1.
DONE BY
MANOJ
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The word "vitamin" comes from the Latin word vita,
means "life".
Vitamins are chemicals found in very small amounts in
many different foods.
 “vitamins have been defined as organic compounds
which are required in minute amounts to maintain
normal health of organisms’.
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A Short History
 From about 1500 BC it was of Vitamins
known that various diseases
could be treated with specific
foods.
 . In 1880 Christian Eijkman
dutch physician and professor
of physiology
produced vitamin-deficiency
conditions in animals on an
experimental basis and
then reversed the condition
with an appropriate feeding
regimen.

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 Frederick Hopkins, English biochemist said in 1906 that
foods contain a small amount of "growth factors" needed to
sustain growth and life itself.
 The general category of "vitamins" was defined as (1)
substances found to be absolutely necessary for life (i.e., vital)
and which (2) the body cannot synthesize on its own.
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 In 1912 Kaziemirz funk Polish-British-American
biochemist named these growth factors “vitamines”
vit + amine
 Funk's original term "vitamine" was changed to "vitamin"
when many scientists identified, purified, and synthesized all
of the vitamins and discovered they did not all contain
nitrogen.
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 In the 1930s a scientific discovery demonstrated the
biochemical functions of the vitamins and established the
body's requirements for them. From then on, they have been
commercially produced.
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Classification of Vitamins
FAT SOLUBLE WATER SOLUBLE
A  B1- Thiamine
D  B2 - Riboflavin
E  B3 – Niacin
K  B5 – pantothenic acid
 B6 –Pyridoxine
 B8 – biotin
 B 9-Folic acid
 B12 -CyanoCobalamin
 C vitamin (ascorbic acid)
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Fat soluble Vitamins
 They are soluble in fat.
 Bile salts are essential for there absorption.
 They are generally stored in liver.
 They are not excreted in urine.
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Vitamin A
It is recorded in the history that Hippocrates(about
500 B.C.) cured night blindness.
He prescribed to the patients ox liver (in
honey),which is now known to contain high quantity
of vitamin A.
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VITAMIN A :- Is widely distributed in animal and plant
foods
animals –pre-formed – Retinol.
plants – pro-formed - carotene
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CHEMISTRY
Retinol (vitamin A alcohol) :
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Retinal (vitamin A aldehyde) :
This is an aldehyde form obtained by the oxidation of
retinol.
Retinal and retinol are interconvertible.
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Retinoic acid (vitamin A acid) :
produced by the oxidation of retinal.
However,retinoic acid cannot give rise to the formation
of retinal or retinol.
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Beta-Carotene (provitamin A) :
Found in plant foods.
lt is cleaved in the intestine to produce two moles of
retinal.
ln humans, this conversion is inefficient, hence beta-
carotene possesses about one-sixth vitamin A activity
compared to that of retinol.
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Dietary Sources of Vitamin A
Plant sources Animal sources
Sweet potatoes Chicken liver
Carrots Cod liver oil
Pumpkin Fish oil
Winter squash Canned beef stew
Cantaloupe Eggs
Pink Grapefruit Fish
Mangoes Shellfish
Apricots Butter
Oranges Fortified margarine
Spinach Cheese
Kale Whole milk
Beet greens Fortified skim milk
Broccoli Fortified low fat dairy
Dark green leafy products
vegetables 16

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DAILY REQUIRMENT
 Men and women – 600 mcg.
 Pregnancy and lactation – 950 mcg.
 Infants – 350mcg.
 Children – 600mcg.
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ABSORPTION & STORAGE
 The liver has enoromous capacity
to store – in the form of retinol
palmitate.
 Free retinol is highly active but
toxic & therefore transported in
blood stream in combination with
retinol binding protein (liver)
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Physiological Functions of Vitamin A
 Vision
 Epithelial cell
"integrity’
 Reproduction
 Resistance to
infectious disease
 Bone remodeling
 Growth
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Vision
 Retinal is a necessary
structural component of
rhodopsin , the light
sensitive pigment within
rod and cone cells of the
retina.
Rods are involved in
dim light vision
Cones are responsible
for bright light &
colour vision
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Wald's visual cycle
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colour vision
The colour vision is governed by colour sensitive
pigments porphyropsin (red), iodopsin
(green) and cyanopsin (blue).
All these pigments are retinalopsin
complexes.
When bright light strikes the retina, one or more of
these pigments are bleached,depending on the
particular colour of light.
The pigments dissociate to all-trans-retinal and opsin.
And this reaction passes on a nerve impulse to brain 24

