Vitamin D deficiency causes the bone disease rickets in children or osteomalacia in adults. It is characterized by skeletal abnormalities and soft, weak bones. Vitamin D is important for calcium absorption from the gut and deposition in bones. It is produced in the skin upon exposure to sunlight and undergoes conversions in the liver and kidney to become active. Deficiency can be caused by lack of vitamin D in diet, sunlight exposure, kidney/liver disorders, or genetic factors. Symptoms depend on age and severity but include bone deformities, fractures, and radiological changes like widened growth plates. Treatment involves daily high dose vitamin D and calcium supplements.

1. Vitamin D
Soumya Ranjan Parida
Basic B.Sc. Nursing 4th
year
Sum Nursing College

2. Rickets
 It is a syndrome of Vit-D deficiency
 It is characterised by various skeletal
abnormalities
 It is a disease of growing bones.

3. Vitamin D
Physiology
 Several compounds have vit-D activity but important
is vit-D3 (cholecalciferol)
 Exposure of skin to ultraviolet rays causes conversion
of 7-dehydrocholesterol to previt-D3
 Pre vit-D3 is converted by a nonezymatic process to
vit-D3
 vit-D3 is converted to 25-hydroxycholecalciferol in the
liver
 This 25-hydroxycholecalciferol is finally converted in
active form 1,25-dihydroxycholecalciferol in the kidney
& this step is controlled by parathormone

4. Functions of Vit-D
 Absorption of calcium from the gut.
 Deposition of cal phosphate in the prepratory
zone of calcification.
 Reabsorption of bones with excretion of
phosphate from the kidney along with
parathormone.

5. Biochemical changes
 In vitamin D deficiency, calcium levels in the blood
decrease because vitamin D is necessary for
absorption of this mineral.
 The level of parathyroid hormone, which increases
the calcium level in the blood, may increase as the
body tries to compensate for the vitamin D
deficiency.(feedback mechanism)
 Because not enough calcium and phosphate are
available to maintain healthy bones, vitamin D
deficiency may result in a bone softenning called
rickets in children or osteomalacia in adults.

6. Vitamin D deficiency can be caused by
 Lack of vitamin D in the diet
 By inadequate exposure to sunlight.
 A pregnant woman with vitamin D deficiency may develop
osteomalacia, and the newborn has a high risk of
developing rickets.
 People with kidney or liver disorders may be unable to
convert vitamin D into a usable form, they are at risk of
osteomalacia.
 Malabsorption disorders
 The use of certain anticonvulsants increase the risk of
vitamin D deficiency.
 Several rare hereditary forms of rickets develop because
the body cannot process (metabolize) vitamin D normally.

7. Clinical Features
Depends on :
 Age of child
 Severity of disease
 Underlying cause of deficiency

8.  Skull
-asymmetrical contours
-craniotabes
-widening of sutures
-persistence of ant & post fontanelle.
-frontal bossing
-caput quadratum or not cross-
bun skull.
 Thorax
-rachitic rosary
-asymmetrical flattening of one or other
hemithorax
-pectus carinatum
-harrisons groove

9.  Abdomen
-ricketic pot belly
 Spine
- ricketic cat back
-scoliosis &kyposis
 Extremities
-profound hypotonia
-limb may be deformed
-bow legs & knock knees
-widening of wrist, elbow,knee,ankle
joint -pathological fracture of long
bones

10. Radiological changes
X-ray wrist
 Widening of distal ends of radius and ulna
 Cupping and fraying of distal ends
 Increases distance b/w distal ends of forearm
bones & metacarpals
 Decreased bone density of shaft with
prominent trabecular pattern

11. Diagnosis
 The diagnosis of rickets or osteomalacia is
based on symptoms.
 Radiological- the appearance of bones on x-
rays
 Biochemical

12. Treatment
 involves taking daily vitamin D and calcium
supplements by mouth.
-Oral low dose -1500-5000 IU/d 6-12 weeks
f/b 400 IU/d
-Massive dose 6 lac IU oral or injection &
repeat in 3-4 weeks
 People with a chronic liver or kidney disorder
may require special formulations of vitamin D
supplements

13. VITAMIN D EXCESS
 Early symptoms are loss of appetite, nausea,
and vomiting, followed by excessive thirst,
weakness, nervousness, and high blood
pressure.
 Because the calcium level is high, calcium
may be deposited throughout the body,
particularly in the kidneys, blood vessels,
lungs, and heart.
 The kidneys may be permanently damaged
and malfunction

14.  Vitamin D excess is usually diagnosed when blood
tests detect a high calcium level in a person who
takes high doses of vitamin D.
 The diagnosis is confirmed by measuring the level
of vitamin D in the blood.
 Treatment consists of discontinuing vitamin D
supplements, following a low-calcium diet for a while
to offset the effects of a high calcium level in the
body, and taking drugs to suppress the release of
calcium from the bones.

15. Refractory rickets
 Develop rickets inspite of intake of vit-D
 Do not show evidence of healng rickets after
2 weeks of parentral therapy
 Causes
-Renal causes
-Malabsorbtion
-Hepatic dysfunction
-Miscellanous causes

16. Differential diagnosis
 Craniotabes-hydrocephalus
 Osteogenesis imperfecta
 Rosary-scurvy,chondrodystrophies

17. Complications
 Respiratory infections
 Pulmonary atelectesis
 Chronic GIT disturbances
 Anemia

18. Prevention
 Exposure to sunlight
 Oral administration of vit-D