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1. Introduction
2. Source
3. Daily allowance
4. Deficiency
5. Treatment
6. Toxicity
1. Micronutrients play a central part in metabolism
and in maintenance of tissue function.
2. Vitamins and minerals.
BACKGROUND
Vitamins are organic substances that
are essential for several enzymatic
functions in human metabolism
A compound is called vitamin when it
cannot be synthesized in sufficient
quantities by an organism, and must be
obtained from the diet.
Functions
 Acts as hormones (vitamin D)
Acts as antioxidant (vitamin E)
 Acts as mediators of cell signalling
and regulators of cell and tissue
growth and differentiation(vitamin
A)
Acts as precusors for enzyme
cofactor biomolecules(coenzymes)
that help act as catalysts and
substrates in metabolism
VITAMINS
 Vitamins are classified according
to solubility into fat soluble & water
soluble.
 13 vitamins are known, 4 fat
soluble (KEDA) & 9 water soluble
(C, Folate & the B group).
VITAMINS
 water soluble-dissolve easily in water
readily excreted from the body.
 fat soluble-absorbed through the
intestinal tract with the help of
lipids(fats).
VITAMIN A-Vitamin A is a
generic term for many related
compounds.
Retinol (alcohol), Retinal (aldehyde)
are often called preformed vitamin A.
Retinal can be converted
by the body to retinoic
acid which is known to
affect gene transcription.
Body can convert b-carote
ne to retinol, thus called provitamin A.
FUNCTIONS
•Immunity: important for activation of T
lymphocyte, maturation of WBC &
integrity of physiological barrier.
•Vision: integrity of eye & formation of
rodopsin necessary for dark adaptation.
•Regulation of gene expression: vital to
cell differentiation & physiologic processes
• Growth & development
Animal Foods Plant Foods
Cod liver oil Sweet potato
Liver & kidney Carrots
Egg Cantaloupe
Butter Spinach
Milk & cheese Apricot
Fish & meat Papaya
RICH DIETARY SOURCES
Life stage mg/day
Infants 300-400
Children 400-600
Adolescent 900M- 700F
Recommended Allowance
Vitamin A deficiency
•Deficiency of vitamin A leads to:
1. Ocular change-Night blindness &
xerophthalmia
2. Extra ocular changes
Growth retardation
Acquired immune deficiency
Keritinization of epithelia in RT, GIT &
UT with increased risk of
RTI, malabsorption & UTI.
WHO CLASSIFICATION OF XEROPTHALMIA
PRIMARY SIGNS SECONDARY SIGNS X1A conjunctival
xerosis
 X1B Bitot’s spot
 X2 Corneal xerosis
 X3A Corneal
ulceration
 X3 B Keratomalacia
 XN Night blindness
 XF Fundal changes
 XS Corneal scarring
 Rhodopsin-protein scotopsin and 11-cis retinal.
 light sensitive- rodopsin decomposed
 11-cis retinal--- >11-trans retinal and splits off from
scotopsin
 In dark-retiene isomerase– reverse reaction
 11-cis retinal combines with scotopsin te regenerate
rhodopsin (vit. A dependent)
 Xeropthalmia-pigmentation of caruncle with loss of
normal lusture and moist apperance of palpebral
conjunctiva-dry and wrinlked.
 Bitots spot-chalky grey spots on the temporal side of
corneas -cleral junction
 Keratomalacia-cornea is soft and ulcerated. Eventually
infected and perforation of cornea occurs resulting in
opacification and blindness.
Treatment
•For treatment of xerophthalmia,
according to WHO guidelines.
>1 year-2,00,000 IU orally on
presentation
the following day.
1 to 4 weeks later.
6mths-1yr 1,00,000 IU
<6mths-50,000 IU
TOXICITY- Children and adults ingesting
>50,000 IU/day for several month.
•Vitamin A in excess leads to:
•Dermatitis with xanthosis cutis
•Hepatosplenomegaly
•Fatigue, malaise, anorexia, vomiting
•Bone pain & increased risk of fracture
•Pseudotumor Cerebri
•Xray-hyperostosis of the shafts of long
bones
PREVENTION
 The National vitamin A prophylaxis programme
 1-5 yrs , every 6 mths
 2,00,000 IU
 Fortification of food(wai wai, dalda ghee).
VITAMIN D
 Vitamin D comprises a group of sterols; the
most important of which are cholecalciferol
(vitamin D3) & ergosterol (vitamin D2).
 Humans & animal utilize only vitamin D3 &
they can produce it inside their bodies from
cholesterol.
 Cholesterol is converted to 7-dehydro-
cholesterol (7DC), which is a precursor of vitamin
D3.
VITAMIN D
 Exposure to the ultraviolet rays in the
sunlight convert 7DC to cholecalciferol.
Vitamin D3 is metabolically inactive until it is
hydroxylated in the kidney & the liver to the
active form 1,25 Dihydroxycholecalciferol.
 1,25 DHC acts as a hormone rather than a
vitamin endocrine & paracrine properties.
FUNCTIONS
•Calcium metabolism: vitamin D enhances
ca absorption in the gut & renal tubules.
•Cell differentiation: particularly of
collagen & skin epithelium
•Immunity: important for Cell Mediated
Immunity & coordination of the immune
response.
Sources of Vitamin D
Sunlight is the most important
source
 Fish liver oil
 Fish & sea food (herring & salmon)
 Eggs
 Plants do not contain vitamin D3
Human milk deficient in vit. D,
contains only 30-40 IU per liter mostly
from 25(OH)D3
Vitamin D deficiency
•Deficiency of vitamin D leads to:
 Rickets in small children.
