1. Liver Diseases

2. Function of the liver

3. 1.Production of bile, which helps break down fats in the small intestine during digestion 2.Production of certain proteins for blood plasma( albumin) 3.Production of cholesterol and special proteins to help carry fats through the body 4.Conversion of excess glucose into glycogen for storage 5.Regulation of blood levels of amino acids, which form the building blocks of proteins

4. 6.Processing of hemoglobin for use of its iron content (The liver stores iron.) 7.Conversion of poisonous ammonia to urea (Urea is one of the end products of protein metabolism that is excreted in the urine.) 8.Clearing the blood of drugs and other poisonous substances 9.Regulating blood clotting

5. Fatty Liver( hepatic steatosis) Fatty Liver : An accumulation of fat in the liver tissue

6. Ordinary, the liver triglycerides are packaged into VLDL and exported to the blood stream. The exact cause of fatty liver is unknown. Fatty liver represents an imbalance between the amount of fat synthesized in the liver or picked up from the blood and the amount exported to the blood via VLDL

7. Fatty liver is common to many conditions: 1.Alcoholic liver disease 2.Exposure to drugs and toxic metals 3.Accompanies obesity, diabetes mellitus, kwashiorkor and Marasmus 4.Long-term total parenteral nutrition

8. Consequences fatty liver In many individuals, fatty liver causes no harm. But in other cases it may accompanied by : 1.Liver enlargement ( hepatomegaly) 2.Liver inflammation 3.Fatigue 4.Liver damage 5.Liver failure 6.Liver cancer

9. Consequences fatty liver Abnormal elevation liver enzyme levels ALT( alanine aminotransferase) and AST ( aspartate aminotransferase) Increased triglycerides Elevated cholesterol levels Elevated blood glucose levels

10. Treatment Fatty Liver Elimination of factors that cause it Alcohol abuse Drug treatment Weight reduction – no rapid – may accelerate progression of liver disease Physical activity Reduction of blood lipid levels Medications to improve insulin sensitivity

11. Insulin resistance promotes fat accumulation in the liver by : 1.Stimulating fatty acid synthesis 2.Inhabiting fatty acid oxidation 3.Blokking VLDL secretion into the blood stream.

12. Hepatitis Hepatitis : Inflammation of the liver Acute Hepatitis : lasts less than six months Chronic Hepatitis: lasts six months or longer

13. Causes of Hepatitis 1.Infection with specific viruses, which are designated by the letters A, B, C, D, and E. 2.Contact with infected persons 3.Ingesting contaminated food or water 4.Excessive alcohol intake 5.Exposure to certain drugs and toxic chemicals

14. Viral hepatitis Hepatitis A ( HAV) : spread via fecal – oral route, is due to the contamination of foods with fecal materials. It usually resolves within a few months and dose not cause chronic illness or permananent liver damage.

15. Hepatitis B ( HAB) : Is transmitted by infected blood or needles Hepatitis C ( HAC) : Is transmitted by blood contact. Both can cause cirrhosis and liver cancer.

16. Symptoms of Hepatitis Fatigue Nausea Anorexia Pain in the liver area Fever Headache Muscle pain Skin rashes Elevated serum levels of ALT & AST Jaundice

17. Jaundice Results when liver dysfunction impairs the metabolism of bilirubin, a breakdown of hemoglobin that is normally eliminated in bile. Accumulation of bilirubin in the bloodstream leads to yellow discoloration of tissues.

18. Treatment of Hepatitis Bed rest Appropriate diet Avoid substances that may aggravate the liver – alcohol and drugs or dietary supplements that cause liver toxicity Hepatitis A usually resolves without use of medications Antiviral agents – hepatitis B, hepatitis C

19. Medical Nutrition Therapy of Hepatitis Nutrition care varies according to patients symptoms and nutrition status If malnourished :a diet adequate in protein (1.0 – 1.2 g/kg) and energy Small, frequent meals

20. Medical Nutrition Therapy: If fluid retention – avoid high-sodium foods Low-fat diet (<30% kcalories) if steatorrhea present Fluid and electrolyte replacement for persistent vomiting Liquid supplements may improve nutrient intake

21. Cirrhosis

22. Cirrhosis : End-stage condition that results from long-term liver disease in which gradually destroys liver tissue. extensive scarring replaces healthy liver tissue causing impairment liver function and liver failure

23. Normal Liver Tissue Cirrhotic Liver is often shrunken and has irregular appearance

24. Consequences of cirrhosis 1.Initial disease: mild or asymptomatic, fatigue, weakness, anorexia, weight loss 2.Later disease: decline in liver function, anemia, impaired blood clotting, increased susceptibility to infection, jaundice, fat malabsorption 3.Advanced disease: disruption of kidney & lung function, altered liver enzymes, bilirubin levels, lowered albumin levels, extended clotting times and elevated blood ammonia levels

25. Cirrhosis - Consequences 1.Portal hypertension: resistance to blood flow in liver causes a rise in pressure within the portal vein

26. Cirrhosis - Consequences 2.esophageal varices :dilated vessels develop throughout the gastrointestinal tract that become enlarged and engorged.it may rupture and cause sever bleeding

27. Cirrhosis - Consequences 3.Ascites : abnormal accumulation of fluid in the abdominal cavity caused by: Portal hypertension forces fluids to leak from the blood into abdominal cavity Water retention due to altered kidney function Reduced albumin synthesis by the diseased liver which helps to retain the fluid in blood vessels.

