Hepatobiliary and Pancreatic Disorders

I. Liver Disorders

Cirrhosis chronic, progressive disease of the liver in which fibrous connective tissue replaces the functioning liver cells
Characteristics:
-liver cells are damaged to the point that they cannot regenerate, liver function falters, and finally fails
-scar tissue forms within the liver to alter the structure of liver cells so that blood flow is interrupted

A. Causes
1. Chronic alcoholism (Laennecs cirrhosis): the most common cause of cirrhosis
2. Infections include infections leading to chronic hepatitis (post-necrotic cirrhosis)
3. Diseases of the bile ducts, including biliary atresia and primary biliary cirrhosis, or obstruction of the bile
ducts due to a stone or tumor (obstructive cirrhosis)
4. Later stages of congestive heart failure (cardiac cirrhosis)
5. Inherited metabolic disorders, including those that cause excessive accumulation of iron
(hemochromatosis) or copper (Wilsons disease) in the liver or alter the livers ability to use glucose
(glycogen storage disease)

B. Symptoms
1. Impaired circulation portal hypertension leads to ascites and esophageal varices which cause
haemorrhage when ruptured
2. Anorexia, vomiting, epigastric pain, distention, steatorrhea, jaundice
3. Nutritional deficiency anemia, negative nitrogen balance, albuminuria due to poor intake

C. Consequences of Cirrhosis
1. Portal hypertension
2. Collaterals and Esophageal Varices
Collaterals small branches of a blood vessel that develop when blood flow through the liver is obstructed
Esophageal varices varices are blood vessels that have become twisted and distended; collaterals
develop in the esophagus; esophageal varices bulge into the limen of the esophagus which can rupture
and result in massive bleeding that can be fatal
3. Ascites and Edema the pressure in the portal vein forces plasma out of the livers blood vessels into the
abdominal cavity, causing the abdomen to swell
Ascites a type of edema characterized by the accumulation of fluid in the abdominal cavity
4. Elevated ammonia levels
5. Hepatic encephalopathy and hepatic coma
6. Clotting abnormalities
-Persons with cirrhosis bruise and bleed easily since the liver is not able to make an adequate supply of
clotting factors
7. Insulin resistance
-the condition can lead to fatty liver which can progress to cirrhosis
8. Malnutrition and wasting

Possible causes of wasting in liver diseases
Reduced nutrient intake Excessive nutrient losses Raised nutrient needs
Abdominal pain
Anorexia
Early satiety
Esophageal varices
Medications
Nausea
Blood loss through GI bleeding
Diarrhea
Malabsorption
Medications
Steatorrhea
Vomiting
Ascites (raises metabolic rate)
Infections
Inflammation
Malnutrition
Medications

Reduced nutrient intake Excessive nutrient losses Raised nutrient needs
Restrictive Diet
Vomiting

D. Nutritional Care
Objectives of dietary treatment:
1. To promote healing and regeneration of liver tissue
2. To prevent fat stasis and formation of fibrous tissues

Diet:
1. High kcal: 45-50kcal/kg DBW to counteract weight loss and attain DBW
2. High PRO: 1.5-2.0g/kg DBW; 100-150g/day to regenerate and repair hepatic cells; formation of bile acids
3. High CHO: 300-400g to spare protein; to aid in recovery
4. Moderate to low fat; MCT to reduce steatorrhea
5. Use the water-soluble forms of Vitamins A, D, and E if steatorrhea is severe and supplement with vitamin K if
hypoprothrombinemia exists
6. Low Na: 500-1000mg/day (ascites and edema are present)
7. Alcohol is not allowed
8. Supplemental vitamin C, the B-complex vitamins, Mg, K, and Zn may be needed

Hepatitis inflammation of the liver marked by degenerative changes
A. Causes
1. Infectious agents such as viruses and bacteria
2. Transfusion of incompatible blood
3. Toxic drugs such as arsenicals or toxic solvents such as carbon tetrachloride

B. Types
1. Hepatitis A caused by Hepatitis A virus (HAV); transmitted by fecal-oral route through contaminated
water, food, and sewage
Symptoms: anorexia, nausea, vomiting, right upper quadrant abdominal pain; dark urine; and jaundice
(icterus)
Recovery is almost complete
2. Hepatitis B: caused by Hepatitis B Virus (HBV) and Hepatitis C (HCV)
-both can lead to chronic and carrier states
-transmitted via blood, blood products, semen, and saliva; contaminated needles, blood transfusion, open
cuts or wounds, splashes into the mouth or eyes
-Chronic active hepatitis can develop leading to cirrhosis and liver failure
3. Hepatitis D: Hepatitis D virus depends on HBV to survive and propagate in humans
-HDV may be a coninfection (occurring at the same time as HBV) or a superinfection (super-imposing itself
on the HBC carrier state)
-can become chronic
4. Hepatitis C, D, E and non-A and non-B caused by hepatitis C, D, E and non-A and non-B viruses
-conditions currently under study
-fecal-oral, parenteral, or sexual routes of transmission are implicated

