A.

Carbohydrate metabolism

Formation and storage of glycogen in glycogenesis Conversion of galactose and fructose to glucoses

A. Carbohydrate metabolism Conversion of amino acid residues to glucose in gluconeogenesis Formation of many important chemical compounds from carbohydrate intermediates.

B.

Protein metabolism

Deamination of amino acids

Provision of lipotropic factor for fat conversion to lipoproteins Formation of plasma proteins Urea formation for removal of ammonia from body fluids

B. Protein metabolism

Many amino acid interconversions: transamination and amination; and synthesis of nonessential amino acids, purines, pyrimedines, creatine phosphates, etc.

C.

Fat metabolism

Fat conversion to transport form with formation of lipoproteins Oxidation of fatty acids to aceto-acetic acids which then is metabolized to acetyl coenzyme A

C. Fat metabolism

(CoA), and enters the citric acid cycle to yield energy. Formation of cholesterol and phospholipids Formation of bile salts Conversion of carbohydrate and protein intermediates to fat through lipogenesis.

D.

Other related functions Storage of Vitamin A, D, K, B12, and other B vitamins Blood coagulation factors : form prothrombin in presence of Vitamin K, also form other blood factors such as fibrinogen, accelerator, factor VII.

D. Other related functions

Storage of iron as ferritin Conjugation and excretion of steroid hormones Detoxification of certain drugs, such as morphine and barbiturates.

A. Hepatitis B. Cirrhosis C. Hepatic Encephalopathy (Hepatic Coma) D. Ascitis E. Esophageal Varices F. Fatty Liver G. Portal Hypertension

1. Characteristics a. Inflammation of the cells accompanied by rapid destruction of the cells b. Types 1) Acute - viral, drug-induced, toxic 2) Chronic - active or persist c. Anorexia, fever, headache d. Weight loss, jaundice, hepatomegaly, tenderness of the liver

2. Etiology a. Acute 1) Viral Type A : infectious hepatitis, transmitted by the fecal-oral route Type B : Serum hepatitis, blood transfusion from infected donors.

2) Toxic and drug induced Carbon Tetrachloride Trichloroethylene Mushroom Poisoning Acetominophen Halothane Isoniazide Chlorpromazine Oral Contraceptive.

b. Chronic 1) Active : a disorder characterized by continuing hepatic necrosis, active inflammation and fibrosis which may lead to cirrhosis. Etiologic agents are hepatitis B virus and chemical or drug agents. 2) Persistent : Rare extra-hepatic involvement, may be secondary to viral hepatitis.

3.

Dietary management Rationale To minimize protein losses Prevent ketosis To replace fluids and electrolytes. To counteract weight loss and for maximum protein utilization. To spare protein, ensure

Diet 1) During acute phase: 5 10% dextrose intravenously and/ or protein parenterally. 2) High calories

A. Hepatitis
3. Dietary management
Diet 5) Moderate fat, MCT preferred over LCT (restrict fat if there is biliary obstruction) 6) High vitamins Rationale To meet high energy needs, at the same time preventing fatty liver To maintain liver functions

7) Frequent small feedings For better tolerance. in cases of anorexia

A. Hepatitis
3. Dietary management
Diet Rationale
to patients 8) Consistency : liquid to soft in acute attacks; Adjusted more liberal in tolerance convalescence

9) Low sodium

In cases of ascites Detoxification function 10) Alcohol prohibited (liver is impaired by alcohol)

1.

Characteristics Slow destruction of liver cells and proliferation of fibrous tissues eventually leading to scarring of the liver tissues. The liver is reduced in size, the shape is distorted after scarring has taken place.

a.

b.

1. Characteristics
c.

Jaundice, ascites, central nervous system dysfunction, cachexia, portal venous hypertension, esophageal and gastric varices, splenomegaly are characteristic findings.

B. Cirrhosis
2.

Etiology

Alcoholism with long-standing malnutrition : Laemecs cirrhosis b. Post necrotic cirrhosis - viral hepatitis c. Biliary cirrhosis - chronic impairement of bile excretion (cholestasis)
a.

2. Etiology Hemochromatosis - increased iron absorption e. Cardiac cirrhosis severe right sided congestive heart failure secondary to Cor pulmonale or constrictive pericarditis. f. Cirrhosis of unknown etiology
d.

