Dietary tips for liver disease

Click to edit Master title style
1
Dr. Kalpna Lahade
(Teaching Associate)
Department of Food Science & Nutrition
College of Community Science
Vasantrao Naik Marathwada Krishi Vidyapeeth
Parbhani-431402

2
Dietary Management for Liver disease

3
Introduction
• Liver is the largest gland and internal organ of
the body.
• The liver is a soft and reddish brown in colour
and is shaped like a wedge.
• Liver serve as our body’s internal chemical
power plant.
• It is located beneath the rib cage below the
lungs in the right upper abdomen.
• It weight between 3 and 3.5 pounds. (1.5 kg)
• Liver is the most metabolically active and at
any given movement , 36000 functions are
being carried out in the liver.

4
Structure of Liver
• The liver is consist of two lobes. Each lobe
is made up of thousands of hexagonally
shaped lobules.
• Numerous liver lobules which are the
smallest functional units of the liver.
• Each lobule is itself made up of numerous
liver cells, called hepatocytes.
• The lobules are connected to small bile
ducts that connect with larger ducts to
ultimately from the hepatic duct.
• Hepatic duct transports bile produced by
the liver cells to the gallbladder &
duodenum.
• The gallbladder, a separate organ that
attached to bile duct.
• The gallbladder stores bile and releases it
back into the duct on cues from the
stomach.

5

6
• Hepatic cells, hepatocytes or
parenchymal calls are arranged in rows
called Hepatic cord.
• Spaces present between hepatic cord
are filled with blood and Sinusoid.
• There are specialise phagocytic
macrophages called Kuffer cells in the
wall of the sinusoids which are
responsible for removing bacteria and
worn out red blood cells and destroying
them.
• Oxygen rich blood from the hepatic
artery and nutrient rich blood from the
small intestine flow down the sinusoids
towards the central vein.
• Hepatocytes remove oxygen and
nutrients from the blood and put in their
waste products.

7
Functions of the Liver
1. Stores vitamins and minerals:
• The liver stores significant amount of vitamins A, D, E, K and B12 as well as
iron and copper.
2. Regulate blood clotting:
• Blood clotting coagulants are created using vitamin K, which can only be
absorbed with the help of bile, a fluid the liver production.
• Fibrinogen and prothrombin produce by liver.
3. Resists infections:
• As part of the filtering process, the liver also removes bacteria from the
bloodstream.
4. Processes glucose:
• The liver removes excess glucose from the bloodstream and stores it as
glycogen.
• As needed, it can convert glycogen back into glucose.

8
Functions
5. Bile production:
• Hepatocytes produce a bile which is a fluid that helps to the digestion and
absorption of fats in the small intestine.
6. Detoxification:
• Liver is the body’s natural detoxifier, as it cleanses the body toxins and
produces bile to support healthy digestion.
• The liver filters toxns through the sinusoid channels, which are linked with
immune calls called Kupffer cells. These engulf the toxin, digest it and
excrete it.
7. Regulation of body temperature:
8. Deamination:
• Deamination is the removal of amino group from the amino acid and
converted to ammonia.
9. Formation and destruction of RBC:
• In fetal, liver do the function of formation of RBC and after in adult stage
liver destruction of RBC.

9
Agents Responsible for Liver Damage
1. Dietary deficiency:
• Fatty changes in kwashiorkor due to low protein and reduced capacity to produce
lipoprotein.
• The liver is often grossly enlarged in children with kwashiorkor, containing 30- 50%
fat by weight, in the form of triglycerides.
• Triglycerides can build up in hepatocytes in the liver mitochondrial - oxidation and
VLDL production are insufficient to handle the fatty acid load.
• The intrahepatic accumulation of fat results due to excess delivery of fatty acids to
the liver and/ or enhanced lipogenesis.
• This is combined with impaired lipid transport from the liver secondary to apoprotein
deficiency.
• When protein is supplied fat clears from the liver within a short time.
• Fatty changes in the liver are common whenever there is a high proportion of fat in
the metabolic mixture, e.g. in uncontrolled diabetes, in starvation, in some cases of
obesity & when too much carbohydrate has been infused during intravenous feeding.

