DISEASES OF

PANCREAS AND GALL

BLADDER
GALL BLADDER

• It is an accessory organ
to Gastrointestinal
tract.
 FUNCTION OF GALL BLADDER

The normal function of the gallbladder is to concentrate and store

the bile derived from the liver.

The liver produces 600 to 800 milliliters of bile per day, and the
gallbladder concentrates and stores 40 to 70 milliliters.

Bile is composed of water, bile salts, cholesterol, phospholipids

(primarily lecithin), proteins, and bile pigment (bilirubin).

During storage in the gallbladder, bile’s concentration increases

approximately 10-fold as its water content is extracted.
 FUNCTION OF GALL BLADDER

When fat enters the duodenum, it stimulates the secretion of a hormone,

cholecystokinin, which is carried by the blood to the gallbladder.

This hormone directs the gallbladder to contract, so that bile is released

into the common duct and then travels to the duodenum.

The function of bile is to emulsify fats so that they can be broken down
or digested by fat-splitting enzymes, the lipases.

Any interference with the flow of bile impairs fat digestion.

DISORDERS OF GALL BLADDER

• The two major disorders of the gallbladder are cholecystitis and cholelithiasis.
Cholecystitis: usually results from a low-grade chronic infection.
Cholelithiasis: It is an end result of cholecystitis, when the gallbladder mucosa becomes
inflamed or infected, the cholesterol may precipitate, forming gallstones of almost pure
cholesterol crystals.
• Gallstone formation, or cholelithiasis, results from the excessive concentration and
crystallization of compounds in bile.
• Mechanism: Increase in bile’s cholesterol concentration or a reduction in gallbladder
motility, thereby promoting gallstone crystallization or subsequent stone growth.
RISK FACTORS OF THE DISEASE

• Aging: Older men and women, and especially women who have borne children.
• Gender: Twice more common in females.
• Ethnicity: Native Americans, pima Indians
• Pregnancy: Stress of pregnancy and hormonal changes
• Medication: Individuals using oral contraceptives and drugs that lower blood cholesterol
levels.
• Diet: Excess use of polyunsaturated fats can increase the incidence of GB disease.
RISK FACTORS OF THE DISEASE

• Obesity and Weight Loss: Obesity predisposes to gallstone formation because it is associated
with increased cholesterol synthesis in the liver, which results in higher cholesterol
concentrations in bile.
• Gallstones may also develop as a result of rapid weight loss, which both increases the secretion of
cholesterol into bile and decreases gallbladder motility.
• Another effect of rapid weight loss is an increased production of the gallbladder’s mucin proteins,
which are a major component of biliary sludge and also serve as a matrix for cholesterol crystals
during stone growth.
• Heredity.
• Other contributing factors include intestinal diseases that involve the malabsorption of bile salts.
TYPES OF GALLSTONES

Cholesterol Gallstones:
• In about 90 percent of cases, gallstones are composed primarily of cholesterol, although they
also contain calcium salts and bilirubin.
• The cholesterol in bile can precipitate out of solution and form small crystals, which eventually
coalesce to form stones.
• Cholesterol stones are usually yellow green in color.
• It develops after the bile concentrate thickens and forms a type of sludge that cannot be easily
expelled by gallbladder contraction.
• Biliary sludge may develop after rapid weight loss or fasting, gastric bypass surgery, or long-
term total parenteral nutrition, and it can also occur during pregnancy.
TYPES OF GALLSTONES

Pigment Gallstones:
• Pigment stones are primarily made up of the calcium salt of bilirubin (calcium bilirubinate).
• They often develop as a result of bacterial infection, which alters the structure of bilirubin and
causes it to precipitate out of bile and form stones.
• Other cases result from excessive red blood cell breakdown, leading to an abnormal accumulation
of bilirubin.
• Conditions associated with pigment stone formation include biliary tract infections, pancreatitis,
and red blood cell disorders, such as sickle-cell anemia. Pigment stones may form in either the
gallbladder or a bile duct.
• Pigment stones can be brown or black.
GALLSTONE SYMPTOMS

