involves addressing symptoms, preventing complications, and possibly liver transplantation.<\/li>\n<\/ul>\n","protected":false},"author":1370,"menu_order":22,"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-5410","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\/5410","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":19,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5410\/revisions"}],"predecessor-version":[{"id":5578,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5410\/revisions\/5578"}],"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\/5410\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=5410"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=5410"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=5410"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=5410"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}