C. Symptoms
*anorexia, malaise, weakness, nausea, vomiting, diarrhea, headaches, fever, enlarged liver and spleen, jaundice,
impaired immunocompetence



D. Nutritional Care
Objectives: (1) to aid the regeneration of the liver tissue; (2) to assist in maintaining nitrogen balance; and (3) to
ensure glycogen storage
1. High protein: 1.0-1.5g/kg BW or 70-100g to achieve positive nitrogen balance and to promote liver tissue
repair
2. High CHO: 50-55% of total kcalories or about 300-400 g/day to provide sufficient available glucose and o
spare protein
3. Moderate fat: 30-35% of kcal or about 80-150g daily to make food more palatable and thus encourage the
anorexic person to eat
4. MCT oil for a brief time if steatorrhea is present
5. May be given in liquid form initially

*During the acute phase of the disease: give a full liquid diet, progressing to a soft diet, and eventually to a regular
diet
*6-8 small feedings are recommended
*Encourage the intake of fluids, but alcoholic drinks must be avoided
*Supplementation with vitamins and minerals (Vitamin C, B-complex vitamins, Vitamin K, and Zn)

Hepatic Encephalopathy (HE) a type of brain damage caused by ammonia intoxication die to failure of the liver to
convert ammonia into urea, which accumulate in the blood
Symptoms: Clinical signs include personality changes, disorientation, flapping tremor in the hands, and spasticity

A. Etiology: accumulation of serum ammonia

B. Characteristics
1. Symptoms of impending hepatic coma: confusion, apathy, drowsiness, personality changes, muscle
contractions and spams
2. Electrolyte imbalance
3. Breath has fecal odor

C. Nutritional Care
Objective: to reduce ammonia production and avoid tissue catabolism
Diet
1. Adequate calories to prevent tissue breakdown
2. Low protein
a. Zero protein for not more than 3 days to reduce sources of nitrogenous wastes
b. Gradual increase by 0.5g/kg BW to 1g/kg BW as condition improves
c. Branched chain amino acids (BCAA) supplementation and less aromatic amino acids (AAA) at 2:1
ratio; aromatic amino acids are implicated in hepatic encephalopathy
3. Tube feeding if oral feeding is insufficient or not tolerated

Hepatic Coma a neurologic disorder indicating extensive liver damage, characterized by varying degrees of
consciousness, stupor and lethargy
Symptoms: personality changes, trembling of the hands, loss of memory, hyperventilation, convulsions, and
respiratory alkalosis

Diet
1. Protein restriction: about 30g/day or less (0.3-0.5g/kg body weight)
-protein restriction should be used for a short period of time only
-as the patients condition improves, gradually increase the protein intake to normal levels
2. Provide sufficient calories from CHO and fat (2000 kcal/day or more) to keep body tissue breakdown to a
minimum
3. Supplement with branched chain amino acids to improve nitrogen balance
Standards for laboratory tests used to diagnose and monitor liver disease
Test Normal Values Values in Liver Disease
Albumin
Aklaline phosphatase
ALT (formerly SGPT)
b

Ammonia
AST (formerly SGOT)
b

Bilirubin (direct)
Prothrombin time
3.5-5.0 g/dL
Varies
a

Varies
a

<50 g/dL
Varies
a

0.1-0.3 mg/dL
10-13 seconds
Decreased
Normal or elevated
Elevated
Elevated
Elevated
Elevated
Prolonged
Note: to convert albumin (g/dL) to standard international (SI) units, multiply by 10; to convert ammonia (g/dL) to SI units,
multiply by 0.5872; to convert bilirubin (g/dL) to SI units (mol/L), multiply by 17.10.
a
Reference ranges vary depending on the test used. Consult laboratory report for normal ranges
b
ALT=alanine transaminase; SGPT=serum glutamic pyruvic transaminase; AST=aspartate transaminase; SGOT=serum
glutamic oxaloacetic transaminase

II. Diseases of the Gallbladder
Cholecystitis inflammation of the gallbladder
Function of the gallbladder: to concentrate, store, and excrete bile produced in the liver

A. Types
1. Acute cholecystitis without stones can occur in critically ill patients or when the gallbladder and its bile are
stagnant
Symptoms: epigastric pain that radiates to the shoulder and lower abdominal region; nausea and vomiting;
chills and fever; jaundice
2. Chronic cholecystitis caused by diminished spontaneous contractile activity and decreased contractile
responsiveness to the hormone cholecystokinin
-walls of the gallbladder become inflamed and distended and infection can occur
Symptoms: colicky pain; belching, and flatulence

B. Cause
*gallstones blocking the bile ducts, leading to the backup of bile

C. Diet
Acute cholecystitis
*NPO for 24 hours or more
*Progress from a clear to full liquid diet for 2-3 days, followed by a low-fat diet (30g/day)
*The diet progresses to a moderate fat intake (50-60 g/day) to promote the flow of bile and induce drainage
of the biliary tract

