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6 MICRONUTRIENT DEFICIENCY 73$.ppt
1. Birhanu G.
Pediatrics and Child Health
Resident
COMMON MICRONUTRIENT
DEFICIENCIES IN CHILDREN
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2. Micronutrients include vitamins and minerals.
Vitamins –organic compounds
- growth ,health and reproduction
Minerals – inorganic elements ,from earth’s crust
- form 5% of typical human diet.
- growth and normal functioning
important public health problems in a number of developing
countries
30% of world’s population unable to use their full mental and
physical potential as a result of micronutrient deficiencies
children are susceptible to micronutrient deficiency.
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3. A vitamin can have several functions & involved in
fundamental functions in the body, such as growth,
maintenance of health, and metabolism.
Based on their chemical properties, they are classified as
either water-soluble or fat-soluble.
The water-soluble vitamins (except vitamin C) are members
of the B complex.
Gross vitamin deficiency may be recognized by obvious
clinical syndromes
Minerals: iron, Zinc ,copper, iodine ,selenium ,
manganese, chromium
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9. Vitamin A is an essential micronutrient because it
cannot be biogenerated de novo by animals.
Vitamin A (retinol) is fat soluble vitamin found
widely in animal tissue
Retinol and its naturally occurring relatives are
member of a large class known as retinoid
There are now over 1000 new retinoid
VITAMIN A DEFICIENCY
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10. Vitamin A exists in two forms
Preformed vitamin A and
Provitamin A form
Vitamin A has role in:
Vision
Reproduction
Growth & embryonic & fetal development
Bone development
Respiratory, gastrointestinal, hematopoietic, and immune
functions.
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11. EPIDEMIOLOGY
Is a major public health problem in developing countries
More than 350,000 cases of childhood blindness are reported
annually due to severe vitamin A deficiency
Improving Vit.A status reduce young child mortality by 25%
diarrhea-specific mortality by 30%.
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12. Infants and young children under 5 year of age are at
highest risk because
Poor stores at birth
Milk and supplementary food ( low vit.A)
Infection including diarrheal disease and
Growth sets requirement high
In Ethiopia it is a major public health problem
The prevalence bitot’s spots is 1% nationwide(1990)
In Harerge and Tigray – as high as 2%
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15. PLANT SOURCE
Source (per 100gm) vit.A(mic.gm)
Carrot, raw 1100
Mango 400
Lettuce 325
Sweet potato, raw 510
Avocado, raw 90
Tomatoes, raw 75
Papaya, raw 75
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16. CAUSES
Inadequate consumption of vitamin A
Problem of absorption, like disorders associated with fat
malabsorption
Problem in conversion or utilization of vitamin A
Repeated infections or diseases such as measles or
diarrhea
Absence of food containing oil or fat in the diet
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17. CLINICAL MANIFESTATION
Eye
Functional retinal rod cell changes occur before
structural lesion
Night blindness –failure of the eye to adapt to dim
light
Epithelial changes lead to-
Conjunctival xerosis –earliest lesion
Bitot’s spots – foamy, bubbly, or cheesy accumulation,
(triangular areas of abnormal squamous cell proliferation
and keratinization of the conjunctiva)
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19. Xerosis of the cornea - haziness due to stromal
infiltration, epithelial keratinization and often early
vascularization
Corneal ulcer - followed by scar which is irreversible
Keratomalacia - implies deformity and loss of corneal
substances leading to eye ball infection and corneal
opacity
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22. Lesions due to vitamin A deficiency develop insidiously and
rarely occur before 2 yr of age
An early symptom is delayed adaptation to the dark; later when
vitamin A deficiency is more advanced, it leads to night
blindness
Mental retardation
Retardation of physical growth
Apathy
Follicular hyperkeratosis of the skin
Susceptibility to infections
Anemia
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24. THERAPY
Vitamin A capsule on two consecutive days immediately
and another dose within 1-4 weeks
Dose -200,000IU above one year
-100,000IU 6 – 12 month
-50,000IU less than 6 months
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25. PREVENTION
Increase consumption of dark green leafy vegetables,
Egg, livers, fat of fish and meat and cod liver oil can be
provided
Vitamin A should be supplemented in malnutrition,
diarrhea, measles and acute respiratory infection.
Distribution of vitamin A capsule should be given to the
community.
One capsule every 6 months up to 6 year of age
One drop of vitamin A (25,000IU) for every child with
immunization schedule
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27. RICKETS
Bone consists of a protein matrix called osteoid and a mineral
phase, principally composed of calcium and phosphate, mostly in
the form of hydroxyapatite.
Rickets refers to deficient mineralization at the growth plate, as
well as architectural disruption of this structure.
Osteomalacia refers to impaired mineralization of the bone
matrix.
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28. Rickets and osteomalacia usually occur together as
long as the growth plates are open; only osteomalacia
occurs after the growth plates have fused.
Because growth plate cartilage and osteoid continue to
expand but mineralization is inadequate, the growth
plate thickens.
There is also an increase in the circumference of the
growth plate and the metaphysis increasing bone width
at the location of the growth plates.
