{"id":5173,"date":"2025-12-04T00:44:43","date_gmt":"2025-12-04T05:44:43","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=5173"},"modified":"2026-01-12T18:38:38","modified_gmt":"2026-01-12T23:38:38","slug":"alcoholic-cirrhosis-patient-medical-education-pamphlet-student-activity","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/alcoholic-cirrhosis-patient-medical-education-pamphlet-student-activity\/","title":{"raw":"Alcoholic Cirrhosis - Patient Medical Education Pamphlet - Student Activity","rendered":"Alcoholic Cirrhosis &#8211; Patient Medical Education Pamphlet &#8211; Student Activity"},"content":{"raw":"<h1><strong>Etiology: <\/strong><\/h1>\r\nThe liver tolerates low levels of alcohol consumption.\u00a0 However, daily consumption of 30-50 grams of alcohol can cause alcoholic liver in approximately 5 years.\r\n\r\nFYI:\u00a0 The definition of 1 alcohol drink is 13.7 grams alcohol (i.e. the equivalent of 12oz. 5% alcohol beer, or 8oz 7% alcohol liquor, or 5oz 12% alcohol wine, or 1.5oz 40% hard-liquor).\r\n<h1><strong>Risk Factors:<\/strong><\/h1>\r\n<strong>Non-modifiable risk factors<\/strong>: include:\u00a0 genetic, metabolic, and immunological\r\n\r\n<strong>Modifiable risk factors include:<\/strong> high-fat diet and at-risk drinking behaviours\r\n\r\nAt risk drinking behaviours include:\r\n<ul>\r\n \t<li>Males: over 14 drinks per week or more than 4 drinks per occasion<\/li>\r\n \t<li>Females and adults over 65ys old: over 7 drinks per week or more than 3 drinks per occasion<\/li>\r\n<\/ul>\r\n\u201cDefinitions of significant drinking from a liver toxicity standpoint are as below (this history is essential to differentiate non-alcoholic fatty liver disease (NAFLD)\u00a0 from alcoholic fatty liver disease (AFLD)\r\n<ul>\r\n \t<li>Men: more than 21 drinks per week<\/li>\r\n \t<li>Women: over 14 drinks per week\u201d<\/li>\r\n<\/ul>\r\nReference for above information:\u00a0 <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK546632\/\">https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK546632\/<\/a>\r\n<h1><strong>Pathogenesis - Steps of Development:\u00a0\u00a0\u00a0 <\/strong><\/h1>\r\n<ol>\r\n \t<li><strong>Stage One of Alcoholic Fatty Liver Disease (AFLD) is \u201cFatty Liver\u201d or \u201cHepatic Steatosis\u201d (steatos is Greek for fat)<\/strong>\r\n<ol>\r\n \t<li>Alcohol metabolism increases triglyceride (lipid) formation which accumulates in liver cells (hepatocytes)<\/li>\r\n \t<li>Lipolysis decreases during alcohol consumption and fat droplets increase inside hepatocytes.<\/li>\r\n \t<li>Hepatomegaly; hepatocytes accumulate triglyceride fat in vacuoles as they are no longer able to process it.<\/li>\r\n \t<li>Asymptomatic and reversible with reduced alcohol intake<\/li>\r\n \t<li>Hepatocytes normally turn over every 5 months, making the liver fairly regenerative, however, when the amount of damage exceeds the ability of the hepatocytes to regenerate, damage becomes permanent.<\/li>\r\n<\/ol>\r\n<\/li>\r\n \t<li><strong>Stage Two of Alcoholic Fatty Liver Disease (AFLD) is \u201cAlcoholic Hepatitis\u201d (hepatitis = liver inflammation)<\/strong>\r\n<ol>\r\n \t<li>As hepatocytes become less functional and injured, WBCs are activated<\/li>\r\n \t<li>Neutrophils begin to attack hepatocytes and the Inflammatory response is triggered by Mast Cells and Basophils. Inflammation and cell necrosis occurs.