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Epithelial cell "integrity
 Many epithelial cells appear to require vitamin A for
proper differentiation and maintenance.
 Lack of vitamin A leads to dysfunction of many epithelia
 The skin becomes keratinized and scaly, and mucus secretion
is suppressed
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Reproduction:
 Normal levels of vitamin A is required for sperm production,
 Normal reproductive cycles in females require adequate
availability of vitamin A.
Bone remodeling:
 Normal functioning of osteoblasts and osteoclasts is dependent
upon vitamin A.
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Resistance to infectious disease
 vitamin A deficiency has been shown to increase the frequency
and severity of disease.
 Several large trials with malnourished children have
demonstrated dramatic reductions in mortality from diseases
such as measles by the simple and inexpensive procedure of
providing vitamin A supplementation.
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Deficiency symptoms
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Deficiency of Vitamin A
Most susceptible
populations:
Preschool children with
decreased intake
Poor persons
Older adults
Alcoholism
Liver disease (limits
storage)
Fat malabsorption

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The signs of vitamin A deficiency
Ocular
Extra ocular
 Night blindness.
 Retarded growth
 Conjunctival xerosis
 Skin disorders
 bitot’s spot
 Effect on reproductive
 Corneal xerosis
organs.
 keratomalacia
 Effect on bone
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Xerophthalmia WHO classification
Night blindness (XN)
Conjunctival xerosis (X1A)
Bitot‘s spot (X1B)
Corneal xerosis (X2)
Corneal ulceration/keratomalacia (X3A) <1/3 of
corneal surface
Corneal ulceration/keratomalacia (X3B) ≥1/3 of
corneal surface
Corneal scar (XS)
Xerophthalmic fundus (XF)
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Night blindness
Lack of vitamin A
causes night blindness
or inability to see in
dim light as a result of
inadequate pigment in
the retina.
Earliest symptom
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Conjunctival xerosis
 Conjunctiva becomes dry, lustureless and non wettable.
 Described as “emerging like sand banks at receding tide”
 Commonly involves the interpalpebral area of temporal
quadrants
 Advanced cases > entire bulbar
conjunctiva involved
 Conjunctival thickening,
wrinkling & pigmentation.
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Bitot's spots
 Raised, silvery white,
foamy, triangular patch of
keratinised epithelium.
 Usually bilateral and
temporal aspect.
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Corneal xerosis
Earliest change is
punctate keratopathy
followed by haziness
and/or granular pebbly
dryness
Lower nasal quadrant
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keratomalacia
 Stromal defects occurs due to
colliquative necrosis
 Small ulcers occurs
peripherally
 Circular, steep margins & are
sharply demarcated
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Corneal scars
Healing of stromal
defects results in
corneal scars of
different densities &
sizes which may or
may not cover the
pupilarry area.
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Xerophthalmic fundus
Seed like, raised, whitish lesions scattered
uniformly over part of fundus at level of optic
disc
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SKIN CHANGES
Dry, lustureless appearance occurs
Phrynoderma results: occurs due to plugging of
hair follicles by keratotic plugs ,
which consist of keratinised epithelium
projecting outwards from follicles.
Skin -> scaly & toad like.
Seen on outer side of legs, buttocks, elbow &
back of forearm
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phr ynoder ma
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RESPIRATORY TRACT: squamous metaplasia of
respiratory mucosa & ciliary damage
GASTROINTESTINAL SYSTEM: reccurent
diarrhoea
REPRODUCTIVE SYSTEM: atrophy of germinal
epithelium
GROWTH: retardation occurs
IMMUNOLOGICAL SYSTEM: decreased immune
response
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TREATMENT
LOCAL OCULAR THERAPHY VITAMIN A
Artificial tears Oral administration is
(0.7% hydroxypropyl methyl recommended
cellulose or 0.3 %
hypromellose) In case of side effects, IM
• Should be instilled every 3-4 injections of water miscible
hours preparations prefered
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Above
age of 1
year
Under
age of 1
year
Women
of
reprodu
ctive
age
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PROPHYLAXIS
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SHORT TERM
APPROACH
Infants 6-12 months old & any older 1,oo,ooo IU orally every 3-6 months
children who weigh less than 8 kg
Children over 1 yr & under 6 yrs of age 2,00,000 IU every 6 months
Lactating mothers 20,000 IU at delivery
Infants less than 6 months not being 50,000 IU orally- should be given
breast fed before they attain 6 months of age
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A revised schedule being followed in india since 1992,
under the programme named as “CHILD SURVIVAL
AND SAFE MOTHERHOOD” is as follows
AT 9 MONTHS OF AGE
FIRST DOSE (1 LAKH IU) ALONG WITH MEASLES
VACCINE
AT 18 MONTHS OF AGE
SECOND DOSE(2 LAKH ALONG WITH BOOSTER
IU) DOSE OF DPT/OPV
THIRD DOSE(2 LAKH IU) AT 2 YEARS OF AGE
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MEDIUM TERM APPROACH:
food fortification with vitamin A
• LONG TERM APPROACH:
promotion of adequate intake of
vit A rich foods.
nutritional health education
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HYPERVITAMINOSIS A:
ACUTE TOXICITY CHRONIC TOXICITY
Headache & dizziness  Anorexia
 Dry skin
Nausea
 Pruritis
Vomiting  Sparse hair
Abdominal pain  Bone pain
 Weight loss
Pseudotumour cerebri{bulging
anterior fontanel}  Benign intracranial
hypertension
 hepatosplenomegaly
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VITAMIN D
it is also called SUNSHINE VITAMIN.
it is available in 2 forms
D3 – cholecalciferol
D2 - ergocalciferol
Cholecalciferol (vitamin D3)
is made from 7-dehydrocholesterol in the skin of
animals and humans.
Ergocalciferol - D2
obtained artificially by irradiation of ergo- sterol
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chemical origins of vitamin D
 Precursors of vitamin D are found in both yeast and animal tissues.
 In yeast, a sterol precursor (ergosterol) is converted to vitamin D2
(ergocalciferol).
 In the dermal tissue of animals, the precursor is 7-dehydrocholesterol which
is converted first to a pre-vitamin D3, then to vitamin D3 (cholecalciferol).
 Vitamin D2 and vitamin D3 are both converted to similar active compounds
(calcidiol and calcitriol) in the liver and kidney.
 D2 and D3 are sometimes referred to as vitamers.
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Dietary Sources of Vitamin D
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DAILY REQUIRMENT
Men and women-100 IU
Pregnancy and lactation – 400IU
Infants & Children –200IU
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Vitamin-D Production and
Metabolism
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Press F5 to view as a
slide show.
skin
7-dehydrocholesterol
D3 (Cholecalciferol)
blood
DBP-D3 DBP (vit. D binding protein)
Ca++ transport Ca++ resorption
(intestine) (bone)
D3
liver
kidney
25-OH D3 1, 25-OH D3 (active)
(calcidiol) (calcitriol)
25-OH D3
DBP-calcidiol
24, 25-OH D3 (inactive)
(tight binding) 56