 Osteomalacia
 Osteoporosis
TOXICITY
•Hypervitaminosis D – infants-2,000-3,000 IU/day,
adults-10,000 IU/day for several months.
causes hypercalcemia,hyperphosphatemia,
hypertension which manifest as:
Nausea & vomiting
Excessive thirst & polyuria
Severe itching
Joint & muscle pains
Azotemia, nephrolithiasis, ectopic
calcification.
Disorientation & coma.
RICKETS
Lack of adequate mineralisation of growing bone
RICKETS
Sign and symptoms-
•Skeletal deformity-bowed legs(genu varum) in
toddlers, knock knees (genu valgum) in older
children, craniotabes (soft skull), spinal and pelvic
deformities, growth disturbances, costochondral
swelling(rickety rosary), harrisons groove, double
malleoli, greenstick fractures, bone pain and
tenderness, muscle weakness and dental problems.
INVESTIGATIONS
Radiologic changes-loss of normal zone of provisional
calcification adjacent to metaphysis.
Widening of the growth plate.
Splaying and cupping of metaphysis.
Generalised reduction in bone density.
Low circulating levels of 25(OH)D3.
Elevated serum alkaline phosphate.
Calcium level may be normal or low
Phosphate level usually are unchanged or low.
RICKETS
TREATMENT
-Vitamin D administered orally either
in a single dose of 60,000 or over 10
days(60,000 IU daily for 10 days)
followed by a maintenance dose of 400
IU/day.
Oral calcium suppliments(50-
75mg/kg/day)
Vitamin E
 Anti oxidant
 Free radical scavanger
 Antineoplastic effect and may raise the concentration
of high density lipoprotein cholesterol.
 Transported in the body by lipoprotein.
 sources-nuts, seeds, whole wheat grain.
 Recommended daily allowance-15-25 IU/day-
6wks(preterm),infants-3mg alfa-tocopherol, adults-
10mg/day.
Deficiency
 Observed in low birth weight infants.
 Anemia, reticulocytosis, thrombocytopenia, and
abnormal erythrocyte metabolism.
 Low levels of vitamin e in premature infants is
associated with hemolytic anemia,
hyperbilirubinemia and intraventricular
hemorrhage.
 Prophylaxis reduces retinopathy of prematurity.
 Clinical menifestation-loss of reflexes, ataxia of
trunks and limbs, dimnished priopioception,
muscle weakness, ptosis, pes cavus, scoliosis and
dysarthria.
Vitamin K
 It is a cofactor of the enzyme that catalyzes one
step in the formation of prothrombin.
 Needed for the generation of several clotting
factors in the liver.
 Source- green leafy vegetables.
 Deficiency-coagulation defect due to
hypoprothrombinemia and deficiency of factor VII
resulting in hemorrhagic disease of the newborn.
 1mg IM –newborn.
 In severe deficiency-2.5 to 5 mg parenterally.
The B VitaminsB-1, B-2, B-3, B-6, B-12
WATER SOLUBLE VITAMINS
 VITAMIN B GROUP
 Thiamine(Vitamin B1)-SOURCES-
 Unrefined or fortified cereal grains, enriched bakery
products, organ meats (liver, kidney) and legumes
 Thiamine content of human milk is relatively low
compared to cow’s milk. Pork
 Fish, Liver, Legumes, Nuts, Whole grain or enriched
breads and cereals
B-1 Thiamin
 Important in:
 Producing energy from carbohydrates
 proper nerve function
 stabilizing the appetite
 promoting growth and good muscle tone
 ATP production
Recommendations
 Men 14+
1.2 mg/day
 Women 14-18
1.0 mg/day
 Women 19+
1.1 mg/day
 1 broiled pork chop,
 1.25 cups corn flakes
OR
 1 baked potato (w/
skin)
 0.5 cup of lentils
 1 cup raisin bran
Warnings
 B-1 is nontoxic even at high dosages
B-1 Deficiency(beri beri)
 Occurs in adults when the intake drops below 1mg/day.
 Three forms-dry, wet, acute
 Dry-no edema, severe muscle wasting, and cardiomegaly.
 Wet-peripheral edema, ocular paralysis, ataxia and mental
impairment.
 Infantile beriberi more subtle than adults occurs in
breastfed infants of thiamine deficient mothers.
 Cardiac involvement with
cardiomegaly, cyanosis, dyspnea, and aphonia if untreated
results in death.
Diagnosis of thiamine deficiency
 Suspected in all cases of malnutrition.
 The diagnosis may be confirmed by measurement of
24hrs urine thiamine excretion-normal 40-100
microgram/day.
 <15/day-deficient range.
 Can also be based on response of red cell transketolase
to the adition of thiamine in vitro. An increase in
transketolase activity of <15%-normal.
 15%-25%- mild deficiency.
 >25%-severly deficient.
Thiamine requirements
 Functions primarily in the metabolism of
carbohydrate.
 RDA-0.4mg/1000 kcal consumed.
 TREATMENT OF BERIBERI
 Resolution of neurologic and cardiac symptoms within
24-48 hrs.
 Mild beriberi-5mg/day PO.
 Severly ill-10mg iv BD.
 In presence of heart failure treatment of heart failure.
SCURVY (VIT. C DEFICIENCY)
 Prolonged vitamin c deficiency results in scurvy.
 Usually occurs in those who are deprived of citrus
fruit, fresh vegetables, or vitamins.
