Liver is the largest organ of
the body.
 Sets in the right side of the
belly.
 Weighs between 1.0-2.5
kg.
 Heavier in males than
females.
 It is reddish in color & feel
rubbery to touch.
 Have two sections-right &
left lobe.
 The right lobe is further
divided into the interior
and posterior segments

The externally visible falciform ligament divides
the left lobe into the medial and
lateral segments.
 Liver is supplied with blood from two sources –the
hepatic artery & portal vein.
 Responsible for 25 %of the basal metabolism &
intimately concerned with the metabolism of
fats,protiens & CHO.
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Shortcut to img_illust_normalLiver_en[1].lnk
Composed of 50,000100,000 lobules.
 Each lobule consist of
a central vein
surrounded by tiny liver
cells grouped in the
sheet or bundle.
 Small branch of hepatic
vein extends through
their centre. .
 Space b/w these cells
contain sinusoids
(blood vessels that are
irregular in shape,
incomplete in size
&wider than blood
capillaries .)
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the liver receives blood containing oxygen from the heart. This
blood enters the liver through the hepatic artery.
The liver also receives blood filled with nutrients, or digested food
particles, from the small intestine. This blood enters the liver
through the portal vein.
In the liver, the hepatic artery and the portal vein branch into a
network of tiny blood vessels that empty into the sinusoids.
The liver cells absorb nutrients and oxygen from the blood as it
flows through the sinusoids. At the same time, they secrete sugar,
vitamins, minerals, and other substances into the blood.
The sinusoids drain into the central veins, which join to form the
hepatic vein. Blood leaves the liver through the hepatic vein.
Each lobule also contains bile capillaries, tiny tubes that carry the
bile secreted by the liver cells. The bile capillaries join to form bile
ducts, which carry bile out of the liver. Soon after leaving the liver,
the bile ducts join together, forming the hepatic duct.
Excess bile flows into the gall bladder, where it is stored for later
use.
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Secretion of bile
Storage of glycogen
Metabolism of fats
Deamination of amino acids
Production of the plasma protiens.
Storage & transport of vitamins &
minerals.
Storage of iron .
Production of clotting factors .
Production of heat .
Detoxification.
Acts as filter
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..
major hypothesis for the pathogenesis of portal systemic
encephalopathy has been termed the altered neurotransmitter
Theory.
A plasma amino acid imbalance existsin ESLD in which the
branched-chain amino acids( BGAAs) valine, leucine, and isoleucine
are decreased, and aromatic amino acids (AAAs) tryptophan,
phenylalanine, and tryrosine,plus methionine, glutamine,
asparagine, and histidine are increased.
The BCAAs furnish as much as 30% of energy requirements for
skeletal muscle, heart, and brain when gluconeogenesis and
ketogenesis are depressed .
This causes serum BCAA levels to fall. At the same time, plasma
AAA’S and methionine are released into circulation by muscle
proteolysis, but the synthesis into protein and liver clearance of
AAAs is depressed .
This changes the plasma molar ratio of BCAAs to AAA’S and may
contribute to the development of hepatic
encephalopathy.
AAAs may limit the cerebral uptake of BCAA because they compete
for carrier-mediated transport at the blood-brain barrier.
Amino Acids Commonly Altered in Liver Disease
Aromatic
. Amino Acids: serum levels are increased.
Tyrosine
Phenylalanine*
Free tryptophan*
Branched €hain Amino Acids: levels are decreased.
Valine*
Leucine"
Isoleucine*
Ammonlogenic Amino Acids: levels are increased.
Glycine
Serine
Threonine*
Glutamine
Histidine*
Lysine"
Asparagine
Methionine*
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Located in cytosol and mitochondria of
hepatocyte also in cardiac and skeletal muscle,
brain, pancreas, kidney and leukocytes.
An enzyme similar to ALT but less specific for
liver disease.
Levels of AST are increased with liver damage or
death of hepatocytes.
In some cases viz alcoholic hepatitis or shock liv
the elevation in serum AST level may be, higher
than the elevation in serum ALT level.
AST Normal range – 2-40 U/L.
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It is located in cytosol of hepatocytes found in several
other body tissues.
It is highest in liver.
ALT level is increased in case of liver cell death, caused
due to, Hepatitis, any shock, injury or excess alcohol or
drug toxicity.
Normal range – 2-40 U/L
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An enzyme that is widely distributed in liver, bone,
placenta, intestine, kidney, leukocytes.
It is mainly bound to canalicular membranes of liver
produced in the bile ducts.
This enzyme activity can be increased with bone
disorders, pregnancy , normal growth & some
malignancies.
40 - 129 U/L
 Bilirubin
is a yellow breakdown product of
the normal heme catabolism .
 It is excreted in bile & urine and elevated
levels may indicate certain diseases.
 It is responsible for the yellow color of the
bruises ,urine & brown color of feces &
yellow discoloration of skin.

