The above ppt contains physiological aspects of liver, pancreas, gall bladder and stressed more on disorders and how nutritionally they are managed.

1. Physiology and functions of liver

2. Anatomy of liver -Introduction
It is the largest gland of the body.
• Occupying much of the right upper part of the abdominal cavity.
• It consists of both exocrine and endocrine parts.
• The liver performs a wide range of metabolic activities necessary for homeostasis, nutrition, and
immune response

3. Location Shape, Size, And Colour
The liver almost fully occupies the right hypochondrium, Upper part of the epigastrium.
part of the left hypochondrium up to the left lateral (midclavicular) line.
Shape : The liver is wedge shaped and resembles a four-sided pyramid laid on one side
with its base directed towards the right and apex directed towards the left.
Colour : It is red-brown in colour.
Weight : In males 1.4 to 1.8kg.
In females 1.2 to 1.4kg.
At birth 125- 150 g. ( 255g at the age of 1 year , 430g at 2 years , 530g at 5 years )

5. External Features
The wedge-shaped liver presents Two well-defined surfaces:
 diaphragmatic
 visceral.
One well-defined border: Inferior Border
Diaphragmatic Surface
 The dome-shaped diaphragmatic surface includes smooth peritoneal areas which
face superiorly, anteriorly and to the right.
 And a rough bare area (devoid of the peritoneum) which faces posteriorly.
 The inferior vena cava (IVC) is embedded in the deep sulcus in the left part of the
bare area.

6. Visceral Surface (Inferior Surface):
 Relatively flat or concave.
 It is directed downward, backward, and to the left.
 It is separated in front from the diaphragmatic surface by the sharp inferior border and
behind from the diaphragm by the posterior layer of coronary ligament.
 The notable features on the visceral surface are: 1. Fossa for the gallbladder. 2. Fissure
for the ligamentum teres hepatis. 3. Porta hepatis.
 The visceral surface is covered by the peritoneum except at the fossa for gallbladder
and the porta hepatis.

7. Inferior Border
 The features of the inferior border are as follows:
 It separates the diaphragmatic surface from the visceral surface.
 It is rounded laterally where it separates the right lateral surface from the inferior
surface.
It is thin and sharp medially where it separates the anterior surface from the inferior
surface.
 It presents two notches:
(a) Notch for ligamentum teres or interlobar notch: It is located just to the right of the
median plane.
(b) Cystic notch: It is located about 5 cm to the right of the median plane and often
corresponds to the fundus of the gallbladder.

8. Lobes Of The Liver
On the diaphragmatic surface: the liver is divided into two lobes, right and left, by the
attachment of the falciform ligament. The right lobe which forms the base of the wedge-
shaped liver is approximately six times larger than the left lobe.
On the visceral surface: the liver is divided into four lobes: 1. Right lobe: to right of the
fossa for gallbladder. 2. Left lobe: to the left of the fissures for ligamentum teres and
ligamentum venosum. 3. Quadrate lobe: between the fossa for gallbladder and the fissure
for ligamentum teres below the porta hepatis. 4. Caudate lobe: between the groove for
IVC and the fissure for ligamentum venosum

10. Ligaments
False Ligaments: are actually peritoneal folds and include: 1. Falciform ligament. 2. Coronary
ligament. 3. Right triangular ligament. 4. Left triangular ligament.
True Ligaments: are actually the remnants of fetal structures and include: 1. Ligamentum teres
hepatis. 2. Ligamentum venosum.
Blood Supply : The liver is a highly vascular organ. It receives blood from two sources. The
arterial blood (oxygenated) is supplied by the hepatic artery and venous blood (rich in nutrients)
is supplied by the portal vein. Through the liver. About 80% of this is delivered through the
portal vein and 20% is delivered through the hepatic artery.
Nerve Supply : The liver is supplied by both sympathetic and parasympathetic fibres.
Factors Keeping The Liver In Position :
• Hepatic veins connecting the liver to the IVC.
• Intra-abdominal pressure maintained by the tone of abdominal muscles.
• Peritoneal ligaments connecting the liver to the abdominal walls.

11. Functions of liver

12. The liver has the ability to regenerate itself.
Only 10% to 20% of functioning liver is required to sustain life, although removal
of the liver results in death, usually within 24 hours.
The liver is integral to most metabolic functions of the body and performs more
than 500 tasks.
The main functions of the liver include
(1)Metabolism of carbohydrate, protein, and fat
(2)Storage And Activation Of Vitamins And Minerals;
(3)Formation and excretion of bile
(4)Conversion of ammonia to urea
(5)Metabolism of steroids
(6)Detoxification of substances such as drugs, alcohol, and organic compounds;
(7)Function as a filter and flood chamber

13. Metabolic functions
Carbohydrate metabolism
• The liver plays a major role in carbohydrate metabolism. Galactose and
fructose, products of carbohydrate digestion, are converted into glucose in
the hepatocyte or liver cell.
• The liver stores glucose as glycogen (glycogenesis) and then returns it to
the blood when glucose levels become low (glycogenolysis).
• The liver also produces “new” glucose (gluconeogenesis) from precursors
such as lactic acid, glycogenic amino acids, and intermediates of the
tricarboxylic acid cycle.

14. Protein metabolism
• Important protein metabolic pathways occur in the liver. Transamination (transfer of an
amino group from one compound to another) and oxidative deamination (removal of an
amino group from an amino acid or other compound) are two such pathways that convert
amino acids to substrates that are used in energy and glucose production as well as in the
synthesis of nonessential amino acids.
• Blood-clotting factors such as fibrinogen and prothrombin as well as serum proteins
including albumin, alpha-globulin, beta-globulin, transferrin, ceruloplasmin, and
lipoproteins are formed by the liver.
Fat metabolism
• Fatty acids from the diet and adipose tissue are converted in the liver to acetyl-coenzyme A
by the process of beta-oxidation to produce energy. Ketones also are produced.
• The liver synthesizes and hydrolyzes triglycerides, phospholipids, cholesterol, and
lipoproteins as well.