 IN INFANCY- clinical features-
 Anorexia, diarrhea, pallor, irritability and increased
susceptibility to infections, sub-periosteal
hemorrhages and long bone tenderness can occur.
 OLDER CHILDREN-hemorrhagic sign predominate.
 Bleeding of gums, conjunctiva and the intestinal tract.
diagnosis
 By characteristric physical findings and history of
inadequate dietary intake.
 X-ray of long bones-infantile scurvy
TREATMENT
Supplimentation of vitamin c resolves symptoms in 24-
48hrs.
RDA-30-40 mg /day-infants
40-70 mg/day- children.
Folic acid
 Essential for the normal growth and maintenance of
all cells .
 Vital for the reproduction of the cells within fetus.
 Deficiency affects normal cell division and protein
synthesis impairing growth.
 Reduces blood levels of homocysteine so lowers risk
of heart disease.
 Also maintains nervous system integrity and intestinal
tract functions.
 Involved in the production of serotonin.
 SOURCES
 Leafy vegetable- spinach, turnip, lettuce, dried beans
and peas, fortified cereal products, sunflower seeds
certain other fruits and vegetables.
 DEFICIENCY- limits cell function( cell division and
protein synthesis).
 Megaloblastic anemia
 Memory problems.
 Deficiency in pregnant women-neural tube defect.
 RDA- infants--70 microgram/day
 1-3 yrs--100 4-6 yrs---150
 7-9 yrs– 200 10-12 yrs--250
 13-15 yrs-300 pregnant and lactating-400

Who’s at Risk?
 Homeless & Malnourished
 Alcoholics
 People with malabsorption conditions
B-2 Riboflavin
 Important in:
 energy production
 carbohydrate, fat, and protein metabolism
 formation of antibodies and red blood cells
 cell respiration
 maintenance of good vision, skin, nails, and hair
 alleviating eye fatigue
Sources of B-2
 Large amounts in
 dairy
 eggs
 meats
 Small amounts in
 leafy green vegetables
 enriched grains
Recommendations
 Men 14-70
1.3 mg/day
 Women 14-70
1.0 mg/day
 71+
Larger doses
 1 cup raisin bran
 1 cup milk
 1 egg
OR
 1 small extra lean hamburger
 1 cup plain yogurt
 0.5 cup fresh cooked spinach
 1 cup cottage cheese
B-2 Deficiency
 Itching and burning eyes
 Cracks and sores in mouth and lips
 Bloodshot eyes
 Dermatitis
 Oily skin
 Digestive disturbances
Warnings
 B-2 is nontoxic at supplemental and dietary levels.
 Light can destroy riboflavin, so purchase milk in
opaque containers.
Who’s at Risk?
 People with cataracts
 People with Sickle Cell Anemia
 Alcoholics
B-3 Niacinamide & Niacin
 Important in:
 energy production
 maintenance of skin and tongue
 improves circulation
 maintenance of nervous system
 health of the digestive track
B-3 Niacinamide & Niacin
 Two Types
 Niacinamide (Nicotinamide)
 does not regulate cholesterol
 Niacin (Nicotinic Acid)
 highly toxic in large doses
 Inosital Hexaniacinate is a supplement that gives the
cholesterol regulation without high toxicity
Recommendations
 Men 14+
16 mg/day
 Women 14+ 14
mg/day
 1 cup rice
 4 oz. broiled salmon
 1 tbsp peanut butter
 1 bagel
 OR
 1 small extra lean hamburger
 0.5 cup grape nuts cereal
Warnings
 In doses of only 50-100 mg nicotinic acid can cause
dilation of blood vessels and potentially painful
tingling (“niacin flush”), diarrhea, nausea,
vomiting, and long term liver damage.
 Nicotinamide is almost always safe to take,
although a few cases of liver damage have been
reported in doses of over 1000 mg/day.
B-3 Deficiency
 Pellegra
 disease caused by B-3 deficiency
 rare in Western societies
 gastrointestinal disturbance, loss of appetite
 headache, insomnia, mental depression
 fatigue, aches, and pains
 nervousness, irritability
Who’s at Risk?
 Most people get plenty of B-3 from their diet because it
is added to white flour.
B-6 Pyridoxine
 Important in:
 Production of red blood cells
 conversion of tryptophan to niacin (B-3)
 immunity
 nervous system functions
 reducing muscle spasms, cramps, and numbness
 maintaining proper balance of sodium and
phosphorous in the body
Recommendations
 Men 14-50
1.3 mg/day
 Men 50+
1.7 mg/day
 Women 14-18
1.2 mg/day
 Women 19-50
1.3 mg/day
 Women 50+
1.5 mg/day
 1 chicken breast
 0.5 cup cooked spinach
 1 cup brown rice
OR
 1 baked potato with skin
 1 banana
 4 oz. lean sirloin
Warnings
 High doses of B-6 may be recommended to treat
carpal tunnel syndrome, and sleep disorders, but
continued use of high doses may result in permanent
nerve damage.
 Pregnant women should always consult their doctor
before taking this supplement and all others.
B-6 Deficiency
 nervousness, insomnia
 loss of muscle control, muscle weakness
 arm and leg cramps
 water retention
 skin lesions
Who’s at Risk?
 very rare
 alcoholics
 patients with kidney failure
 women using oral contraceptives
B-12 Cobalamin
 Important in:
 proper nerve function
 production of red blood cells
 metabolizing fats and proteins
 prevention of anemia
 DNA reproduction
 energy production?