<\/li>\r\n \t<li>Fibrous (collagen scar) tissue formation (scarring replaces hepatocytes)\u2014irreversible change<\/li>\r\n \t<li>Mild symptoms \u2013 anorexia, nausea, liver tenderness; bout of heavy alcohol consumption can lead to liver failure, encephalopathy &amp; death<\/li>\r\n<\/ol>\r\n<\/li>\r\n \t<li><strong>Stage Three of Alcoholic Fatty Liver Disease (AFLD) is End-Stage Cirrhosis<\/strong>\r\n<ol>\r\n \t<li>Depicted by increased necrosis of hepatocytes and scarring (fibrosis). Liver shrinks in size<\/li>\r\n \t<li>Little normal function of liver remains<\/li>\r\n \t<li>Extensive diffuse fibrosis interferes with blood supply ; Bile may back up; Loss of lobular organization (nodules of regenerated hepatocytes may appear, but are not functional due to distorted blood vessels &amp; biliary ducts)<\/li>\r\n \t<li>Degenerative changes may be asymptomatic until disease is well advanced (80-90% of liver destroyed).<\/li>\r\n \t<li>Signs of portal hypertension (e.g. ascites), impaired digestion &amp; absorptions<\/li>\r\n<\/ol>\r\n<\/li>\r\n<\/ol>\r\n<h1>Why Portal Hypertension?<\/h1>\r\n<ul>\r\n \t<li><strong>Portal Hypertension<\/strong> <span style=\"font-size: 1em\">occurs because the fibrosis within the liver impinges the blood vessels within the liver creating resistance to blood flow.\u00a0<\/span><\/li>\r\n \t<li>Therefore the portal vein becomes engorged and exhibits high pressure.<\/li>\r\n \t<li>The portal vein carries blood from the esophagus, stomach, small &amp; large intestines, spleen, pancreas and gallbladder meaning that the engorgement and hypertension builds up within those tissues as well.<\/li>\r\n \t<li>This leads to: <strong>varices<\/strong> (engorged veins) which can rupture and bleed.<\/li>\r\n \t<li>Engorged blood vessel cause splenic congestion and enlargement of the spleen <strong>(splenomegaly)<\/strong> and\r\n<ul>\r\n \t<li><strong>esophageal varices<\/strong> (which are easily torn by food passage, causing hemorrhaging).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Congestion of spleen increases hemolysis (RBC lysis) and drop in WBC and platelet numbers.<\/li>\r\n \t<li>Congestion in intestinal walls &amp; stomach Impairing digestion &amp; absorption.<\/li>\r\n \t<li><strong>Decreased blood volume into kidneys<\/strong>\r\n<ul>\r\n \t<li>stimulates activation of <strong>renin, aldosterone<\/strong> and <strong>ADH,<\/strong> leading to increase Na+ and water retention,<\/li>\r\n \t<li>contributing to increases in blood volume and portal hypertension, leading to <strong>ascites.<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Blocked lymphatics<\/strong> as well as decreased liver\u2019s synthesis of plasma protein <strong>albumin<\/strong> contribute to decreased plasmas <strong>osmotic pressure,<\/strong>\r\n<ul>\r\n \t<li>which increase fluid shift from blood into peritoneal cavity creating more <strong>ascites.<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Signs &amp; Symptoms (and why each occurs):<\/strong><\/h1>\r\n<strong>Loss of hepatocyte function causes:<\/strong>\r\n<ol>\r\n \t<li><strong>Ascites: <\/strong>due to portal hypertension, elevated renin, aldosterone and ADH levels, decreased serum albumin level and decreased plasma osmotic pressure, lymphatic obstruction in liver.<\/li>\r\n \t<li><strong>General edema:<\/strong> also due to elevated renin, aldosterone and ADH levels, decreased serum albumin level and decreased plasma osmotic pressure, lymphatic obstruction in liver<\/li>\r\n \t<li><strong>Esophageal varices and hemorrhoids<\/strong> (engorged blood vessels) and possible tears:\u00a0 due to portal hypertension<\/li>\r\n \t<li>Splenomegaly<\/li>\r\n \t<li>Anemia, Fatigue<\/li>\r\n \t<li>Anorexia, Indigestion, Weight Loss:<\/li>\r\n \t<li>Leukopenia, Thrombocytopenia<\/li>\r\n \t<li>Increased bleeding<\/li>\r\n \t<li>Purpura<\/li>\r\n \t<li>Hepatic encephalopathy, tremors, confusion, coma<\/li>\r\n \t<li>Gynecomastia, impotence, irregular menses<\/li>\r\n \t<li>Jaundice<\/li>\r\n \t<li><strong>Impaired<\/strong><strong> conversion of protein breakdown product, ammonia to urea (to be excreted in urine)<\/strong><\/li>\r\n \t<li><strong>Decreased<\/strong><strong> inactivation of hormones and drugs<\/strong>\r\n<ul>\r\n \t<li><strong>Drug dosages must be carefully monitored to avoid toxicity.