15. Storage And Activation Of Vitamins And Minerals
• The liver is involved in the storage, activation, and transport of many vitamins
and minerals. It stores all the fat-soluble vitamins in addition to vitamin B12
and the minerals zinc, iron, copper, and manganese.
• Hepatically synthesized proteins transport vitamin A, iron, zinc, and copper in
the bloodstream.
• Carotene is converted to vitamin A, folate to 5-methyl tetrahydrofolic acid, and
vitamin D to an active form (25-hydroxycholecalciferol) by the liver
Formation and excretion of bile
• In addition to functions of nutrient metabolism and storage, the liver forms and
excretes bile.
• Bile salts are metabolized and used for the digestion and absorption of fats and
fat-soluble vitamins.
• Bilirubin is a metabolic end product from red blood cell destruction; it is
conjugated and excreted in the bile

16. Conversion of ammonia to urea , metabolism of
steroids and detoxification function
• Hepatocytes detoxify ammonia by converting it to urea, 75% of which is
excreted by the kidneys. The remaining urea finds its way back to the
gastrointestinal tract (GIT).
• The liver also metabolizes steroids. It inactivates and excretes aldosterone,
glucocorticoids, estrogen, progesterone, and testosterone.
• It is responsible for the detoxification of substances, including drugs and
alcohol as well as toxins such as pollutants, pesticides and herbicides,
herbal products, and toxic mushrooms.
• Finally, the liver acts as a filter and flood chamber by removing bacteria and
debris from blood through the phagocytic action of Kupffer cells located in
the sinusoids

17. Liver function tests

18. No one test reflects overall hepatic function.
Each test generally reflects one aspect of hepatic function and must be interpret in
conjunction with other tests with clinical assessment of patient.
Liver abnormalities can be divided into
1. Obstructive – affect biliary excretion of substances
2. Parenchymal – result in generalised hepatocellular dysfunction

19. Major liver function tests may be classified as follows
1. Tests based on excretory function – Measurement of bile pigments, bile salts from
bilirubin
2. Tests based on serum enzymes derived from liver - Determination of
transaminases, alkaline phosphatase, γ – glutamyltranspeptidase.
3. Tests based on synthetic functions – Prothrombin time, serum albumin.
4. Tests based on detoxification: formation of urea

20. Based on excretory function
Normal plasma bilirubin: 0.2–0.8 mg/dl.
Unconjugated bilirubin: 0.2–0.6 mg/dl.
Conjugated bilirubin: 0–0.2 mg/dl.
If the plasma bilirubin level exceeds 1mg/dl, the condition is called
hyperbilirubinemia.
Levels between 1 & 2 mg/dl are indicative of latent jaundice.
When the bilirubin level exceeds 2 mg/dl, it diffuses into tissues producing
yellowish discoloration of sclera, conjunctiva, skin & mucous membrane resulting
in jaundice.
 Icterus is the Greek term for jaundice.

21. Based on serum enzymes
A large number of enzyme estimations are available which are used to ascertain liver function
AST ( aspartate amino transferase) or SGOT (serum glutamate oxaloacetate transaminase)
Normal range: 10-45 U/L.
AST is found in both cytoplasm & mitochondria
AST/GOT also reflects damage to the hepatic cells & is less specific for liver disease. It can
also be released with heart, muscle & brain disorders.
AST help diagnose various heart, muscle or brain disorders, such as a myocardial infarct (heart
attack). Acute hemolytic anemia, cirrhosis of the liver , Hepatitis , Acute pancreatitis or
inflammation of pancreas, Acute renal failure or loss of kidney function, Heart attack ,
primary muscle disease , Recent surgery

22. ALT ( alanine amino transferase ) or SGPT (serum glutamate pyruvate transaminase)
ALT is a cytoplasmic enzyme, Normal Range: 5-40 U/L. SGPT is elevated with
Alcoholic liver disease, Cancer of liver, Hepatitis or inflammation of the liver ,
Noncancerous tumour of the liver , Use of medicines or drugs toxic to the liver,
Cirrhosis or scarring of the liver ,Death of liver tissue.
ALP alkaline phosphatase , occurs in all tissues, especially liver, bone, bile duct, kidney
& the placenta.
The ALP used to help diagnose certain liver diseases and bone disorders.
Normal range: 30 - 95 IU/L
Most effective in an alkaline environment. Levels are significantly higher in growing
children.
A rise in serum ALP , usually associated with elevated serum bilirubin is an indicator of
biliary obstruction (obstructive/posthepatic jaundice).
ALP is also elevated in cirrhosis of liver & hepatic tumors.

23. γ - glutamyl transpeptidase (GGT)
This is a microsomal enzyme widely distributed in body tissues, including liver.
Measurement of γ - glutamyl transpeptidase (GGT) activity provides a sensitive
index to asses liver abnormality. The activity of this enzyme almost parallels that of
transaminases in hepatic damage.
Normal range: 10-15 U/L
Serum GGT is highly elevated in biliary obstruction & alcoholism.
Several drugs (e.g. phenytoin) induce & increase this enzyme in circulation.

24. Based on synthesis function
• Serum albumin: normal range is about 3.0 -5.5 g/dl
• Albumin is solely synthesized by the liver.
• It has a half-life of about 20-25 days.
• It is a good marker to assess chronic (& not acute) liver damage. Low serum
albumin is commonly observed in patients with severe liver damage.
• Albumin is also decreased in malnutrition.
• Functional impairment of liver is frequently associated with increased synthesis of
globulins.
• Cirrhosis of the liver causes a reversal of albumin/globulin ratio (A/G ratio).
Liver dysfunction causes activation and proliferation of circulating plasma cells , and
the liver is unable to dispose the gut antigens and endotoxins, which results in elevated
levels of globulins

25. Prothrombin Time
Normal level is 11 to 14secs. (Measures the activity of fibrinogen & factors V, VII & X)
prolonged period of blood clotting reflects liver damage and also the vitamin deficiency
Based on detoxification function
liver is the major site of detoxification
Blood Ammonia
Significant increase of blood ammonia levels usually reflect disruption of hepatic urea
synthesis.
Normal whole blood ammonia levels are 47 to 65mmol/L
Increase usually reflect severe hepatocellular damage.

