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This guide provides detailed information on the anatomy, physiology, and functions of the liver for nursing professionals. It covers topics such as glucose metabolism, ammonia conversion, protein metabolism, fat metabolism, vitamin storage, drug metabolism, bile formation, bilirubin excretion, lab tests, liver biopsy, and manifestations of liver dysfunction.
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Liver Dysfunction and Pancreatitis Nursing 210
Liver Anatomy and Physiology • Largest internal organ • Weighs about 1500 grams • Located right upper quadrant • Figure 39-1 p.1075
Anatomy and Physiology • Approximately 75% of the blood supply comes from the portal vein • Drains the GI tract and is rich in nutrients • Remainder of blood supply enters by hepatic artery • Rich in oxygen • All blood leaves the liver through hepatic vein to the inferior vena cava
Liver Functions • Glucose metabolism • Important role in metabolism of glucose and regulation of blood glucose • Converts glucose to glycogen (storage) • Breaks down glycogen into glucose (energy) • Additional glucose is synthesized through gluconeogenesis (amino acids or lactate)
Liver Functions • Ammonia Conversion • Ammonia (potential toxin) is byproduct of gluconeogenesis • Liver converts ammonia into urea • Also removes ammonia produced by intestinal bacteria from portal blood • Urea is excreted in urine
Liver Functions • Protein Metabolism • Synthesizes all plasma proteins except gamma globulin • Albumin (osmotic pressure) • Alpha and beta globulins • Blood clotting factors • Specific transport proteins • Prothrombin: liver needs vitamin K
Liver Functions • Fat Metabolism • Fatty acids broken down into ketones • Provide source of energy for muscles and other tissues • Occurs when glucose is limited as in starvation or uncontrolled diabetes • Fatty acids also used for synthesis of cholesterol, lipoproteins and other complex lipids
Liver Functions • Vitamin and Iron Storage • Vitamins A, B12, D and several B-complex vitamins stored in liver • Iron and copper
Liver Functions • Drug Metabolism • Liver metabolism generally results in loss of activity of the medication • Certain oral meds absorbed by GI tract may be metabolized by liver to such a great extent (first-pass effect) that bioavailability is decreased
Liver Functions • Bile Formation • Mainly water and electrolytes (potassium, calcium, bicarbonate, chloride) • Continuously made by hepatocytes and stored in gallbladder • Emptied into intestine when needed for digestion
Liver Functions • Bilirubin Excretion • Pigment derived from breakdown of hemoglobin • Modified by hepatocytes through conjugation to be more soluble in aqueous solutions • Conjugated bilirubin is carried by bile into duodenum for excretion
Liver Function and Lab Tests • Blood Studies (review Brunner p. 1079) • Serum Aminotransferase • AST • ALT • Elevated levels usually indicate cellular damage to the liver • > 70% of liver cells may be damaged before LFT’s become elevated
Blood Studies, cont. • Pigment studies • Serum bilirubin, direct • Serum bilirubin, total • Urine bilirubin • These studies measure ability of liver to conjugate and excrete bilirubin • Abnormal results are seen in liver and biliary tract disease
Blood Studies, cont. • Serum Ammonia • Liver converts ammonia to urea. Ammonia rises in liver failure • Protein Studies • Serum albumin • Low levels seen with liver disease • Serum globulin • Elevated levels with advanced cirrhosis and chronic active hepatitis
Blood Studies, cont. • Tumor Marker • Alpha-fetoprotein (AFP) • Increased levels are seen with hepatic carcinoma • Prothrombin Time (PT) • Time required for a firm fibrin dot to form • In liver dysfunction, increase clotting time with increased risk of bleeding
Liver Biopsy • Used to obtain a specimen of liver tissue • Done under local anesthesia • Complications: • Pneumothorax • Peritonitis • Hemorrhage
Manifestations of Liver Dysfunction • Jaundice • Ascites • Portal Hypertension • Esophageal Varices • Hepatic Encephalopathy • Nutritional Deficiencies
Jaundice • Also known as icterus, a yellow discoloration of the skin, sclerae and mucous membranes • Caused by elevated bilirubin levels in the blood • Jaundice becomes clinically evident when the serum bilirubin level exceeds 2.5mg/dL • Several types of Jaundice: Hemolytic, Hepatocellular, Obstructive, and Hereditary Hyperbilirubinemia
Jaundice, cont. • Symptoms • Yellow discoloration of the skin, sclerae and mucous membranes • Itching (pruritus) due to deposits of bile salts on the skin • Stool becomes light in color • Urine becomes deep orange and foamy
Portal Hypertension • Elevated pressure in the portal venous blood • Blood flow through the liver is obstructed • Vessels enlarge, collateral circulation develops to take blood back to the systemic circulation • Two major sequelae result • Ascites • Varices
Ascites • This is the accumulation of fluid in the peritoneal cavity • Decrease albumin levels cause decreased oncotic pressure • Fluid leaves the plasma and leaks in to the peritoneal cavity and interstitial spaces • Decrease volume causes activation of the Renin-Angiotensin system – Na & H2O retained in attempt to return intravascular volume to normal– more edema and ascites
Portal Hypertension and Ascites • Symptoms • Portal HTN not evident unless bleeding from collateral blood vessels or ascites occurs • Ascites – increase abdominal girth, unexplained rapid weight gain • Striae and distended veins over abdomen • Fluid and electrolyte imbalances • Respiratory difficulty may occur due to pressure on the diaphragm
