Malnutrition - UH



Topic C: Medical Nutrition Therapy

1 b Questions 5-9

5. Malnutrition: Protein, calorie, vitamin, and mineral

Definition of malnutrition: A condition caused by inadequate intake or inadequate digestion of nutrients. It may result from eating an inadequate or unbalanced diet, digestive problems, absorption problems, or other medical conditions.

Protein:

Definition: Protein is the main component of muscles, organs, and glands. Every living cell and all body fluids, except bile and urine, contain protein. The cells of muscles, tendons, and ligaments are maintained with protein. Children and adolescents require protein for growth and development.

Protein Energy Malnutrition (PEM): In its most severe states, takes the form of kwashiorkor or marasmus

|Variable |Kwashiorkor |Marasmus |

|Skeletal muscle |No major loses |Signifcant losses |

|Serum proteins |Significantly decreased |Relatively normal |

|Adipose tissue |Preserved |Signifcant loss |

|Body weight |Relatively normal |Significant loss |

|Edema |Pitting edema common |Absent |

|Predisposing factors |Ample energy with little or no protein |Starvation, lack of both protein and total |

| | |energy |

Kwashiorkor and Marasmus not often seen in developed countries. Severe cases can still occur, especially as a result of AIDS, certain cancers, some GI diseases, alcoholism and other instances of substance abuse.

Cachexia- the emaciated condition of the body and general ill health resulting from these and other disesases.

In children:

The severity of PEM can be classified in children and adolescents using weight for height measurements or height for age.

Wasting: a term for a deficit in weight for height

Stunting: a term for deficient in height for age

Pts with PEM can be classified into four categories:

1. Normal

2. Wasted, but not stunted (indicating acute PEM)

3. Wasted and stunted (indicating acute and chronic PEM)

4. Stunted but not wasted (indicating past PEM with adequate nutrition at present)

Calculations:

% weight for height= Actual body weight x 100

Reference weight for height

% height for age= Actual height or length x 100

Reference height for age

* The reference is the median (or 50th percentile) for the subjects age and

sex.

Treatment of PEM:

In patients with severe PEM, the first stage of treatment consists of correcting fluid and electrolyte imbalances, treating infection with antibiotics that don't affect protein synthesis, and addressing related medical problems.

The second phase involves replenishing essential nutrients slowly to prevent taxing the patient's weakened system with more food than it can handle.

Malnutrition/Deficiencies in Vitamins:

The fat soluble vitamins:

1. Vitamin A: is a fat-soluble vitamin, and helps in the formation and maintenance of healthy teeth, skeletal and soft tissue, mucous membranes, and skin. It is also known as retinol because it generates the pigments in the retina.

• Vitamin A deficiency can increase the susceptibility to infectious diseases, as well as cause vision problems.

• Clinical sign: Hyperkeratosis: dry, bumpy skin associated with Vitamin A deficiency

2. Vitamin D: is a fat soluble vitamin and may be absorbed from food by the intestines or may be produced by the skin when the skin is exposed to sunlight. In its active form, vitamin D acts as a hormone to regulate calcium absorption from the intestine and to regulate levels of calcium and phosphate in the bones.

• Vitamin D deficiency is manifest as rickets in children and osteomalacia in adults.

• Rickets: Diseae involving impaired mineralization of growing bones. It can result from Vitamin D, but also from deficiencies in Calcium and Phosphorous. Rickets characterized by: structural abnormalities of weight bearing bones, bone pain, muscular tenderness, hypocalemic tetany. May appear bow-legged.

• Osteomalacia: Generalized reductions in bone density and the presence of psuedofractures especially of the spine, femur, and humerus.

3. Vitamin E: is a fat soluble vitamin and an antioxidant that protects body tissue from the damage of oxidation. It is important in the formation of red blood cells and the use of vitamin K.

• Vitamin E deficiency can occur in the neuromuscular, vascular, and reproductive systems. May cause impaired position sensation, changes in balance and coordination, muscle weakness, and visual disturbances.

