Resource Person:-Prof.Dr.A.K.Dutta
Presented by:- Prateek Singh
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
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
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 .
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.
These lead to:-
 Learning disability
 Impaired work capacity.
 Increased susceptibility to infection
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.
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
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.
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
 2 nd stage:-

                  Relative Hyperparathyroidism



                        Phosphaturia




                 Negative phosphorus balance




                      Hypophosphatemia
 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
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
 Bowed legs (genu varum)         Costochondral swelling
                                   ( "rickety rosary" or "rachitic
                                   rosary")




 Knock-knees (genu valgum) or
  "windswept knees.               Harison’s sulcus and pot belly
Diagnosis:
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
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
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 &
References :-
   Essential Pediatrics by O . P . Ghai

Textbook of Preventive & social medicine by K .
                      Park

     www.mc.vanderbilt.edu
THANK YOU

vitamin D deficiency

  • 1.
  • 2.
    Vitamin D isa 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 VitaminD 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 Ddeficiency 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:-  Inchildren :- 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
  • 11.
     2 ndstage:- Relative Hyperparathyroidism Phosphaturia Negative phosphorus balance Hypophosphatemia
  • 12.
     3 rdstage:- 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
  • 15.
  • 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 needsare 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
  • 20.