26. Diseases of Liver – Alcoholic Liver Disease

27. Alcoholic Liver Disease
• Alcoholic liver disease is one of the most common liver diseases
• 48% of deaths from cirrhosis were related to alcohol
• Acetaldehyde is a toxic byproduct of alcohol metabolism that causes damage to
mitochondrial membrane structure and function.
• Acetaldehyde is produced by multiple metabolic pathways, one of which
involves alcohol dehydrogenase
• Several variables predispose some people to alcoholic liver disease.
• These include genetic polymorphisms of alcohol metabolizing enzymes, gender
(women more than men), simultaneous exposure to other drugs, infections with
hepatotropic viruses, immunologic factors, obesity, and poor nutrition status.
• The pathogenesis of alcoholic liver disease progresses in three stages
 Hepatic Steatosis
 Alcoholic Hepatitis,
 Cirrhosis.

28. Alcohol Acetaldehyde Hepatoxicity Decreased vitamin activation Hypo vitaminemia
Inflammation and necrosis
Hydrogen
Hydrogen replaces fat as a
fuel source and it accumulates
Fatty liver Hepatitis (stage 2)
(Stage 1 )
Cirrhosis (stage 3)

30. Metabolic consequences of alcohol
• Ethanol is metabolized primarily in the liver by alcohol dehydrogenase.
• This results in acetaldehyde production with the transfer of hydrogen to nicotinamide
adenine dinucleotide (NAD), reducing it to NADH.
• The acetaldehyde then loses hydrogen and is converted to acetate, most of which is
released into the blood.
• Many metabolic disturbances occur because of the excess of NADH, which overrides the
ability of the cell to maintain a normal redox state.
• These include hyper lactic acidemia, acidosis, hyperuricemia, ketonemia, and
hyperlipemia.
• The tricarboxylic acid (TCA) cycle is depressed because it requires NAD.
• The mitochondria, in turn, use hydrogen from ethanol rather than from the oxidation of
fatty acids to produce energy via the TCA cycle, which leads to a decreased fatty acid
oxidation and accumulation of triglycerides.
• In addition, NADH may actually promote fatty acid synthesis.
• Hypoglycemia also can occur in early alcoholic liver disease secondary to the suppression
of the TCA cycle, coupled with decreased gluconeogenesis resulting from ethanol

31. Fatty liver
Fatty infiltration, known as hepatic steatosis or fatty liver, is caused by a
culmination of these metabolic disturbances: (1) an increase in the mobilization of
fatty acids from adipose tissue; (2) an increase in hepatic synthesis of fatty acids;
(3) a decrease in fatty acid oxidation; (4) an increase in triglyceride production;
and (5) a trapping of triglycerides in the liver. Hepatic steatosis is reversible with
abstinence from alcohol. Conversely, if alcohol abuse continues, cirrhosis can
develop. Patients with alcoholic fatty liver disease usually are asymptomatic but
can have symptoms such as fatigue, poor appetite, right upper quadrant
discomfort, or hepatomegaly.
Alcoholic hepatitis
Alcoholic hepatitis generally is characterized by hepatomegaly, modest elevation
of serum transaminase levels, increased serum bilirubin concentrations, normal or
depressed serum albumin concentrations, or anemia. Patients also may have
abdominal pain, anorexia, nausea, vomiting, weakness, diarrhea, weight loss, or
fever. Some patients can develop jaundice, coagulopathy, ascites, or
encephalopathy. If patients discontinue alcohol intake, hepatitis may resolve;
however, the condition often progresses to the third stage.

32. Alcoholic cirrhosis
• Clinical features of alcoholic cirrhosis, the third stage, vary. Symptoms
can mimic those of alcoholic hepatitis; or patients can develop
complications of cirrhosis such as gastrointestinal bleeding, hepatic
encephalopathy, or portal hypertension (elevated blood pressure in the
portal venous system caused by the obstruction of blood flow through the
liver). Patients with alcoholic cirrhosis often develop ascites, the
accumulation of fluid, serum protein, and electrolytes within the
peritoneal cavity caused by increased pressure from portal hypertension
and decreased production of albumin (which maintains serum colloidal
osmotic pressure). A liver biopsy usually reveals micronodular cirrhosis,
but it can be macronodular or mixed. Prognosis depends on abstinence
from alcohol and the degree of complications already developed. Ethanol
ingestion creates specific and severe nutritional abnormalities

33. Malnutrition in alcoholics
• Several factors contribute to the malnutrition common in individuals with chronic alcoholic
liver disease:
• 1. Alcohol can replace food in the diet of moderate and heavy drinkers, displacing the intake
of adequate calories and nutrients. In light drinkers, it is usually an additional energy
source, or empty calories. Although alcohol yields 7.1 kcal/g, when it is consumed in large
amounts it is not used efficiently as a fuel source. When individuals consume alcohol on a
regular basis but do not fulfill criteria for alcohol abuse, they are often overweight because
of the increased calories (alcohol addition). This is different from the heavy drinker who
replaces energy-rich nutrients with alcohol (alcohol substitution).
• 2. In the alcoholic, impaired digestion and absorption are related to pancreatic insufficiency,
as well as morphologic and functional alterations of the intestinal mucosa. Acute and
chronic alcohol intake impairs hepatic amino acid uptake and synthesis into proteins,
reduces protein synthesis and secretion from the liver, and increases catabolism in the gut.
• 3. Use of lipids and carbohydrates is compromised. An excess of reduction equivalents
(e.g., nicotinamide adenine dinucleotide phosphate [NADH]) and impaired oxidation of
triglycerides result in fat deposition in the hepatocytes and an increase in circulating
triglycerides. Insulin resistance is also common.