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29. Mineralization defects are classified according to the
predominant mineral deficiency.
Calcipenic rickets is caused by calcium deficiency,
which usually is due to insufficient intake or
metabolism of vitamin D, and insufficient intake or
absorption of calcium in the setting of normal
vitamin D levels.
Phosphopenic rickets usually is caused by renal
phosphate wasting.
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30. PATHOGENESIS
Growth plate thickness is determined by two
opposing processes:
chondrocyte proliferation and hypertrophy on the one
hand, and
vascular invasion of the growth plate followed by
conversion into primary bone spongiosa on the other .
Vascular invasion requires mineralization of the
growth plate cartilage and is delayed or prevented
by deficiency of calcium or phosphorus.
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31. In these circumstances, growth plate cartilage
accumulates and the growth plate thickens.
In addition, the chondrocytes of the growth plate become
disorganized, losing their columnar orientation with
characteristic expansion of the hypertrophic zone.
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34. NUTRITIONAL VITAMIN D DEFICIENCY
Nutritional rickets – Calcipenic rickets is usually
caused by dietary deficiency of vitamin D.
Occasionally, nutritional rickets is caused by
deficiency of dietary calcium or a mixed deficiency of
vitamin D and calcium.
Vitamin D deficiency remains the most common cause
of rickets globally and is prevalent, even in
industrialized countries.
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35. Vitamin D-deficiency rickets typically presents between
3 months and 3 years of age, when growth rates (and
calcium needs) are high, and exposure to sunlight may be
limited.
The recommended intake of vitamin D to prevent
deficiency is 400 international units daily in healthy
infants and 600 int. units daily for children 1 to 18 years.
CONT’D…
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36. Risk factors
Maternal vitamin D deficiency
Breast feeding
Skin pigmentation & low sunlight exposure
Malabsorptive disorders
Anti-convulsant drugs
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37. Vitamin D3
Naturally present in human skin as
7-dehydrocholestrole activated photochemically to
cholecalciferol and transferred to the liver
In the liver by 25-hydroxylase to 25-OH
cholecalciferol then
In the renal cortical cells by1,25 hydroxylase to
1,25 - OHcholecalciferol
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39. Functions of 1,25-dehydroxycholecalciferol
Facilitates intestinal absorption of calcium and
phosphorus
Reabsorption of phosphorus in the kidney
Control serum ca and P together with parathyroid
hormone and cacitonin
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40. CLINICAL MANIFESTATION
Craniotabes - softening of the cranial bones, can be
detected by applying pressure at the occiput or over the
parietal bones -earliest sign of rickets
Rachitic rosary -the beads of a rosary as the examiner's
fingers move along the costochondral junctions
Growth plate widening is also responsible for the
enlargement at the wrists and ankles
Harrison groove horizontal depression along the lower
anterior chest
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41. Large anterior fontanell
Caput quadratum
Pigeon chest
Delayed eruption of temporary teeth
Bow leg or knock knee
Greenstick fracture
Rachitic dwarfism
Hypotonia
Sweating
Delayed tooth eruption
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46. LABORATORY FINDING
Serum Ca= normal or low
Serum Phosphorus= low
Serum alkaline phosphatase= increased
Serum 25-OH cholecalciferol decreased
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47. Radiology
Generalized decrease in the skeletal radiodensity
Widening, capping and fraying at the end distal of the bones,
best seen at the end of radius and ulna.
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50. TREATMENT
Vitamin D adminstration
-Stoss dose of vit D 300,000-600,000 IU IM in 2-4 doses over
one day or,
Daily intake of 2000-5000IU of vit D for 4-6 wks
-Both should be accompanied by adequate administration of
Ca and P
-After treatment continue with the daily requirement i.e 400IU
of vit D daily
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51. PREVENTION
Most cases of nutritional rickets can be prevented by
universal administration of a daily multivitamin
containing 400 IU of vitamin D to children who are
breast-fed
Adequate sunlight exposure.
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52. READING ASSIGNMENT
Rickets of Prematurity
Congenital rickets
Vitamin D–Dependent Rickets, Type 1
Vitamin D–Dependent Rickets, Type 2
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53. include thiamine, riboflavin, niacin, vitamin B6,
folate, vitamin B12, biotin, and pantothenic acid.
serve as coenzymes in many metabolic pathways
that are functionally closely related
VITAMIN B COMPLEX DEFICIENCIES
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57. VITAMIN C DEFICIENCY
Vitamin C
is a water-soluble micronutrient essential for human health
synthesized by plants and most animals , not by humans and
other primates .
Vegetables and fruits, especially citrus, are the best food
sources of vitamin C
Absorbtion (small intestine) tissues ( pitutary ,adrenal )
Infants on cow milk or evaporated milk –need supplement
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58. FUNCTIONS
Collagen formation
Dopamin nor epinepherin
Cholestrol steroid
Important antioxidant
Enhances iron absorption ,transfer of iron from
transferrin to ferritin , & formation of
tetrahydrofolicacid affect the functions of
the hematopoietic system (immune response,
leukocytes, macrophages, red blood cells).
