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3. 3
it is also called SUNSHINE VITAMIN.
it is available in 2 forms
D3 – cholecalciferol
D2 - calciferol

4. 4

5. Cholecalciferol (vitamin D3)
is made from 7-dehydrocholesterol in the skin
of animals and humans.
calciferol - D2
obtained artificially by irradiation of ergo-
sterol and is called ergocalciferol

6. It is a steroid hormone.
Biologically active form
is Calcitriol
SOURCES
 Fish liver oil
 Egg yolk
 Milk
 Butter
 Cheese
 Margarine
RDA: 100 IU/day in adults
pregnancy, lactation, infant and children ( 220 IU)

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 Sunshine
 Fish liver oils
 Oily fish
 Margarine

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 The kidney, as well as liver further
converts this precursor into 1,25-
hydroxyvitamin D, the most
physiological active vitamin-D
metabolite, which is also called
calcitrol.

12.  Traditionally, calcitrol is understood as a
hormone that, together with parathyroid
hormone, regulates blood calcium levels and,
in turn, bone density.,
 calcitrol targets the intestine, where it
promotes calcium absorption; and bone, where
it catalyzes calcium deposition.

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 Sunlight causes an opening of the sterol ring
structure, leading to formation of pre-vitamin
D3. A slow process (1-2 days) converts pre-
vitamin D3 to cholecalciferol. Daily exposure
to sunshine is not necessary.

14.  Continued exposure to sunshine causes the
reversible formation of inactive
components. There can be no
overproduction (hence no toxicity) of
naturally-produced cholecalciferol since any
excess is converted to these inactive
compounds.

15.  Ability to form cholecalciferol depends
upon availability in skin of 7-
dehydrocholesterol. Although this
molecule is generally plentiful in skin,
reduction with aging can diminish
cholecalciferol production, necessitating
vitamin D supplementation in the elderly.

16.  Since vitamin D from foods is transported to
the liver in chylomicrons. All free vitamin D
metabolites are transported in the blood, as
D-binding protein (DBP). In the mitochorndria
of the renal proximal tubular cells, 1,25-
(OH)2-D reaches its target organs through
the bloodstream where it circulates bound to
proteins.

17.  Hydroxylation in the liver at C25 yields
the intermediate 25-hydroxy-
cholecalciferol. This is transformed into
the active form of the vitamin by
further hydroxylation at C1 to 1,25-
dihydroxy-cholecalciferol (1,25-(OH)2-
D-3), a steroid hormone. Additionally, a
multitude of synthetic vitamin D
analogues exist that are used for the
treatment of disturbances in a Ca

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 Precursors of vitamin D are found in both
yeast and animal tissues. In yeast, a sterol
precursor (ergosterol) is converted to vitamin
D2 (ergocalciferol). Ergocalciferol is the
compound most commonly found as the
additive to fortify milk.

21.  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.

22.  circulating calcitrol enters cells and
complexes with the genes in the cell nucleus.
 This affects DNA expression and, in turn,
overall cell functioning and growth.
 Because calcitrol maintains normal cell
proliferation, it inhibits cancerous growth.

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 In addition, calcitrol influences immune-
cell activity, helping to explain vitamin
D’s seemingly beneficial role in
infectious disease and immune-related
disorders, such as multiple sclerosis,
rheumatoid arthritis, and diabetes.

24.  How is vitamin D transported and
stored?
This depends upon the source of the vitamin D.
Vitamin D that is taken into the gut (vitamin D-
containing foods or nutritional supplements) are
absorbed by intestinal mucosal cells in the
duodenum and jejunum and packaged, along
with dietary fat, into lipoproteins called
chylomicrons (CM).

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 These CM are first put into the lymph, then
deposited into the blood stream. The CM carry
the vitamin to the liver or adipose for storage
and eventual use.
 Vitamin D synthesized in skin through the
action of sunlight is bound to a blood protein
called (vitamin) D binding protein (DBP),
which transports it to the liver.

27. 1. Vitamin-D promotes absorption of Ca++
and P by the intestine. It stimulates
the synthesis of a specific Ca++
binding protein by intestinal
epithelium.

28. 1. Vitamin-D induces the synthesis of
specific Ca++
binding protein in
bones
2. Vitamin-D regulates the Ca++
level by
reabsorbing Ca++
through the kidney

29. 4. Vitamin-D promotes mineralization of
bones through deposition of Ca++
and
P in growing bones.
5. Vitamin-D increases the reabsorption
of PO4 through renal tubules.

30. 4. Vitamin-D acts as coenzyme for
alkaline phosphatase
5. Vitamin-D is responsible for
enameling of the teeth. Its
deficiency leads to irregular and
rough teeth

31. 8. Vitamin-D promotes growth in general
and is essential for normal health.
BMR is decreased in vitamin-D
deficiency. The deficiency of vitamin-
D leads to the repeated attacks of
respiratory diseases.

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 Men and women- 0.01 mg.
 Pregnancy and lactation – 0.01 mg
 Infants & Children –0.01 mg

34. DEFICIENCY
Rickets
Osteomalacia

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 Rickets was once considered an extremely
common disorder of childhood. The term
itself is derived from the old English word
for "twist,”

37.  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.

38.  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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Bow Legs
Frontal & Parietal Bossing
Pigeon Chest
Soft & fragile bones
Prominence of sternum
DEFICIENCY
RICKETS
Harrison’s groove

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Frontal bossing
Harrison's sulcus
and pot belly

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Rib beading
rickety rosary
Bowleg deformity

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ScoliosisWrist enlargement

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Knock knee deformity
Wrist enlargement
Rib beading
(rachitic rosary
Harrison's sulcus
and pot belly Chest deformity Frontal bossing
Scoliosis
X-ray in rickets

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Rickets can be caused by lack of
sunlight, but also from
insufficient calcium. Vitamin D
linked to calcium absorption.

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Osteomalacia
 it is also known as adult rickets and 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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 Teeth – developmental abnormalities of
dentine & enamel.
 Caries – higher risk of caries
 Enamel – there may be hypoplasia of enamel,
may be mottled, yellow gray in color
 Pulp – high pulp horns, large pulp chamber,
delayed closure of root apices

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 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.
 Patient with 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

55. Effects are mainly due to hypercalcaemia
IMMEDIATE DELAYED
Anorexia Urinary lithiasis. Thirst
Metastatic calcification Lassitude
Constipation
Polyuria

56. Toxicity:
 Malaise, drowsiness, nausea, abdominal
pain, thirst, constipation and loss of
appetite.
 Long term effect – ectopic calcification
anywhere in the body, renal damage,
renal calculi.
 Prolonged use in infants can cause
mental and physical retardation, kidney
failure and death.

57.  Dangerous to exceed 10,000
units daily vit D in an adult more
than 12 weeks.
 Vit D supplements should be
avoided in individuals especially
infants and children.
 Should not exceed 400 units a
day.