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NUTRITIONAL DISORDERS
HA MWAKYOMA, MD
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MALNUTRITION A pathological state resulting from a relative or absolute deficiency or excess of one or more essential nutrients; clinically manifested or detected only by biochemical, anthropometric or physiological tests.
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Forms of Malnutrition Undernutrition: Marasmus
Overnutrition: Obesity, Hypervitaminoses Specific Deficiency: Kwashiorkor, Hypovitaminoses, Mineral Deficiencies Imbalance: Electrolyte Imbalance
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ETIOLOGY
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Classification of Undernutrition
Gomez Classification: uses weight-for-age measurements; provide grading as to prognosis Weight-for-Age% Status Normal st degree nd degree < rd degree
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Wellcome Classification: simple since based on 2 criteria only - wt loss in terms of wt for age% & presence or absence of edema Wt-for-Age% Edema No Edema Kwashiorkor Undernutrition < 60 Marasmic- Marasmus Kwashiorkor
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Waterlow Classification: adopted by WHO; can distinguish between deficits of weight-for-height% (wasting) & height-for-age% (stunting) N Mild Mod Severe Ht-for-Age% > <80 Wt-for-Ht% > <70
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Protein Energy Malnutrition Iceberg
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Marasmus Common in the 1st year of life Etiology:
“Balanced starvation” Insufficient breastmilk Dilute milk mixture or lack of hygiene
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Marasmus Clinical Manifestations: Wasting Muscle wasting
Growth retardation Mental changes No edema Variable-subnormal temp, slow PR, good appetite, often w/diarrhea, etc. Laboratory Data: Serum albumin N Urinary urea/ gm crea N Urinary hydroxyproline/ gm crea low, early Serum essential a.a. index N Anemia uncommon Glucose tolerance curves diabetic type K+ deficiency present Serum cholesterol low Diminished enzyme activity Bone growth delayed Liver biopsy N or atrophic
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Kwashiorkor Between 1-3 yrs old Etiology:
Very low protein but w/calories from CHO In places where starchy foods are main staple Never exclusively dietary
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Kwashiorkor Clinical Manifestations: Diagnostic Signs Edema
Muscle wasting Psychomotor changes Common Signs Hair changes Diffuse depigmentation of skin Moonface Anemia Occasional Signs: Flaky-paint rash Noma Hepatomegaly Associated Laboratory: Decreased serum albumin EEG abnomalities Iron & folic acid deficiencies Liver biopsy fatty or fibrosis may occur
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Kwashiorkor
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Obesity Definition: Generalized, excessive accumulation of fat in subcutaneous & other tissues Classification according to “desirable” weight standard: Overweight ~ >10% while Obese ~ >20% The Centers for Disease Control (CDC) avoids using "obesity" instead suggest two levels of overweight: 85th percentile of BMI ~ "at risk" level & 95th percentile of BMI ~ the more severe level
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Obesity Appears most frequently in the 1st year, 5-6 years & adolescence Etiology: Excessive intake of food compared w/ utilization Genetic constitution Psychic disturbance Endocrine & metabolic disturbances rare Insufficient exercise or lack of activity
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Obesity Clinical Manifestations:
Fine facial features on a heavy-looking taller child Larger upper arms & thighs Genu valgum common Relatively small hands & fingers tapering Adiposity in mammary regions Pendulous abdomen w/ striae In boys, external genitalia appear small though actually average in size In girls, external genitalia normal & menarche not delayed Psychologic disturbances common Bone age advanced
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Obesity
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Complication of Obesity
Pickwickian Syndrome Rare complication of extreme exogenous obesity Severe cardiorespiratory distress & alveolar hypoventilation Includes polycythemia, hypoxemia, cyanosis, CHF & somnolence
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The Energy-Releasing Vitamins
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Thiamine, Riboflavin, Niacin, Pyridoxine are cofactors to enzymes in energy metabolism, hence, deficiencies show up in quickly growing tissues such as epithelium. Typical symptoms for the group include: Dermatitis Glossitis Cheilitis Diarrhea Nerve cells use lots of energy, so symptoms also show up in the nervous tissue: Peripheral neuropathy Depression Mental confusion Lack of motor coordination Malaise
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Thiamine (Vitamin B1) Deficiency Beriberi
Pathology: Biochemically, there is accumulation of pyruvic and lactic acid in body fluids causing: Cardiac dysfunction such as cardiac enlargement esp right side, edema of interstitial tissue & fatty degeneration of myocardium Degeneration of myelin & of axon cylinders resulting in peripheral neuropathy and In chronic deficiency states, vascular dilatation & brain hemorrhages of Wernicke’s Disease, resulting in weakness of eye movement, ataxia of gait and mental disturbance
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Thiamine Deficiency (Beriberi)
