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Vit. A def report edited.pptx

Apr 04, 2018

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    Vitamin A deficiency, according to WHO is tissue concentration of Vitamin

    A low enough to have adverse health consequences even if there is no

    evidence of clinical Xerophthalmia.

    Vitamin A deficiency can occur at any age but it is most common amongchildren under 6 years of age. Over 100 million preschool-age children are

    thought to be affected.

    Lack of vitamin A in children causes severe visual impairment and

    blindness, and significantly increases the risk of severe illness, and even

    death, from such common childhood infections as diarrheal disease.

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    Vitamin A Deficiency

    leading cause of preventable blindness in

    children

    increases the risk of disease and death from

    severe infections

    In pregnant women VAD causes night

    blindness and may increase the risk of

    maternal mortality.

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    Vitamin A Deficiency

    For children

    causes severe visual impairment and blindness

    significantly increases the risk of severe illness, andeven death, from such common childhood infections

    as diarrhoeal disease and measles.

    For pregnant women in high-risk areas, vitamin Adeficiency occurs especially during the lasttrimester when demand by both the unborn child

    and the mother is highest. demonstrated by the high prevalence of night

    blindness during this period.

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    Vitamin A Deficiency

    common in many developing countries

    typically begins during infancy, when infants

    do not receive adequate supplies of colostrum

    or breast milk

    Chronic diarrhea

    leads to excessive loss of vitamin A in young

    children, and vitamin A deficiency increases the

    risk of diarrhea

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    ETIOLOGY OF VITAMIN

    A DEFICIENCY

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    o PRIMARY VITAMIN A DEFICIENCY

    - prolonged dietary deprivation- endemic in Southeast Asia

    o SECONDARY VITAMIN A DEFICIENCY

    - decreased bioavailability of provitamin A

    - interference with absorption, storage or

    transport

    - common in prolonged protein-energy

    undernutrition

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    VITAMIN A DEFICIENCY CLINICAL

    MANIFESTATIONS

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    1. NYCTALOPIA

    - Difficulty to adjust to dim light

    - Insufficient adaptation to darkness

    - Inhibits Rhodopsin production

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    2. XEROPHTHALMIA

    - Dry eyes- Conjunctiva becomes dry and thick and wrinkled

    - Loss of goblet cells in the conjunctiva which is

    responsible for mucus secretion

    - Eyes fail to produce tears

    - Dead epithelial and microbial cells accumulate on

    the conjunctiva and form debris

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    most common symptom of vitamin A deficiency in

    young children and pregnant women

    Corneal ulceration and necrosis

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    3.) BITOTS SPOT

    - Foamy, cheesy accretions of desquamated

    keratin and saprophytic bacilli overlying an area of

    conjunctival xerosis

    -Build up of keratinized epithelial debris and

    secretions found in the conjunctiva

    - Usually associated with night blindness

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    - In advanced deficiency, cornea becomes hazy and

    develop erosions

    - Liquefactive corneal necrosis

    4.) KERATOMALACIA

    -Softening of the cornea

    - Leads to corneal scarring

    that blinds at least a quarter

    of a million each year

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    5.) FOLLICULAR

    HYPERKERATOSIS

    -Rough

    keratinized skin

    -Resembles

    goosebumps

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    6.) Increased the severity and mortality risk

    of infections (particularly diarrhea and

    measles) malaria, and respiratory disease

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    TREATMENTS FORVITAMIN A

    DEFICIENCY

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    TIMING VITAMIN A DOSE

    Immediately on diagnosis

    < 6 mos. of age 50,000 IU

    6-12 mos. of age 100,000 IU

    >12 mos. of age 200,000 IU

    Next day Same age-specific dose

    Atleast 2 weeks later Same age-specific dose

    TREATMENT FOR XEROPHTHALMIA

    For all age groups except for women of reproductive age

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    For women of reproductive age:

    Night Blindness/ Bitots Spot: ---- 10,000 IU

    daily for atleast 2 weeks or weekly doses of

    25,000 IU

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    VITAMIN A TOXICITY

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    ACUTE VITAMIN A TOXICITY

    Accidental ingestion by children (>300,000)

    Eating of polar bear or seal liver by arctic explorers

    Headaches, drowsiness, irritability, nausea and vomiting,

    skin peeling

    CHRONIC VITAMIN A TOXICITY

    Mega therapy/ massive daily doses (150,000-350,000 IU)

    Coarse hair, cracked lips, dry, rough skin, alopecia of theeyebrows, frail bone

    In children, hepatomegaly, splenomegaly and pseudotumor

    cerebri

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    PREVENTION

    i i h l i S h d l

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    Individual Oral dose Timing

    Children 6-11 mos.old 55 mg. Retinylpalmitate (100,00 IU) Once every 4-6 mos.

    Children > 12 mos.

    old

    100 mg.

    (200,000 IU)

    Once every 4-6 mos.

    Infants 0-6 mos. old 1375 mg.

    (25,000 IU)

    1-3 times over the

    first 6 mos. of life

    Women ofchildbearing age

    110 mg.(200,000 IU)

    Within 1-2 months atmost of giving birth

    Pregnant and

    Lactating women

    275 mg. (5,000-

    10,000 IU)

    Daily

    Vitamin A Prophylaxis Schedule

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    RDA of Vitamin A for different age group:

    1 year or younger 375 mcg

    1-3 years old 400 mcg

    4-6 years old 500 mcg

    7-10 years old 700 mcg

    All males older than 10 years old 1000 mcg

    All females older than 10 years old 800 mcg