Bilirubin is created by the activity
of biliverdin
reductase on biliverdin, a green
tetrapyrrolic bile pigment that is
also a product of heme
catabolism. Bilirubin, when
oxidized, reverts to become
biliverdin once again. This cycle,
in addition to the demonstration
of the potent antioxidant activity
of bilirubin, has led to the
hypothesis that bilirubin's main
physiologic role is as a cellular
antioxidant.
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Unconjugated bilirubin (indirect)
Erythrocytes (red blood cells)
generated in the bone
marrow are disposed of in the
spleen when they get old or
damaged. This
releases hemoglobin, which is
broken down to heme as the
globin parts are turned
into amino acids. The heme is
then turned into unconjugated
bilirubin in the
reticuloendothelial cells of the
spleen. This unconjugated
bilirubin is not soluble in water,
due to intramolecular hydrogen
bonding. It is then bound
to albumin and sent to the liver

Conjugated bilirubin(direct)

In the liver it is conjugated
with glucuronic acid by the
enzyme glucuronyltransferase, making it
soluble in water. Much of it goes into
the bile and thus out into the small
intestine. However 95% of the secreted
bile is reabsorbed by the small
intestine. This bile is then resecreted by
the liver into the small intestine. This
process is known as enterohepatic
circulation. About half of the
conjugated bilirubin remaining in the
large intestine(about 5% of what was
originally secreted) is metabolized by
colonic bacteria to urobilinogen, which
can be further metabolized
to stercobilinogen, and finally oxidized
to stercobilin. Stercobilin gives feces its
brown color
 Bilirubin
is broken down by light. Tubes
containing blood or (especially) serum to be
used in bilirubin assays should be protected
from illumination.
 Total bilirubin ("TBIL") measures both BU and
BC. Total and direct bilirubin levels can be
measured from the blood, but indirect bilirubin
is calculated from the total and direct bilirubin.
 Indirect bilirubin is fat-soluble and direct
bilirubin is water-soluble.
 Bilirubin (in blood) is in two forms.
Abb.
"BC"
"BU"
Name(s)
Watersoluble?
"Conjugated" or
"Direct bilirubin"
Reacts quickly when dyes (diazo
Yes (bound
reagent) are added to the blood
toglucuronic
specimen to
acid)
produceazobilirubin "Direct bilirubin"
"Unconjugated" or
No
"Indirect bilirubin"
Reaction
Reacts more slowly. Still produces
azobilirubin. Ethanol makes all bilirubin
react promptly then calc: Indirect
bilirubin = Total bilirubin - Direct
bilirubin
μmol/L
mg/dL
0.2-1.9,[
Total bilirubin
5.1–17.0
0.3–1.0
0.1-1.2
Direct bilirubin
1.0–5.1
0-0.3
0.1–0.3
0.1-0.4
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Hyperbilirubinemia results from a higher than normal level of bilirubin in the blood.
Mild rises in bilirubin may be caused by:

Hemolysis or increased breakdown of red blood cells

Gilbert's syndrome - a genetic disorder of bilirubin metabolism that can result in mild
jaundice, found in about 5% of the population
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Rotor syndrome: non-itching jaundice, with rise of bilirubin in the patient's serum, mainly
of the conjugated type.
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Moderate rise in bilirubin may be caused by:

Pharmaceutical drugs (especially antipsychotic, some sex hormones, and a wide range of
other drugs)

Sulfonamides are contraindicated in infants less than 2 months old as they increase
unconjugated bilirubin leading to kernicterus.