4. Vitamin K: Vitamin K is known as the clotting vitamin, because without it blood would not clot. Some studies indicate that it helps in maintaining strong bones in the elderly.

• Clinical sign of deficiency: Hemorrhage, but very rare.

The water soluble vitamins:

1. Thiamin (Vitamin B1): plays essential metabolic roles in CHO metabolism and neural function. Deficiency is characterized by weight loss, cardiac and neurologic signs. In humans, this will eventually lead to Beriberi.

▪ There are two types of Beriberi: Wet and Dry

o Cardiovascular disease (Wet Beriberi)

▪ Wet beriberi is characterized by swelling (edema), increased heart rate (tachycardia), lung congestion, and enlarged heart related to congestive heart failure.

o Nervous system disease (Dry Beriberi)

▪ Symptoms of dry beriberi include pain, tingling, or loss of sensation in hands and feet (peripheral neuropathy), muscle wasting with loss of function or paralysis of the lower extremities, and potentially brain damage and death.

* Beriberi most commonly occurs in developed countries in patients who abuse alcohol, because drinking heavily can lead to malnutrition and poor absorption and storage of thiamine.

2. Riboflavin (Vitamin B2): Works with the other B vitamins. It is important for body growth and red cell production, and helps in releasing energy from carbohydrates. Also required by the body for health, growth and reproduction.

• Early symptoms of deficiency: burning and itching of the eyes, soreness or burning of lips, mouth, and tongue. A purple, or swollen tongue may be a clinical sign.

3. Niacin: a generic term for nicotinamide and nicotinic acid, functions as a component of NAD and NADP in metabolism

• A disease caused by a deficient diet or failure of the body to absorb niacin or an amino acid (tryptophan). Common in certain parts of the world (in people consuming large quantities of corn), the disease is characterized by scaly skin sores, diarrhea, mucosal changes, and mental symptoms (especially a schizophrenia-likedementia). It may develop after gastrointestinal diseases or alcoholism.

4. Vitamin B6 (pyridoxine): Vitamin B-6 plays a role in the synthesis of antibodies in the immune system. It helps maintain normal nerve function and acts in the formation of red blood cells. It is also required for the chemical reactions of proteins. The higher the protein intake, the more the need for vitamin B6.

• Deficiency: leads to metabolic abnormalities: weakness, sleeplessness, peripheral neuropathies, glossitis, stomatitis. Very rare.

5. Folate: Folic acid acts as a coenzyme (with vitamin B-12 and vitamin C) in the breakdown (metabolism) of proteins and in the synthesis of new proteins. It is necessary for the production of red blood cells and the synthesis of DNA (which controls heredity), as well as tissue growth and cell function. It also increases the appetite and stimulates the formation of digestive acids.

• Deficiency: Impaired biosynthesis of DNA and RNA, which can manifest anemia. Clinical signs can include: general weakness, depression, and polyneuropathy.

• Preconceptual folate consumption can reduce the risk of serious birth defects such as neural tube defects.

6. Vitamin B12: plays important roles in metabolism and function of all cells, especially for those in the GI tract, bone marrow, and nervous tissue.

• Deficiency: impaired cell division, pernicious anemia

• Clinical signs: lemon-yellow tint resulting from concurrent anemia and jaundice from ineffective erythropoeisis, smooth, beefy red tongue, or neurologic disorders.

7. Vitamin C (Ascorbic Acid): serves several metabolic functions: enzyme cofactor, a protective agent, and as a reactant with transition metal ions. Vitamin C can also promote the resistance to infection

• Scurvy: impaired wound healing, edema, hemorrhages, weakness of bone and cartilage, swollen bleeding gums, tooth loss, muscular atrophy and skin lesions.

Minerals:

Symptoms of mineral Deficiency

[pic]A deficincy of calcium results in rickets in children and osteomalacia, both of which display a lack of bone mineralization. Calcium deficiency may also contribute to osteoporosis. Toxicity is rare except in certain diseases involving vitamin D or the parathyroid gland.