34. • 4. Vitamin and mineral deficiencies occur in alcoholic liver disease as a
result of reduced intake and alterations in absorption, storage, and ability
to convert the nutrients to their active forms. Steatorrhea resulting from
bile acid deficiency is also common in alcoholic liver disease and affects
fat-soluble vitamin absorption. Vitamin A deficiency can lead to night
blindness. Thiamin deficiency is the most common vitamin deficiency in
alcoholics and is responsible for Wernicke encephalopathy, Folate
deficiency can occur as a result of poor intake, impaired absorption,
accelerated excretion, and altered storage and metabolism. Inadequate
dietary intake and interactions between pyridoxal-5-phosphate (active
coenzyme of vitamin B6) and alcohol reduce vitamin B6 status.
Deficiency of all B vitamins and vitamins C, D, E, and K is also
common. Hypocalcemia, hypomagnesemia, and hypophosphatemia are
not uncommon among alcoholics; furthermore, zinc deficiency and
alterations in other micronutrients can accompany chronic alcohol intake

35. Liver Cirrhosis

36. Definition Of Cirrhosis
Chronic liver damage from a variety of causes leading to scarring and liver failure
WHO definition: A diffuse process characterized by liver necrosis and fibrosis and
conversion of normal liver architechture into structurally abnormal nodules that lack
normal lobular organisation.
Common Causes
1. Chronic alcoholism & NASH
2. Chronic hepatitis B& C
3. Autoimmune diseases: autoimmune hepatitis.
4. Biliary disease
5. Cholestatic liver disease : PBC, PSC
6. Hemochromatosis (Iron overload)
7. Wilson's disease,
8. Alpha-1 anti-trypsin deficiency.
9. Obesity
10. Inherited diseases
11 .Drugs & toxins

37. • Predisposing/ Precipitating Factors
Malnutrition
 Effects of Alcohol abuse
Chronic impairment of Bile excretion – Biliary Obstruction in the
Liver and Common bile duct (Gallbladder Stones)
 Necrosis from Hepatotoxins or Viral Hepatitis
Congestive Heart Failure

38. • Pathophysiology
Modularity(regenerating nodules).
Fibrosis(deposition of dense fibrous septa)-fragmentation of sample.
Abnormal liver architecture
Hepatocyte abnormalities : pleomorphism, dysplasia, hyperplasia
Gross pathology: irregular surface ,yellowish colour, small, firm

42. Assessment
• Clinical Manifestations
• Sign/Symptoms - early
• anorexia, nausea, indigestion
• aching or heaviness in right upper quadrant
• weakness & fatigue

43. Late signs:
• abnormal liver function tests:
• bilirubin (N=0-0.9mg/dl),
• AST (N=4.8-19U/L)
• ALT (N= 2.4-17U/L)
• Serum alkaline phosphatase (N=30-40U/L)
• Ammonia (plasma) (N= 15-45umol/L)
• AST / ALT ratio > 1
• Low albumin (< 3.8 g/dL)
• Prolonged prothrombin time
• Low platelet count (< 175 x1000/ml)
• intermittent jaundice, edema, ascites,
• Ecchymosis, bleeding tendencies ,anemia
• Infection
• Gynecomastia, testicular atrophy
• Neurologic changes

45. • Diagnosis Of Cirrhosis
Clinical +laboratory +radiologic +liver biopsy

47. Nutritional Assessment
• Subjective Global Assessment
• Anthropometric measurements
• Bioelectric impedance analysis

48. Dietary management
The measures in dietetic treatment are:
• Assuring the adequate intake of protein and of the correct types of
proteins
• Assuring an adequate supply of energy
• Increased dietary intake of fiber
• Administration of branched-chain amino acids
• Reduced intake of sodium
• Restriction of fluid
• Increased intake of potassium

49. Energy Requirements
 Patients usually need 35-45 kcal/kg/day.
They should supply 60-70% of non nitrogen calories.
Cirrhosis is a disease of accelerated starvation ,so patients should avoid
long time without feeding.
Patients often do better on multiple small meals with alate bed-time
meal.

50. Lipids
Around 20- 30% of total calorie intake should be supplied as fat.
MCT oil are preferred as they are easily digestible and assimilable
A mixed fuel system improves nitrogen balance compared to glucose alone.
Even in decompensated cirrhosis, high lipid containing parenteral mixtures were
found to be well tolerated and improve encephalopathy.
 Thus lipid restriction has no scientific basis in patients with cirrhosis.
 Fat should be provided as polyunsaturated fatty acids, with less than 50% long chain
triglycerides.
 Fat helps make food tastier. This is important for people who suffer from a
suppressed appetite due to chronic liver disease.
fat need in order to properly absorb the four fat-soluble vitamins—A, D,E, and K.
Without some fat, these vitamins may become deficient in the body, even if they are
taken in supplemental form.

51. Proteins
 Proteins should not be restricted in patients with liver disease unless
they become protein intolerant due to encephalopathy.
 Protein intake should be in the range of 1-1.5 g/kg/day.
Several studies have shown that a daily protein supply of 1.0-
1.2g/kg/day may be sufficient to prevent negative N2 balance in cirrhosis
 With mild stress, this has to increase to 1.5 g/kg/day, and with acute
exacerbations of hepatitis or decompensation to 2.0g/kg/day
Special attention should be paid to patients on beta-blockers for
prevention of variceal bleeding.
Beta-blockers increase protein oxidation (an alternative method of
protein metabolism without energy production), and may increase protein
requirement.

52. BCAAs
• Oral BCAAs in cirrhosis with or without chronic encephalopathy
• BCCAs supplement can only be recommended in patients At high risk
of encephalopathy.
• branched-chain amino acids, at doses of 12 to 14 grams per day
• BCAA-enriched formulations can be useful in pt who are intolerant to
protein and malnourished, which can improve protein synthesis and
reduce post injury catabolism.
• Leucine is the most active in promoting protein synthesis and inhibiting
protein breakdown.
• Isoleucine and valine increase nitrogen balance and increase tissue
concentration of leucine

53. Probiotics
• 25% of cirrhotics have small intestinal bacterial overgrowth
• Probiotics decrease intestinal pH, inhibiting growth of pathogenic
bacteria
• Probiotics with fructo-oligosaccharides equal to lactulose for hepatic
encephalopathy is generally safe and well

54. Fluid balance
• fluid intake 30-40mL/kg/day maintains fluid balance
• Dilutional hyponatremia develops due to decreased renal blood flow
and greater free water accumulation
• Fluid restriction of 1.5L/day only if with ascites and hyponatremia
<120mEq/L