Three forms: Wet beriberi: generalized edema, acute cardiac symptoms and prompt response to thiamine administration Dry beriberi: edema not present, condition similar to peripheral neuritis w/ neurological disorders present Infantile beriberi divided into: Acute cardiac - ages 2-4 months; sudden onset of cardiac s/sx such as cyanosis, dyspnea, systolic murmur & pulmonary edema w/ rales Aphonic - ages 5-7 months; insidious onset of hoarseness, dysphonia or aphonia Pseudomeningeal - ages 8-10 months; signs of meningeal irritation w/ apathy, drowsiness & even unconsciousness; occurs more often
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Thiamine Deficiency (Beriberi)
Prevention: Richest sources are pork, whole grain, enriched cereal grains and legumes Improved milling of rice conserve thiamine Excessive cooking of vegetables or polishing of cereals destroy In breast-fed infants, prevention achieved by maternal diet w/ sufficient amounts
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Thiamine Deficiency (Beriberi)
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Thiamine Deficiency (Beriberi)
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Riboflavin (Vitamin B2) Deficiency
Functions: Acts as coenzyme of flavoprotein important in a. a., f. a. & CHO metabolism & cellular respiration Needed also by retinal eye pigments for light adaptation Clinical Manifestations: Characteristic lesions of the lips, the most common of which are angular stomatitis and cheilosis Localized seborrheic dermatitis of the face may result such as nasolabial seborrhea or angular palpebritis
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Clinical Manifestations:--cont--
Scrotal or vulvar dermatosis may also occur Ocular s/sx are photophobia, blurred vision, itching of the eyes, lacrimation & corneal vascularization
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Riboflavin Deficiency
Prevention: Best sources: eggs, liver, meat, fish, milk, whole or enriched ground cereals, legumes, green leafy vegetables Impaired absorption in achlorhydria, diarrhea & vomiting
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Riboflavin Deficiency
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Niacin (Vitamin B3) Deficiency Pellagra
Etiology: Diets low in niacin &/or tryptophan Amino acid imbalance or as a result of malabsorption Excessive corn consumption Clinical Manifestations: Start w/ anorexia, weakness, irritability, numbness & dizziness Classical triad of dermatitis, diarrhea & dementia
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Clinical Manifestations: ---cont---
Dermatitis may develop insidiously to sunlight or heat First appears as symmetrical erythema Followed by drying, scaling & pigmentation w/ vesicles & bullae at times Predilection for back of hands, wrists, forearms (pellagrous glove), neck (Casal’s necklace) & lower legs (pellagrous boot) GIT s/sx are diarrhea, stomatitis or glossitis; feces pale, foul milky, soapy or at times steatorrheic
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Clinical Manifestations: ---cont---
Mental changes include depression, irritability, disorientation, insomnia & delirium
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Niacin Deficiency (Pellagra)
Prevention: Rich sources include meat, peanuts and legumes, whole grain and enriched breads and cereals Avoid too large a proportion of corn
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Pyridoxine (Vitamin B6) Deficiency
Functions: Vitamin B6 is involved in the synthesis and catabolism of amino acids, synthesis of neurotransmitters, porphyrins and niacin Plays important role in clinical conditions such as anemia, hyperemesis gravidarum, cardiac decompensation, radiation effects, skin grafting, INH therapy & seborrheic dermatitis
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Pyridoxine (Vitamin B6) Deficiency
Etiology: Losses from refining, processing, cooking & storing Malabsorptive diseases such as celiac disease may contribute Direct antagonism might occur between INH & pyridoxal phosphate at the apoenzyme level
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Pyridoxine Deficiency
Clinical Manifestations: Three different types Neuropathic, due to insufficient neurotransmitter synthesis, such as irritability, depression & somnolence Pellagrous, due to low endogenous niacin synthesis, such as seborrheic dermatitis, intertrigo, angular stomatitis & glossitis
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Clinical Manifestations:---cont--
Anemic, due to low porphyrin synthesis, such as microcytic anemia & lymphopenia In genetic diseases involving pyridoxal phosphate enzymes also xanthurenic aciduria, cystathioninuria & homocystinuria
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Pyridoxine Deficiency
Prevention: Rich sources include yeast, whole wheat, corn, egg yolk, liver and lean meat Toxicity at extremely high doses has been described; infants whose mothers received large doses during pregnancy should be observed for seizures due to dependency Children receiving INH therapy should be observed for neurologic s/sx in w/c case pyridoxine should be given
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The Hematopoietic Vitamins
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Folic Acid (Vitamin B9) Deficiency
Functions: Needed for RBC & DNA formation, cell multiplication esp. GI cells Newly discovered functions: Prevents neural tube defects Prevents heart disease (reduces homocysteine levels) Prevents colon cancer
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Folic Acid (Vitamin B9) Deficiency
Etiology: Peak incidence 4-7 months Deficient dietary intake: goat’s milk deficient & powdered milk poor source Deficient absorption as in celiac disease, achlorhydria, anticonvulsant drugs, zinc deficiency & bacterial overgrowth
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Folic Acid (Vitamin B9) Deficiency - aetiology
Impaired metabolism w/ ascorbic acid deficiency, hypothyroidism, drugs like trimethoprim & alcoholism Increased requirement during rapid growth & infection Increased excretion/loss may occur subsequent to vitamin B12 deficiency & chronic alcoholism Increased destruction possible in cigarette smoking
