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Premium member Presentation Transcript Vitamin and Trace Mineral Deficiency and Excess: Vitamin and Trace Mineral Deficiency and ExcessIntroduction: Introduction Vitamins and trace minerals are required constituents of the human diet since they are inadequately synthesized or not synthesized in the human body. Only small amounts of these substances are needed to carry out essential biochemical reactions (e.g., by acting as coenzymes or prosthetic groups). Overt vitamin or trace mineral deficiencies are rare in Western countries due to a plentiful, varied, and inexpensive food supply; however, multiple nutrient deficiencies may appear together in persons who are chronically ill or alcoholic. After gastric bypass surgery, patients are at high risk for multiple nutrient deficiencies. Moreover, subclinical vitamin and trace mineral deficiencies, as diagnosed by laboratory testing, are quite common in the normal population, especially in the geriatric age group .Principal Clinical Findings of Vitamin Malnutrition: Principal Clinical Findings of Vitamin MalnutritionThiamine, Riboflavin, Niacin, Pyridoxine are cofactors to enzymes in energy metabolism, hence, deficiencies show up in quickly growing tissues such as epithelium.: 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 MalaiseThiamine (Vitamin B1) Deficiency Beriberi: 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 disturbanceThiamine Deficiency (Beriberi): 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 oftenThiamine Deficiency (Beriberi): Thiamine Deficiency (Beriberi) Diagnosis: Clinical manifestations not conclusive Therapeutic test w/ parenteral thiamine = dramatic improvement Blood lactic & pyruvic acid levels elevated after oral load of glucose Decreased red cell hemolysate transketolase RDA: Infants 0.4mg Older children 0.6-1.2mg Nursing mothers 1.5mg Adults 1-1.3mg 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 Treatment: Children: 10mg p. o. daily for several weeks Adults 50mgThiamine Deficiency (Beriberi): Thiamine Deficiency (Beriberi)Thiamine Deficiency (Beriberi): Thiamine Deficiency (Beriberi)Riboflavin (Vitamin B2) Deficiency: 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 dyssebacia and angular palpebritis Scrotal or vulvar dermatosis may also occur Ocular s/sx are photophobia, blurred vision, itching of the eyes, lacrimation & corneal vascularizationRiboflavin Deficiency: Riboflavin Deficiency Diagnosis: Urinary riboflavin determination RBC riboflavin load test RDA: Infants & children <10yrs 0.6-1.4mg Children >10yrs 1.4-2mg depending on food intake Adults 0.025mg/gm dietary protein Prevention: Best sources: eggs, liver, meat, fish, milk, whole or enriched ground cereals, legumes, green leafy vegetables Also present in beer Impaired absorption in achlorhydria, diarrhea & vomiting Treatment: Riboflavin 2-5mg p. o. daily w/ increased B complex Parenteral administration if relief not obtainedRiboflavin Deficiency: Riboflavin DeficiencyNiacin (Vitamin B3) Deficiency Pellagra: 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 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 Mental changes include depression, irritability, disorientation, insomnia & deliriumNiacin Deficiency (Pellagra): Niacin Deficiency (Pellagra) Diagnosis: History & manifestations of diet poor in niacin or tryptophan In niacin deficiency, urinary levels of N-methyl-nicotinamide low or absent Differential diagnoses: Kwashiorkor, Infantile Eczema, Combination deficiencies of amino acids & trace minerals such as zinc RDA: Infants & children <10yrs 6-10mg Older individuals 10-20mg Prevention: Rich sources include meat, peanuts and legumes, whole grain and enriched breads and cereals Avoid too large a proportion of corn Treatment: Niacin 50-300mg daily which may be taken for a long time Skin lesions may be covered w/ soothing lotionsNiacin Deficiency (Pellagra): Niacin Deficiency (Pellagra)Pyridoxine (Vitamin B6) Deficiency: 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 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 levelPyridoxine Deficiency: 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 Anemic, due to low porphyrin synthesis, such as microcytic anemia & lymphopenia In genetic diseases involving pyridoxal phosphate enzymes also xanthurenic aciduria, cystathioninuria & homocystinuriaPyridoxine Deficiency: Pyridoxine Deficiency Diagnosis: As screening test, tryptophan load test done -100mg/kg BW tryptophan will give large amount of xanthurenic acid in urine Prevention: Firm requirement not established but usually recommended: Infant 0.1-0.5mg, Child 0.5-1.5mg & Adult 1.5-2mg 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 Treatment: Pyridoxine 100mg IM injection for seizures due to deficiency Children w/ pyridoxine dependency should be given 2-10mg IM injection or 10-100mg oral vitamin B6Folic Acid (Vitamin B9) Deficiency: 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 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 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 smokingFolic Acid Deficiency: Folic Acid Deficiency Clinical Manifestations: Megaloblastic anemia w/ irritability, failure to gain wt & chronic diarrhea Thrombocytopenic hemorrhages advanced cases Scurvy may be present Laboratory Findings: Anemia macrocytic Serum folic acid <3ng/ml, normal