The liver is the largest gland in the body, located in the upper right portion of the abdominal cavity. It performs many critical functions, including metabolism of carbohydrates, proteins, and fats, production of bile and blood proteins, storage of vitamins and minerals, and detoxification of toxins. Liver disease can result from viral infections, alcoholism, toxins, metabolic disorders, drugs, and other causes. Complications of liver disease include malnutrition, ascites, encephalopathy, and others. Nutrition therapy aims to correct nutritional deficiencies and fluid/electrolyte balance while avoiding complications like hyperglycemia or encephalopathy.

1. PRIYA AGARWAL

2.  Largest gland in the body, weighing 1500 gms.
 Location : Upper right hand portion of abdominal
cavity below diaphragm.
 Colour: Reddish brown
 It consists of two lobes right and left both of which
are made up of 8 segments. The segments are made
up of a thousand lobules. The lobules are connected
to small ducts that connect with larger ducts to
ultimately form the common hepatic duct.

4.  CHO metabolism: Glucose converted to
glycogen and stored in liver
 Protein metabolism: Amino acids converted
to glucose ( Gluconeogenesis) and synthesis
of non EAA.
 Fat metabolism: Fatty acid and triglyceride
production(from excess CHO) synthesis of
phospholipids, cholesterol and ketone
bodies.

5.  Blood protein manufactured: Albumin, Prothrombin
and Fibrinogen.
 Detoxification: Alcohol and drugs, ammonia
converted to urea.
 Erythropoietic function: Production of platlets
 Bile Formation: bile consists of bile pigment, bile
salts, protein, cholesterol and inorganic salts.
 Vitamin and mineral storage: storage of A,D, K and
B12 conversion of carotene to vit A. Zinc, iron,
copper and magnesium stored in liver.

6.  Acute Viral Hepatitis: Widespread
inflammation caused by hepatitis viruses A,B,
C, D and E.
 A and E are infectious forms spread by oral
fecal route. Jaundice is common symptom.
 B,C and D are serum forms spread by blood
and body fluids.

7.  Chronic Hepatitis: 6 mths of hepatitis, biochemical
and clinical signs of liver disease and hepatic
inflammation.
 Fulminant Hepatitis: Liver dysfunction with
Hepatic Encephalopathy(altered consciousness and
neuromuscular disturbances)
 NASH: Nonalcholic Steatohepatitis. Accumulation
of Fat in hepatocytes. Causes Drugs, inborn errors
of metabolism and acquired metabolic disorders
(Type 2 DM, obesity, malnutrition)

8.  Alcoholic liver Disease: three stages as follows:
1. Hepatic Steatosis : metabolic disturbances like
Increase in fatty acid synthesis, increase T.G
production and trapping of T.G in liver.
2. Alcoholic Hepatitis: hepatomegaly . Reverts back
if patients discontinue alcohol.
3. Alcoholic Cirrhosis: Symptoms same as alcoholic
hepatitis. Hepatic Encephalopathy, Portal HT and
Ascitis.

9.  Cholestatic Liver Disease:
1. Primary Biliary Cirrhosis: Chronic cholestatic disease
caused by destruction of small and intermediate size
intrahepatic bile ducts.
2. Sclerosing cholangitis: inflammation and scarring of
bile ducts
3. Hepatic osteodystrophy: Vitamin D and calcium
malabsorption.
 Inherited disorders: Hemochromatosis (altered iron
metabolism) and wilson’s disease ( impaired copper
excretion and its accumulation in liver)
 Other Liver Diseases: tumors (benign or malignant).
Carcinoma develops in cirrhotic liver.

10.  It is characterized by destruction of liver cells,
distortion of normal lobules and prolonged fatty
degeneration with fibrous connective tissues replacing
destroyed liver cells. This then blocks the flow of blood
through the liver.
 Cirrhotic liver is contracted and lost most of its
functioning.
Cirrhotic changes are of three types:
 Diffuse hepatic fibrosis or portal laennac’s cirrhosis seen
in alcholics.
 Post necrotic scarring seen in acute infective hepatitis
 Biliary cirrhosis : obstruction in the bile duct

12.  Viral infections : A,B, C, D and E
 Chronic alcoholism
 Toxins in food : Aflatoxin , chillies and spices
are irritant foods that may damage liver cells
 Blocked bile duct
 Metabolic disturbances: Haemochromatosis
and wilson’s disease.
 Drugs: chronic use of hepatotoxic drugs
 NAFLD( NASH)

