Liver Dysfunction and Pancreatitis

1. Liver Dysfunction and Pancreatitis Nursing 210

2. Liver Anatomy and Physiology • Largest internal organ • Weighs about 1500 grams • Located right upper quadrant • Figure 39-1 p.1075

3. 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

4. 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)

5. 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

6. 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

7. 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

8. Liver Functions • Vitamin and Iron Storage • Vitamins A, B12, D and several B-complex vitamins stored in liver • Iron and copper

9. 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

10. 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

11. 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

12. 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

13. 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

14. 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

15. 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

16. Liver Biopsy • Used to obtain a specimen of liver tissue • Done under local anesthesia • Complications: • Pneumothorax • Peritonitis • Hemorrhage

17. Manifestations of Liver Dysfunction • Jaundice • Ascites • Portal Hypertension • Esophageal Varices • Hepatic Encephalopathy • Nutritional Deficiencies

18. 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

20. 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

21. 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

22. 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

24. 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

25. Portal Hypertension and Ascites • Treatment • Portal HTN – treat underlying cause • Ascites • Na and fluid restrictions • Diuretic agents (Aldactone, Lasix) • Albumin therapy • Paracentesis

26. 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

27. 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

28. 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

29. 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

30. 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

31. 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

32. Viral Hepatitis • Types • Hepatitis A (HAV) • Hepatitis B (HBV) • Hepatitis C (HCV) • Hepatitis D (HDV) • Hepatitis E (HEV)

33. 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

34. 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

35. HAV • Outcome – usually mild with recovery • Fatality rate less than 1% • No carrier state • No increased risk of chronic hepatitis, cirrhosis or hepatic cancer

36. 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

37. 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

38. 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

39. 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

40. HCV • Treatment with interferon and ribavirin • HCV accounts for 30% of liver transplants in US

41. 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

42. HEV • Transmitted through fecal – oral route • Similar to HAV • Incubation variable 15-65 days • Jaundice usually always present • No chronic state

43. 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

44. Toxic and Drug Induced Hepatitis • Drug Induced Hepatitis • Tylenol • Aspirin • Thorazine • INH • Valium

45. 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

46. 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)

47. 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

49. Cirrhosis • Clinical manifestations • Liver enlargement • Ascites • Infection and Peritonitis • Varices • Edema • Vitamin deficiency • Mental deterioration

50. 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