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Nutrition and Liver Diseases: Fatty Liver, Hepatitis, Cirrhosis
- 1. Nutrition and Liver Diseases 1919 Copyright © 2017 Cengage Learning. All Rights Reserved.
- 2. © Cengage Learning 2017 Introduction • Liver – Most metabolically active organ in the body • Produces most of the proteins circulating in plasma • Produces bile to emulsify fat during digestion • Detoxifies drugs and alcohol • Processes excess nitrogen for excretion as urea • What is the difficulty in early diagnosis of liver disease? Copyright © 2017 Cengage Learning. All Rights Reserved.
- 3. © Cengage Learning 2017 Fatty Liver and Hepatitis • Fatty liver – Accumulation of fat in liver tissue • Amount of fat produced in the liver or picked up from the blood exceeds the amount the liver can use or export to the blood via VLDL – Causes • Metabolism defects, excessive alcohol intake, exposure to drugs and toxins • Insulin resistance in nonalcoholic fatty liver disease Copyright © 2017 Cengage Learning. All Rights Reserved.
- 4. © Cengage Learning 2017 Fatty Liver and Hepatitis: Fatty Liver (cont’d.) • Consequences of fatty liver – Asymptomatic for many – Steatohepatitis: liver inflammation – Hepatomegaly: liver enlargement – Fatigue – May progress to more serious conditions • Cirrhosis, liver failure, or liver cancer Copyright © 2017 Cengage Learning. All Rights Reserved.
- 5. © Cengage Learning 2017 Fatty Liver and Hepatitis: Fatty Liver (cont’d.) • Treatment of fatty liver – Eliminate causative factors • Discontinue alcohol or drug use • Lower blood lipid levels • Weight reduction, increased activity, medications to improve insulin sensitivity – Lifestyle modifications not always successful in patients lacking the usual risk factors Copyright © 2017 Cengage Learning. All Rights Reserved.
- 6. © Cengage Learning 2017 Fatty Liver and Hepatitis (cont’d.) • Hepatitis: liver inflammation – Causes • Specific viral infections (A, B, C, D, and E) • Excessive alcohol intake • Exposure to drugs or toxic chemicals • Fatty liver disease • Autoimmune disease • Certain herbal remedies Copyright © 2017 Cengage Learning. All Rights Reserved.
- 7. © Cengage Learning 2017 Fatty Liver and Hepatitis: Hepatitis (cont’d.) • Viral hepatitis – Features listed in Table 19-1 – Hepatitis A virus (HAV) • Primarily spread via fecal-oral transmission – Hepatitis B virus (HBV) • Transmission: infected blood or needles, sexual contact with an infected person, or mother to infant during childbirth Copyright © 2017 Cengage Learning. All Rights Reserved.
- 8. © Cengage Learning 2017 Fatty Liver and Hepatitis: Hepatitis (cont’d.) • Viral hepatitis – Hepatitis C virus (HCV) • Spread via infected blood or needles • Not readily spread by sexual contact or childbirth • Symptoms and signs of hepatitis – Onset of acute hepatitis • Fatigue, malaise, nausea, vomiting, anorexia, and pain in the liver area Copyright © 2017 Cengage Learning. All Rights Reserved.
- 9. © Cengage Learning 2017 Fatty Liver and Hepatitis: Hepatitis (cont’d.) • Symptoms and signs of hepatitis – Slightly enlarged, tender liver – Jaundice – Elevated ALT and AST serum levels • Treatment of hepatitis – Supportive care: bed rest and diet – What substances should be avoided? – Antiviral agents for HBV or HCV Copyright © 2017 Cengage Learning. All Rights Reserved.
- 10. © Cengage Learning 2017 Fatty Liver and Hepatitis: Hepatitis (cont’d.) • Nutrition therapy for hepatitis – Most individuals: no dietary changes required – Nutritional support as needed • Small, frequent meals (for anorexia, abdominal discomfort) • Electrolyte replacement (persistent vomiting) • Adequate protein (1.5-2 g/kg/day) and energy to replenish nutrient stores (malnourished) • Oral supplements Copyright © 2017 Cengage Learning. All Rights Reserved.
- 11. © Cengage Learning 2017 Cirrhosis • Late stage of chronic liver disease – Extensive scarring replaces healthy liver tissue – Impaired liver function and liver failure • What are the chief causes of cirrhosis in the United States? Copyright © 2017 Cengage Learning. All Rights Reserved.