<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Decreased<\/strong><strong> removal of toxic substances (<em>ammonia, drugs<\/em>)<\/strong><\/li>\r\n \t<li><strong>Blood Chemistry is altered (<em>abnormal electrolytes, amino acids, \u2191 ammonia<\/em>) causing hepatic encephalopathy, &amp; increased clotting times (due to \u2193 clotting proteins).<\/strong><\/li>\r\n<\/ol>\r\n<h1><strong>Signs &amp; symptoms:<\/strong><\/h1>\r\n<strong>Initial manifestations\u00a0<\/strong><strong>often mild &amp; vague: <\/strong>\r\n<ul>\r\n \t<li>Fatigue, anorexia, weight loss, anemia, diarrhea<\/li>\r\n \t<li>Dull aching pain may be present in RUQ (right upper quadrant).<\/li>\r\n<\/ul>\r\n<strong>Advanced cirrhosis: <\/strong>\r\n<ul>\r\n \t<li>Ascites &amp; peripheral edema; pruritus<\/li>\r\n \t<li>\u2191 bruising; \u2193 healing &amp; tissue maintenance<\/li>\r\n \t<li>Esophageal varices - May rupture, leading\u00a0 to hemorrhage, circulatory shock, Jaundice<\/li>\r\n \t<li>Obstruction of bile ducts &amp; blood flow by fibrous tissue causes:<\/li>\r\n \t<li>Reduction of bile entering the intestine\u00a0 \u2192\u00a0 Impairs digestion and absorption!<\/li>\r\n \t<li>Backup of bile in the liver \u2192 Leads to obstructive jaundice (note that intrahepatic jaundice now co-exists with obstructive jaundice!)<\/li>\r\n \t<li>Sex hormone imbalance \u2192 spider nevi, testicular atrophy, impotence, gynecomastia, irregular menses.<\/li>\r\n \t<li>Acute encephalopathy (asterixis\/hand-flapping, confusion, convulsions, coma) or<\/li>\r\n \t<li>Chronic encephalopathy (personality changes, memory lapses, irritability, disinterest in personal care)<\/li>\r\n<\/ul>\r\n<h1><strong>Diagnostic Tools:<\/strong><\/h1>\r\n<ol>\r\n \t<li>Imaging,<\/li>\r\n \t<li>Blood tests for blood counts and abnormal presence of liver proteins\/enzymes in blood (indicating hepatocyte death\/dysfunction)<\/li>\r\n<\/ol>\r\n<h1><strong>Treatments:<\/strong><\/h1>\r\n<ol>\r\n \t<li>Avoid fatigue &amp; exposure to infection<\/li>\r\n \t<li>Avoidance of alcohol or specific cause<\/li>\r\n \t<li>Supportive or symptomatic treatment<\/li>\r\n \t<li>Dietary restrictions on protein &amp; salt<\/li>\r\n \t<li>Increased intake of carbohydrate &amp; vitamin supplements<\/li>\r\n \t<li>Balancing serum electrolytes (possibly with diuretics)<\/li>\r\n \t<li>Paracentesis to remove excess fluid<\/li>\r\n \t<li>Albumin transfusions to prevent third spacing<\/li>\r\n \t<li>Antibiotics to reduce intestinal flora<\/li>\r\n \t<li>Emergency treatment if esophageal varices rupture<\/li>\r\n \t<li>Portocaval shunts to reduce portal hypertension<\/li>\r\n \t<li>Liver transplantation (can be from living donors!)<\/li>\r\n<\/ol>\r\n<h1><strong>3 Types of Jaundice:<\/strong><\/h1>\r\n<strong>Compare Prehepatic Jaundice, Intrahepatic Jaundice and Posthepatic Jaundice giving an example of a cause of each:<\/strong>\r\n<ul>\r\n \t<li><strong>Jaundice: <\/strong>The yellowish colour of sclera of eyes, skin &amp; other tissues due to hyperbilirubinemia<strong>.<\/strong><\/li>\r\n \t<li>Is a sign of a disease or disorder.