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FUNCTIONS
 Calcium Balance
 Cell Differentiation
 Immunity
 Blood Pressure Regulation

 Development of Bones & Teeth
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Endocrine, paracrine and intracrine
functions of Vitamin D

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vitamin D - deficiency
 RICKETS  Children's
OSTEOMALACIA  Adults
 Increase the risk of Osteoporosis
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Rickets
 Rickets derived from the old English word for "twist," or "wrick,“
 Rickets is caused by a deficiency in vitamin D.
 During growth, human bone is made and maintained by the interaction of
calcium, phosphorus, and vitamin D. Calcium is deposited in immature
bone (osteoid) in a process called calcification, which transforms immature
bone into its mature and familiar form.
 In order to absorb and use the calcium available in food, the body needs
vitamin D. In rickets, the lack of this important vitamin leads to low
calcium, poor calcification, and deformed bones.
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DEFICIENCY
RICKETS
Frontal & Parietal Bossing
Pigeon Chest
Prominence of sternum
Harrison’s groove
Bow Legs
Soft & fragile bones
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X-ray in rickets
Knock knee deformity Bowleg deformity Wrist enlargement Scoliosis
Rib beading Harrison's sulcus
(rachitic rosary and pot belly Chest deformity Frontal bossing
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Osteomalacia
 it is also known as adult rickets
 Flat bones and diaphysis of long bones are affected
it is most commonly seen in post menopause female
with history of low dietary calcium intake.
The majority of patient have bone pain &muscle
weakness..
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Oral manifestation
 Teeth – developmental abnormalities of dentine & enamel.
 Caries – higher risk of caries
 Enamel – there may be hypoplasia, may be mottled, yellow
gray in color
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MANAGEMENT
Dietary enrichment of vitamin D in the form of milk
Curative treatment includes 2000 to 4000 IU of
calcium daily for 6 to 12 weeks.
osteomalacia due to intestinal malabsorption require
larger dose of vitamin D & calcium i.e.
40,000 to 1,00,000 IU of vitamin
D
15 to 20 gms of calcium lactate .
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Before treatment After treatment
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HYPERVITAMINOSIS D
Anorexia, nausea & vomiting
Constipation
Hypertension
Drowsiness, irritability & hypotonia
Polyuria & polydipsia
Renal damage
Hyperkalaemia
CLOUDING OF
CORNEA
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TREATMENT
Decrease the intake of vitamin d
Oral aluminium hydroxide
Cortisone
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Tocopherol or vitamin E
 It is also called anti-aging factor.
 The word tocopherol is derived from the word toco meaning
child birth and pheros meaning to bear.
 It is yellow oily liquid freely soluble in fat solvent.
 Tocopherol alpha,beta,gamma,lambda have been obtained
from the natural sources
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SOURCES
EGG, FISH, BUTTER ,LIVER
Palm oil
 Nuts
 sunflower
 sunflower seeds
 corn  green leafy
 soybean vegetables
 olive  whole grain
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DAILY RECOMMENDED DOSE
 men - 8 – 10mg
 women – 5- 8mg
 Children – 8.3mg

