CIRRHOSIS OF LIVER

PRIYA AGARWAL

STRUCTURE OF LIVER 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.

FUNCTIONS 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.

CONT 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.

DISEASES OF LIVER 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.

CONT… 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)

CONT…. 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.

CONT…. 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.

CIRRHOSIS OF LIVER 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

ETIOLOGY 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)

CLINICAL MANIFESTATIONS

LIVER FUNCTION TESTSTest 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 ammonia to urea.

COMPLICATIONS Malnutrition Ascites Hyponatremia Hepatic encephalopathy Glucose alterations Hepatorenal syndrome OsteopeniaAll these complications have nutritional

implications.

MANAGEMENT OF CIRRHOSIS Nutrition Assessment Medical Management Nutritional Management (MNT)

NUTRITION ASSESSMENTMalnutrition is common in liver disease patients

because of following reasons: Inadequate oral intake Anorexia Dysgeusia, early satiety Nausea and vomiting Maldigestion and malabsorption. Restricted dietsBefore 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)

MEDICAL MANAGEMENT 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.

MEDICAL NUTRITION THERAPY

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.

NUTRIENT REQUIREMENTSENERGY 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).

CONT…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.

CONT….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

CONT…FLUIDOnly 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.