55. Nutritional supplementations
Vitamins A, D, E, and K, zinc and selenium supplementation for all
cirrhotics
 If with chronic cholestasis, check serum levels of vitamin A and
25(OH)-D annually
Alcoholics need folate and thiamine supplements
Strict low sodium diet (1 g of table salt per day) • Low sodium diet (3
g of table salt per day) • Sodium-reduced diet (4-5 g of table salt per
day)

56. CONCLUSION
Adequate caloric intake (35 kcal per kg body weight daily)
Adequate intake of protein (1.2–1.5 g per kg body weight daily)
Adequate intake of vegetable fiber or roughage
 Regular exercise to maintain muscle mass
Timely addition of enteral dietary supplementation
 Timely addition of branched-chain amino acids

57. Viral - Hepatitis

58. Hepatitis
• Hepatitis is an inflammation of the liver that results in diffuse hepatic cell
death and may lead to areas of liver necrosis.
• It can be classified as acute or chronic (lasting > 6 months) and may progress
to fulminant liver failure, cirrhosis, and, in some cases, hepatocellular
carcinoma.
• Hepatitis may result from infectious causes (e.g., bacterial, viral, parasitic,
fungal) and noninfectious causes (e.g., drugs, metabolic diseases, alcohol,
autoimmune diseases).
• Viral hepatitis is most commonly caused by hepatitis viruses (especially
hepatitis A, hepatitis B, and hepatitis C) and herpes viruses (cytomegalovirus,
Epstein-Barr virus, varicella-zoster virus, herpes simplex virus).
• These viruses are quite divergent in their structure, epidemiology, routes of
transmission, incubation period, clinical presentations, natural history,
diagnosis, and preventive and treatment options.

59. Indian Scenario
• Viral hepatitis, caused by hepatitis viruses A through E, still remains a
major public health problem in India. India has “intermediate to high
endemicity” for Hepatitis B surface antigen and an estimated 40 million
chronic HBV infected people, constituting approximately 11% of the
estimated global burden. Population prevalence of chronic HBV
infection in India is around 3-4 %. There is a wide variation in HBsAg
prevalence in different geographical regions in India with highest
prevalence recorded in natives of Andaman’s and Arunachal Pradesh.
• Population prevalence of chronic HCV infection in India is around 1 %.
However, there are pockets of areas where prevalence of Hepatitis C has
been observed to be relatively higher in Punjab, Haryana, Andhra
Pradesh, Puducherry, Arunachal Pradesh and Mizoram

60. • Common symptoms include fever, nausea, vomiting, fatigue, jaundice,
right-upper-quadrant abdominal tenderness, and dark urine and pale
stools.
• Extrahepatic manifestations may occur, particularly with chronic
hepatitis. These include amenorrhea, arthritis, skin rash, vasculitis,
thyroiditis, gynecomastia, glomerulonephritis, polyarteritis nodosa,
• Complications of chronic hepatitis include end-stage liver disease,
decompensated cirrhosis, and development of hepatocellular carcinoma.

61. • Hepatitis A (HAV) - is a self-limited cause of acute hepatitis and does
not result in a carrier state or chronic disease.
• Hepatitis A virus spreads from person to person most commonly by fecal-
oral route. Contaminated water and food, including shellfish collected
from sewage contaminated water are the chief sources of infection. The
virus may also spread via sexual (anal) contact
• Disease is usually mild, with symptoms present in 70% of patients,
starting abruptly and lasting 6-24 weeks. However, fulminant liver failure
may occur in patients with underlying liver disease.

62. • Hepatitis B (HBV) generally causes a mild or subclinical acute hepatitis but
may result in chronic hepatitis or an asymptomatic carrier state. Most
symptoms last 1-3 months, although fatigue can last longer. Progression to
chronic hepatitis is most common in perinatal infections and young children.
• Hepatitis B virus can be transmitted both via parenteral and sexual route, most
often by mucous membrane or percutaneous exposure to infective serum or
visceral fluids. Saliva, serum, and semen have also been found to be infectious.
• Percutaneous exposures leading to the transmission of HBV include blood
products transfusion, iv drug abusers, hemo-dialysis, and needlestick injuries
in health care workers. Vertical transmission of HBV is one of the major
source of transmission to neonates.
• The greatest risk of perinatal transmission occurs in infants of HBeAg-positive
women. By age 6 months, these children have a 70-90% risk of infection, and
of those who become infection, about 90% will go on to develop chronic
infection with HBV.

63. • Hepatitis C (HCV) is the most common cause of chronic hepatitis and
the most common indication for liver transplantation. Acute hepatitis C
is usually asymptomatic, but many cases do progress to chronic
hepatitis.
• Hepatitis C patients may remain asymptomatic for 20-25 years before
developing cirrhosis, which occurs in about 20-30% of chronic cases.
• Hepatitis C virus can be transmitted parentally, perinatally or sexually.
Transmission can occur by percutaneous exposure to infected blood
products, transplantation of organs from infected donors, and sharing of
contaminated needles among IV drug abusers

64. Risk Factors
• Hepatitis A. Contact with an infected person (either living in close contact or via
sexual contact), poor hygiene, traveling to areas with inadequate sanitation,
contaminated food (especially shellfish), and illicit drug use.
• Hepatitis B. Exposure to blood or body fluids (e.g., intravenous drug use, high-
risk sexual activity, blood transfusion and/or organ transplant, occupational needle
stick exposure).
• Hepatitis C. Same as HBV, with intravenous drug use being the greatest risk
factor.
• Underlying liver disease. Patients with underlying liver disease (e.g.,
autoimmune hepatitis, hemochromatosis, Wilson’s disease, alpha-1 antitrypsin
deficiency) are at increased risk of developing symptomatic hepatitis.
• Alcohol use, smoking, HIV infection, and fatty liver are risk factors for
progression of hepatitis.