<\/li>\r\n<\/ul>\r\n<strong>Three types of disorders can cause jaundice<\/strong>\r\n\r\n<strong>1. <span style=\"text-decoration: underline\">Pre-hepatic jaundice<\/span>: <\/strong>\r\n<ul>\r\n \t<li><strong>Caused by excessive destruction of red blood cells (<em>&amp; liver can\u2019t keep up in breaking down of bilirubin \u2013 which is a breakdown product of hemoglobin\u2019s heme pigment<\/em>)<\/strong><\/li>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Characteristic of hemolytic anemias or transfusion reactions<\/strong><\/li>\r\n \t<li><strong>Physiological jaundice of the newborn \u2013 common 2-3 days after birth \u2026. Treated with phototherapy (bili light)<\/strong><\/li>\r\n \t<li><strong>Prehepatic Jaundice is a result of: \u2191 unconjugated bilirubin in serum<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<strong>2. <span style=\"text-decoration: underline\">Intra-hepatic jaundice<\/span>: <\/strong>\r\n<ul>\r\n \t<li><strong>Occurs with disease or damage to hepatocytes (<em>can no longer uptake bilirubin and\/or can no longer conjugate bilirubin<\/em>)\u00a0 <\/strong><\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Hepatitis<\/strong><strong> or cirrhosis<\/strong><\/li>\r\n \t<li><strong>Intrahepatic jaundice results in \u2191 unconjugated &amp; conjugated bilirubin in serum<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<strong>3. <span style=\"text-decoration: underline\">Post-hepatic jaundice<\/span>: <\/strong>\r\n<ul>\r\n \t<li><strong>Caused by obstruction of bile flow into gall-bladder or duodenum &amp; subsequent backup of bile into the blood\u2026 causes pruritus (itchiness) of the skin (due to bile salt deposits) and \u2193 digestion.<\/strong><\/li>\r\n<\/ul>\r\n<ol>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Caused by Tumor<\/strong><strong>, or choledocholithiasis <\/strong><\/li>\r\n \t<li><strong>Posthepatic Jaundice is due to \u2191 conjugated bilirubin in serum<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>","rendered":"<h1><strong>Etiology: <\/strong><\/h1>\n<p>The liver tolerates low levels of alcohol consumption.\u00a0 However, daily consumption of 30-50 grams of alcohol can cause alcoholic liver in approximately 5 years.<\/p>\n<p>FYI:\u00a0 The definition of 1 alcohol drink is 13.7 grams alcohol (i.e. the equivalent of 12oz. 5% alcohol beer, or 8oz 7% alcohol liquor, or 5oz 12% alcohol wine, or 1.5oz 40% hard-liquor).<\/p>\n<h1><strong>Risk Factors:<\/strong><\/h1>\n<p><strong>Non-modifiable risk factors<\/strong>: include:\u00a0 genetic, metabolic, and immunological<\/p>\n<p><strong>Modifiable risk factors include:<\/strong> high-fat diet and at-risk drinking behaviours<\/p>\n<p>At risk drinking behaviours include:<\/p>\n<ul>\n<li>Males: over 14 drinks per week or more than 4 drinks per occasion<\/li>\n<li>Females and adults over 65ys old: over 7 drinks per week or more than 3 drinks per occasion<\/li>\n<\/ul>\n<p>\u201cDefinitions of significant drinking from a liver toxicity standpoint are as below (this history is essential to differentiate non-alcoholic fatty liver disease (NAFLD)\u00a0 from alcoholic fatty liver disease (AFLD)<\/p>\n<ul>\n<li>Men: more than 21 drinks per week<\/li>\n<li>Women: over 14 drinks per week\u201d<\/li>\n<\/ul>\n<p>Reference for above information:\u00a0 <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK546632\/\">https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK546632\/<\/a><\/p>\n<h1><strong>Pathogenesis &#8211; Steps of Development:\u00a0\u00a0\u00a0 <\/strong><\/h1>\n<ol>\n<li><strong>Stage One of Alcoholic Fatty Liver Disease (AFLD) is \u201cFatty Liver\u201d or \u201cHepatic Steatosis\u201d (steatos is Greek for fat)<\/strong>\n<ol>\n<li>Alcohol metabolism increases triglyceride (lipid) formation which accumulates in liver cells (hepatocytes)<\/li>\n<li>Lipolysis decreases during alcohol consumption and fat droplets increase inside hepatocytes.