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Vitamin-D
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Vitamin - D
(antirachitic vitamin)
BY
R.PARTHSARATHY
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Introduction
Vitamin D is a steroid.
It is present in animals, plants and yeast.
Insoluble in water, soluble in fat and organic
solutions.
Sensitive to oxygen, light and iodine.
Heating and mild acidity can convert into inactive
form.
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Chemical structure
MOST IMPORTANT FORM
It is considered as
prohormone.
BECAUSE
From which
1,25-dehydrocholesterol
synthesized. (active form)
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Sources
Liver and viscera of fish.
Liver of animals which feeds on fish.
Eggs, butter and milk.
But the cheapest is the sunlight.
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Functions
Vitamin D acts on organs such as bone, kidneys, intestinal
mucosa for regulation of calcium and phosphorus metabolism.
It promotes intestinal absorption of calcium and phosphorus.
It promotes bone resorption and calcium mobilization to
increase the levels of calcium and phosphorus.(PTH)
Mineralization of bone is promoted by 1,25-dihydroxy D3.
It is necessary for the development of bones and normal
growth of the body.
It also increases the citrate level of blood, bone, kidneys and
heart tissues.
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Daily requirements
Children and infants : 400IU/day
Adults : 200IU/day
Plasma concentration of 25-OH D3
Average 25-30 ng/mL
Range 8 - 60 ng/mL
Levels < 10 ng/mL indicative of deficiency
Levels > 150 ng/mL associated with toxicity
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Deficiency manifestations
Deficiency of vitamin D produces rickets in growing children
with characteristic defects in bone growth.
Deficiency of vitamin D in adults is called osteomalacia which
is characterized by
- poor intestinal absorption of calcium and phosphorus.
- rise in urinary phosphorous.
- negative calcium balance.
- muscular weakness and early fracture of bone.
- loss of calcium and bowed legs.
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Toxicity
Vitamin D is fat soluble, and accumulation (from diet) in
the body can be toxic.
The long-term safe dose of vitamin D is not known,
however, 10,000 IU /day is safe in healthy adults
All known cases of vitamin D toxicity have involved
intake of or over 40,000 IU/day.
The LD50 in man is unknown – there are no reported
deaths from acute toxicity.
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Hyper-vitaminosis
Excess of vitamin D causes toxicity characterized by
Nausea
Anorexia
Digestive disturbances and calculi formation.
Elfin facies
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Factors that influence
vitamin D status
Genetics
Vitamin D resistant rickets (hypophosphatemic rickets)
Vitamin D dependent rickets (type I)
Vitamin D dependent rickets (type II)
Drugs
Anticonvulsant drugs such as Diphenylhydatoin, phenobarbital
Alcohol
low 25(OH)D level
Age
Low epidermal con of 7-dehydrocholesterol
1-hydroxylase: less responsive to PTH
Sex