- 12. © Cengage Learning 2017 Cirrhosis (cont’d.) • Consequences of cirrhosis – Metabolic disturbances • Anemia; bruise easily; susceptible to infections – Bile obstruction • Jaundice, fat malabsorption, and pruritis (itchy skin) – Fluid accumulation in blood vessels and body tissues – Figure 19-3: clinical effects of liver cirrhosis Copyright © 2017 Cengage Learning. All Rights Reserved.
- 13. Copyright © 2017 Cengage Learning. All Rights Reserved.
- 14. © Cengage Learning 2017 Cirrhosis (cont’d.) • Portal hypertension – Rise in blood pressure due to increased portal blood coupled with obstructed blood flow through the liver • Collateral vessels and gastroesophageal varices – Collaterals: blood vessels that enlarge or newly form • Allow an alternative pathway for diverted blood Copyright © 2017 Cengage Learning. All Rights Reserved.
- 15. © Cengage Learning 2017 Cirrhosis (cont’d.) • Collateral vessels and gastroesophageal varices – Varices: abnormally dilated blood vessels – Esophageal and gastric varices • Vulnerable to rupture • Bleeding may be fatal Copyright © 2017 Cengage Learning. All Rights Reserved.
- 16. © Cengage Learning 2017 Cirrhosis (cont’d.) • Ascites – Large accumulation of fluid in the abdominal cavity – Indicates a critical stage of liver damage – Causes: • Portal hypertension • Sodium and water retention in kidneys • Reduced albumin synthesis in liver Copyright © 2017 Cengage Learning. All Rights Reserved.
- 17. © Cengage Learning 2017 Cirrhosis (cont’d.) • Hepatic encephalopathy – Abnormal neurological functioning – Signs: adverse changes in personality, behavior, mood, mental ability, and motor functions – Fully reversible with treatment – Exact etiology unknown • What are current theories surrounding hepatic encephalopathy? Copyright © 2017 Cengage Learning. All Rights Reserved.
- 18. Copyright © 2017 Cengage Learning. All Rights Reserved.
- 19. © Cengage Learning 2017 Cirrhosis (cont’d.) • Elevated ammonia levels – Healthy liver converts blood ammonia to urea – In advanced disease, liver is unable to process the ammonia sufficiently – Ammonia-laden blood bypasses the liver via collateral vessels • Reaches the general blood circulation and thereby, brain tissue Copyright © 2017 Cengage Learning. All Rights Reserved.
- 20. © Cengage Learning 2017 Cirrhosis (cont’d.) • Malnutrition and wasting – Some degree of wasting in most patients with advanced cirrhosis – Possible causes of malnutrition (Table 19-4) • Reduced nutrient intake • Malabsorption or nutrient losses • Altered metabolism or increased nutrient needs Copyright © 2017 Cengage Learning. All Rights Reserved.
- 21. © Cengage Learning 2017 Cirrhosis (cont’d.) • Treatment of cirrhosis – Objectives: correct the underlying cause of disease; prevent or treat complications – Supportive care • Appropriate diet • Avoidance of liver toxins – Medications to treat complications • Be aware of diet-drug interactions (Box 19-6) Copyright © 2017 Cengage Learning. All Rights Reserved.
- 22. © Cengage Learning 2017 Cirrhosis (cont’d.) • Nutrition therapy for cirrhosis (Table 19-5) – Customized to each patient’s needs – Energy • 25 to 40 kcal/kg dry body weight per day • Four to six small meals • Oral supplements • Box 19-7 offers tips for improving intakes Copyright © 2017 Cengage Learning. All Rights Reserved.
- 23. © Cengage Learning 2017 Cirrhosis: Nutrition Therapy for Cirrhosis (cont’d.) • Protein – 1.0 to 1.5 g/kg dry body weight/day – Branched-chain amino acids (BCAA) • Carbohydrate and fat – Medications or insulin to treat insulin resistance – Carbohydrate and glucose control – Fat may be restricted to <30% of kcal with steatorrhea Copyright © 2017 Cengage Learning. All Rights Reserved.