65. Natural history:
• The clinical presentation of infectious hepatitis varies with the
individual, as well as with the specific causative virus, as depicted in
Table 1.0.
• Some patients may be entirely asymptomatic or only mildly
symptomatic at presentation. Others may present with rapid onset
fulminant hepatic failure. The classic presentation of infectious
hepatitis involves four phases, as follows:
• Phase-1 (viral replication phase): Patients are asymptomatic during
this phase. Laboratory studies demonstrate serological and enzyme
markers of hepatitis

66. • Phase II (prodromal phase): Patients experience anorexia, nausea,
vomiting, alterations in taste, arthralgia, malaise, fatigue, urticaria, and
pruritus, and some develop an aversion to cigarette smoke. When seen
by a health care provider during this phase, patients are often diagnosed
as having gastroenteritis or a viral syndrome.
• Phase III (Icteric phase): Patients note dark urine, followed by pale-
coloured stools, in addition to the predominant gastrointestinal
symptoms and malaise. Patients become icteric and may develop right
upper quadrant pain with hepatomegaly.
• Phase IV (convalescent phase): Symptoms and icterus resolve and liver
enzymes return to normal

67. • Table 1.0: Natural history of viral hepatitis
Features HAV HBV HCV HDV HEV
IP (mean) 30 days 60-90 days 50 days 60-90 days 40 days
Onset Acute Insidious Acute Insidious Acute
Age Child &
young
Young adults Any age Any age Young adults
Severity Mild Occ severe Moderate Occ severe Mild
Fulminant 0.1 % 0.1 -1% 0.1% 5-20% 1-2%
Chronicity None 1-10% 85% Common None
Cancer None + + + None
Prognosis Excellent Worse with
age
Moderate Acute-good
chronic-poor
good

68. • So, natural history of different hepatitis viruses can be spontaneous resolution,
chronic HBV infection, fulminant hepatitis, or hepatocellular carcinoma (HCC).
• Chronicity: There are 100% chances of chronicity in patients with HDV
superinfection over HBV (HBV-HDV co-infection have 1-10% chances), while
perinatal HBV and HCV has 90% and 85% chances of chronicity, respectively.
• Fulminant hepatitis: The highest chances of viral hepatitis to culminate into
FHF (fulminant hepatic failure) are with HDV superinfection over pre-existing
HBV infection; and HEV infection in pregnant females (20% chances in each),
while HBV-HDV co-infection have 5% chances for FHF. The order of chances
of FHF in decreasing order is as follows: HDV super-infection& HEV in
pregnancy (20%) > HBV-HDV co-infection (5%) > HEV infection in non-
pregnant female
• Hepatocellular Carcinoma: HCV infection, HBV infection and HDV infection
have chances to complicate as hepatocellular carcinoma in long standing cases

69. Diagnosis
• A complete history and physical examination are important for assessing
exposures and risk factors. Blood tests are essential for a proper
diagnosis. Abnormal liver function tests are common in viral hepatitis
patients, especially during the acute phases of infection. Serum
transaminases (aspartate aminotransferase [AST] and alanine
aminotransferase [ALT]), bilirubin, and alkaline phosphatase are
generally elevated. Coagulation studies, such as prothrombin time (PT)
and partial thromboplastin time (PTT), and albumin are often normal,
except in severe disease.

70. Hepatitis Virus Serology
• Hepatitis A. Anti hepatitis A virus IgM reflects acute infection. IgG, in patients with no acute clinical
symptoms, reflects past exposure or vaccination and confers lifelong immunity.
Three serological markers are available for the diagnosis of hepatitis A. These are
Hepatitis A Total(IgG and IgM) antibody
Hepatitis A IgM
Hepatitis A IgG
• Hepatitis A IgM is generally detectable 5-10 days before onset of symptoms and can persist for upto
6 months. Therefore presence of Hepatitis A IgM indicates acute infection.
• Hepatitis A IgG: It becomes the predominant antibody during convalescence and remains detectable
indefinitely, and therefore patients with serum anti-HAV total ( IgG and IgM) or specific IgG ( but
negative for anti-HAV IgM) denotes immunity to the infection either because of post infection or
vaccination.
• Other tests available for the diagnosis of Hepatitis A are detection of virus or viral components in
fecal samples by immune-electron microscopy (IEM) or by detection of HAV RNA in fecal samples
by RT-PCR during the late incubation period and the pre icteric phase, but seldom later, but these are
not commonly used in routine

71. • Hepatitis B. Surface antigen HBs and core antigen HBc signal acute
infection. Hepatitis B envelope antigen (HB e Ag) indicates high
infectivity. In patients who have received immunization, only surface
antibody is present, whereas core antibody and surface antibody are
present in patients with past exposure who have recovered. Elevation of
ALT for a period longer than 6 months indicates chronic infection. It is
important to test for superinfection with hepatitis D virus.
• Hepatitis C. Testing includes serology, polymerase chain reaction (PCR),
and genotyping. Hepatitis C antibodies are usually present and indicate
chronic infection. PCR indicates viral replication and active disease.
Chronic HCV is diagnosed if RNA via PCR remains positive for more
than 6 months.

72. Nutritional Considerations
The following nutrition considerations apply to prevention and treatment of viral hepatitis:
• Hygiene and sanitation. Persons who travel are at higher risk for hepatitis A (HAV) through the
consumption or handling of contaminated uncooked fruits and vegetables. Boiling or cooking food and
water for ≥ 1 minute to 85°C (185°F) is necessary to inactivate HAV.
• Avoiding contaminated shellfish and game meats. Most acute HAV infections are due to
contaminated shellfish consumption. Shellfish are often taken from wastewater-polluted areas of the sea
and can concentrate the microbial pathogens in seawater. Those taken from near the shoreline (e.g.,
clams, oysters) are particularly likely to be pathogenic. Hepatitis E (HEV) has been identified in
contaminated shellfish and produce, as well as animal meats, particularly wild game, and contaminated
pork.
• Avoiding high-iron foods and iron supplements. Hepatitis C progression occurs in patients as a result
of accelerated hepatic iron uptake and the oxidative stress caused by iron-catalyzed (When excessive
iron changes to Fe3+ from Fe2+,) free radicals are produced and the oxidative stress causes injury
of cell-membrane and DNA, leading to hepatitis progression. Along with phlebotomy, a low-iron
diet helps lower the risk for hepatocellular carcinoma (HCC) in these patients.
• Nutritional supplementation may be required. Treatment with interferon can cause digestive
complaints with a subsequent reduction in appetite and food intake and has been reported to result in
weight loss in 11-29% of treated patients.