Recommendations
 Men and Women
14+
2-3 mcg/day
 1 chicken breast
 1 hard boiled egg
 1 cup plain low fat yogurt
OR
 1 cup milk
 1 cup raisin bran
Warnings
 Vegetarians need to look for fortified sources (soy
milk, supplements).
 Elderly often have trouble absorbing.
B-12 Deficiency
 anemia
 nerve damage
 hypersensitive skin
Who’s at Risk?
 pernicious anemia
 B-12 injections often taken regularly
 HIV
 Chronic Fatigue Syndrome
Calcium and magnesium
Calcium
 most abundant mineral in the body.
 Located primarily in bone tissue(98%)
 Coagulation cascade, nerve conduction, and
muscle stimulation.
 Absorption depends on intake and Vitamin D .
 Absorption is decreased by fiber, phytate,
oxalate, fat and lactose.
 SOURCE-
 milk and dairy products, grains and fruits.
 Deficiency –vegeterians, steatorrhea, chronic
malabsorption syndromes, or intestinal and renal
abnormalities.
Requirement
 1-10yrs 500-800mg/day
 Purberty 1000-1200 mg/day
 Pregnant and lactating women 400mg/day.
 DEFICIENCY
 Tetany- muscle cramps, numbness and tingling in
limbs.
 Rickets and osteoporosis –chronic deficiency
MAGNESIUM
 Essential for bioenergic reactions controlling fuel
oxidation, membrane transport, and signal
transmission.
 Over 80% in bone and skeletal muscle.
 SOURCES- legumes, nuts banana and whole
grains.
 Regulation of magnesium balance depends on
renal tubular absorption.
 Deficiency –secondary to intestinal
malabsorption, excessive gastrointestinal losses
through fistulae or continuous suction or renal
disease affecting tubular reabsorption.
 Manifestations –irritability, tetany, hypo or hyper
reflexia.
 Requirement –
 0-6mths 40-50mg/day
 6-12mths 60mg/day
 >12mths 200mg/day
Trace elements
 ZINC
 COPPER
 SELENIUM
 CHROMIUM
 IODINE
 IRON
ZINC
 FUNCTIONS- functions as an intracellular hormone
contributing to the regulation of cellular growth and
also impacts on nucleic acid metabolism and protein
synthesis
 ABSORPTION AND METABOLISM-
Absorbed throughout the small intestine.
Metabolises in liver – transported in portal system
attached to albumin or transferrin.
Distributed in most tissues, 90% of total body zinc is
localised in bone and skeletal muscle.
Excreted through feces.
DEFICIENCY
 Develops as a part of malnutrition or malabsorption
syndrome due to low intake or intestinal disease.
 FEATURES
 Poor physical growth
 Delayed sexual maturation
 The typical syndrome of zinc deficiency consists of-
growth retardation, hypogonadism, anemia
 Other symptoms consists of-diarrhea, hair
loss, anorexia, dermatitis, impaired immune function
and skeletal abnormalities.
 Acrodermatitis enteropathica.
 Eye lesions-photophobia, blepharitis, corneal
opacities.
requirement
 3.5-5.0 mg/day.
 TREATMENT-0.5-1 mg elemental zinc/kg/day for several
weeks or months.
 1 mg elemental zinc=4.5 mg zinc sulphate or 3 mg zinc
acetate.
 IV 50 microgram of elemental zinc/kg body weight /day.
 TOXICITY-relatively nontoxic
 Acute ingestion of large amounts may cause liver and
kidney failure.
 Competitive interaction of zinc with other minerals may
lead to copper deficiency in person receiving chronic zinc
supplementation at high doses.
COPPER
 Is a component of several metalloenzymes that are
required for oxidative metabolism
 ABSORPTION AND METABOLISM-
40% of ingested copper is absorbed in the stomach and
small intestine.
Transported to the liver attached to albumin.
Excreted via biliary system to feces and urine.
SOURCES- meats, liver, seafood, nuts and seeds.
use of copper-containing pesticides, contamination of
water by copper pipes and copper cooking utensils.
DEFICIENCY-primary deficiency infrequent
Secondary deficiency in –malabsorption syndrome, liver
disease, peritoneal dialysis.
 CLINICAL MENIFESTATIONS
 Microcytic, hypochromic anemia unresponsive to iron
therapy, neutropenia, and osteoporosis.
 Periosteal elevation, cupping and flaring of long
bones metaphysis with spur formation
, submetaphyseal fractures, flaring of anterior
ribs, and spontaneous fractures of the ribs.
 Pallor, depigmentation of skin and hair, prominent
dilated superficial veins, skin lesions resembling
seborrheic dermatitis, anorexia, diarrhea, and failure
to thrive.
 Copper transport is disrupted-wilson disease and
menkes disease-defect in copper transporting
membrane protein.
toxicity
 Acute ingestion of large doses of copper cause
diarrhea, abdominal pain, and may lead to liver and
kidney failure.
 Chronic intoxication occurs from copper released from
water piping , by extensive use of topical copper
containing medications, or hemodialysis with
solutions that have high copper content.
IODINE
 iodine deficiency during pregnancy can result in
stillbirth, spontaneous abortion, congenital
abnormalities such as cretinism, increased perinatal
mortality, endemic cretinism
 In neonate-neonatal goiter, neonatal hypothyroidism,
endemic mental retardation
 Child and adolescent-goiter, subclinical
hypothyroidism, impaired mental function and
retarded physical development.
Recommended daily intake
 90 microgram for preschool children (0-59 mth)
 120 microgram for school children (6-12 yrs)
 150 microgram for adults (above 12 years)
 200-250 microgram for pregnant and lactating women.
correction
 Iodised salt intake 5g/day.