 Infants – 4- 5mg
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ABSORPTION ,STORAGE, EXCRETION
ABSORPTION
 small intestine
 it is incorporated into
lipoproteins [VLDL & LDL] &
transported through the blood
stream via the lymph.
STORAGE  liver & fatty
tissue
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FUNCTIONS
 REPRODUCTIVE FUNCTION
it has got protective effect on reproduction and
prevention of sterility.
 BLOOD FLOW AND CLOTTING MECHANISM
it dilates the capillaries & enables the blood to
flow freely.
 ELECTRON TRANSPORT SYSTEM -
it functions as co factor in electron transport system
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Protects liver from being damaged by toxic compounds
such as carbon tetrachloride.
Prevents the oxidation of vitamin A and carotenes.
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DEFICIENCY
 REPRODUCTIVE – abortion of fetus in females & atrophy
of spermatogenic structure in males leading to permanent
sterility.
 HEART - there is necrosis & fibrosis of heart muscle.
 BLOOD CAPILLARIES – may lead to degenerative changes
in the blood capillaries
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ORAL MANIFESTATION –
 loss of pigmentation ,
 atrophic degenerative changes in enamel
OCULAR MANIFESTATION
PTOSIS, OPHTHALMOPLEGIA AND PIGMENTED
RETINOPATHY
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MANAGEMENT –
vitamin E is given in the doses of
100 to 400mg.
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VITAMIN K (PHYLOQUINONE)
 It is essential for production prothrombin & other factor
involve in blood clotting mechanism.
 Hence it is known as anti – hemorrhagic vitamin.
 it is also known as PHYLOQUINONE
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Forms
 It is available in 3 forms - NAPHTHOQUINONE
 K1 – it is the form occurs in
plant origin.
 K2 –is synthesized by
intestinal bacteria.
 K3 - synthetic form
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Source
MILK
MEAT
FISH
SPINACH
CABBAGE
CAULIFLOWER
SOYA BEAN
WHEAT GERM
CARROTS
POTATOES
TOMATOES
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DAILY REQUIRMENT
 men and women – 70 – 140 mcg.
 children – 35 – 75mcg
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ABSORPTION ,STORAGE, EXCRETION
 ABSORPTION small
intestine
 STORAGE  liver
adipose tissue
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FUNCTIONS
 it is essential for the hepatic synthesis of coagulation factor II,
V, VII, IX, X.
 CLOTTING – it prevents hemorrhage only in cases when
there is defective production of prothrombin
Serves as a essential cofactor in carboxylation of glutamic
acid residues in vit k dependent proteins
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DEFICIENCY
Causes
Decrease
synthesis of
factor 2,7,9,10 Increase clotting time
After antibacterial Prolong bleeding
therapy,
Surgical operations-
Cholecystectomy Hemorrhagic
Conditions like
Malabsorption conditions
Obstructive
jaundice
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SYMPTOMS OF VIT K DEFICIENCY
Bruising from bleeding into the skin
Nose bleeds
Bleeding gums
Bleeding in stomach
Blood in stool
Black tarry stool
Extremly heavy menstrual bleeding
Intracranial bleeding
NEWBORNS: . HEMORRHAGIC DISEASE OF
NEWBORN
. HYPOPROTHROMBINEMIA
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MANAGEMENT
Vit k can be given orally
In case of someone who improperly absorbs fat or at
risk of excessive bleeding, can be given im
In case of associated liver disorder, vit k is
insufficient , blood transfusion may be neccesary
All newborns are recommended to give vit k IM to
prevent intracranial bleed after delivery
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