B. Cirrhosis
3. Dietary management
Rationale To regenerate hepatic cells Prevent hypoproteinemia a) High Supply lipotropic factors protein Form cholic acids and other bile acids. b) High CHO (300 500 To spare protein. grams per day) c) Moderate fat To prevent fatty liver. MCTs do (Use MCT) require bile salts for absorption. Diet

3. Dietary management
Diet d)Vitamins supplements 1)Thiamine 2)Fat soluble A, D, K e) Low sodium :1 to 2 gm NaCl f) restriction Water

B. Cirrhosis
Rationale To prevent complications Wernicke-Korsakoff syndrome Osteomalacia hypoprothrombinemia

&

To prevent ascites and edema If hypernatremia is present

B. Cirrhosis
3. Dietary management
Diet Rationale

g) Small frequent better tolerance feedings h) Smooth diet or To prevent irritation of full liquid esophageal varices

1. Characteristics A complex organic brain syndrome secondary to liver diseases is characterized by : a) Disturbance of awareness and mental function: forgetfulness and confusion >>> Stupor >>> coma. b) Neurologic changes, rigidity, flapping tremor (asterixis )

1. Characteristics c) Fetor hepaticus : fecal odor of breath d) Distinctive electroencephalographic changes e) Hyperammonemia

Effects of increased blood ammonia level:

Ammonia intoxication due to the failure of the liver to convert ammonia to nontoxic urea Failure of glutamic acid to function in the normal brain metabolism due to its combination with ammonia.

2.

Etiology

a) Ammonia theory : Cirrhotic changes in the liver bring about diminished portal blood circulation and development of collateral circulation, bypassing the liver and its urea cycle for the removal of ammonia from the blood and conversion to urea for excretion

2.

Etiology b) Amino acid neurotransmitter theory - the failing liver induces amino imbalance, with an accumulation of more aromatic amino acids (phenylanine, tyrosine, and tryptophan), methionine, and histidine in the CNS.

2. Etiology

These amino acids are all aminergic neutotransmitter precursors, and the imbalance of their products leads to encephalopathy

3. Precipitating factors
a)

Gastrointestinal bleeding b) Increased dietary protein c) Acute infections d) Deterioration of liver function as in hepatitis, cirrhosis, trauma of surgery.

3.

Precipitating factors e) Electrolyte disturbances, e.g. hypokalemic acidosis, which increases renal ammonia production, increase of unchanged ammonia which can readily cross the blood brain barrier, and accumulate in the CNS.

4) Sources of Ammonia a) Protein deamination b) Massive hemorrhages from esophageal varices followed by digestion of blood proteins c) Intake of ammonia containing drugs.

5) Management a. Dietary
Diet 1)Protein intake Initially : non-protein diet Progress to : 20 30 gm /day, if condition improves until the normal protein allowance is tolerated. 2) Calories : 1500 to 2000 / day, mostly from CHO and fat. Rationale To eliminate completely a source of nitrogen for ammonia synthesis. To minimize tissue protein breakdown which is a source of ammonia.

5) Management a. Dietary

C. Hepatic Encephalopathy (Hepatic Coma)

Diet Rationale 3) Liberal vitamins For adequate nutrition and minerals 4) Low sodium To prevent ascites. Given when oral feeding is not 5) Tube feeding possible Less ammoniagenic, and contains 6) Use of smaller amounts of methionine and vegetable-derived aromatic amino acid; protein source of fiber which alters bacterial N

C. Hepatic Encephalopathy 5) Management (Hepatic Coma) a. Dietary

Rationale These are not catabolized by the liver, 7)Use of branched but are taken up preferentially by extrahepatic tissues; improve plasma chain amino acid levels of valine, isoleucine, and leucine Hypokalemia increases renal vein 8) Parenteral or ammonia due to increased renal ammonia production and increased back diffusion of oral potassium ammonia from alkaline urine Diet

5) Management b. Medical
Diet 1) Neomycin 2) Lactulose 3) Enemas 4) Caution on the use of drugs causing CNS depression 5) Avoid excessive

C. Hepatic Encephalopathy (Hepatic Coma)

Rationale To inhibit the action of GI flora that convert protein and urea to ammonia. Acidify bowel contents with resultant ammonia trapping, or increased motility. To control constipation, and cleanse bowel. Direct depressant affect on brain.

1.

Characteristics : - Accumulation of fluid in the abdominal cavity due to impaired circulation >>> portal hypertension.

2.

Etiology a) Portal hypertension obstruction secondary fibrosis.

a)

and lymphatic to intrahepatic

Reduced osmotic pressure of the plasma due to a failure of the liver to synthesize plasma albumin.

b)

Increased retention of sodium and due to :

water

1. Secondary hyperaldosteronism - due to a reduction in renal blood flow and impaired hepatic metabolism and excretion of aldosterone. 2. Reduced renal vascular flow and excessive serum levels of anti-diuretic hormone

3)

Management
Rationale Individual vary in needs To prevent further retention of sodium To provide high protein but low in sodium supplement; to correct hypoalbuminuria. Due to impaired water excretion May cause hypokalemic acidosis, which enhances hepatic encelopathy.