 Administration of iodine solutions such as Lugol,s
iodine at regular interval and iodization of water
supplies dy direct addition of iodine solution or via a
special delivery mechanism.
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Micronutrients

  • 1. 1. Introduction 2. Source 3. Daily allowance 4. Deficiency 5. Treatment 6. Toxicity
  • 2. 1. Micronutrients play a central part in metabolism and in maintenance of tissue function. 2. Vitamins and minerals.
  • 3. BACKGROUND Vitamins are organic substances that are essential for several enzymatic functions in human metabolism A compound is called vitamin when it cannot be synthesized in sufficient quantities by an organism, and must be obtained from the diet.
  • 4. Functions  Acts as hormones (vitamin D) Acts as antioxidant (vitamin E)  Acts as mediators of cell signalling and regulators of cell and tissue growth and differentiation(vitamin A) Acts as precusors for enzyme cofactor biomolecules(coenzymes) that help act as catalysts and substrates in metabolism
  • 5. VITAMINS  Vitamins are classified according to solubility into fat soluble & water soluble.  13 vitamins are known, 4 fat soluble (KEDA) & 9 water soluble (C, Folate & the B group).
  • 6. VITAMINS  water soluble-dissolve easily in water readily excreted from the body.  fat soluble-absorbed through the intestinal tract with the help of lipids(fats).
  • 7. VITAMIN A-Vitamin A is a generic term for many related compounds. Retinol (alcohol), Retinal (aldehyde) are often called preformed vitamin A. Retinal can be converted by the body to retinoic acid which is known to affect gene transcription. Body can convert b-carote ne to retinol, thus called provitamin A.
  • 8. FUNCTIONS •Immunity: important for activation of T lymphocyte, maturation of WBC & integrity of physiological barrier. •Vision: integrity of eye & formation of rodopsin necessary for dark adaptation. •Regulation of gene expression: vital to cell differentiation & physiologic processes • Growth & development
  • 9. Animal Foods Plant Foods Cod liver oil Sweet potato Liver & kidney Carrots Egg Cantaloupe Butter Spinach Milk & cheese Apricot Fish & meat Papaya RICH DIETARY SOURCES
  • 10. Life stage mg/day Infants 300-400 Children 400-600 Adolescent 900M- 700F Recommended Allowance
  • 11. Vitamin A deficiency •Deficiency of vitamin A leads to: 1. Ocular change-Night blindness & xerophthalmia 2. Extra ocular changes Growth retardation Acquired immune deficiency Keritinization of epithelia in RT, GIT & UT with increased risk of RTI, malabsorption & UTI.
  • 12. WHO CLASSIFICATION OF XEROPTHALMIA PRIMARY SIGNS SECONDARY SIGNS X1A conjunctival xerosis  X1B Bitot’s spot  X2 Corneal xerosis  X3A Corneal ulceration  X3 B Keratomalacia  XN Night blindness  XF Fundal changes  XS Corneal scarring
  • 13.  Rhodopsin-protein scotopsin and 11-cis retinal.  light sensitive- rodopsin decomposed  11-cis retinal--- >11-trans retinal and splits off from scotopsin  In dark-retiene isomerase– reverse reaction  11-cis retinal combines with scotopsin te regenerate rhodopsin (vit. A dependent)  Xeropthalmia-pigmentation of caruncle with loss of normal lusture and moist apperance of palpebral conjunctiva-dry and wrinlked.  Bitots spot-chalky grey spots on the temporal side of corneas -cleral junction  Keratomalacia-cornea is soft and ulcerated. Eventually infected and perforation of cornea occurs resulting in opacification and blindness.
  • 14.
  • 15. Treatment •For treatment of xerophthalmia, according to WHO guidelines. >1 year-2,00,000 IU orally on presentation the following day. 1 to 4 weeks later. 6mths-1yr 1,00,000 IU <6mths-50,000 IU
  • 16. TOXICITY- Children and adults ingesting >50,000 IU/day for several month. •Vitamin A in excess leads to: •Dermatitis with xanthosis cutis •Hepatosplenomegaly •Fatigue, malaise, anorexia, vomiting •Bone pain & increased risk of fracture •Pseudotumor Cerebri •Xray-hyperostosis of the shafts of long bones
  • 17. PREVENTION  The National vitamin A prophylaxis programme  1-5 yrs , every 6 mths  2,00,000 IU  Fortification of food(wai wai, dalda ghee).
  • 18. VITAMIN D  Vitamin D comprises a group of sterols; the most important of which are cholecalciferol (vitamin D3) & ergosterol (vitamin D2).  Humans & animal utilize only vitamin D3 & they can produce it inside their bodies from cholesterol.  Cholesterol is converted to 7-dehydro- cholesterol (7DC), which is a precursor of vitamin D3.
  • 19.
  • 20. VITAMIN D  Exposure to the ultraviolet rays in the sunlight convert 7DC to cholecalciferol. Vitamin D3 is metabolically inactive until it is hydroxylated in the kidney & the liver to the active form 1,25 Dihydroxycholecalciferol.  1,25 DHC acts as a hormone rather than a vitamin endocrine & paracrine properties.
  • 21. FUNCTIONS •Calcium metabolism: vitamin D enhances ca absorption in the gut & renal tubules. •Cell differentiation: particularly of collagen & skin epithelium •Immunity: important for Cell Mediated Immunity & coordination of the immune response.