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Folic Acid Deficiency Clinical Manifestations:
Megaloblastic anemia w/ irritability, failure to gain wt & chronic diarrhea Thrombocytopenic hemorrhages advanced cases Scurvy may be present
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Folic Acid Deficiency Laboratory Findings: Anemia macrocytic
Serum folic acid <3ng/ml, normal level=5-20ng/ml RBC folate levels indicator of chronic deficiency, normal level= ng/ml Serum iron & vitamin B12 normal or elevated
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Folic Acid Deficiency Laboratory Findings:
Formiminoglutamic acid in urine esp after oral histidine Serum LDH markedly high Bone marrow hypercellular
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Folic Acid Deficiency
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Cobalamine (Vitamin B12) Deficiency
Absorption: Vitamin B12 + glycoprotein (intrinsic factor) from parietal cells of gastric fundus terminal ileum absorption + intrinsic factor + Ca++ blood Function: Needed in reactions affecting production of methyl groups
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Cobalamine (Vitamin B12) Deficiency
Etiology: Congenital Pernicious Anemia: Lack of secretion of intrinsic factor by stomach manifest at 9 months-10 years as uterine stores become exhausted Inadequate intake or dietary deficiency rare Strict vegetarian diet Not commonly seen in kwashiorkor or marasmus Breast-fed infants whose mothers had deficient diets or pernicious anemia Consumption or inhibition of the B12-intrinsic factor complex Vitamin B12 malabsorption from disease of ileal receptor sites or other intestinal causes
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Cobalamine Deficiency
Clinical Manifestations: Megaloblastic anemia that becomes severe Neurological includes ataxia, paresthesias, hyporeflexia, Babinski responses, clonus & coma Tongue smooth, red & painful
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Cobalamine Deficiency
Laboratory Findings: Anemia macrocytic Serum vitamin B12 <100pg/ml but serum iron & folic acid normal or elevated Serum LDH activity markedly increased Urinary excess of methylmalonic acid, a reliable & sensitive index
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Cobalamine Deficiency
Laboratory Findings: Schilling test to assess the absorption of vitamin B12: Normal person ingests small amount of radioactive vitamin B12 none in urine **If flushing dose injected parenterally, 1000mcg of non-radioactive vitamin B12 10-30% of previous radioactive vitamin B12 appears in the urine Pernicious anemia 2% or less **If modified: 30 mg intrinsic factor administered along normal amounts Disease of ileal receptor sites or other intestinal causes no improvement even w/ intrinsic factor
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Cobalamine Deficiency
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Ascorbic Acid (Vitamin C) Deficiency Scurvy
Functions: Collagen is the major connective tissue in the body & hydroxyproline, found only in collagen, is formed from proline requiring ascorbic acid If there is defective collagen formation, endochondral bone formation stops since oste, intercellular substance is no longer formed Vitamin C is involved in hydroxylation reactions in the synthesis of steroids and epinephrine Ascorbic acid also aids iron absorption by reducing it to ferrous state in the stomach, spares vitamin A, vitamin E and some B vitamins by protecting them from oxidation, and enhances the utilization of folic acid by aiding the conversion of folate to tetrahydrofolate
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Ascorbic Acid (Vitamin C) Deficiency Scurvy
Etiology: More common 6-24 months May develop in breastfed infant if mother’s diet deficient Improper cooking practices produce significant nutrient losses & faulty dietary habits
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Ascorbic Acid Deficiency (Scurvy)
Clinical Manifestations: Early stages are vague symptoms of irritability, digestive disturbances & anorexia Mild vitamin C deficiency signs include ecchymoses, corkscrew hairs and the formation of petechiae due to increased capillary fragility resulting from weakened collagen fibrils Severe deficiency results in decreased wound healing, osteoporosis, hemorrhaging, bleeding into the skin and friable bleeding gums with loosened teeth A presenting feature is an infant w/ painful, immobile legs (pseudoparalysis), edematous in “frog position” & occasionally w/ mass
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Ascorbic Acid Deficiency (Scurvy)
Clinical Manifestations: There is depression of sternum w/ a “rosary of scorbutic beads at the costochondral junction due to subluxation of the sternal plate Orbital or subdural hemorrhages, melena & hematuria may be found Low grade fever & anemia usually present Impairment of growth & development
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Ascorbic Acid Deficiency (Scurvy)
Diagnosis: History of vitamin C-deficient diet Clinical picture Therapeutic test
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Diagnosis: X-ray findings in the long bones:
Most prominent & early change is simple knee atrophy Shaft trabeculae cannot be distinguished giving “ground glass appearance” Cortex reduced to “pencil-point thinness” Zone of well-calcified cartilage, white line of Fraenkel, seen as irregular & thickened white line w/c Zone of rarefaction, a linear break in bone proximal & parallel to white line under at metaphysis Calcifying subperiosteal hemorrhages cause bone to assume a dumb-bell or club shape
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Ascorbic Acid Deficiency (Scurvy)
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Ascorbic Acid Deficiency (Scurvy)
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