Hepatitis (levels may be moderate or high)

Chemotherapy

Biliary stricture (benign or malignant)

Very levels of bilirubin may be caused by:

Neonatal hyperbilirubinaemia, where the newborn's liver is not able to properly process
the bilirubin causing jaundice

Unusually large bile duct obstruction, e.g. stone in common bile duct, tumour obstructing
common bile duct etc.
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Severe liver failure with cirrhosis (e.g. primary biliary cirrhosis

Choledocholithiasis (chronic or acute)presence of gallstone in the common bile duct
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An enzyme associated with microsomes and plasma
membranes in hepatocytes also present in kidney,
pancreas, heart , brain.
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An enzyme produced in the bile ducts that like alkaline
phosphatase, may be elevated in the serum of patients
with bile duct disease.
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It is increased with liver disease, pulmonary disease,
diabetes mellitus and during alcohol ingestion by many
drugs.
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Main export protein synthesized in the liver and most imp. factor in
plasma osmotic pressure maintenance, secreted in the blood.
Major protein circulating in blood stream.
Low serum albumin levels indicate poor liver function.
Serum albumin concentration is usually normal in chronic liver diseases
until cirrhosis and liver damage is present.
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Albumin – 3.4 - 4.8 g%.
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Albumin levels can be low in conditions other than, liver disease like
malnutrition.
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Albumin is a better index of chronic liver disease.
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Increased losses occur with protein losing enteropathy, nephrotic
syndrome burns, GIT bleeding, exfoliative dermatitis.
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Most blood coagulation factors are synthesized in the liver.
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When liver function is severely abnormal, their synthesis and secretion
into blood is decreased.
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PT is a type of blood clotting test and is prolonged when blood
concentration of some clotting factors made by liver are low.
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In chronic liver disease, PT is not usually elevated until cirrhosis is
present and liver damage is significant.
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In acute liver disease, PT can be prolonged with severe liver damage.
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Decreased synthesis of clotting factors increase prothrombin time and
risk of bleeding.
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Major protein in the serum are separated in an
electric field and their concentrations are
determined.
Four major types of serum proteins measured
are albumin, alpha- globulins, beta- globulins
and gamma- globulins.
Alpha and gamma globulins are synthesized in
liver. Levels increase with chronic liver disease.
In cirrhosis, the albumin may be decreased and
the gamma - globulins elevated.
Gamma- globulins can be significantly elevated
in some types of autoimmune hepatitis also.
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Platelets are the smallest of the blood cells, involved in
blood clotting.
With liver disease the spleen becomes enlarged as
blood flow through the liver is impeded.
This can lead to platelets being sequestered in the
enlarged spleen.
The platelet count can be abnormal in many conditions
other than liver disease.
 It
is a thin walled
reservoir situated on
the under surface of
liver.
 It can store about 4050ml of bile.
 It concentrates bile
formed in the liver.
 Stores it , until needed
for digestion.
 Interference with the
flow of bile in
gallbladder diseases
may cause impaired fat
digestion.
Acts as a reservoir for the
storage of bile .
 Mucosal lining of gall bladder
reabsorbs the fluid &
electrolytes ,thus
concentrating the bile
constituents.
 Hormone cholecystokinin
secreted by the duodenal
walls, cause muscular walls
of the gall bladder to
contract and expel the bile.
 Duodenal peristalsis inhibits
the sphincter of oddi & cause
it to relax & allow the bile to
enter the duodenum.
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Bile is the external secretion of the liver .
 Produced in the diluted form .
 Concentrated later by the gall bladder to a
viscid greenish fluid .
 It consists of Water
 Bile salts(sodium glycocholate &sodium
taurocholate)
 Bile acids
 Bile pigment( bilirubin).
 Cholesterol
 Mucus