Diet 1) Protein varies 2) Sodium restriction 3) Low sodium milk, such as Lonalac, or Casilan 4) Limit fluid intake to 1500 ml per day 5)Brisk diuresis avoided

1.

Characteristics a. Presence of varicose veins in the lower third of esophagus and stomach. b. Hemorrahage with excessive dietary roughage Etiology - Due to impaired portal circulation

2.

3.

Management

DIET a. Low fiber diet; smooth bland diet Liquids in cases of severe hemorrhage. b. Tube feeding or gastrostomy

RATIONALE To prevent irritation Depends tolerance on

1.

Characteristics : - Fatty infiltration of the liver associated with starvation, malnutrition, deficiency and toxic factors causing cellular necrosis.

2.

Etiology Chronic Alcoholism Protein Malnutrition Diabetes Mellitus Obesity Large Doses Of Corticosteroid Chronic Illness With Malabsorption.

3. Management ( dietary ) Protein as tolerated > To provide lipotropic factors necessary for Fat transport

1.

Characteristics

a. Increased portal pressure due to impairment in blood flow b. May lead to varicose veins in the lower end of esophagus and stomach (esophageal Varices) encephalopathy and ascites.

2. Etiology a. Cirrhosis which impedes blood flow b. Mechanical obstruction, e.g. thrombosis or tumor invasion. c. Occlusion of the major hepatic vein d. Portal vein thrombosis

3) Management

DIET RATIONALE of a. Same as in cirrhosis Treatment disorder and esophageal varices. underlying may lead in fall of portal pressure and disappearance of varices b. Iron To replace losses due

III. DISEASES OF THE GALLBLADDER

Gallbladder - concentrates and stores bile. * Components of bile 1. Acids - taurocholic and glycocholic 2. Pigments - bilirubin and biliverdin 3. Cholesterol 4. Lecithin 5. Inorganic substances Na, K, Ca, Cl, HCO3 6. Water

* Action of bile

Decreases surface tension of fat Activates lipases and increases solubility of soaps and fatty acids Carries fat soluble vitamins A, D, E, and K Accelerates action of pancreatic enzymes.

A. B. C. D. E. F.

Cholecystitis Cholelithiasis Cholecystolithiasis Choledocholelithiasis Biliary Dyskinesia Jaundice or Icterus

1.

Characteristics a. Inflammation of the wall without any sign of infection b. Epigastric pain radiating to right shoulder c. Impaired fat digestion d. Sense of fullness, nausea

1.

Characteristics Jaundice unusual f. Low grade fever g. Stomach distention with intake of gasforming vegetables and strongly flavored foods.
e.

2. Etiology a. Cystic duct obstruction e.g. gallstones trigger inflammation caused mechanically or chemically. b. Chronic infections

3. Management
DIET

A. Cholecystitis
RATIONALE To rest inflamed gallbladder, prevent and correct dehydration, volume depletion, and electrolyte abnormalities Reduce discomfort by preventing stimulation of sphicter of oddi, and contraction of gallbladder. Decrease mechanical and chemical stimulation To prevent dyspepsia

a. IV fluids and electrolytes; progress to clear liquid

b. Low Fat c. Bland low fiber d. Low calorie for obese patients e. Small, frequent feedings

1 Characteristics a. Presence of gallstones without infection b. Constituent of stones : cholesterol, bile pigments, calcium. 2. Etiology a. Cholesterol sterolone : increased biliary secretion of cholesterol

b. Bile pigment stone : 1) hemolysis which leads to increased biliary secretion of conjugated bilirubin, which combines with calcium to form calcium bilirubinate 2) Bacterial infection of bile

3.

Predisposing factors a. Obesity b. Multiparity c. Clofibrate, oral contraceptives and estrogens

3. Predisposing factors Vagotomy and diabetes mellitus delayed emptying of the gallbladder e. Chronic hemolytic disorders. f. Biliary infection g. Age
d.

4. Dietary management Low Fat , Bland diet > To prevent undue stimulation and contraction Of the gallbladder, which causes pain.

1.

Characteristics - Presence of gallstones with infection

2. Management - Same as for cholelithiasis.

1.

Characteristics The stones slip into the common bile duct, producing obstruction partially or completely, or obstruct intermittently.

a.

1. Characteristics
b.

May be without symptoms or with:

1) Biliary colic - due to increased biliary pressure due to sudden interference in bile flow

3.