level=5-20ng/ml RBC folate levels indicator of chronic deficiency, normal level=150-600ng/ml Serum iron & vitamin B12 normal or elevated Formiminoglutamic acid in urine esp after oral histidine Serum LDH markedly high Bone marrow hypercellular RDA: 20-50mcg/24 hrs Treatment: Parenteral folic acid 2-5mg/24 hrs, response in 72 hrs, therapy for 3-4 wks Transfusions only when anemia severe Satisfactory responses even w/ low doses of 50mcg/24 hrs, have no effect on primary vitamin B12 deficiency If pernicious anemia present, prolonged use of folic acid should be avoidedFolic Acid Deficiency: Folic Acid DeficiencyCobalamine (Vitamin B12) Deficiency: 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 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 causesCobalamine Deficiency: Cobalamine Deficiency Clinical Manifestations: Megaloblastic anemia that becomes severe Neurological includes ataxia, paresthesias, hyporeflexia, Babinski responses, clonus & coma Tongue smooth, red & painful 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 indexCobalamine Deficiency: Cobalamine Deficiency 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 RDA: Infants 0.5 mcg/day Older children & adults 3mcg/day Treatment: Prompt hematological response w/ parenteral vitamin B12 1-5mcg/24hrs If there is neurological involvement 1mg IM daily for at least 2wks Pernicious Anemia: Monthly vitamin B12 1mg IM necessary throughout patient’s lifeCobalamine Deficiency: Cobalamine DeficiencyAscorbic Acid (Vitamin C) Deficiency Scurvy: 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 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 habitsAscorbic Acid Deficiency (Scurvy): 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 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 & developmentAscorbic Acid Deficiency (Scurvy): Ascorbic Acid Deficiency (Scurvy) Diagnosis: History of vitamin C-deficient diet Clinical picture Therapeutic test 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 shapeAscorbic Acid Deficiency (Scurvy): Ascorbic Acid Deficiency (Scurvy) Laboratory tests not helpful: Ascorbic acid concentrate of buffy layer of centrifuged oxalated blood; latent scurvy gives zero level in this layer Diminished urinary excretion of vitamin C after loading Differential Diagnosis: Bleeding, swollen gums: Chronic gingivitis & pyorrhea w/ pus & respond to good dental hygiene Pseudoparalysis: Syphilis negative x-ray; Poliomyelitis absent tenderness of extremities Tenderness of limbs: RF age >2 yrs; Suppurative arthritis & osteomyelitis positive blood cultures Bleeding manifestations: Blood dyscracias positive blood exams “Rosary of scorbutic beads”: RicketsAscorbic Acid Deficiency (Scurvy): Ascorbic Acid Deficiency (Scurvy) Prognosis: Recovery rapid w/ adequate treatment & permanent deformity rare Pain ceases in a few days but swelling caused by subperiosteal hemorrhages may last several months Prevention : A minimum daily intake of 30mg is recommended by WHO for all age levels. Every infant should receive supplement starting 2nd week of life. Lactating mothers should have at least 50mg vitamin C daily. Guava & papaya richer in vitamin C than citrus fruits, also in most green leafy vegetables, tomatoes & fresh tubers but absent in cereals, most animal products & canned milk. Treatment: Ascorbic acid 200-500mg daily or 100-150ml of fruit juice.Ascorbic Acid Deficiency (Scurvy): Ascorbic Acid Deficiency (Scurvy)Ascorbic Acid Deficiency (Scurvy): Ascorbic Acid Deficiency (Scurvy)Vitamin A: Vitamin A Vitamin A , in the strictest sense, refers to retinol. However, the oxidized metabolites, retinaldehyde and retinoic acid, are also biologically active compounds. The term retinoids includes all molecules (including synthetic molecules) that are chemically related to retinol. Retinaldehyde (11- cis ) is the essential form of vitamin A that is required for normal vision, whereas retinoic acid is necessary for normal morphogenesis, growth, and cell differentiation. Retinoic acid does not function in vision and, in contrast to retinol, is not involved in reproduction. Vitamin A also plays a role in iron utilization, humoral immunity, T cell–mediated immunity, natural killer cell activity, and phagocytosis. Vitamin A is commercially available in esterified forms (e.g., acetate, palmitate ) since it is more stable as an ester.Vitamin A: Vitamin A Vitamin A deficiency is endemic in areas where diets are chronically poor, especially in southern Asia, sub-Saharan Africa, some parts of Latin America, and the western Pacific, including parts of China. Vitamin A status is usually assessed by measuring serum retinol [normal range, 1.05–3.50 mol /L (30–100 g/ dL )] or blood spot retinol or by tests of dark adaptation. There are stable isotopic or invasive liver biopsy methods to estimate total body stores of vitamin A. Based on deficient serum retinol [<0.70 mol /L (20 g/ dL )], there are >90 million preschool-age children with vitamin A deficiency, among whom >4 million have an ocular manifestation of deficiency termed xerophthalmia . This condition includes milder stages of night blindness and conjunctival xerosis (dryness) with Bitot's spots (white patches of keratinizedepithelium appearing on the sclera) as well as rare, potentially blinding corneal ulceration and necrosis. Keratomalacia (softening of the cornea) leads to corneal scarring that