[pic]The widespread abundance of phosphorus in food makes a deficiency uncommon except in certain diseases. With excessive intake of aluminum, calcium or magnesium containing antacids or laxatives, a phosphate deficiency can occur because these substances prevent phosphate from being absorbed from the intestine.

[pic]A deficiency of magnesium is rare. Drugs that cause potassium depletion, such as certain diuretics, may also cause low magnesium levels. A deficiency can occur in diabetics, alcoholics and in the presence of gastrointestinal disorders where absorption is impaired, such as prolonged diarrhea. Magnesium appears to be involved in the regulation of calcium levels; therefore if magnesium levels are low, calcium levels may also be low and unresponsive to treatment unless magnesium levels are corrected. Signs of a deficiency include loss of appetite, irritability, disorientation, convulsions, and abnormal behavior.

[pic]Too little potassium (hypokalemia) results in cardiac arrhythmias, muscle weakness, sodium loss in the urine, alterations in acid base balance and the inefficient use of carbohydrate.

Symptoms of Trace Mineral Deficiency

[pic]Iron deficiency generally occurs during the growth period or when intake fails to replace iron loss that is associated with blood loss. When iron stores are depleted and there is inadequate production of heme (the portion of hemoglobin associated with the iron), the red blood cells become small (microcytic) and have decreased capacity to carry oxygen. There is also a drop in iron-containing enzymes that are important in cellular metabolism. This results in decreased work capacity, fatigue and altered behavior such as irritability.

[pic]A zinc deficiency may be associated with diets high in unrefined cereal and unleavened bread, long term TPN, or diseases of the intestine such Crohn's disease,

[pic]Iodine Deficiency is manifest by a decreased metabolic rate, lethargy and obesity. A prolonged deficiency of iodine causes the thyroid gland to increase in size such that a large nodule referred to as a goiter, protrudes from the neck. In many countries inorganic iodides are added to table salt to prevent the deficiency. Iodine deficiency in infants and children results in mental retardation. Inadequate maternal intake causes a deficiency in the fetus and newborn.

[pic]Signs of a chromium deficiency are usually only seen in adults eating highly refined foods or in people who are receiving long-term TPN that lack chromium. With a chromium deficiency, blood sugar levels are generally high. There may also be abnormalities of nerve stimulation of the extremities (arms, hands, legs and feet) and alterations of brain tissue.

[pic]Although a copper deficiency is rare, it can occur in people with prolonged diarrhea or other disorders of intestinal absorption. It can also occur in the presence of high dose zinc supplementation. Signs of a deficiency include anemia, a decrease in certain white blood cells, skeletal demineralization, loss of hair color, and skin pallor. Children with copper deficiencies may experience ruptured blood vessels, central nervous system abnormalities, growth retardation, and poor temperature regulation.

[pic]Manganese deficiency has not been well documented in humans. A few people on manganese deficient diets showed signs of elevated calcium and phosphorus, suggesting that dissolution of bone to release manganese stores may also release calcium and phosphorus into the blood. As such, it is speculated that a manganese deficiency may be a contributing factor for osteoporosis. In animals, a deficiency has been associated with abnormal reproductive ability, growth retardation, birth defects, abnormal formation of bone and cartilage, dermatitis, and impaired glucose handling.

[pic]Although selenium deficiency is uncommon in the United States, low levels in the body may be associated with acute illness and prolonged TPN. Symptoms of selenium deficiency include muscle weakness and pain, inflammation of the muscles, fragile red blood cells, degeneration of the pancreas, and abnormal coloration. There have also been associations of selenium deficiency with several diseases affecting the heart muscle, but a protective effect against heart disease has not been proven. In geographic areas where selenium is deficient in the soil and therefore in food, human deficiencies have been reported to cause dilation of the heart and congestive heart failure.