73. • A low-fat, low-cholesterol diet may be helpful. Chronic hepatitis C (CHC)
infection increases the risk for hepatic steatosis. A higher intake of dietary
cholesterol contributes to this problem and is associated with the progression of
hepatitis C-related liver disease. Individuals on a dietary regimen that is
reduced in fat (23% of calories) and cholesterol (185 mg/day) experienced a
reduction in liver enzyme elevations and an improvement in immunological
abnormalities known to contribute to liver inflammation in patients with CHC.
• Increase in the intake of PUFA , MUFA, suppresses the progression of the virus
• Adequate vitamin D status. Vitamin D deficiency is common in patients with
chronic liver disease, and these patients may have a reduced ability to convert
vitamin D to its active form. An inverse relationship seems to exist between
vitamin D concentrations and viral load in patients with CHC. vitamin D
supplementation improves the probability of response to treatment.
• Avoidance of extremes in B12 status. Adequate B12 status helps with
clearance of hepatitis virus from the circulation of infected patients. However,
overly high serum B12 levels may also foster viral replication and are
associated with concentrations of hepatitis C RNA levels.

74. • Various nutrients have lately been identified to be associated with
suppression or promotion of HCV proliferation and attract
considerable notice
• It is known that β-carotene, vitamin D, linoleic acid, arachidonic
acid, eicosapentaenoic acid, docosahexaenoic acid, iron, and zinc
have suppressive effects,
• while retinol, vitamin E, vitamin K, vitamin C, cholesterol, and
selenium have promoting effects on HCV proliferation.
• For example, when the serum concentration of vitamin D was
maintained at 32 ng/mL or more by daily administration of 2,000 IU
vitamin D3, the antiviral effect of IFN-based treatment in CHC
patients was markedly improved.

75. Diseases of Gall bladder and Pancreas

77. Diseases of gall bladder
Cholelithiasis
Pathophysiology
• The formation of gallstones (calculi) is cholelithiasis.
• Virtually all gallstones form within the gallbladder. Gallstone disease affects
millions of people each year and causes significant morbidity. In most cases
gallstones are asymptomatic. Gallstones that pass from the gallbladder into the
common bile duct may remain there indefinitely without causing symptoms,
or they may pass into the duodenum with or without symptoms.
• Choledocholithiasis develops when stones slip into the bile ducts, producing
obstruction, pain, and cramps. If passage of bile into the duodenum is
interrupted, cholecystitis can develop. In the absence of bile in the intestine,
lipid absorption is impaired, and without bile pigments, stools become light in
color (acholic). If uncorrected, bile backup can result in jaundice and liver
damage (secondary biliary cirrhosis). Obstruction of the distal common bile
duct can lead to pancreatitis if the pancreatic duct is blocked.

78. Types of gallstones
• Most gallstones are unpigmented cholesterol stones composed primarily of
cholesterol, bilirubin, and calcium salts. Bacteria also play a role in gallstone
formation. Low-grade chronic infections produce changes in the gallbladder
mucosa, which affect its absorptive capabilities. Excess water or bile acid may be
absorbed as a result. Cholesterol may then precipitate out and cause gallstones
• Risk factors for cholesterol stone formation include, High dietary fat intake over
a prolonged period may predispose a person to gallstone formation because of
the constant stimulus to produce more cholesterol for bile synthesis required in
fat digestion.
• Rapid weight loss (as with jejunoileal and gastric bypass and fasting or severe
calorie restriction) is associated with a high incidence of biliary sludge and
gallstone formation
• cholelithiasis and fatty liver disease share risk factors, including central obesity,
insulin resistance, and diabetes, female gender, pregnancy, older age, family
history, obesity and truncal body fat distribution, inflammatory bowel disease,
and drugs (lipid-lowering medications, oral contraceptives, and estrogens).

79. • Pigmented stones typically consist of bilirubin polymers or calcium
salts. They are associated with chronic hemolysis. Risk factors
associated with these stones are age, sickle cell anemia and
thalassemia, biliary tract infection, cirrhosis, alcoholism, and long-term
PN

80. Medical Nutrition Therapy
• Gallstones are more prevalent in low-fiber, high-fat, westernized diets.
Consumption of large amounts of animal protein and animal fat, especially
saturated fat, and a lack of dietary fiber, promote gallstone development.
• There also may be some benefit in replacing simple sugars and refined
starches with high-fiber carbohydrates. Individuals consuming refined
carbohydrates have a 60% greater risk for developing gallstones, compared
with those who consumed the most fiber, in particular insoluble fiber.
• Thus plant-based diets may reduce the risk of cholelithiasis. Vegetarian diets
are high in fiber and low in fat, consisting primarily of unsaturated fat.
Vitamin C, which is generally high in vegetarian diets, affects the rate-
limiting step in the catabolism of cholesterol to bile acids and prevent the
formation of gall stones

81. Diseases of pancreas
The pancreas is an elongated, flattened gland that lies in the upper
abdomen behind the stomach. The head of the pancreas is in the right
upper quadrant below the liver within the curvature of the duodenum, and
the tapering tail slants upward to the hilum of the spleen
This glandular organ has an endocrine and exocrine function. Pancreatic
cells manufacture glucagon, insulin, and somatostatin for absorption into
the bloodstream (endocrine function) for regulation of glucose
homeostasis. Other cells secrete enzymes and other substances directly into
the intestinal lumen, where they aid in digesting proteins, fats, and
carbohydrates (exocrine function).

82. • In most people the pancreatic duct, which carries the exocrine pancreatic
secretions, merges with the common bile duct into a unified opening through
which bile and pancreatic juices drain into the duodenum at the ampulla of
Vater.
• Many factors regulate exocrine secretion from the pancreas. Neural and
hormonal responses play a role, with the presence and composition of ingested
foods being a large contributor.
• The two primary hormonal stimuli for pancreatic secretion are secretin and
CCK. Factors that influence pancreatic secretions during a meal can be divided
into three phases:
(1) the cephalic phase, mediated through the vagus nerve and initiated by the
sight, smell, taste, and anticipation of food that leads to the secretion of
bicarbonate and pancreatic enzymes
(2) gastric distention with food initiates the gastric phase of pancreatic secretion,
which stimulates enzyme secretion
(3) the intestinal phase, mediated by the release of CCK, with the most potent
effect.