Chronic cholecystitis
*moderate fat intake
*Protein kept at 1g/kg BW
*adjust kilocalories to achieve and maintain desirable weight

Cholelithiasis formation of stones in the gallbladder; stones are made up of cholesterol, bile acids, calcium, and other
inorganic salts, and bilirubin

A. Causes
1. Stones slip into the bile ducts, producing obstruction, pain and cramps
2. Bacteria can result in gallstone formation
-low grade chronic infections can produce changes in the gallbladder mucosa, affecting its absorptive
capabilities; in turn, excess water or excess bile acid may be absorbed, causing cholesterol to precipitate
out and result in gallstone formation

B. Risk Factors for Gallstones
1. Body weight obesity increases the risk of gallstones
2. Gender women between the ages of 20 60 year have twice the risk of developing gallstones as men
3. Age the risk of gallstones increases with age for men and women
4. Other risk factors
a. People with diabetes
b. People using cholesterol-lowering medications
c. Those on total parenteral nutrition
d. People with short bowel movement
e. Dietary factors:
-dietary fibers protect against gallstones by reducing the saturation of cholesterol in the bile
-simple sugars, alcohol, diets rich in animal fats and low in vegetable fats may promote gallstones

C. Diet
With acute gallstone attack:
-Low-fat to decrease gallbladder contraction and lessen the pain
With a sluggish gallbladder:
-Moderate fat intake to stimulate gallbladder contraction and prevent stagnation of bile
-High fiber

III. Diseases of the Pancreas

Pancreatitis inflammation of the pancreas characterized by edema, cellular exudates, and fat necrosis
Symptoms: range from continuous or intermittent pain of varying intensity to severe upper abdominal pain which
may radiate to the back
Clinical signs: nausea, vomiting, abdominal distention and steatorrhea

A. Types
1. Acute pancreatitis characterized by severe epigastric pain, nausea, vomiting, fever, and decreased
peristalsis
2. Chronic pancreatitis characterized by a disturbance in the functioning of the pancreas leading to
inadequate production of digestive enzymes

B. Causes
1. Chronic alcoholism
2. Biliary tract disease
3. Gallstones (most common cause)
4. Certain drugs
5. Trauma
6. Hypertriglyceridemia
7. Hypercalcemia
8. Some infections such as viruses

C. Diet
Objective: to rest the pancreas by restricting foods that stimulate its actions and reduce pancreatic secretions and
bile


For acute pancreatitis:
1. Withhold oral and enteral feeding
2. Support with IV fluids
3. If oral nutrition cannot be initiated in 5 to 7 days, start nutrition support
4. For less severe cases of prolonged acute pancreatitis, tube feeding can be initiated
5. For severe acute pancreatitis, parenteral nutrition should be initiated
6. With the start of oral nutrition, provide:
*easily digestible foods
*low fat diet
*6 small meals
*adequate protein intake
*increased calories

For chronic pancreatitis:
1. Provide oral diet as in acute phase
2. Tube feeding can be used when oral is inadequate
3. Supplement pancreatic enzymes
4. Supplement fat-soluble vitamins and vitamin B12

Cystic Fibrosis a hereditary disorder characterized by the production of thick mucus that affects many organs, including
the pancreas, lungs, liver, heart, gallbladder, and small intestine
-a life-threatening congenital disease occurring in infants and young children
-a common cause of pancreatic insufficiency

A. Characteristics
1. Generalized dysfunction of the exocrine glands involving the pancreas, respiratory system, salivary glands,
gastrointestinal tract, biliary system, and paranasal glands
2. The sweat contains large amounts of sodium chloride and potassium to a lesser extent
3. Thick mucus secretion causes obstruction of mucus-producing cells or organ passages, resulting in
asthma, recurrent pneumonia, and sinusitis
4. Lack of pancreatic enzymes interferes with protein, fat, and carbohydrate utilization
5. Vitamin deficiencies

B. Consequences of Cystic Fibrosis
1. Chronic lung disease
2. Malabsorption
3. Loss of electrolyte in the sweat
*the thick, sticky mucus clogs the lungs airways, the pancreatic ducts and liver
*damage to the pancreas as bile duct interferes with the secretion of digestive enzymes, pancreatic juices,
pancreatic hormones, and bile

C. Diet
*high calorie, high protein, liberal fat and high sodium diet, supplemented with fat-soluble vitamins
-increase dietary intakes to 120%-150% of required need for calories and 150%-200% for protein
-supplement with fat-soluble vitamins if there is fat malabsorption
-increase daily salt intake (1/8 tsp for infants and -1 tsp for children) when there is excessive loss
during strenuous physical activity, extremely hot weather, and febrile illness
-monitor K, Ca, Mg, Cu, Fe, Zn and Se supplement if needed
-fat may not be restricted if pancreatic enzyme is taken with each meal