• Gallstone pain (often called biliary colic) usually arises when a gallstone temporarily
blocks the cystic duct, which leads from the gallbladder to the common bile duct.
• The pain is steady and severe and may last for several minutes or several hours. Although
the pain is usually located in the upper abdomen, it may radiate to the chest, back, or
shoulder. Pain may also occur during the night and awaken a person from sleep.
• Nausea and vomiting may also be present. Symptoms usually develop after meals,
especially after eating fatty foods.
COMPLICATIONS OF GALLSTONES

• If a gallstone remains lodged in the cystic duct, it can obstruct bile flow to the duodenum
and cause cholecystitis—distention and inflammation of the gallbladder.
• Cholecystitis can lead to infection or to more severe complications, including
perforation of the gallbladder, peritonitis, and fistulas.
• If gallstones obstruct the common bile duct, they can block bile flow from the liver and
lead to jaundice or damage to liver tissue.
• An impacted stone within the bile ducts may lead to infection and the condition known as
bacterial cholangitis, which causes severe pain, sepsis, and fever and is often a medical
emergency.
• Gallstones can block the pancreatic duct as well—a primary cause of acute pancreatitis.
TREATMENT

• Asymptomatic gallstones generally do not require treatment.

• Gallstones that cause symptoms or complications are usually treated with
gallbladder surgery or nonsurgical procedures that dissolve or fragment the
stones.
SURGERY

• Gallbladder removal, or cholecystectomy, is the primary treatment for patients with recurring
gallstones.
• The standard surgical approach is a laparoscopic method, which relies on narrow surgical
telescopes (laparoscopes) to view and perform the necessary procedures via small incisions in
the abdomen. The procedure takes only one or two hours, and many patients are discharged on
the same day as the surgery.
• Open cholecystectomy—which requires opening the abdominal cavity
• Once the gallbladder has been removed, the common bile duct collects bile between meals and
releases it into the duodenum at mealtimes.
NON-SURGICAL PROCEDURE

Litholysis: in patients who have small cholesterol stones and transient conditions associated
with gallstone formation. The gallstones can be treated by oral intake of ursodeoxycholic acid
(ursodiol), a bile acid that reduces the bile’s cholesterol content and eventually allows the
cholesterol crystals in gallstones to dissolve.
• Used for 6 to 18 months

Shock-wave lithotripsy, a procedure that is also used to fragment kidney stones. This
technique uses high-amplitude sound waves (called shock waves) to break gallstones into
pieces that are small enough to either pass into the intestine without causing symptoms or be
dissolved with ursodeoxycholic acid.
DIET MODIFICATION BEFORE SURGERY

• Before the gallbladder or gallstones are removed, a low-fat diet (with less than 30 percent
of total kcalories from fat) may be prescribed.
• Fat modification involves only its quantity, approximately 40 to 50 g intake per day.
• some individuals may tolerate small, frequent meals better than large meals.
• If weight loss is indicated, calories will be reduced accordingly.
OBESITY, DIETING, AND GALL STONES

• As BMI increases, the risk for developing gallstones also rises.

• People who are obese may also have large gallbladders that do not empty normally or
completely.
• Rapid weight loss may also cause silent gallstones to become symptomatic.
• Dieting may cause a shift in the balance of bile salts and cholesterol in the gallbladder.
• Weight cycling, or losing and regaining weight repeatedly, may increase the risk of
developing gallstones.
• Gallstones are common among people who undergo gastrointestinal surgery to lose weight,
also called bariatric surgery.
PANCREAS

• Pancreas is an important
accessory organ of the GI tract.
• Function: major producer of
digestive enzymes, any
pancreatic disorder can seriously
impair the body’s ability to
digest food.
DISEASE OF PANCREAS