1
0
2. Infective agents:
• Virus can cause infections and damage to liver. Type A, B, C, D, E and G can cause
hepatitis.
• Type E is dangerous during pregnancy.
• Hepatitis A and E virus contaminants through faecal - oral route leading jaundice and
liver enlargement.
• Hepatitis B, C, D and G virus cause homogenous serum jaundice with low blood or
blood products of carrier, unsterilized needles.
• Most patients recover. In 10% of people the disease may reach a chronic stage.
• Type B & D can cause extreme jaundice.
• Hepatitis B vaccination is now part of the routine immunisation programme.
Vaccinations are available for Type A & B.

11
3. Toxic agents:
Alcohol:
• A chronic alcohol is often deficient in protein, carbohydrates and vitamins.
• These make up the liver highly vulnerable to any infection or toxin.
• Alcohol is known to as direct action on the lipid metabolism in the liver by enhancing fatty acid
synthesis, decreasing fatty acid oxidation and producing Specific stimulation to triglycerides
formation leading to fatty liver, decreased release of lipoprotein and enhanced uptake of
circulating lipids.
Drugs and chemicals:
• Every drug that is consumed reaches the liver & its chemical nature is altered before being
eliminated from the body.
• Drugs like Paracetamol, INH and oestrogen may damage the liver.
• Workers in chemical industry like organic hydrocarbons may develop liver damage.
• Toxicity due to liver damage has also been observed with several commercially available herbal
preparations.
• Excess stores of iron, copper, galactose, glycogen may
accumulate in liver and in time lead to Cirrhosis.

1
2
4. In born error of metabolism
• Children with heredity tyrosinaemia, galactosaemia and
hereditary fructose intolerance may develop liver damage.
• Successful management depends on early diagnosis & exclusive of
the offending substances from the diet.

13
Damage caused to liver
• Fatty globulation:
• Droplets of triglycerides are formed and the function of liver is impaired.
• Fatty liver is third leading cause of chronic liver disease and liver cancer.
Obesity, diabetes, hypertension are the main cause of fatty liver.
• Necrosis:
• Due to excessive alcohol intake, the liver may become tender and enlarged.
• This is due to inflammation reaction provoked by necrosis or death of
hepatocytes due to excessive fatty globulation or to a direct toxic effect.

1
4
Liver Diseases
• Jaundice
• Hepatitis
• Cirrhosis
• Hepatic encephalopathy
• Cholelithiasis
• Cholecystits

15
Jaundice
• Damage to liver cells leads to increase in bilirubin resulting in jaundice.
• It is a symptoms common to many diseases of the liver and binary tract and
consists of a yellow pigmentation of conjunctiva, skin and body tissues
because of accumulation of bile pigments in the blood.
• Level of bilirubin in jaundice – more than 3 mg/ dL
• Bilirubin
• Bilirubin is yellow colour pigment which develop due to break down of RBCs
and Haemglobin. When bilirubin level is rise leads to jaundice.
• Types of jaundice
• Prehepatic/ hemolytic jaundice-
• Hepaic jaundice-.
• Post hepatic/ obstructive jaundice
• Neonatal jundice

1
6

17
Hepatic jaundice
Post- Hepatic jaundice
Water soluble

1
8
Pre-hepatic/ hemolytic jaundice
• Due to excess breakdown of RBC or Haemoglibon,
unconjugated bilirubin or indirect bilirubin level
becomes increased.
Cause
• Anaemia
• Thalasimia
• Maleria
• Excessive RBC breakdown
• Iron or Vitamin B12 deficiency

1
9
Hepatic jaundice
• In hepatocellular or intrahepatic jaundice, due to
dysfunctioning of the hepatic cell, the liver losses
the ability to conjugate bilirubin.
• This conjugated bilirubin / direct bilirubin level get
increased called hepatic jaundice.
Post- Hepatic/ Obstructive jaundice
• The bilirubin that is not excreted will have been
conjugated by the liver, hence the result is a
conjugated hyperbilirubinamia.

2
0
Neonatal jaundice
• Excessive breakdown of RBCs (hemolysis)
• Fetal hemogobin replace with adult hemoglobin
Unconjugated bilirubin /
Indirect bilirubin
0.2 to 0.8 mg/dL Pre-Hepatic
conjugated bilirubin /
direct bilirubin
0.1 to 0.4 mg/dL Hepatic
Total bilirubin 0.1 to 1.2 mg/dL Post- Hepatic
New born infants > 5 mg/dL Neonatal
Normal Bilirubin Value

2
1
Diagnosis
• LFT (Liver Function Test)
• Serum Bilirubin Test
• Urine Routine Test
• CBC Test
• Hepatitis Test (A,B and C)
• Ultrasound
• CT scan

2
2
Symptoms:
If jaundice is caused by an
infection-
• Fever
• Chills
• Abdominal pain
• Flu-like symptoms
• Change in skin colour
• Dark coloured urine and/ or
clay coloured stool.
If jaundice isn’t caused by an
infection, then person have
symptoms such as-
• Chronic hepatitis or inflammation
of the liver.
• Pyoderma gangrenosum
• Acute hepatitis A, B or C
• Polyarthralgias (inflammation of
joints).

