Liver cirrhosis and liver toxicity diet plan

This deals with the dietary recommendation for liver cirrhosis and what causes liver toxicity

1. LIVER CIRRHOSIS AND LIVER TOXICITY AMREEN FATHIMA A 23FSM03

2. LIVER CIRRHOSIS 01

3. INTRODUCTION Each time you liver is injured, it tries to repair itself. Chronic liver disease –progresses to cirrhosis Cirrhosis is characterized by fibrosis and nodule formation of the liver, secondary to a chronic injury, which leads to alteration of the normal lobular organization of the liver.

4. ETIOLOGY CLASSIFICATION VIRAL TOXINS AUTOIMMMUNE CHOLESTATIC MAETABOLIC VASCULAR

5. Decompensated cirrhosis CLINICAL SYMPTOMS A wide range of signs and symptoms arising from a combination of liver dysfunction and portal hypertension . The diagnosis of ascites, jaundice, hepatic encephalopathy, variceal bleeding, or hepatocellular carcinoma in a patient with cirrhosis signifies the transition from a compensated to a decompensated phase of cirrhosis. Compensated cirrhosis P atients are asymptomatic , and their disease is detected incidentally by labs, physical exam, or imaging.  One of the common findings is mild to moderate elevation in aminotransferases or gamma glutamyl transpeptidase with possible enlarged liver or spleen on examination. Patients with cirrhosis can be asymptomatic or symptomatic , depending on whether their cirrhosis is clinically compensated or decompensated.

6. TREATMENT/MANAGEMENT Damage to the liver is permanent , thus f urther injury to the liver should be avoided General management to prevent chronic liver disease includes avoidance of alcohol , vaccination for HBV and HCV , good nutrition with a balanced diet , weight reduction , and early treatment of precipitating factors like dehydration, hypotension, and infections . R outine monitoring of volume status, kidney function, varices development, and progression to HCC.  Specific therapy usually targets the etiology including antiviral medications in viral hepatitis , steroids and immunosuppressant agents in autoimmune hepatitis , ursodeoxycholic acid and obeticholic acid in primary biliary cholangitis, copper chelation in Wilson disease , and iron chelation and phlebotomy in hemochromatosis.  Weight loss of at least 7% is beneficial in NASH, and alcohol abstinence is crucial in alcoholic cirrhosis.

7. PRINCIPLE OF THE DIET A high calorie, high carbohydrate, moderate or restricted fat, high vitamin diet helps in regeneration of liver and helps to prevent the formation of ascites.  Low fat with supplementation of fat soluble vitamins and minerals should be given.  Sodium should be restricted only when there is ascites.  Fibre should be restricted when there is danger of oesophageal varices and portal hypertension.  The diet should be attractive and palatable .

8. ENERGY Consumption of food is difficult because of anorexia and ascites . The patients are usually emaciated by the time cirrhosis of liver is diagnosed. The patient requires highly nutritious food i.e., high calorie diet is necessary because of prolonged undernourishment. The calorie requirement should be between 2000 – 2500 Kcals . CARBOHYDRATES Carbohydrates should be supplied liberally so that the liver may store glycogen.  Liver function improves when an adequate store of glycogen is present in liver cells, 60% of the calories should come from carbohydrate so that the liver damage is minimised .

9. PROTEINS: The serum albumin , which is exclusively synthesised by the liver cells, is low in cirrhosis and aggravated by the loss of a considerable amount into the ascitic fluid.  A high protein diet is helpful for regeneration of the liver. It also helps to compensate for the considerable loss of albumin in the ascitic Fluid.  In hepatic coma , a high protein intake of 1.2 g/kg of body weight can be given. If the patient is in precoma or breakdown of liver cells.  The protein content of the diet varies according to the symptoms.  The increased amounts of protein can be met by the addition of casein (milk protein concentrate) which can be added in milk, soups and ice creams.  Vegetable proteins containing more valine is beneficial in preventing encephalopathy. 

10. FATS About 20 g of fat is given.  Medium chain triglycerides containing C8 and C10 fatty acids can be given as these are digested and absorbed in the absence of bile salts , Coconut oil contains medium chain fatty acids.

11. VITAMINS AND MINERALS The liver is the major site of storage and conversion of vitamins into their metabolically active form.  In cirrhosis the liver concentration of folate, riboflavin, nicotinamide, vitamin B12 and vitamin A are decreased which may be due to decreased synthesis of retinol binding proteins.  Since vitamin D is converted to calcidiol in the liver, oral administration or injection of vitamin D in biliary cirrhosis is not successful in raising the serum level of calcidol .  Vitamin supplementation especially of B vitamins is required to prevent anaemia .  Choline and methionine are useful if fatty infiltration is present.  Sodium is restricted in oedema and ascites.