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59. VIT. C DEFICIENCY
Very low intake of vitamin C Scurvy
onset of clinical manifestations of scurvy is 6–24 mo
early symptoms - low-grade fever, irritability, tachypnea,
digestive disturbances, loss of appetite, and
generalized tenderness, particularly in the legs, which is
noticeable when the diaper is changed.
Pseudoparalysis,( with the hips and knees semi-flexed and
the feet rotated outward )
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60. An infant with scurvy characteristically lies with
the legs flexed at the knees and the hips partially
flexed and externally rotated
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61. A “rosary” and depression of the sternum
changes in the gums are manifested as bluish purple, spongy
swellings of the mucous membrane, especially over the upper
incisors .
Anemia - related to impaired ability to use iron or folate
swollen joints, purpura and ecchymoses, poor wound and
fracture healing, petechiae, perifollicular hemorrhages ,
hyperkeratosis of hair follicles, arthralgia, and muscle
weakness
osteoblasts cannot form osteoid brittle bone that fracture
easily
Severe vitamin C deficiency degeneration of skeletal
muscles, cardiac hypertrophy, bone marrow depletion, and
adrenal atrophy.
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62. DIAGNOSIS
characteristic clinical picture, the radiographic
appearance of the long bones, and a history of poor
vitamin C intake.
distal ends of the long bones (knee)
Radiological changes – simple bone atrophy ,ground
glass apperance ,thin cortex ,white line of fraenkel ,
Dx – zone of rarefaction under the white line at the
metaphysis
Plasma and serum vitamin C
Scurvy is often misdiagnosed as arthritis
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63. A, An early scurvy “white line” is visible
on the ends of the shafts of the tibia and
fibula; rings are shown around the
epiphyses of the femur and tibia.
B, More advanced scorbutic changes;
zones of destruction (ZD) are evident in
the femur and tibia
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64. TREATMENT
Daily intake of 3–4 oz of orange or tomato juice
produces healing in children with scurvy
Vitamin C supplements of 100–200 mg orally or
parenterally
TOXICITY – limited data on children (1–3 yr, 400 mg;
4–8 yr, 650 mg; 9– 13 yr, 1200 mg, and 14–18 yr, 1800
mg. )
Daily intake of >2 g of vitamin C in adults is unsafe
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65. ZINC DEFICIENCY
Zinc essentiality in humans was established in 1961.
Zinc deficiency is common in the developing world
often associated with malnutrition or other micronutrient
deficiencies (iron).
Source -Organ and flesh of mammals, fish.
-Eggs and dairy foods
- Cereals and legumes contain a modest amount of
Zn,but less absorbed
-Fruits and vegetables are low in Zn.
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66. 10 to 40 % is absorbed in the small bowel
The primary stores of zinc include the liver and kidney
Phytate ( cereals and legumes), irreversibly binds Zn in
the intestinal lower efficiency of absorption from
plant foods
animal protein (e.g., beef, eggs, and cheese) improves the
bioavailability of Zn from plant food .
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67. 86 % of the total-body Zn is in skeletal muscle and bone
95% of body Zn is intracellular,
Zinc supplementation reduces the incidence and severity
of diarrhea, pneumonia, and possibly malaria.
Children with diarrhea in developing countries have been
treated with zinc (20 mg/day orally for 14 days), with
improved morbidity and mortality rates.
Function
apoptosis regulation;
cell proliferation and growth
immune regulation.
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68. DEFICIENCY
Causes
inadequate intake, increased requirements,
malabsorption, increased losses, or impaired utilization
True prevalence is unknown
characterized by skin lesions, reductions in growth, delayed
puberty, hypogonadism, host defense defects and poor appetite
Chronic zinc deficiency is associated with dwarfism,
hypogonadism, dermatitis, and T-cell immunodeficiency.
Repletion of a Zn deficiency appears to be rapid
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69. ACRODERMATITIS ENTEROPATHICA ( ZINC
MALABSORBTION)
• is a rare autosomal recessive disorder caused by an
inability to absorb sufficient zinc from the diet
• is associated with severe zinc depletion
• signs and symptoms in 1st few mo of life
cutaneous eruption ..vesiculobullous, eczematous,
dry, scaly, or psoriasiform skin lesions
symmetrically distributed in the perioral, acral, and
perineal areas and on the cheeks, knees, and elbows
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70. Alopecia
Ocular manifestations include photophobia,
conjunctivitis,
Associated chronic diarrhea, stomatitis,
glossitis, nail dystrophy, growth retardation,
irritability,
delayed wound healing, intercurrent bacterial
infections, and superinfection with Candida
albicans.
Impaired lymphocyte function
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71. Acrodermatitis enteropathica in an infant.
Moist erythematous plaques on the cheeks and
buttocks.
The buttock lesions are typically symmetrical
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72. TREATMENT
Oral therapy with zinc compounds is the
treatment of choice(50 mg-150mg /24hrs) . or
Replacement doses of 3 mg/kg/day of elemental
zinc (13.2 mg/kg/day of zinc sulfate) are
recommended.
zinc levels are measured every three to six
months and the dose is adjusted up or down as
needed.
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