  • 22. Sources of Vitamin D Sunlight is the most important source  Fish liver oil  Fish & sea food (herring & salmon)  Eggs  Plants do not contain vitamin D3 Human milk deficient in vit. D, contains only 30-40 IU per liter mostly from 25(OH)D3
  • 23. Vitamin D deficiency •Deficiency of vitamin D leads to:  Rickets in small children.  Osteomalacia  Osteoporosis
  • 24. TOXICITY •Hypervitaminosis D – infants-2,000-3,000 IU/day, adults-10,000 IU/day for several months. causes hypercalcemia,hyperphosphatemia, hypertension which manifest as: Nausea & vomiting Excessive thirst & polyuria Severe itching Joint & muscle pains Azotemia, nephrolithiasis, ectopic calcification. Disorientation & coma.
  • 25. RICKETS Lack of adequate mineralisation of growing bone
  • 26. RICKETS Sign and symptoms- •Skeletal deformity-bowed legs(genu varum) in toddlers, knock knees (genu valgum) in older children, craniotabes (soft skull), spinal and pelvic deformities, growth disturbances, costochondral swelling(rickety rosary), harrisons groove, double malleoli, greenstick fractures, bone pain and tenderness, muscle weakness and dental problems.
  • 27. INVESTIGATIONS Radiologic changes-loss of normal zone of provisional calcification adjacent to metaphysis. Widening of the growth plate. Splaying and cupping of metaphysis. Generalised reduction in bone density. Low circulating levels of 25(OH)D3. Elevated serum alkaline phosphate. Calcium level may be normal or low Phosphate level usually are unchanged or low.
  • 29. TREATMENT -Vitamin D administered orally either in a single dose of 60,000 or over 10 days(60,000 IU daily for 10 days) followed by a maintenance dose of 400 IU/day. Oral calcium suppliments(50- 75mg/kg/day)
  • 30. Vitamin E  Anti oxidant  Free radical scavanger  Antineoplastic effect and may raise the concentration of high density lipoprotein cholesterol.  Transported in the body by lipoprotein.  sources-nuts, seeds, whole wheat grain.  Recommended daily allowance-15-25 IU/day- 6wks(preterm),infants-3mg alfa-tocopherol, adults- 10mg/day.
  • 31. Deficiency  Observed in low birth weight infants.  Anemia, reticulocytosis, thrombocytopenia, and abnormal erythrocyte metabolism.  Low levels of vitamin e in premature infants is associated with hemolytic anemia, hyperbilirubinemia and intraventricular hemorrhage.  Prophylaxis reduces retinopathy of prematurity.  Clinical menifestation-loss of reflexes, ataxia of trunks and limbs, dimnished priopioception, muscle weakness, ptosis, pes cavus, scoliosis and dysarthria.
  • 32. Vitamin K  It is a cofactor of the enzyme that catalyzes one step in the formation of prothrombin.  Needed for the generation of several clotting factors in the liver.  Source- green leafy vegetables.  Deficiency-coagulation defect due to hypoprothrombinemia and deficiency of factor VII resulting in hemorrhagic disease of the newborn.  1mg IM –newborn.  In severe deficiency-2.5 to 5 mg parenterally.
  • 33. The B VitaminsB-1, B-2, B-3, B-6, B-12
  • 34. WATER SOLUBLE VITAMINS  VITAMIN B GROUP  Thiamine(Vitamin B1)-SOURCES-  Unrefined or fortified cereal grains, enriched bakery products, organ meats (liver, kidney) and legumes  Thiamine content of human milk is relatively low compared to cow’s milk. Pork  Fish, Liver, Legumes, Nuts, Whole grain or enriched breads and cereals
  • 35. B-1 Thiamin  Important in:  Producing energy from carbohydrates  proper nerve function  stabilizing the appetite  promoting growth and good muscle tone  ATP production
  • 36. Recommendations  Men 14+ 1.2 mg/day  Women 14-18 1.0 mg/day  Women 19+ 1.1 mg/day  1 broiled pork chop,  1.25 cups corn flakes OR  1 baked potato (w/ skin)  0.5 cup of lentils  1 cup raisin bran
  • 37. Warnings  B-1 is nontoxic even at high dosages
  • 38. B-1 Deficiency(beri beri)  Occurs in adults when the intake drops below 1mg/day.  Three forms-dry, wet, acute  Dry-no edema, severe muscle wasting, and cardiomegaly.  Wet-peripheral edema, ocular paralysis, ataxia and mental impairment.  Infantile beriberi more subtle than adults occurs in breastfed infants of thiamine deficient mothers.  Cardiac involvement with cardiomegaly, cyanosis, dyspnea, and aphonia if untreated results in death.
  • 39. Diagnosis of thiamine deficiency  Suspected in all cases of malnutrition.  The diagnosis may be confirmed by measurement of 24hrs urine thiamine excretion-normal 40-100 microgram/day.  <15/day-deficient range.  Can also be based on response of red cell transketolase to the adition of thiamine in vitro. An increase in transketolase activity of <15%-normal.  15%-25%- mild deficiency.  >25%-severly deficient.
  • 40. Thiamine requirements  Functions primarily in the metabolism of carbohydrate.  RDA-0.4mg/1000 kcal consumed.  TREATMENT OF BERIBERI  Resolution of neurologic and cardiac symptoms within 24-48 hrs.  Mild beriberi-5mg/day PO.  Severly ill-10mg iv BD.  In presence of heart failure treatment of heart failure.