2
3
Dietary Modification
• Aim to repair damage of liver cells and to improve proper
functioning of the liver.
• Fat should be restricted.
• Provide good quality protein to repair cell damage and
prevent the liver from further damages.
• Good amount of carbohydrates should be given to provide
energy.
• In case of hypertension, oadema, sodium should be
restricted.
• Easily digested, attractive and nutritious foods should be
given.
• Avoid oily, bakery foods, butter, ghee, whole milk, raw &
uncooked foods.
•

2
4
Infective Hepatitis
•Infective hepatitis is otherwise known as viral hepatitis.
•This is common cause of jaundice.
• Hepatitis can be due to type A and E or due to B, C, D and G virus.
Cause
1. Viral Hepatitis
2. Alcoholic Hepatitis
3. Toxic Hepatitis
4. Autoimmune
Hepatitis

2
5
Symptoms:
• Fever
• Loss of appetite
• Fatigue
• Nausea and vomiting and abdomen discomfort
• Pain in abdomen
• Body pain, joint pain
• Colour of urine change dark yellow to red and faeces become
whitish.
• Symptoms may continue for 4-8 weeks. Neglected viral hepatitis
leads to cirrhosis of liver.

2
6
Diagnosis
• Medical history and symptoms
• Physical examination
• Blood test (jaundice and viruses)
• Ultrasound

27
Dietary Management
• Principle of diet: A high protein, high carbohydrate and moderate fat diet.
• Nutritionally adequate diet and bed rest.
• The main aim is to ensure recovery of damaged tissues and to prevent further
damage.
• Energy:
In Nasogastric feeding – 1000kcal.
In severe cases- 1600 to 2000kcal.
• Proteins:
For the liver cells to generate an adequate supply of proteins is needed.
Requirement vary according to the severity of the disease.
Severe jaundice – 40g
Mild jaundice- 60 – 80g.
Patient with hepatic coma and coma, protein containing foods are recommended.

2
8
• Fats:
Severe- 20gm, Moderate- 20 -30gm
in other cases of jaundice, fats needs to be restricted only if there is obstruction to
bile flow that does not permit fat digestion and produces fatty diarrhoea.
• Carbohydrate:
When fever, nausea and vomiting are present, intravenous glucose is suggestion.
when patient can take oral feeds, intravenous feeding should be stopped and fruits
juices, sugar, jaggery and honey are given to provide carbohydrates and electrolytes.
• Vitamins: are essential to regenerate liver cells.500mg vitamin C, 10 mg vitamin K,
supplements of B complex are essential to meet daily needs.
• In case of vomiting or nausea and anorexia, vitamins may be given by injections.
• Minerals: oral feeds of fruits juices, vegetable and meat soups with added salt are
given orally or through a nasogastric tube to maintaing electrolyte balance.
• Intravenous feeding: in case of severe nausea and vomiting 10% glucose solution is
recommended.

2
9
Treatment
• Acute hepatitis
• Bed rest
• Plenty of fluids
• Good balanced
nutrition
• Symptomatic
medication
Chronic hepatitis
•Need Antiviral drug
(Hepatitis B & C)
•Complication like
liver failure or cancer ,
need to liver
transplant

3
0
Foods included Foods avoided
• Cereal porridge
• Soft chapathis
• Bread
• Rice
• Skimmed milk
• Potato
• Fruit and fruit juices
• Sugar, jaggery. Honey
• Biscuits, soft custards without butter
cream and non- stimulant beverages
• Meat, fish, chicken,egg, meat Soups
• Sweet preparation where ghee, butter
or oil are used
• Fried preparations
• Bakery products
• Dried fruits
• Spices
• Papads, chutney
• Alcoholic beverages
• Whole milk and cream

31
• Patient should be given enough fluid to prevent
dehydration.
• As patient with severe hepatitis may not be able
excrete a water load, very carefully monitoring of fluid
balance is necessary.
• Patients tend to prefer small meal and these should be
given frequently throughout the day.