12. DIETARY CONSIDERATIONS If patient cannot maintain a sufficient intake by eating, supplementation with sip feeding should be considered.  If this is inadequate , enteral supplementation should be considered.  Parenteral nutrition should be reserved for patients in whom enteral nutrition is unsuccessful and to be given only for short time .  Due to risk of catheter sepsis and poor resolution of ascites parenteral nutrition is not the best choice of feeding.  Hepatic herbal supportives , antioxidants and maintenance of adequate calorie, fluid and electrolytes, fat soluble vitamins are routinely recommended 

13. Sample Diet for liver cirrhosis Breakfast  1 cup scrambled egg + 2 multigrain toasted bread + 1 cup skim milk Mid-morning 1 cup coconut water/ 1 bowl fruit salad Lunch 1 cup dal + 1 cup mix veg + 1 cup parboiled rice + veg salad Evening 1 cup skim milk/ tea Dinner 1 cup cabbage and peas vegetable + 2 chapatti + veg salad

14. LIVER TOXICITY 02

15. Toxic hepatitis occurs when your liver develops inflammation because of exposure to a toxic substance . Toxic hepatitis may also develop when you take too much of a prescription or over-the-counter medication . The liver normally removes and breaks down most drugs and chemicals from your bloodstream. Breaking down toxins creates byproducts that can damage the liver. Although the liver has a great capacity for regeneration, constant exposure to toxic substances can cause serious, sometimes irreversible harm . One of the most important causes of liver dysfunction is drug-induced liver injury (DILI) which can lead to a wide spectrum of symptoms ranging from mild non-specific symptoms like asymptomatic transaminitis, acute hepatitis, chronic hepatitis, cholestasis to liver failure. LIVER TOXICITY

16. ETIOLOGY Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Anti-infective Drugs (Anti-tubercular Drugs) Anti-cancer Drugs Hormonal Drugs Immunosuppressive Agents Sedative and Neuropsychiatric Drugs Antibiotics Herbal Supplements

17. PATHOPHYSIOLOGY Liver damage can be hepatocellular , cholestatic , or mixed (includes features of both). Cholestatic damage commonly occurs due to the drug or the drug metabolite . They inhibit hepatobiliary transporter systems which are essential for bile formation and secretion of cholephilic substances and xenobiotics. Hepatocellular injury occurs through multiple pathways including direct hepatotoxicity, and innate and adaptive immune responses. Drug-induced liver injury can be dose-dependent/intrinsic , and on most occasions, it is dose-independent/idiosyncratic .

18. CLINICAL SYMPTOMS Fatigue Decreased appetite Aversion to oily food Epigastric discomfort Tender liver Patients with cholestatic type can present with jaundice, light coloured faeces and pruritis . Occasionally, they can also have allergic manifestations like fever, rash and aching in joints.

19. RISK FACTORS Taking over-the-counter pain relievers or certain prescription drugs Having a liver disease Having hepatitis Aging Drinking alcohol Being female Having certain genetic mutations

20. DRUG CAUSING TOXICITY Acetaminophen (Tylenol) Statins Nicotinic acid (Niacin) Amiodarone ( Cordarone ) Methotrexate ( Rheumatrex , Trexall ) Antibiotics Nonsteroidal anti-inflammatory drugs (NSAIDs) Nitrofurantoin Augmentin Tacrine (Cognex) Disulfiram (Antabuse) Vitamins and Herbs

21. EVALUATION It can cause elevation of liver enzymes including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and total bilirubin . However, there is currently no single test that can predict. In 2011, the International Serious Adverse Events Consortium ( iSAEC ) recommended modified biochemical criteria for identification of drug-induced liver injury as reaching any of the following items: Alanine transferase greater than or equal to 5 ULN Alkaline Phosphatase greater than or equal to 2 ULN , Alanine transferase greater than or equal to 3 ULN and Total bilirubin greater than or equal to 2 ULN

22. TREATMENT/DIET MANAGEMENT Discontinuing the suspected drug is the first step in the management of drug-induced liver injury. N-acetylcysteine is the antidote for acetaminophen poisoning Carnitine has been used in valproate injury. Steroids have been proposed as a therapeutic option for liver injury but have not been well studied . Currently, glucocorticoids are used for immune-mediated drug-induced liver injury. Silymarin alone or silymarin combination with benzylpenicillin has been used in mushroom toxicity In patients with cholestasis , ursodeoxycholic acid can be tried. Patients should be followed until the resolution of symptoms and normalization of labs.

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