14. Test Alteration significance Normal value
Total bilirubin Elevated Bile formation and excretion 0.3- 1.2mg/dl
Serum Albumin Decreased Inability to synthesize
protein
3.5- 5.5gm/dl
Prothrombin time Increased Prothrombin and fibrinogen
production decreased
11-15 secondsf
Alanine
aminotransferase
ALT (SGPT)
Increased Enzyme found in
hepatocytes.
5-40 IU/L
Aspartate
aminotransferase
AST (SGOT)
Increased Present in hepatocytes also
in cardiac and skeletal
muscle, brain, kidney
5-45 IU/L
Alkaline
Phosphatase
Incrreased Present in liver, bone
placenta, kidney, intestine..
30-115 IU/L
Ammonia Increased Liver cannot convert

15.  Malnutrition
 Ascites
 Hyponatremia
 Hepatic encephalopathy
 Glucose alterations
 Hepatorenal syndrome
 Osteopenia
All these complications have nutritional
implications.

16. Nutrition Assessment
Medical Management
Nutritional Management (MNT)

17. Malnutrition is common in liver disease patients
because of following reasons:
 Inadequate oral intake
 Anorexia
 Dysgeusia, early satiety
 Nausea and vomiting
 Maldigestion and malabsorption.
 Restricted diets
Before MNT nutritional assessment is important to
determine extent and cause of malnutrition.
The Nutrition assessment tool used for liver disease
patients is Subjective Global Assessment (SGA)

19.  Primary treatments are removal of causative agent
examples alcohol, drugs etc
 Drug therapy limited because of a reduced ability
of liver to metabolise drugs
 Antibiotics such as neomycin or ampicillin are given
to decrease colonic bacteria which produce
ammonia from protein thereby decreasing the
amount of nitrogenous waste. However
malabsorption may occur.
 Lactulose (synthetic disacc) reduces the absorption
of ammonia.

20. Objectives of nutrition therapy:
 To correct fluid and electrolyte balance
 To promote regeneration of liver cells
 To correct nutritional deficiencies
 To avoid potential complications that may occur
as a result of inappropriate nutrition support
like hypo and hyperglycemia, hepatic
encephalopathy, hypertriglyceridemia.

21. ENERGY
REE x 1.2-1.4 (factor for stress and activity) which is equal
to 25-30 kcal /kg dry gbody wt. dry body weight is an
estimate of actual body weight without ascitis. Under
conditions of metabolic stress such post operative period,
sepsis, hepatic failure the energy needs may be 35-45 kcal
/kg dry body weight.
PROTEIN
Essential for building new tissues and liver cells. For
nitrogen balance 0.6-1 gm /kg dry wt per day. For positive
balance 1.2-1.3 gm. Since catabolism of Aromatic amino
acids leads to more ammonia production. Since liver is
damaged ammonia cannot be converted to urea so emphasis
should be on inclusion of vegetable proteins (pulses).

22. CARBOHYDRATES AND FATS
Determining CHO needs is often challenging as liver is
involved in its metabolism. Daily intake of 300 g mainly in the
form of simple sugars like glucose, sugar fruits and fruit
juices, starches and roots and tubers is advised.
Many cirrhotic patients suffer from malabsorption of fat due
to impaired bile secretion. So a fat restricted diet is
recommended. In acute stage only 15-20% of the total
calories should be from fat later on it can be increased.
Emulsified fat and MCTs are better tolerated but EFA
deficiency may develop in prolonged absence of long chain
TGs.

23. VITAMINS AND MINERALS
Fat soluble vitamins are affected due to impaired
absorption. Thus diet should contain beta carotene rich
foods. Folate and B12 deficiency can lead to macrocytic
anemia. Deficiency of thiamine, pyridoxine and B12 can
result in neuropathy. Intramuscular Vit K injections
given to rule out deficiency.
Serum calcium and magnesium levels are lowered in
cirrhotic patients so adequate amounts should be
provided in diet. Zinc deficiency is also common.
Presence of ascitis and edema requires restriction in
sodium . It is restricted to 2gm/d. When diuretic
therapy is recommended a more liberal sodium intake
may be advised

24. FLUID
Only mild restriction is advised to correct ascitis and edema.
Diet and Feeding pattern
 With ascitis early satiety is common complaint so small
meals at regular intervals are recommended.
 For esophageal varices soft and fibre restricted diet is
prescribed.
 Restrict animal proteins and include more of plant proteins.
 Sodium restriction so avoid cooking salt, baking powder and
processed foods and salted pickles.
 Energy dense foods are recommended.
 Fat should not be restricted unless patient has steatorrhea
 Supplement protein if patient is undergoing paracentesis.