  • 41. SCURVY (VIT. C DEFICIENCY)  Prolonged vitamin c deficiency results in scurvy.  Usually occurs in those who are deprived of citrus fruit, fresh vegetables, or vitamins.  IN INFANCY- clinical features-  Anorexia, diarrhea, pallor, irritability and increased susceptibility to infections, sub-periosteal hemorrhages and long bone tenderness can occur.  OLDER CHILDREN-hemorrhagic sign predominate.  Bleeding of gums, conjunctiva and the intestinal tract.
  • 42. diagnosis  By characteristric physical findings and history of inadequate dietary intake.  X-ray of long bones-infantile scurvy TREATMENT Supplimentation of vitamin c resolves symptoms in 24- 48hrs. RDA-30-40 mg /day-infants 40-70 mg/day- children.
  • 43. Folic acid  Essential for the normal growth and maintenance of all cells .  Vital for the reproduction of the cells within fetus.  Deficiency affects normal cell division and protein synthesis impairing growth.  Reduces blood levels of homocysteine so lowers risk of heart disease.  Also maintains nervous system integrity and intestinal tract functions.  Involved in the production of serotonin.
  • 44.  SOURCES  Leafy vegetable- spinach, turnip, lettuce, dried beans and peas, fortified cereal products, sunflower seeds certain other fruits and vegetables.  DEFICIENCY- limits cell function( cell division and protein synthesis).  Megaloblastic anemia  Memory problems.  Deficiency in pregnant women-neural tube defect.  RDA- infants--70 microgram/day  1-3 yrs--100 4-6 yrs---150  7-9 yrs– 200 10-12 yrs--250  13-15 yrs-300 pregnant and lactating-400 
  • 45. Who’s at Risk?  Homeless & Malnourished  Alcoholics  People with malabsorption conditions
  • 46. B-2 Riboflavin  Important in:  energy production  carbohydrate, fat, and protein metabolism  formation of antibodies and red blood cells  cell respiration  maintenance of good vision, skin, nails, and hair  alleviating eye fatigue
  • 47. Sources of B-2  Large amounts in  dairy  eggs  meats  Small amounts in  leafy green vegetables  enriched grains
  • 48. Recommendations  Men 14-70 1.3 mg/day  Women 14-70 1.0 mg/day  71+ Larger doses  1 cup raisin bran  1 cup milk  1 egg OR  1 small extra lean hamburger  1 cup plain yogurt  0.5 cup fresh cooked spinach  1 cup cottage cheese
  • 49. B-2 Deficiency  Itching and burning eyes  Cracks and sores in mouth and lips  Bloodshot eyes  Dermatitis  Oily skin  Digestive disturbances
  • 50. Warnings  B-2 is nontoxic at supplemental and dietary levels.  Light can destroy riboflavin, so purchase milk in opaque containers.
  • 51. Who’s at Risk?  People with cataracts  People with Sickle Cell Anemia  Alcoholics
  • 52. B-3 Niacinamide & Niacin  Important in:  energy production  maintenance of skin and tongue  improves circulation  maintenance of nervous system  health of the digestive track
  • 53. B-3 Niacinamide & Niacin  Two Types  Niacinamide (Nicotinamide)  does not regulate cholesterol  Niacin (Nicotinic Acid)  highly toxic in large doses  Inosital Hexaniacinate is a supplement that gives the cholesterol regulation without high toxicity
  • 54. Recommendations  Men 14+ 16 mg/day  Women 14+ 14 mg/day  1 cup rice  4 oz. broiled salmon  1 tbsp peanut butter  1 bagel  OR  1 small extra lean hamburger  0.5 cup grape nuts cereal
  • 55. Warnings  In doses of only 50-100 mg nicotinic acid can cause dilation of blood vessels and potentially painful tingling (“niacin flush”), diarrhea, nausea, vomiting, and long term liver damage.  Nicotinamide is almost always safe to take, although a few cases of liver damage have been reported in doses of over 1000 mg/day.
  • 56. B-3 Deficiency  Pellegra  disease caused by B-3 deficiency  rare in Western societies  gastrointestinal disturbance, loss of appetite  headache, insomnia, mental depression  fatigue, aches, and pains  nervousness, irritability
  • 57. Who’s at Risk?  Most people get plenty of B-3 from their diet because it is added to white flour.
  • 58. B-6 Pyridoxine  Important in:  Production of red blood cells  conversion of tryptophan to niacin (B-3)  immunity  nervous system functions  reducing muscle spasms, cramps, and numbness  maintaining proper balance of sodium and phosphorous in the body
  • 59. Recommendations  Men 14-50 1.3 mg/day  Men 50+ 1.7 mg/day  Women 14-18 1.2 mg/day  Women 19-50 1.3 mg/day  Women 50+ 1.5 mg/day  1 chicken breast  0.5 cup cooked spinach  1 cup brown rice OR  1 baked potato with skin  1 banana  4 oz. lean sirloin
  • 60. Warnings  High doses of B-6 may be recommended to treat carpal tunnel syndrome, and sleep disorders, but continued use of high doses may result in permanent nerve damage.  Pregnant women should always consult their doctor before taking this supplement and all others.
  • 61. B-6 Deficiency  nervousness, insomnia  loss of muscle control, muscle weakness  arm and leg cramps  water retention  skin lesions
  • 62. Who’s at Risk?  very rare  alcoholics  patients with kidney failure  women using oral contraceptives
  • 63. B-12 Cobalamin  Important in:  proper nerve function  production of red blood cells  metabolizing fats and proteins  prevention of anemia  DNA reproduction  energy production?
  • 64. Recommendations  Men and Women 14+ 2-3 mcg/day  1 chicken breast  1 hard boiled egg  1 cup plain low fat yogurt OR  1 cup milk  1 cup raisin bran
  • 65. Warnings  Vegetarians need to look for fortified sources (soy milk, supplements).  Elderly often have trouble absorbing.