3
2
Cirrhosis of Liver
• Cirrhosis is a condition in which there is destruction of the liver due to necrosis, fatty
infiltration, fibrosis and nodular regeneration.
• Cirrhosis is extensive scarring of liver.
• The cirrhosis process may commence many years before it becomes clinically obvious and
usually the patient when first seen is at a very late stage with complications, such as
ascites, reputured oesophageal varices or hepatic coma.
• almost 85-90% of liver damage also do not produce symptoms.
• The initial change in cirrhosis is widespread liver cell necrosis due to viral hepatitis,
alcohol, etc.
• This necrosis results in collapse of the liver cells and intrahepatic shunt, due to the
proximity of hepatic artery and portal vein to the central vein.
• The necrosis and collapse also stimulate nodular regeneration and fibrosis.
• Cirrhosis of liver is the structural & functional end result of nutritional, infective or toxic
changes in the liver.

33
Causes
• Chronic Alcoholism
• Viral infection:
Hepatitis B, C, D & G more likely to produce cirrhosis.
• Nutrition:
Malnutrition aggravates any injury to the liver particularly vitamin A, β-
carotene and vitamin E & C.
• Toxin of food:
Alfatoxin may be one of the cause of cirrhosis.
Chillies and spices are irritant foods which when absorbed are likely to damage
the liver cells.
However, the effect of such substances on the liver is as yet unknown.
Metabolic disturbances such as haemochromatosis (no control on iron
absorption) or Wilson’s disease (disturbance in copper metabolism) can lead to
cirrhosis of liver.
Childhood cirrhosis is a common in India. The clinical and histological features
are similar to those of adult cirrhosis.
Usually they are seen between age of 1-3 years but even babies less than old
may show an advances stage of the disese.

3
4
Symptoms and clinical finding
• The onset of cirrhosis may be gradual with disturbances such as-
Anorexia, Nausea & vomiting, Pain and distension
• The patient may be suffer from –Weakness, Muscle cramps,
Weight loss and fever.
• As the disease progress Jaundice & other serious changes occur.
• Ascites may develop as a consequence of portal vein
hypertension, obstruction of hepatic vein, increased sodium
retention or impaired water excretion.
• Oesophageal varices or varicose veins in the oesophagus and
upper part of the stomach may develop as a complication of
portal hypertension.
• Haemorrhage is then an ever present danger and may be
provoked by roughage of any kind.
•

35
Dietary management
• Principle of diet: high calorie, high protein, high carbohydrate,
moderate or restricted fat, high vitamins.
• Energy: consumption of food is difficult because of anorexia and
ascites. The patient requires highly nutritious food i.e. high calorie diet
because of prolonged undernourishment. The calorie requirement
should be between 2000 to 2500kcal.
• Protein: the serum albumin which is exclusively synthesizes by the liver
cells, is low in cirrhosis and aggravated by the loss of considerable
amount of albumin into ascitic fluid. A high protein diet is helpful for
regeneration of the liver. 1.2 g/ kg body weight can be given in the
absence of hepatic coma.
• The increased amount of proteins can be met by the addition of casein
which can be added in milk, soups and ice-creams.
• Vegetable protein containing more valine is beneficial in preventing
encephalopathy.

3
6
• Fat: about 20gm of fat is given. Even if changes are present in the liver,
fat should be given provided adequate amount of protein is supplied.
Medium chain triglycerides (e.g. coconut oil) containg C8 to C10 fatty
acid can be given as these are digested and absorbed in the absence of
bile salts.
• Carbohydrate:
• Carbohydrate 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% calories should come from carbohydrates so that liver
damage is minimised.
• Vitamins & Minerals: Anaemia is common in cirrhotic patients
hence, Iron supplements should be recommended. Ferrous
sulphate 0.3g tablet 3 times daily after meal. Folic acid 1mg/d.
• Sodium is restricted in oedema and ascites.

37
• If the patient cannot maintain a sufficient intake by eating,
supplementation with sip feeding should be considered.
• If this is inadequate, enteral supplementation should be given.
• Antioxidants and maintenance of calorie, fluid and
electrolyte, fat soluble vitamins are routinely
recommended

3
8
Hepatic Encephalopathy
• Hepatic Encephalopathy: complex syndrome characterized by
neurological disturbance which may develop as a complication of severe
liver disease.
• It result from entrance of certain nitrogen containing substances such as
ammonia into cerebral circulation without being metabolised by the
liver.
• It may be consequance of stunting of the portal blood into systematic
circulation in cirrhosis or of severe damage to liver cells in hepatitis.
Intestine protein breakdown Ammonia Urea
Liver
Cirrhosis
Brain

3
9
Precipitating factors
• Gastrointestinal bleeding
• Severe infection
• Surgical procedure
• Excessive dietary protein and sedatives
• Plasma aromatic amino acids levels and methionine
are elevated while branched chain amino acids are
lowered.