<\/li>\n<li>Hepatomegaly; hepatocytes accumulate triglyceride fat in vacuoles as they are no longer able to process it.<\/li>\n<li>Asymptomatic and reversible with reduced alcohol intake<\/li>\n<li>Hepatocytes normally turn over every 5 months, making the liver fairly regenerative, however, when the amount of damage exceeds the ability of the hepatocytes to regenerate, damage becomes permanent.<\/li>\n<\/ol>\n<\/li>\n<li><strong>Stage Two of Alcoholic Fatty Liver Disease (AFLD) is \u201cAlcoholic Hepatitis\u201d (hepatitis = liver inflammation)<\/strong>\n<ol>\n<li>As hepatocytes become less functional and injured, WBCs are activated<\/li>\n<li>Neutrophils begin to attack hepatocytes and the Inflammatory response is triggered by Mast Cells and Basophils. Inflammation and cell necrosis occurs.<\/li>\n<li>Fibrous (collagen scar) tissue formation (scarring replaces hepatocytes)\u2014irreversible change<\/li>\n<li>Mild symptoms \u2013 anorexia, nausea, liver tenderness; bout of heavy alcohol consumption can lead to liver failure, encephalopathy &amp; death<\/li>\n<\/ol>\n<\/li>\n<li><strong>Stage Three of Alcoholic Fatty Liver Disease (AFLD) is End-Stage Cirrhosis<\/strong>\n<ol>\n<li>Depicted by increased necrosis of hepatocytes and scarring (fibrosis). Liver shrinks in size<\/li>\n<li>Little normal function of liver remains<\/li>\n<li>Extensive diffuse fibrosis interferes with blood supply ; Bile may back up; Loss of lobular organization (nodules of regenerated hepatocytes may appear, but are not functional due to distorted blood vessels &amp; biliary ducts)<\/li>\n<li>Degenerative changes may be asymptomatic until disease is well advanced (80-90% of liver destroyed).<\/li>\n<li>Signs of portal hypertension (e.g. ascites), impaired digestion &amp; absorptions<\/li>\n<\/ol>\n<\/li>\n<\/ol>\n<h1>Why Portal Hypertension?<\/h1>\n<ul>\n<li><strong>Portal Hypertension<\/strong> <span style=\"font-size: 1em\">occurs because the fibrosis within the liver impinges the blood vessels within the liver creating resistance to blood flow.\u00a0<\/span><\/li>\n<li>Therefore the portal vein becomes engorged and exhibits high pressure.<\/li>\n<li>The portal vein carries blood from the esophagus, stomach, small &amp; large intestines, spleen, pancreas and gallbladder meaning that the engorgement and hypertension builds up within those tissues as well.<\/li>\n<li>This leads to: <strong>varices<\/strong> (engorged veins) which can rupture and bleed.<\/li>\n<li>Engorged blood vessel cause splenic congestion and enlargement of the spleen <strong>(splenomegaly)<\/strong> and\n<ul>\n<li><strong>esophageal varices<\/strong> (which are easily torn by food passage, causing hemorrhaging).<\/li>\n<\/ul>\n<\/li>\n<li>Congestion of spleen increases hemolysis (RBC lysis) and drop in WBC and platelet numbers.<\/li>\n<li>Congestion in intestinal walls &amp; stomach Impairing digestion &amp; absorption.<\/li>\n<li><strong>Decreased blood volume into kidneys<\/strong>\n<ul>\n<li>stimulates activation of <strong>renin, aldosterone<\/strong> and <strong>ADH,<\/strong> leading to increase Na+ and water retention,<\/li>\n<li>contributing to increases in blood volume and portal hypertension, leading to <strong>ascites.