blinds at least a quarter of a million children each year and is associated with a fatality rate of 4–25%. However, vitamin A deficiency at any stage poses an increased risk of mortality from diarrhea, dysentery, measles, malaria, and respiratory disease. Vitamin A deficiency can compromise barrier and innate and acquired immune defenses to infection. Vitamin A supplementation can markedly reduce risk of child mortality (23–34%, on average) in areas where deficiency is widely prevalent. About 10% of pregnant women in undernourished settings also develop night blindness, assessed by history, during the latter half of pregnancy, and this moderate vitamin A deficiency is associated with an increased risk of maternal infection and mortality rate.Treatment Vitamin A Deficiency: Treatment Vitamin A Deficiency Any stage of xerophthalmia should be treated with 60 mg of vitamin A in oily solution, usually contained in a soft-gel capsule. The same dose is repeated 1 and 14 days later. Doses should be reduced by half for patients 6–11 months of age. Mothers with night blindness or Bitot's spots should be given vitamin A orally, either 3 mg daily or 7.5 mg twice a week for 3 months. These regimens are efficacious, and they are less expensive and more widely available than injectable water-miscible vitamin A. A common approach to prevention is to supplement young children in high-risk areas with 60 mg every 4–6 months, with a half dose given to infants 6–11 months of age.Vitamin D : Vitamin D Risk factors for vitamin D deficiency are old age, lack of sun exposure, dark skin (especially among those living in northern latitudes), fat malabsorption , and obesity. Rickets represents the classic disease of vitamin D deficiency. Signs of deficiency are muscle soreness, weakness, and bone pain. Some of these effects are independent of calcium intake .Vitamin D: Vitamin D Vitamin D deficiency can be treated by the oral administration of 50,000 IU/week for 6–8 weeks followed by a maintenance dose of 800 IU/d (100 g/d) from food and supplements after achievement of normal plasma levels. The physiologic effects of vitamin D2 and D3 are identical when ingested over long periods.Vitamin E: Vitamin E Vitamin E deficiency causes axonal degeneration of the large myelinated axons and results in posterior column and spinocerebellar symptoms. Peripheral neuropathy is initially characterized by areflexia , with progression to an ataxic gait, and by decreased vibration and position sensations. Ophthalmoplegia , skeletal myopathy, and pigmented retinopathy may also be features of vitamin E deficiency. Either vitamin E or selenium deficiency in the host has been shown to increase certain viral mutations and, therefore, virulence.Vitamin E: Vitamin E Symptomatic vitamin E deficiency should be treated with 800–1200 mg of - tocopherol per day. Patients with abetalipoproteinemia may need as much as 5000–7000 mg/d. Children with symptomatic vitamin E deficiency should be treated with 400 mg/d orally of water-miscible esters; alternatively, 2 mg/kg per d may be administered intramuscularly. Vitamin E in high doses may protect against oxygen-induced retrolental fibroplasia and bronchopulmonary dysplasia as well as intraventricular hemorrhage of prematurity. Vitamin E has been suggested to increase sexual performance, treat intermittent claudication, and slow the aging process, but evidence for these properties is lacking. When given in combination with other antioxidants, vitamin E may help prevent macular degeneration.Vitamin K: Vitamin K The symptoms of vitamin K deficiency are due to hemorrhage, and newborns are particularly susceptible because of low fat stores, low breast milk levels of vitamin K, sterility of the infantile intestinal tract, liver immaturity, and poor placental transport. Intracranial bleeding, as well as gastrointestinal and skin bleeding, can occur in vitamin K–deficient infants 1–7 days after birth. Thus, vitamin K (1 mg IM) is given prophylactically at the time of delivery .Vitamin K: Vitamin K Vitamin K deficiency in adults may be seen in patients with chronic small-intestinal disease (e.g., celiac disease, Crohn's disease), in those with obstructed biliary tracts, or after small-bowel resection. Broad-spectrum antibiotic treatment can precipitate vitamin K deficiency by reducing gut bacteria, which synthesize menaquinones , and by inhibiting the metabolism of vitamin K. In patients with warfarin therapy, the antiobesity drug orlistat can lead to international normalized ratio (INR) changes due to vitamin K malabsorption . The diagnosis of vitamin K deficiency usually is made on the basis of an elevated prothrombin time or reduced clotting factors, although vitamin K may also be measured directly by HPLC. Vitamin K deficiency is treated by using a parenteral dose of 10 mg. For patients with chronic malabsorption , 1–2 mg/d of vitamin K should be given orally, or 1–2 mg/week can be taken parenterally . Patients with liver disease may have an elevated prothrombin time because of liver cell destruction as well as vitamin K deficiency. If an elevated prothrombin time does not improve on vitamin K therapy, it can be deduced that it is not the result of vitamin K deficiency. Be master of your habits, Or they will master you.: Be master of your habits, Or they will master you. You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.