 Bile
acts to some extent as a surfactant, helping to emulsify the
fats in the food.
 Since bile increases the absorption of fats, it is an important part of
the absorption of the fat-soluble vitamins, such as the vitamins D,
E, K and A.
 Bile serves also as the route of excretion for bilirubin, a by-product
of red blood cells, recycled by the liver.
 Bile salts also act as bactericides, destroying many of the microbes
that may be present in the food.
 Bile salt anions have a hydrophilic side and a hydrophobic side,
and therefore tend to aggregate around droplets of fat (triglycerides
and phospholipids) to form micelles, with the hydrophobic sides
towards the fat and hydrophilic towards the outside.
 have
important Function in assisting the
digestive action of the pancreatic enzyme .
 helps in aiding the absorption of fats & fat
soluble vitamins form the small intestine.
 These salts by lowering the surface tension
cause fat droplets to break up or emulsify
into small droplets allowing fat digesting
enzyme to work more efficiently.
 They convert them to fatty acids & glycerol
,the form in which they are absorbed.
 Bile salts do not appear in faeces as they are
reabsorbed from the small intestine &
returned to the liver.
 These
include
 40% cholic acid .
 40% chemodeoxycholic acid.
 18% deooxycholic acid .
 2% lithocholic acid.
 Total bile acid pool is 2.4 g but it is absorbed
& recirculated 6-8 times a day. Thus
providing over 15- 20 gm of bile for
digestion.
Are derived from the breakdown of the haemoglobin of
worn out RBC’s & give the bile its characteristic color.
 The bile pigments are converted in the bowel to
urobilinogen by bacterial action.
 Some urobilinogen is reabsorbed into the blood & is
excreted by the kidneys into the urine.
 Exposure of urine to the air causes urobilinogen to be
oxidized to urobilin.
 In the faeces , urobilinogen is altered 7 oxidized to
form stercobilin which gives the faeces a dark brown
colour.
 If there is an obstruction to the excretion of bile , bile
pigments accumulate in the blood giving the skin ,a
yellow color (jaundice).

 The
liver is constantly secreting bile, up to 1
liter in a 24 hour period, but most of it is
stored in the gallbladder.
 This hollow organ can only hold 30 to 60 ml
of bile and is able to store the large
quantities of bile from the liver by
concentrating it.
 The gallbladder is able to achieve this by
reabsorption of water, sodium, chloride and
other electrolytes through its lining.
 The other constituents of bile, like the bile
salts, cholesterol, lecithin and bilirubin,
stays in the gallbladder.
 The
liver cells (hepatocytes) produce bile which
collects and drains into the hepatic duct.
 From here it can enter the small intestine to act
on fats by traveling down the common bile duct,
or it can enter the gallbladder through the cystic
duct, where it is stored.
 The liver manufactures between 600ml to 1 liter
of bile in a day. As bile travels down the ducts,
the lining of these passages, secrete water,
sodium and bicarbonate ions into the bile,
thereby diluting it.
 These additional substances help to neutralize
the stomach acid which enters the duodenum
with partially digested food (chyme) from the
stomach.
Cholelithiases
 The
formation of gallstones (calculi) in the absence of
infection of the gallbladder is called cholelithiasis.
 all gallstones form within the gallbladder
 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.
 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.
Most gallstones in people are unpigmented cholesterol
stones composed primarily of cholesterol ,bilirubin and
calcium salts.
 Risk factors for cholesterol stone formation include
female gender, pregnancy, older age, family history
obesity diabetes mellitus, inflammatory bowel disease
and drugs (lipid-lowering medications, oral
contraceptives and estrogens).
 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 .
 Bacteria may 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 gallstone formation .

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.
 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( parenteral nutrition).

 treatment
of gallstone disease includes
cholecystectomy, especially if the stones are
numerous, large, or calcified.
 cholecystectomy may be done as a traditional open
laparotomy or as a less invasive laparoscopic
procedure.
 Chemical dissolution with the administration of bile
salt with other acids are used but very less.
 Patients with gallstones that have migrated into
the bile ducts may be candidates for endoscopic
retrograde cholangiopancreatography techniques
 No
specific dietary treatment is available to
prevent cholelithiasism in susceptible persons.
 Nutrition-related factors include obesity ,severe
fasting and these should be corrected when
possible.
 In cholecystitis, dietary treatment includes a lowfat diet to prevent gallbladder contractions.
 After surgical removal of the gallbladder, oral
feedings are usually resumed with the return of
bowel movement.
 after that the diet can be advanced to a regular
diet as tolerated.
 In the absence of the gallbladder, bile is secreted
directly by the liver into the intestine.
 Inflammation
of the
gallbladder is known as
cholecystitis.
 it may be chronic or
acute. It is usually caused
by gallstones obstructing
the bile ducts , leading to
the backup of bile.
 Bilirubin, the main bile
pigment, gives bile its
greenish color.
 When biliary tract
obstruction prevents bile
from reaching the
intestine, it backs up and
returns to the circulation.
 Due
to infection of gall bladder.
 It occurs in association with obstruction to
the cystic duct or neck of the gall bladder.
 Gall stones are the cause of obstruction
 The walls of the gallbladder become
inflamed and distended and infection can
occur.
 During such episodes, the patient
experiences upper quadrant abdominal pain
accompanied by nausea, vomiting, and
flatulence.
In an acute attack, oral feedings are discontinued.
Parenteral nutrition may be indicated if the patient is
malnourished.
 When feedings are resumed, a low-fat diet is
recommended to decrease gallbladder stimulation
 Patient should be kept in bed & given analgesics.
 Large quantities of fluids should be drunk.
 For acute cases, an entirely fluid of at least 2 -3 litres
daily given in small feeds at hourly or two hourly
intervals is advisable for few days.