  • 66. B-12 Deficiency  anemia  nerve damage  hypersensitive skin
  • 67. Who’s at Risk?  pernicious anemia  B-12 injections often taken regularly  HIV  Chronic Fatigue Syndrome
  • 68. Calcium and magnesium Calcium  most abundant mineral in the body.  Located primarily in bone tissue(98%)  Coagulation cascade, nerve conduction, and muscle stimulation.  Absorption depends on intake and Vitamin D .  Absorption is decreased by fiber, phytate, oxalate, fat and lactose.
  • 69.  SOURCE-  milk and dairy products, grains and fruits.  Deficiency –vegeterians, steatorrhea, chronic malabsorption syndromes, or intestinal and renal abnormalities. Requirement  1-10yrs 500-800mg/day  Purberty 1000-1200 mg/day  Pregnant and lactating women 400mg/day.
  • 70.  DEFICIENCY  Tetany- muscle cramps, numbness and tingling in limbs.  Rickets and osteoporosis –chronic deficiency
  • 71. MAGNESIUM  Essential for bioenergic reactions controlling fuel oxidation, membrane transport, and signal transmission.  Over 80% in bone and skeletal muscle.  SOURCES- legumes, nuts banana and whole grains.  Regulation of magnesium balance depends on renal tubular absorption.
  • 72.  Deficiency –secondary to intestinal malabsorption, excessive gastrointestinal losses through fistulae or continuous suction or renal disease affecting tubular reabsorption.  Manifestations –irritability, tetany, hypo or hyper reflexia.  Requirement –  0-6mths 40-50mg/day  6-12mths 60mg/day  >12mths 200mg/day
  • 73. Trace elements  ZINC  COPPER  SELENIUM  CHROMIUM  IODINE  IRON
  • 74. ZINC  FUNCTIONS- functions as an intracellular hormone contributing to the regulation of cellular growth and also impacts on nucleic acid metabolism and protein synthesis  ABSORPTION AND METABOLISM- Absorbed throughout the small intestine. Metabolises in liver – transported in portal system attached to albumin or transferrin. Distributed in most tissues, 90% of total body zinc is localised in bone and skeletal muscle. Excreted through feces.
  • 75. DEFICIENCY  Develops as a part of malnutrition or malabsorption syndrome due to low intake or intestinal disease.  FEATURES  Poor physical growth  Delayed sexual maturation  The typical syndrome of zinc deficiency consists of- growth retardation, hypogonadism, anemia  Other symptoms consists of-diarrhea, hair loss, anorexia, dermatitis, impaired immune function and skeletal abnormalities.  Acrodermatitis enteropathica.  Eye lesions-photophobia, blepharitis, corneal opacities.
  • 76. requirement  3.5-5.0 mg/day.  TREATMENT-0.5-1 mg elemental zinc/kg/day for several weeks or months.  1 mg elemental zinc=4.5 mg zinc sulphate or 3 mg zinc acetate.  IV 50 microgram of elemental zinc/kg body weight /day.  TOXICITY-relatively nontoxic  Acute ingestion of large amounts may cause liver and kidney failure.  Competitive interaction of zinc with other minerals may lead to copper deficiency in person receiving chronic zinc supplementation at high doses.
  • 77. COPPER  Is a component of several metalloenzymes that are required for oxidative metabolism  ABSORPTION AND METABOLISM- 40% of ingested copper is absorbed in the stomach and small intestine. Transported to the liver attached to albumin. Excreted via biliary system to feces and urine. SOURCES- meats, liver, seafood, nuts and seeds. use of copper-containing pesticides, contamination of water by copper pipes and copper cooking utensils. DEFICIENCY-primary deficiency infrequent Secondary deficiency in –malabsorption syndrome, liver disease, peritoneal dialysis.
  • 78.  CLINICAL MENIFESTATIONS  Microcytic, hypochromic anemia unresponsive to iron therapy, neutropenia, and osteoporosis.  Periosteal elevation, cupping and flaring of long bones metaphysis with spur formation , submetaphyseal fractures, flaring of anterior ribs, and spontaneous fractures of the ribs.  Pallor, depigmentation of skin and hair, prominent dilated superficial veins, skin lesions resembling seborrheic dermatitis, anorexia, diarrhea, and failure to thrive.  Copper transport is disrupted-wilson disease and menkes disease-defect in copper transporting membrane protein.
  • 79. toxicity  Acute ingestion of large doses of copper cause diarrhea, abdominal pain, and may lead to liver and kidney failure.  Chronic intoxication occurs from copper released from water piping , by extensive use of topical copper containing medications, or hemodialysis with solutions that have high copper content.
  • 80. IODINE  iodine deficiency during pregnancy can result in stillbirth, spontaneous abortion, congenital abnormalities such as cretinism, increased perinatal mortality, endemic cretinism  In neonate-neonatal goiter, neonatal hypothyroidism, endemic mental retardation  Child and adolescent-goiter, subclinical hypothyroidism, impaired mental function and retarded physical development.
  • 81. Recommended daily intake  90 microgram for preschool children (0-59 mth)  120 microgram for school children (6-12 yrs)  150 microgram for adults (above 12 years)  200-250 microgram for pregnant and lactating women.
  • 82. correction  Iodised salt intake 5g/day.  Administration of iodine solutions such as Lugol,s iodine at regular interval and iodization of water supplies dy direct addition of iodine solution or via a special delivery mechanism.