2) Acute cholangitis - inflammation of the bile duct caused by sudden, complete or partial common-duct obstruction associated with spiking fever and chills, colic and jaundice, may lead to acute suppurative cholangitis >>> septicemia >>> death. 3) Pancreatitis Management : - Same as for cholelithiasis.

1. Characteristics a. Abnormal function and flow of the bile due to abnormal pressure relationship in the biliary tract. b. Types 1) Hypertonic, spastic common duct 2) Atonic, achalasia: distended and toneless gallbladder while sphincter of Oddi is contracted.

2.

Dietary Management

RATIONALE Bile acid deficiency impairs fat digestion and absorption b. Atonic type: High To stimulate Fat contraction of gallbladder

DIET a. Hypertonic type: Low Fat

1.

Characteristics Yellow pigmentation of the skin and discoloration of the eyes due to the overflow of bile from the bile duct to the general circulation.

a.

b.

Types 1) Hemolytic - due to increased amount of emoglobin released from RBC, producing hyperbilirubinemia.

2) Hepatic - Impaired excretion of bilirubin by the liver infections - Obstruction of the extrahepatic bile ducts obstructive - Symptoms: steatorrhea, malnutrition, osteomalacia.

2. Dietary management
DIET a. High calories High protein ( 1.5 to 2 gm / kg) b. Low Fat c. Vitamins and mineral supplements: Vitamin D, B=complex, fat soluble, Iron, calcium d. Full liquid in acute phase Poor appetite due to colic, vomiting, and fever RATIONALE For adequate nutrition Impaired fat digestion and absorption due to bile acid deficiency

A. Pancreatitis

B.

Cystic Fibrosis

C. Cancer of the Pancreas

1. a. b. c.

Characteristics Inflammation of the pancreatic tissues May be acute or chronic Symptoms : abdominal pain, radiating to the back and chest, nausea, vomiting, abdominal distention, jaundice, steatorrhea, creatorrhea, moderate fever.

2. Etiology a. Alcohol ingestions B. Biliary tract disease C. Gallstone D. Metabolic: renal failure; hyperparathyroidism E. Trauma F. Infectious : mumps G. Drug associated : thiazides.

3.

Pathogenesis Autodigestion of the cells and blood vessels of the pancreas by activated proteolytic enzymes brought about by the toxins, infections and direct trauma. There is a release of vasoactive substances producing vasodilatation and edema.

4. Dietary management
RATIONALE To rest the organ To control steatorrhea and b. Low Fat prevent stimulation for bile production c. Moderate CHO and Prevention of hypoglycemia and protein creatorrhea d. Plus enzyme Utilization of nutrients supplements e. Six small feedings; Avoid undue distention and DIET a. Acute attack : NPO

A. Pancreatitis
4. Dietary management DIET f. Avoidance of alcohol g. Supplements of fat-soluble and calcium h. MCT oil RATIONALE Alcohol may precipitate attack. To prevent deficiencies Better absorbed than LCT

It is the dysfunction of the mucus-producing exocrine glands in the bronchi, pancreas, liver and intestines.

1. Characteristics a. Hereditary, rare but common in Caucasian children, transmitted as an autosomal recessive trait with a gene frequency of 1:20.

b. Recurrent pulmonary infection due to: > abnormally viscous mucous secretion > bronchiolar plugging > obstructive enphysema c. Maldigestion and malabsorption due to : > fibrosed pancreas due to atrophy of exocrine; strictures due to obstruction of the duct system by plugs.

> reduction of pancreatic enzymes d.Malabsorption of fat, protein, oligosaccharides, water and fat soluble vitamins e. Biliary cirrhosis >>> portal HPN f. Intestinal obstruction at birth due to thick, tenacious intestinal secretion; small or large bowel obstruction in adult

g. Sweat with abnormally high content of sodium, potassium and chloride. loss of Na in sweat >>> muscle cramps >>> weakness >>> circulatory collapse >>> shock >>> death.

2.

Management
DIETARY RATIONALE

1) Adequate calories, high > To provide weight gain CHO 2) Low fat, MCT oil > Lack of enzyme to digest LCT

3) Extra sodium chloride (1-4 > To replace sodium loss gm/day) 4) Calcium and magnesium > Due to poor absorption of supplements these minerals > Intact protein cannot be digested due to lack of proteolytic enzymes of the

5) Amino acid supplements

1.

Characteristics

More common in males than females at age 60 70 years Weight loss, abdominal pain, anorexia, and jaundice Hepatomegaly, liver tenderness

C. Cancer of the Pancreas

2. Dietary management Nutrition support to nutritional deficiencies. prevent