<\/strong><\/li>\n<\/ul>\n<\/li>\n<li><strong>Blocked lymphatics<\/strong> as well as decreased liver\u2019s synthesis of plasma protein <strong>albumin<\/strong> contribute to decreased plasmas <strong>osmotic pressure,<\/strong>\n<ul>\n<li>which increase fluid shift from blood into peritoneal cavity creating more <strong>ascites.<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Signs &amp; Symptoms (and why each occurs):<\/strong><\/h1>\n<p><strong>Loss of hepatocyte function causes:<\/strong><\/p>\n<ol>\n<li><strong>Ascites: <\/strong>due to portal hypertension, elevated renin, aldosterone and ADH levels, decreased serum albumin level and decreased plasma osmotic pressure, lymphatic obstruction in liver.<\/li>\n<li><strong>General edema:<\/strong> also due to elevated renin, aldosterone and ADH levels, decreased serum albumin level and decreased plasma osmotic pressure, lymphatic obstruction in liver<\/li>\n<li><strong>Esophageal varices and hemorrhoids<\/strong> (engorged blood vessels) and possible tears:\u00a0 due to portal hypertension<\/li>\n<li>Splenomegaly<\/li>\n<li>Anemia, Fatigue<\/li>\n<li>Anorexia, Indigestion, Weight Loss:<\/li>\n<li>Leukopenia, Thrombocytopenia<\/li>\n<li>Increased bleeding<\/li>\n<li>Purpura<\/li>\n<li>Hepatic encephalopathy, tremors, confusion, coma<\/li>\n<li>Gynecomastia, impotence, irregular menses<\/li>\n<li>Jaundice<\/li>\n<li><strong>Impaired<\/strong><strong> conversion of protein breakdown product, ammonia to urea (to be excreted in urine)<\/strong><\/li>\n<li><strong>Decreased<\/strong><strong> inactivation of hormones and drugs<\/strong>\n<ul>\n<li><strong>Drug dosages must be carefully monitored to avoid toxicity.<\/strong><\/li>\n<\/ul>\n<\/li>\n<li><strong>Decreased<\/strong><strong> removal of toxic substances (<em>ammonia, drugs<\/em>)<\/strong><\/li>\n<li><strong>Blood Chemistry is altered (<em>abnormal electrolytes, amino acids, \u2191 ammonia<\/em>) causing hepatic encephalopathy, &amp; increased clotting times (due to \u2193 clotting proteins).<\/strong><\/li>\n<\/ol>\n<h1><strong>Signs &amp; symptoms:<\/strong><\/h1>\n<p><strong>Initial manifestations\u00a0<\/strong><strong>often mild &amp; vague: <\/strong><\/p>\n<ul>\n<li>Fatigue, anorexia, weight loss, anemia, diarrhea<\/li>\n<li>Dull aching pain may be present in RUQ (right upper quadrant).<\/li>\n<\/ul>\n<p><strong>Advanced cirrhosis: <\/strong><\/p>\n<ul>\n<li>Ascites &amp; peripheral edema; pruritus<\/li>\n<li>\u2191 bruising; \u2193 healing &amp; tissue maintenance<\/li>\n<li>Esophageal varices &#8211; May rupture, leading\u00a0 to hemorrhage, circulatory shock, Jaundice<\/li>\n<li>Obstruction of bile ducts &amp; blood flow by fibrous tissue causes:<\/li>\n<li>Reduction of bile entering the intestine\u00a0 \u2192\u00a0 Impairs digestion and absorption!<\/li>\n<li>Backup of bile in the liver \u2192 Leads to obstructive jaundice (note that intrahepatic jaundice now co-exists with obstructive jaundice!)<\/li>\n<li>Sex hormone imbalance \u2192 spider nevi, testicular atrophy, impotence, gynecomastia, irregular menses.<\/li>\n<li>Acute encephalopathy (asterixis\/hand-flapping, confusion, convulsions, coma) or<\/li>\n<li>Chronic encephalopathy (personality changes, memory lapses, irritability, disinterest in personal care)<\/li>\n<\/ul>\n<h1><strong>Diagnostic Tools:<\/strong><\/h1>\n<ol>\n<li>Imaging,<\/li>\n<li>Blood tests for blood counts and abnormal presence of liver proteins\/enzymes in blood (indicating hepatocyte death\/dysfunction)<\/li>\n<\/ol>\n<h1><strong>Treatments:<\/strong><\/h1>\n<ol>\n<li>Avoid fatigue &amp; exposure to infection<\/li>\n<li>Avoidance of alcohol or specific cause<\/li>\n<li>Supportive or symptomatic treatment<\/li>\n<li>Dietary restrictions on protein &amp; salt<\/li>\n<li>Increased intake of carbohydrate &amp; vitamin supplements<\/li>\n<li>Balancing serum electrolytes (possibly with diuretics)<\/li>\n<li>Paracentesis to remove excess fluid<\/li>\n<li>Albumin transfusions to prevent third spacing<\/li>\n<li>Antibiotics to reduce intestinal flora<\/li>\n<li>Emergency treatment if esophageal varices rupture<\/li>\n<li>Portocaval shunts to reduce portal hypertension<\/li>\n<li>Liver transplantation (can be from living donors!)