28. Ascites can cause Abdominal discomfort and early satiety leading to malnutrition Body weight is difficult to interpret

29. ascites indicates that liver damage has reached a critical stage, as half of patients with ascites die within 2 years

30. Cirrhosis - Consequences 4.Hepatic encephalopathy: disorder characterized by abnormal neurological functioning Caused by elevated ammonia levels Including changes in: personality, mental abilities, motor functions. At worst,hepatic coma may develop.

31. 5.Elevated blood ammonia levels: Much of body free ammonia is produced by bacterial action on unabsorbed dietary protein in the colon Normally, the liver extracts ammonia from portal blood and converts it to urea, most of which is excreted by the kidneys In advanced liver disease, reaches the brain tissue – producing neurological symptoms called hepatic encephalopathy

32. Cirrhosis - Consequences 6- Malnutrition and wasting Most patients with cirrhosis are at high risk of developing protein-energy malnutrition (PEM) caused by combination of several factors: Consume less food due to reduced appetite, fatigue, or gastrointestinal symptoms (ascites – early satiety) taste changes Diet has lack of taste due to limited sodium intake Fat malabsorption – steatorrhea Catabolism, inadequate protein synthesis, reduce nutrient storage

33. Medical nutrition therapy of Cirrhosis

34. MNT is customized to each patients need 1-Energy Calculate resting metabolic rate (RMR) and multiply by stress factor 1.2 initially Nutrient malabsorption, recent weight loss, and infection increase energy needs RMR calculations are based on desirable weight or estimated dry weight (weight without ascites) A value for dry weight can be obtained after diuretic therapy or after a medical procedure that directly removes excess abdominal fluid. Four to six feedings daily

35. Cirrhosis - MNT 2-Protein Protein recommendations 0.8 – 1.2 grams per kg body weight (desirable weight or dry weight) Protein restriction may worsen malnutrition and wasting Patients with hepatic encephalopthy should avoid excessive protein consumption and their protein intake should be modest in quantity and spread throughout the day. Protein restriction is not helpful because it can worsen malnutrition

36. Cirrhosis - MNT 3- Carbohydrate Carbohydrate provides a good portion of energy need. Many patients with cirrhosis are insulin resistant and require medicines or insulin to manage hyperglycemia Patients with diabetes – consume mostly complex carbohydrates at regular intervals

37. Cirrhosis - MNT 4- Fat Patients with fat malabsorption – restricted to less than 30 % of total kcalories or as necessary to control steatorrhea If steatorrhea present, fat intake is restricted, medium-chain triglycerides (MCT) can be used to provide energy but supplementation with essential fatty acids is necessary. Severe steatorrhea – warrants supplementation of fat-soluble vitamins, calcium, magnesium, and zinc

38. Cirrhosis - MNT 5- Sodium and fluid If ascites present – restrict sodium to no more than 2000 mg/day if unpalatable may allow more liberal sodium intake & depend on diuretics to mobilize fluid Diuretic therapy

39. Cirrhosis - MNT 5- Sodium and fluid Patients who are non-responsive to sodium restriction and diuretic therapy fluids may be removed by surgical puncture Monitor potassium intake if on potassium- wasting diuretic If ascites present – restrict sodium to no more than 2000 mg/day Fluid restriction serum sodium <128 meq/L – 1,200-1,500 mL/day serum sodium < 125 meq/L – 1,000-1,200 mL/day

40. Cirrhosis - MNT 6- Vitamins and minerals Vitamin and mineral deficiencies can be a result of the illness, complications of disease, or alcoholism Multivitamin supplementation is recommended If steatorrhea occurs, fat-soluble nutrients provided in water-soluble forms If esophageal varices – liquid form may be preferred

41. 7- Enteral and parenteral nutrition support may be used in patients who are unable to consume enough food. Enteral standard formulas – energy-dense, moderate-protein, low-electrolyte may be necessary for patients with ascites or fluid restriction. Tube feeding may be warranted if varices present so use narrow, flexible tube Parenteral nutrition may be needed if obstruction, gastrointestinal bleeding or uncontrollable vomiting