5. Inborn Errors of Metabolism:

I have never heard of most of these before, but I wanted to give you guys a list of most of them. I’ll go into detail about the more common ones after the table.

|Inborn Error of Metabolism |Suggested Dietary Management |

|Arginosuccinic Aciduria (Urea Cycle Disorders) |Low protein diet, use of special formulas and supplements of |

| |arginine |

|Galactosemia |Galactose elimination diet |

|Glutaric Aciduria Type 1 |Restrictions of amino acids |

|Glycogen Storage Disease |Prevent hypoglycemia by use of a CHO controlled diet |

|Homocystinuria |Restriction of amino acids, use of formulas such as Hominex if |

| |Vitamin B6 nonresponsive |

|Isovaleric Acidemia |Restriction of protein |

|Maple Syrup Urine Disease (MSUD) |Restrictions of amino acids leucine, isoleucine, and valine; use |

| |of special formulas MSUD diet powder |

|Ornithine Transcarbamylase Deficiency (Urea Cycle Acid Disorder) |Low-protein diet; additives such as Moducal may be added to give |

| |CHO calories |

|Phenylketonuria |Phenylalanine-restricted diet |

|Propionic Acidemia and Methylmalonic Acidemia |Low-protein diet |

|Tyrosinemia |Restrictions of tyrosine, phenylalanine, and methionine |

More common Inborn Errors:

1. Homocystinuria: an autosomal-recessive metabolic disorder; a disorder of the amino acid metabolism. If left untreated, it may lead to mental retardation, seizures, altered growth, hepatic disease, or stroke.

Nutritional Implications:

• Reduce methionine in the diet to prevent accumulation of homocystine

• Prevent cardiovascular complications

• Supplement with essential nutrients. Possible that low folic acid intakes aggravate the symptoms

• In B6 nonresponsive group (low levels B6 metabolism or low levels of reductase enzyme may cause methionine to cysteine conversion) dietary control of methionine intake is important. Use a low-protein diet with a supplement of cystine to supply sulfur.

• Increase fluid intake

2. Inborn errors of CHO metabolism: Fructosemia results from a defect in the enzyme converting fructose to glucose, Sucrose/maltose intolerance requires omission of sucrose and maltose from the diet, galactosemia results from lack of galactose-1-phospate ulridyltranferase (GALT) possibly in combination with high levels of galactitol (cataracts can occur if untreated)

Fructosemia: No fructose, sucrose, sorbitol, invert sugar, mayple syrup, honey, and molasses in diet. Caution with TF

Galactosemia: Use a lactose and galactose free diet. No milk, soybeans, peaches, lentils, liver, brains, or breads or cereals containing milk or cream cheese. Fresh blueberries and honeydew melon also excluded. Supplement with Vitamin D, Vitamin E, and riboflavin

Glycogen storage disease: Increase protein intake, Use small, frequest feedings, avoid lactose and sucrose

Sucrose/maltose intolerance: Omit sucrose and maltose from diet

3. Mayple Syrup Urine Disease: results from an autosomal recessive trait, causing an inborn error of metabolism in which BCAA are not degraded through decarboxylation to simple acids. If left untreated: retardation, neuropathy.

• Restrict intake of BCAA’s in diet.

• Use small amounts of milk in the diet

• Replace needed electrolytes

• Provide adequate kcals to spare protein

4. Phenylketonuria (PKU): results from a mutation in the phenylalanine hydroxylase gene. Phenylalanine is not metabolized to tyrosine.

• Use a diet low in Phenylalanine.

• Omit meat, fish, poultry, bread, milk, cheese, legumes, and peanut butter.

• Determine if serum iron or other nutrient levels are low and correct as needed.

• Monitor serum pyridoxine b/c turnover seems to be reduced in PKU and excesses may be retained

• Add calories: jam, jelly, sugar, honey, molasses, syrups, cornstarch, and oils that are Phe-free

7. Oncologic Conditions

• American Cancer Society’s Warning Signs of Cancer

o Change in Bowel/Bladder Habits

o Sore that does not heal

o Unusual bleeding or discharge

o Thickening in lump in brease or elsewhere

o Indigestion or dysphagia

o Obvious change in wart or mole

o Nagging cough or hoarseness

• Other concerns: Weight changes, BMI ................
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