Chronic cholecystitis is long-standing inflammation of the
gallbladder.
 It is caused by repeated mild attacks of acute
cholecystitis.
 This leads to thickening of the walls of the gallbladder.
 The gallbladder begins to shrink and eventually loses the
ability to perform its function: concentrating and storing
bile.
 Eating foods that are high in fat may aggravate the
symptoms of cholecystitis because bile is needed to digest
such foods.
 Chronic cholecystitis occurs more often in women than in
men and the incidence increases after the age of 40.
 Risk factors include the presence of gallstones and a
history of acute cholecystitis.

 Patients
with chronic conditions may require a longterm low-fat diet that contains 25% to30% of total
kilocalories as fat.
 Stricter limitation is undesirable because fat in
the intestine is important for some stimulation and
drainage of the biliary tract.
 The degree of food intolerance varies widely
among persons with gallbladder disorders.
 avoid foods that cause flatulence and bloating.
 Cholestasis
is a condition
in which little or no bile
is secreted or the flow of
bile into the digestive
tract is obstructed.
 This can occur in patients
without oral or enteral
feeding for a prolonged
period and can predispose
to a calculous
cholecystitis.
 Prevention includes
stimulation of intestinal
and biliary motility.
 If this is not possible,
drug therapy is used.
 Most
common test is oral cholecystography.
 Presence of stones then can be visualized by
roentgenogram.
 When stones are not visualized ,intravenous
cholangiography is done. It involves
administration of an iodine contrast dye
 Injection of an iodine contrast medium
permits visualization of biliary duct.
 Ultrasonography & computed tomography (ct
scan) can also be done.
Pathophysiology and medical Management
 Inflammation of the bile ducts is known as
cholangitis.
 Patients with acute cholangitis need resuscitation
with fluids and broad-spectrum antibiotics.
 If the patient does not improve with conservative
treatment, placement of a percutaneous biliary
stent or cholecystectomy may be done.
Sclerosing cholangitis is another chronic cholestatic
liver disease.
 Fibrosing inflammation of segments of extrahepatic
bile ducts, with or without involvement of
intrahepatic ducts.
 Progression of the disease leads to complications of
portal hypertension, hepatic failure and
cholangiocarcinoma.
 Primary Sclerosing cholangitis (PSC) is the most
common type of Sclerosing cholangitis.
 It usually occurs in association with inflammatory
bowel disease.

