2. Vitamin D is a
group of fat-soluble
prohormones.
Two
major forms of
which are vitamin D 2
(or ergocalciferol)
and vitamin D 3 (or
cholecalciferol).
Production is greatest in the
stratum basale and stratum Produced in skin
spinosum . exposed to sunlight,
specifically
3. Functions of Vitamin D
Regulates the calcium and phosphorus levels
in the blood by promoting their absorption
from food in the intestines.
Promotes bone formation and
mineralization .
Inhibits parathyroid hormone secretion
from the parathyroid gland.
Affects the immune system by promoting
immunosuppression, phagocytosis, and
anti-tumor activity
4. Dietary sources of
vitamin-D
Fortified foods especially
dairy products, cereals and
vit. Supplements.
Fish, liver, oils, egg yolk &
butter.
Infants: obtain vit D
supplement from mothers
milk, infant formulas, cow
milk .
5. Why Vitamin D deficiency
occurs?
Due to:-
Inadequate sunlight exposure.
Poor access to micronutrients rich
food.
Disorder that limit its absorption.
Deficient soil quality.
Impaired conversion into active
metabolites.
Possible role of dietary fibers.
6. These lead to:-
Learning disability
Impaired work capacity.
Increased susceptibility to infection
7. Deficiency causes:-
In children :-
RICKETS:- Bone softening diz., deformity
of long bones occur.
In adults :-
OSTEOMALACIA :- Bone thinning
disorder,proximal
muscle weakness & bone fragility.
OSTEOPOROSIS:-Decrease bone
minerilzation & inc. Bone fragility.
8. RICKETS:-
Rickets is characterized by
bone deformities
due to incomplete
mineralization, resulting
in soft & pliable bones and
delay in teeth
formation.
The weight bearing bones
are bent to form bow
legs
9. Risk factors
Breast-fed infants whose mothers are
not exposed to sunlight .
Breast-fed infants who are not exposed to
sunlight .
Lactose intolerant.
Individuals with red hair have a decreased
risk for rickets due to their greater
production of vitamin D in sunlight.
10. Pathogenesis of Rickets
Appears to develop in 3 stages:-
1 st stage Absence of adequate stores
In supply of 1,25 dihydroxy vit D
Intestinal absorption of Ca & P
Release of parathyroid hormone
1,25 (OH)2 vit D3
25(OH) vit D (in kidney)
Absorption of Ca & P Mobilization of Ca & P
from bone
12. 3 rd stage:-
Relative hyperparathyroidism
Depleted 25(OH) vit D
Impaired production of
Adequate quantity of 1,25(OH)2 vit D3
Intestinal absorption of Ca & P
13. Signs and Symptoms
Bone pain or tenderness.
muscle weakness ( rickety
myopathy or "floppy baby
syndrome")
syndrome
Increased tendency for
fractures (easily broken
bones), especially
greenstick fractures
Hypocalcemia
Tetany
Craniotabes (soft skull)
Skeletal deformity:Cranial,
spinal, and pelvic
14. Bowed legs (genu varum) Costochondral swelling
( "rickety rosary" or "rachitic
rosary")
Knock-knees (genu valgum) or
"windswept knees. Harison’s sulcus and pot belly
16. Treatment:-
Natural & artificial light are effective
therapeutically but oral administration
preferred.
Administration of 15,000ugm or 6,00,000
IU of vit.D 3 orally or I.M. induces rapid
healing.
If healing lines of rickets is not seen on x-
ray plate of bone within 3-4 weeks of
therapy, the above dose may be repeated .
Cases who respond to this therapy are further
put on 400 units or 10ugm of vitamin D 3 per
17. Requirement
Body needs are met entirely by
conversion of 7 dehydrocholesterol to
vit D 3 in skin
Or
in absence of exposure to UV light,
it can be met entirely by ingestion
of Vit D
The recommended dietary intake for
vit D by infants has been accepted
as 200IU/day
and children 400IU/day
18. Hypervitaminosis – D
Signs & symptoms - similar to idiopathic
hypercalcemia.
Symptoms include:-
Hypotonia, anorexia, irritability,
constipation,
polyuria, pallor
Aortic stenosis, vomiting
Hypertension
Retinopathy
Urine shows proteinuria
Metastatic calcification as revealed by x-
rays
Generalized osteoporosis
T/t includes discontinuation of vit D &
19. References :-
Essential Pediatrics by O . P . Ghai
Textbook of Preventive & social medicine by K .
Park
www.mc.vanderbilt.edu