<\/li>\n<\/ol>\n<h1><strong>3 Types of Jaundice:<\/strong><\/h1>\n<p><strong>Compare Prehepatic Jaundice, Intrahepatic Jaundice and Posthepatic Jaundice giving an example of a cause of each:<\/strong><\/p>\n<ul>\n<li><strong>Jaundice: <\/strong>The yellowish colour of sclera of eyes, skin &amp; other tissues due to hyperbilirubinemia<strong>.<\/strong><\/li>\n<li>Is a sign of a disease or disorder.<\/li>\n<\/ul>\n<p><strong>Three types of disorders can cause jaundice<\/strong><\/p>\n<p><strong>1. <span style=\"text-decoration: underline\">Pre-hepatic jaundice<\/span>: <\/strong><\/p>\n<ul>\n<li><strong>Caused by excessive destruction of red blood cells (<em>&amp; liver can\u2019t keep up in breaking down of bilirubin \u2013 which is a breakdown product of hemoglobin\u2019s heme pigment<\/em>)<\/strong><\/li>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Characteristic of hemolytic anemias or transfusion reactions<\/strong><\/li>\n<li><strong>Physiological jaundice of the newborn \u2013 common 2-3 days after birth \u2026. Treated with phototherapy (bili light)<\/strong><\/li>\n<li><strong>Prehepatic Jaundice is a result of: \u2191 unconjugated bilirubin in serum<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p><strong>2. <span style=\"text-decoration: underline\">Intra-hepatic jaundice<\/span>: <\/strong><\/p>\n<ul>\n<li><strong>Occurs with disease or damage to hepatocytes (<em>can no longer uptake bilirubin and\/or can no longer conjugate bilirubin<\/em>)\u00a0 <\/strong><\/li>\n<\/ul>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Hepatitis<\/strong><strong> or cirrhosis<\/strong><\/li>\n<li><strong>Intrahepatic jaundice results in \u2191 unconjugated &amp; conjugated bilirubin in serum<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p><strong>3. <span style=\"text-decoration: underline\">Post-hepatic jaundice<\/span>: <\/strong><\/p>\n<ul>\n<li><strong>Caused by obstruction of bile flow into gall-bladder or duodenum &amp; subsequent backup of bile into the blood\u2026 causes pruritus (itchiness) of the skin (due to bile salt deposits) and \u2193 digestion.<\/strong><\/li>\n<\/ul>\n<ol>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Caused by Tumor<\/strong><strong>, or choledocholithiasis <\/strong><\/li>\n<li><strong>Posthepatic Jaundice is due to \u2191 conjugated bilirubin in serum<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ol>\n","protected":false},"author":1370,"menu_order":27,"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-5173","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\/5173","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":8,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5173\/revisions"}],"predecessor-version":[{"id":5181,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5173\/revisions\/5181"}],"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\/5173\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=5173"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=5173"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=5173"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=5173"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}