Portal Hypertension and Ascites • Treatment • Portal HTN – treat underlying cause • Ascites • Na and fluid restrictions • Diuretic agents (Aldactone, Lasix) • Albumin therapy • Paracentesis
Varices • Esophageal, gastric, hemorrhoidal • Due to elevated pressures in veins that drain into portal system • Often source of massive hemorrhage • Potential for bleeding increased by blood clotting abnormalities seen in patients with liver disease
Hepatic Encephalopathy • Impaired neurological function that occurs with profound liver failure • Accumulation of ammonia and other toxic metabolites • GI bleeding, high protein diet, bacterial infections • Other factors unrelated to increased ammonia levels • Dehydration • Surgery • Medications - sedatives, tranquilizers, analgesics,non sparing potassium diuretics
Hepatic Encephalopathy • Symptoms • Stage one • Normal level of consciousness w/periods of lethargy and euphoria • Slowed thought process • Slight confusion • Reversal of day – night sleep pattern • Clinical signs • Asterixis (flapping tremor of hand), impaired writing, normal EEG
Hepatic Encephalopathy • Stage two • Disorientation • Sleeps most of time, but easily aroused • Agitation, mood swings • Clinical signs • Asterixis, fetor hepaticus (musty odor to breath), abnormal EEG • Stage three • Deep sleep, difficult to arouse • Incoherent speech • Clinical signs • Increased deep tendon reflexes, rigidity of extremities, markedly abnormal EEG • Stage four • comatose
Hepatic Encephalopathy • Treatment • Restrict protein intake in early stages • Lactulose • reduce serum ammonia through bowel evacuation • Fecal flora are changed to organisms that do not produce ammonia from urea • D/C sedatives, tranquilizers, analgesics
Viral Hepatitis • Inflammation and necrosis of hepatic cells • Bile flow is impaired • Necrosis occurs in a spotty pattern • Liver cells may regenerate during recovery period
Viral Hepatitis • Types • Hepatitis A (HAV) • Hepatitis B (HBV) • Hepatitis C (HCV) • Hepatitis D (HDV) • Hepatitis E (HEV)
HAV • Also known as “infectious hepatitis” • Mode of transmission is fecal – oral route; poor sanitation • Incubation period 15-50 days • May occur with or without symptoms, flu like • Preicteric phase – headache, anorexia, fever • Icteric phase – dark urine, jaundice of skin, sclera
HAV • 1995 FDA approved vaccine • Recommend for travelers to locations of poor sanitation, high risk groups (homosexual men,IV drug users, day care workers) • Nursing management includes • Stressing good hygiene • Environmental sanitation
HAV • Outcome – usually mild with recovery • Fatality rate less than 1% • No carrier state • No increased risk of chronic hepatitis, cirrhosis or hepatic cancer
HBV • Also known as “serum hepatitis” • Transmission – blood and body fluids, through mucous membranes and breaks in skin • Health care workers at great risk • IV drug users and homosexual activity • Very long incubation period: 1-6 months • May occur without symptoms, may develop arthralgias, rash
HBV • Vaccine used to provide active immunity • Recommended for all health care workers • Passive immunity is provided through hepatitis B immune globulin (HBIG) • Recommended for people exposed to HBV who have not received vaccine or have never had HBV
HBV • Nursing management includes: teaching patient proper nutrition, rest, prevention of spread (blood, body fluids) • Fatality 1-10% • Carrier state possible • Increase risk for cirrhosis, chronic hepatitis and hepatic cancer
HCV • Also known as Non-A, Non-B hepatitis • Transmission through blood transfusion, exposure to blood contaminated equipment or drug paraphernalia,sexual contact • Incubation 15-160 days • Clinical course similar to HBV • Chronic carrier state occurs frequently • Increase risk for chronic liver disease and cancer
HCV • Treatment with interferon and ribavirin • HCV accounts for 30% of liver transplants in US
HDV • Only individuals with HBV are at risk • Sexual contact, IV drug use • Symptoms similar to HBV, more likely to progress to chronic active hepatitis and cirrhosis • Investigation into interferon as treatment
HEV • Transmitted through fecal – oral route • Similar to HAV • Incubation variable 15-65 days • Jaundice usually always present • No chronic state
Toxic and Drug Induced Hepatitis • Toxic hepatitis • Inflammatory condition caused by ingestion or inhalation of certain substances • Dry cleaning fluid • Glue • Insecticides – pesticides • Poisonous mushrooms • Rat poison
Toxic and Drug Induced Hepatitis • Drug Induced Hepatitis • Tylenol • Aspirin • Thorazine • INH • Valium
Toxic and Drug Induced Hepatitis • Symptoms • Similar to those of viral hepatitis • GI and flu type symptoms • Jaundice • Hepatomegaly • Depending of substance, may take days to months for symptoms to appear
Fulminant Hepatic Failure • Sudden and severely impaired liver function in previously healthy person • Liver failure within 8 weeks of first clinical sign • Viral hepatitis is most common cause • Other causes • Acetaminophen • Chemicals • Wilson’s disease (copper build up in liver)
Cirrhosis • Chronic, degenerative process, replacement of normal tissue with scar tissue • Three types • Alcoholic (most common, chronic alcoholism) • Postnecrotic (acute viral hepatitis) • Biliary (chronic biliary obstruction and infection) • Other causes: • Toxic drug or chemical reaction • Unknown cause
Cirrhosis • Clinical manifestations • Liver enlargement • Ascites • Infection and Peritonitis • Varices • Edema • Vitamin deficiency • Mental deterioration
Cirrhosis • Treatment • No alcohol • Well balanced diet, unless: • Hepatic Encephalopathy – restrict protein • Ascites – restrict sodium • Vitamin supplements • B-Complex • Folic acid • A,C,and K