 Sclerosing
cholangitis can result in sepsis
and liver failure.
 Most patients have multiple intrahepatic
strictures, which makes surgical
intervention difficult.
 Patients are generally on broad-spectrum
antibiotics.
 When sepsis is recurrent, patients may
require chronic antibiotic therapy.
 The
pancreas is an
elongated, soft & flattened
gland.
 It lies in the upper abdomen
behind the stomach.
 It is 12-20 cm long in adults &
weighing 75-85 gm.
 The head of the pancreas is
in the right upper quadrant
below the stomach ,adjacent
to the duodenum.
 Main
pancreatic duct extends from tail, collecting it’s vital
secretions of enzymes.
 This portion
consists of about 1 million islets of langerhans, out
of which 80% secrete insulin, 15% secrete glucagon, 5% secrete
somatostatin.
 This
glandular organ has both an endocrine & exocrine
function.
 The
exocrine function is to secrete digestive
enzymes in the inactive form .
 Which only become activated after their release into
the pancreatic juices & the small intestine .
 the endocrine function is the secretion of insulin &
glucagon.
 Insulin is imp for the metabolism of CHO, fats &
proteins & glucagon is concerned with the
breakdown of liver glycogen & with increased
glucogenesis.
TEST
SIGNIFICANCE
SECRETIN
STIMULATION TEST
MEASURES PANCREATIC SECREATION, PARTICULARLY
BICARBONATE, IN RESPONSE TO SECRETIN
STIMULATION.
GLUCOSE TOLERANCE
TEST
ASSESES ENDOCRINE FUNCTION OF THE PANCREAS BY
MEASURING INSULIN RESPONSE TO A GLUCOSE
LEVEL.
72-HOUR STOOL FAT
TEST
ASSESSES EXOCRINE FUNCTION OF THE PANCREAS BY
MEASURING FAT ABSORPTION THAT REFLECTS
PANCREATIC LIPASE SECRETION.
 Pancreatitis
is an inflammation of the pancreas and
is characterized by oedema, cellular exudate and
fat necrosis.
 Pancreatitis is classified as either acute or chronic.
 The symptoms of pancreatitis can range from
continuous or intermittent pain of varying intensity
to severe upper abdominal pain, which may radiate
to the back.
 Symptoms may worsen with the ingestion of food.
 Clinical presentation may also include nausea,
vomiting, abdominal distention, and steatorrhea.
Severe cases are complicated by hypotension,
oliguria, and dyspnea.
causes
Chronic
Alcoholism
Biliary tract
disease
Hypertriglyceridem
ia hypercalcemia
Gall stones
Pancreatitis
Trauma
Certain drugs
some viral
infections
PATHOPHYSIOLOGY
Pancreatitis
Diagnosis
•Test of pancreatic function
•Secretin stimulation test
•Glucose tolerance test
•72 hrs stool fat test
Clinical findings
Symptoms:
•Abnormal pain and
distention
•Nausea
•Vomiting
•Steatorrhea
In severe form:
•Hypotension
•Oliguria
•dyspnea
MANAGEMENT
MEDICAL MANAGEMENT
Acute:
•Withhold oral feeding
•Administer H2-receptor
antagonism, somatstatin
Chronic:
•Manage intestinal pH with:
•Ant acids
•H2 receptor inhibitors
•Administer insulin for
glucose intolerance
NUTRITION MANAGEMENT
P
A
N
C
R
E
A
T
I
T
I
S
Acute:
•Withhold oral and enternal feeding
•If oral nutrition cannot be initiated in 5 to
7 days, start nutrition support
•Once oral nutrition is started, provide:
•Easily digestible foods
•Low fat diet
•6 small meals
•Adequate protein intake
•Increased calories
Chronic:
•Provide oral diet as in acute phase
•Supplement pancreatic enzymes
•Supplement fat soluble vitamins and
vitamin B12
 This
is a serious disorder
which may lead to
haemorrhagic necrosis of
the pancreas, peritonitis &
death.
 Biliary tract stone disease &
alcohol abuse account for 80% of
cases of acute pancreatitis.
 Gall stones & biliary sludge
impaires normal flow of secretion
of pancreatic enzymes.
 Severe acute pancreatitis results
in a hyper metabolic & catabolic
state.
 In
these conditions, the effect of trypsin inhibitor may
be overwhelmed.
 if unchecked the rapidly activated enzymes literally
digest the pancreas in few hours.
 This phase is lethal & may lead to chronic
pancreatic insufficiency.
 Genetic disease like cystic fibrosis may also lead to
pancreatic insufficiency.
 Alcohol
& malnutrition are the major causes of chronic
pancreatitis.
 It
is characterized by recurrent attacks of, epigastric pain of long
duration that may radiate into the back.
 The
pain can be precipitated by meals.
 The
gastric pain is associated with nausea, vomiting or diarrhea.
 Rarely,
chronic pancreatitis is hereditary.
 Principle sign
of chronic pancreatitis is malabsorption caused by
deficiency of pancreatic enzymes& subsequent steatorrhoea.
to prevent further damage to the pancreas.
 decrease the number of attacks of acute
inflammation, alleviate pain, decrease
steatorrhea, and correct malnutrition.
 Dietary intake should be as liberal as possible,
but modifications may be necessary to minimize
symptoms
 Substitution of dietary fat with MCT oil may
relieve steatorrhea and lead to weight gain.
 Antacids, H2-receptor antagonists that reduce
gastric acid secretion may be used to
achieve this effect.