4
0
symptoms
• Confusion
• Restlessness
• Irritability
• Inappropriate behavior
• Delirium and drowsiness
• Convulsion
• Coma
• Flapping tremor of arms and legs when extended.

4
1
Treatment and dietary management
• Treatment is emperical and based on preventing the formation and
absorption of gut- derived toxins/ principally ammonia.
• Daily protein intakes in patient with cirrhosis should be 1 to 1.5 g/kg.
• Dairy protein and vegetable protein are better tolerated,
• In protein intolerant patient, nitrogen should be provided in the form of an
amino acid supplement.
• Plasma arginine and citralline concentrations tend to be higher in patient
on vegetable protein diets.
• This may facilitate ammonia removal via Krebs- Henseleit cycle.
• In general, patient should be encourage to take 30 – 40gm of vegetable
protein.
• Branched chain amino acid can be given to malnourished decompensated
cirrhosis patients with hepatic encephalopathy who are intolerant of
dietary protein.

4
2
Dietary Guideline
• A wholesome well balanced diet maintain the health of
liver and minimise further damage.
• A healthy calorie intake should be maintained.
• Vegetable and dairy proteins are preferred.
• If needed dietary supplements containing certain types of
amino acids can be included.
• Diet should include whole grains at least five servings of
fruits and vegetables of varying colours.
• Salt, sugar and fatty foods should be restricted.
• A minimum of 6 – 8 glasses of fluids/day should br taken. In
addition to water, juices, tea, milk and soups can be taken.
• Small and frequent meals should be taken and long periods
of fasting is avoided.

4
3
• Cholecystitis and cholelithiasis
• Cholelithiasis occurs when gallstones develop.
• If these gallstones block the bile duct from the gallbladder to small
intestine, bile can build up in the gallbladder and cause inflammation.
• This inflammation is called cholecystitis.
• Cause:
• Genetic factors, environmental factors, uncontrolled diabetes, obesity.
• Hypertriglycerideamia is strongly associate with cholelithiasis.
• Dietary guidelines:
• Foods included are cereals in soft form, cooked rice, chapathi, bread
and idli, milk pudding, milk shakes, curd, cooked or pureed vegetables
and khichadi.
• Pulses, beans, meat, fruits, fruit juices, fish & chicken, soft cooked egg
can also be given.
• These foods are high in energy and protein and help in regeneration of
liver cells.

4
4
Pancreatitis
• Acute Pancreatitis:
• It is an inflammatory process of the pancreas that involves peri- pancreatic tissues and
remote organs.
• In mild form, care includes withholding food and drink and administering IV fluids and
parenteral anagesia. Bowel rest reduces pain.
• Small meals composed primarily of carbohydrate may be attempted.
• Carbohydrate causes less pancreatic stimulation than protein and fat.
• Chronic Pancreatitis:
• It is inflammatory disorder that causes anatomic changes, including infiltration of
chronic inflammatory cells and fibrosis of the pancreas.
• Low in fiber oral nutrition because fiber may absorb pancreatic enzymes and delay the
absorption of nutrients.
• Fat soluble vitamins, vitamin B12 and micronutrients including antioxidant should be
replaced as clinically indicated.
• Calcium and vitamin D supplements within the physiologic dosage range are
recommended.
• Lipase supplents reduce steatorrhoea in chronic pancreatitis patients.
• Jejunal feeding improves weight, reduces nacrotic use and improves patient’s quality of
life.
• To keep pancreas healthy, high cholesterol, high calcium diet and excess consumption
of alcohol should be avoided.

4
5
• World Liver Day is on 19th April.
• World Hepatitis Day is on 28th July
Kill the causes of
liver
to
live next day of

Dietary tips for liver disease

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Dietary tips for liver disease

Similar to Dietary tips for liver disease (20)

More from DR KALPANA LAHADE

More from DR KALPANA LAHADE (8)

Recently uploaded

Recently uploaded (20)

Dietary tips for liver disease