Pancreatic Insufficiency: Reduced production of pancreatic enzymes may occur in cystic fibrosis, chronic
pancreatitis, pancreatic cancer, or protein-calorie malnutrition.
Acute and chronic pancreatitis: The pancreas may become inflamed and/or obstructed by chronic alcohol
abuse or GB disease.
• Pancreatitis is a severe disorder, since the enzymes in the immobile juice can cause the pancreas to digest
itself.
• Symptoms: Acute pain and tenderness result, and in critical cases the pancreas may hemorrhage.
• The digestion of starch, fats and protein is reduced and these are excreted resulting in malnutrition.
Absorption of fat soluble vitamins is also reduced.
• In severe cases, there is necrosis and risk to life due to failure of cardiac, renal and/or respiratory systems.
ACUTE PANCREATITIS

• About 80% of all cases are mild and have a favorable outcome.
• Death may occur with severe disease and about one-third of these arise within the first
week, usually from multi-organ failure.
• Acute pancreatitis occurs as a consequence of premature intracellular trypsinogen
activation, releasing proteases that digest the pancreas and surrounding tissue.
• Triggers: alcohol, gallstones and pancreatic duct obstruction
• The severity of acute pancreatitis is dependent on the balance between the activity of
released proteolytic enzymes and antiproteolytic factors.
PATHOPHYSIOLOGY

Causes:
• Gallstones
• Alcohol
• Idiopathic causes
• Post-ERCP
CLINICAL FEATURES

• Severe, constant upper abdominal pain, of increasing intensity over 15–60 minutes,
which radiates to the back. Nausea and vomiting are common. There is marked
epigastric tenderness.
• In severe cases, the patient becomes hypoxic and develops hypovolaemic shock with
oliguria.
• Pancreatic ascites occurs when fluid leaks from a disrupted pancreatic duct into the
peritoneal cavity.
TREATMENT

• The treatment of choice is to inhibit the secretion of the enzymes and to treat for shock
and renal shutdown.
• Management comprises several related steps:
• Establishing the diagnosis and disease severity
• Early resuscitation, according to whether the disease is mild or severe
• Detection and treatment of complications
• Treatment of the underlying cause.
DIET THERAPY FOR ACUTE PANCREATITIS

• The aim of diet therapy is to prevent the secretion of pancreatic enzymes.

Acute life saving measures: IV or TPN feedings, replacement of fluid and electrolytes,
blood transfusions, and drugs for pain and inhibiting gastric secretions. Nasogastric suction.
NBM
First oral diet: Clear liquid with amino acids, predigested fats, and other commercial
preparations added gradually.
Progression: a bland diet given in six small feedings. No stimulants—coffee, caffeine, tea,
colas, alcohol—are allowed
CHRONIC PANCREATITIS

• Chronic pancreatitis is a chronic

inflammatory disease characterized
by fibrosis and destruction of
exocrine pancreatic tissue.
• Occurs possibly as a result of
malnutrition, deficiency of trace
elements and micronutrients, and
cassava consumption.
MANAGEMENT

Alcohol misuse: Avoidance of alcohol

Pain relief: Analgesics particularly NSAIDS
Malabsorption: Treated by dietary fat restriction (with supplementary medium-chain
triglyceride therapy in malnourished patients) and oral pancreatic enzyme supplements.
Management of complication: Surgical or endoscopic therapy may be necessary for the
management of pseudocysts, pancreatic ascites, common bile duct or duodenal stricture and
the consequences of portal hypertension.
DIET THERAPY FOR CHRONIC PANCREATITIS

• The aim of diet therapy is to treat the malabsorption and prevent malnutrition.
• Usually consists of a bland diet of soft or regular consistency in small meals at frequent
intervals (six feedings), and contains no stimulant foods. Pancreatic enzymes are given
orally with food.
• low-fat diet: Vitamin and mineral supplementation may be necessary, especially fat-
soluble vitamins A, E, and K. B complex vitamins may also be replaced.
• Tube feedings or TPN may be necessary.
Thank you!!