83. Pancreatitis
• Pancreatitis is an inflammation of the pancreas and is characterized by
edema, cellular exudate, and fat necrosis. The disease can range from
mild and self-limiting to severe, with autodigestion, necrosis, and
hemorrhage of pancreatic tissue.
• Classification
• Acute pancreatitis
• Sudden inflammation of the pancreas that last for short time
• It may range from mild to severe pancreatitis

84. Etiology
• Gall stones
• Hypertriglyceridemia
• Chronic alcoholism
• Certain drugs
• Some viral infections
• Trauma
• Blocked pancreatic / common bile duct

85. Symptoms
• Upper abdomen pain radiating to back
• Pain aggravated by eating ,especially foods high in fat
• Nausea vomiting
• Fever
Diagnosis
Apply Ranson’s criteria
Medical history
Physical examination
Blood test : Serum amylase ,lipase levels are typically elevated 3 times the
normally levels

86. • Some Tests of Pancreatic Function
• Ranson’s Criteria to Classify the
Severity of Pancreatitis
At Admission or Diagnosis
• Age greater >55 years
• White blood cell count >16,000 m3
Blood glucose level >200 mg/100 mL
Lactic dehydrogenase >350 units/L
Aspartate transaminase >250 units/L
During the Initial 48 Hours
• Haematocrit decrease of >10%
• Blood urea nitrogen increase of >5
mg/dL
• Arterial Po2 <60 mm Hg
• Base deficit >4 mEq/L
• Fluid sequestration >6000 mL
• Serum calcium level <8 mg/mL
Test
Secretin stimulation test
Glucose tolerance test
72-hr stool fat test
Fecal
Significance
Measures pancreatic
secretion, particularly
bicarbonate, in response to
secretin stimulation
Assesses endocrine function
of the pancreas by
measuring insulin response
to a glucose load
Assesses exocrine function of
the pancreas by measuring fat
absorption that reflects
pancreatic lipase secretion
elastase Enzyme most
commonly used to determine
pancreatic function; indirect
test. Levels .200 mcg/g are
considered normal;
concentration ,15 mcg/g of
feces consistent with pancreatic
exocrine insufficiency

87. Chronic pancreatitis
• Long lasting inflammation of the pancreas evolving insidiously over
many years
Etiology
Auto immune conditions
Hypertriglyceridemia
Chronic alcoholism
Cystic fibrosis
Idiopathic
Familial pancreatitis

88. Symptoms
• Recurrent attacks of epigastric pain of long duration , precipitated by
meals
• Steatorrhea
• Diabetes
• Weight loss
• Deficits of lean body mass
• Malnutrition

89. •Diagnosis
1) Structural test : X Ray ,trans abdominal ultrasound , CT scan and
ERCP (For accurate visualization of pancreatic ductal system)
2) Functional test : faecal elastase (less than normal)
Glucose tolerance test (impaired)
3)72 hour stool fat test (more than normal)

90. Objectives and goals of managements
• To prevent further damage to the pancreas
• Decrease the number of attacks of acute inflammation
• To decrease the pain
• Correct malnutrition
• To control blood sugar levels , if diabetic

91. MNT and special dietary recommendations
• Mild acute pancreatitis
• Treat the underlying cause
• Oral feedings can be started immediately, if there is no nausea and vomiting
and pain has resolved
• Feeding start with sips of water to clear liquid proceeding to low fat solid diet
• Gradually shifts to a normal diet (if tolerated by patients)
• Severe acute pancreatitis
• EN is recommended to prevent infectious complications
• PN should be avoided, unless the EN is not available, not tolerated, not
meeting caloric requirements
• Nasogastric / Nasojejunal delivery of enteral feeding is better and safety

92. Nutritional management of acute pancreatitis
• Energy : 25-35kcal/kg IBW/day
• Proteins: 1.2-1.5g / kg IBW/day
• CHOs : 3-6g /kg IBW/day
• (If diabetic restrict refined sugars, include complex CHOs )
• Lipids : up to 2g/kg IBW/ day, corresponds to blood triglycerides levels
If oral nutrition cannot be initiated within 5-7 days, start with tube feeding
• Once the oral nutrition is started provide ,
• Easily digestible ,low fat diet , MCT oils are preferable
• Divide the meals into small six meals
• Increase the calories ( hypermetabolic & catabolic state in severe acute
pancreatitis ) and adequate proteins (BCAAs and High quality proteins )

93. Nutritional management of chronic pancreatitis
• Patients with CP are at increased risk of developing PEM because of
pancreatic insufficiency and inadequate oral intake. Patients with CP
admitted to a tertiary care center usually have malnutrition, increased
energy requirements, weight loss, deficits of lean muscle and adipose
tissue, visceral protein depletion, impaired immune function, and vitamin
deficiencies
• The first goal of MNT is to provide optimal nutrition support
• When pancreatic function is diminished by approximately 90%, enzyme
production and secretion are insufficient; maldigestion and malabsorption
of protein and fat thus become a problem.
• Large meals with high-fat foods and alcohol should be avoided.

94. • pancreatic enzyme replacement is mandatory , Pancreatic enzyme replacements are given
orally with meals
• To promote weight gain, the level of fat in the diet should be the maximum a patient can
tolerate without increased steatorrhea or pain.
• substitution of some dietary fat with MCT oil to improve fat absorption and weight gain
• The diet should be low fat, primarily from vegetable-based oils such as olive oil. Trans fatty
acids, found in commercially baked goods and other processed foods should be eliminated.
• Meals should be small and frequent.
• Malabsorption of the fat-soluble vitamins may occur in patients with significant steatorrhea.
Also, deficiency of pancreatic protease, necessary to cleave vitamin B12 from its carrier
protein, potentially could lead to vitamin B12 deficiency.
• With appropriate supplemental enzyme therapy, vitamin absorption should be improved; but
the patient should be monitored periodically for vitamin deficiencies.
• All these vitamins should be supplemented
• glucose intolerance occurs in 40-90% of all cases with severe pancreatic insufficiency. In this
patients diabetic diet should be given
Reduction in steatorrhea and adequate energy intake are the most important principle of
nutrition therapy in chronic pancreatitis