- 24. © Cengage Learning 2017 Cirrhosis: Nutrition Therapy for Cirrhosis (cont’d.) • Sodium – What restrictions are necessary to control ascites? – Surgical treatments: paracentesis, transjugular intrahepatic portosystemic shunt • Vitamins and minerals – Deficiencies common; nutrient supplementation often necessary Copyright © 2017 Cengage Learning. All Rights Reserved.
- 25. © Cengage Learning 2017 Cirrhosis: Nutrition Therapy for Cirrhosis (cont’d.) • Food safety: to avoid foodborne illness • Enteral and parenteral nutrition support – Tube feedings • Supplement or replace oral intakes • Standard formula; or energy-dense formula for patients with ascites – Parenteral nutrition support for patients unable to tolerate enteral feedings Copyright © 2017 Cengage Learning. All Rights Reserved.
- 26. © Cengage Learning 2017 Liver Transplantation • Overview – Most transplants preceded by chronic hepatitis C or alcoholic liver disease – Five-year survival rate of 54% to 81% • Nutrition status of transplant patients – Why is it difficult to assess nutrition status in transplant candidates? Copyright © 2017 Cengage Learning. All Rights Reserved.
- 27. © Cengage Learning 2017 Liver Transplantation (cont’d.) • Posttransplantation concerns – Immediate concerns • Organ rejection • Infection – Immunosuppressive drugs raise infection risk – Antibiotics and antiviral medications reduce risk • In what ways do immunosuppressive drugs affect nutrition status? Copyright © 2017 Cengage Learning. All Rights Reserved.
- 28. © Cengage Learning 2017 Liver Transplantation (cont’d.) • Posttransplantation concerns – Stress of surgery increases protein and energy requirements • High-kcal, high-protein snacks and oral supplements – Vitamin and mineral supplementation – Food safety measures Copyright © 2017 Cengage Learning. All Rights Reserved.
- 29. © Cengage Learning 2017 Nutrition in Practice: Alcohol in Health and Disease • Guidelines for alcohol consumption • Alcohol metabolism and toxicity • Long-term consequences of excessive intake • Benefits of moderate intake for some populations Copyright © 2017 Cengage Learning. All Rights Reserved.
Editor's Notes
- Answer: Liver disease progresses slowly. Its primary symptom, fatigue, often goes unnoticed. Other symptoms may be so mild that complications develop before liver disease is diagnosed.
- Answer: Substances that irritate the liver, such as alcohol, drugs, and dietary supplements that cause liver damage.
- Answer: Alcoholic liver disease and chronic hepatitis C infection, followed by nonalcoholic fatty liver disease and chronic hepatitis B infection.
- Table 19-2 Laboratory Tests for Evaluation of Liver Disease aThe test for prothrombin time evaluates the clotting ability of blood. Note: U/L = units per liter; dL = deciliter; μg = micrograms; N = nitrogen
- Answer: Elevated blood ammonia levels are thought to play a key role in its development due to ammonia’s neurotoxicity. Other substances that may accumulate in brain tissue and disturb brain function include sulfur compounds, naturally occurring benzodiazepines, short-chain fatty acids, and manganese. Some research shows that severe liver damage may lead to reduced serum levels of the branched-chain amino acids and increased levels of the aromatic amino acids, which may alter the types of neurotransmitters produced in the brain. Most likely, a combination of abnormalities contributes to the disruption in neurological functioning.
- Table 19-3 Clinical Features of Hepatic Encephalopathy
- Answer: Patients with ascites are generally advised to restrict sodium. Because ascites is partly caused by sodium and water retention in the kidneys, treatment usually includes both sodium restriction (to no more than 2000 milligrams of sodium per day) and diuretic therapy to promote fluid loss. Potassium intake should be monitored if a potassium-wasting diuretic (such as furosemide) is used.
- Answer: Liver dysfunction and malnutrition often have similar metabolic effects. If fluid retention is present, it can mask weight loss and alter anthropometric and laboratory values.
- Answer: Gastrointestinal side effects include nausea, vomiting, diarrhea, abdominal pain, and mouth sores. Some medications may alter appetite and taste perception. Some of the drugs may cause hyperglycemia or outright diabetes, which may need to be controlled with insulin. Electrolyte and fluid imbalances are common. Other possible effects include hypertension, hyperlipidemias, kidney toxicity, protein catabolism, and increased osteoporosis risk.