2. Sunlight as a source of vitamin D
Adequate supplies of
vitamin D3 can be
synthesized with sufficient
exposure to solar
ultraviolet B radiation
Melanin, clothing or
sunscreens that absorb
UVB will reduce cutaneous
production of vitamin D3
3.
4.
5. Rickets & Osteomalacia
These are different expression of the same disease.
Lack of available calcium and phosphorus ( or both) for
mineralization of newly formed osteoid .
Rickets-
– Occur in children
– only before fusion of epiphysis
– Leads to softening of bone & deformity
Osteomalacia- occur in adult
-softening of bone
6. Rickets & Osteomalacia
Etiology
Deficiency (vit – D or phosphate)
– Deficient intake in diet
– GI disease
Renal causes
– Vit – D resistent
– Vit –D dependent( type – I & II)
– Renal tubular acidosis
– CRF
Other -Chronic use of anticonvulsant drugs
-fibrous dysplasia and neurofibromatosis
-fibrous or connective tissue tumor
7. Normal bone growth
THERE ARE 4 ZONES :
1.ZONE OF RESTING CARTILAGE : 1 layer
2.ZONE OF PROLIFERATING CART. : 6 layers
3.zone OF PROVISIONAL CALCIFICATION "epiphyseal line " :
the cart. cells in this layer become mature, they contain alkaline phosphatase
release the phosphate in the matrix which already contains ca. & po4 in solution
increase production of ca. & po4 precipitation of ca.phosphate in the matrix
around the cartilage cells death of the cells.
4.ZONE OF BONE FORMATION :
The layer of prov. calc. is invaded by capillaries and osteoblast which deposit a layer of
organic bone matrix "osteoid tis.“ rapidly mineralized and the calcified cartilage
ultimately replaced by bone.
8.
9. PATHOLOGY
1. The mature cartilage cells will not die and the
proliferating zone will be formed of many layers and
invades the adjacent zone of of provis. calc.- irregularity
of epiphyseal line.
2. The prov. calc. zone and newly formed ost. tis. will fail to
calcify or will calcified irregularly.
wide irregular frayed zone of non rigid tis. " RACHITIC
METAPHSIS " is produced.
3. In the shaft the preformed bone is replaced by
uncalcified ost.
soft rarified cortical bone
bone deformities & green stick fractures.
10. Rickets
Disease of infancy &childhood
Dietary deficiency & GI disease are the common causes
Rare before 6 months
Commonly develop b/w 6 mth - 3yr
22. Rickets
Vit-D deficiency vit-D resistant
Acquired Inherited
Muscular weakness No muscular weakness
Normal growth rate Growth seldom become N
Serum Ph3 comes N Serum Ph3 never comes
with t/t normal
27. Rickets
Biochemical finding
Most specific test for vit–D deficiency is 25 vit–D
PTH is under -ve feedback of Calcium
● Decrease serum Ca = increase
PTH
Alkaline phosphatase increase in all cases of rickets and
osteomalacia
28. Rickets1) Biochemical finding
Category Serum
Calcium
Serum
Ph3
Serum
Alkaline
Ph3ase
PTH 25-HC 1, 25-
DHC
Tubular
Reabsrp.
Of Ph3
Urinary
calcium
Vit-D deficiency Low to
normal
Low High High Low Low Low low
Ph3 deficiency normal Low High normal normal normal High High
Gastrointestinal Low Low High High Low to
Normal
Low to
Normal
Low Low
Vit- D resistant
phosphoturia
Normal Low High Normal Normal Norma
l
Low Normal
Type-I dependent Low Low High High Normal Low Low low
Type –II vit-D
dependent
low low High High N- High N- High Low low
Renal tubular acidosis Low Low High High N –High N- High Low high
29.
30. Osteomalacia
Clinical feature
Insidious course
Pt may present with bone pain, backache and bone
tenderness
proximal muscle weakness
Fracture may be first sign of Osteomalacia
Vertebral collapse, kyphosis
31. Osteomalacia
Clinical feature
Long standing case sign of secondary hyperparathyroidism
●
Depression
●
Polyuria
●
Increased thirst
●
Constipation
●
Nephrolithiasis
●
?Peptic Ulcer Disease
37. Osteomalacia
Deferential diagnosis
1. Osteomalacia osteoporosis
Unwell well
Generalized chronic ache pain after #
Muscles weakness muscle normal
Looser’s zone absent
Ph3 decrease normal
Alk. Ph3ase increase normal
40. Rickets
Treatment
Depending on etiology, severity and metabolic
abnormality
In general the combination of Vit-D, Ca and phosphate
Orthopedic measure require in very less no. of cases
1 mg of vit-D = 40,000 IU
1 IU = 0.025 microgram
41. Rickets
Treatment
1. Vit-D deficiency state
Vit –D 300,000-600,000 IU
Im /Orally in a day (2-4dose)
Vit –D 2,000 – 5,000 I.U./day 4- 6 wk
Calcium --- 1g/ day
General nutrition , sunlight ?
Followed by
400 IU / day
42. Rickets
Treatment
2. Absorption defect
Vit- D 1,500 – 25,000 IU / day
Calcium 1 g/ day
Treatment of underling pathology; where appropriat, low
fat or gluten free diet
43. Rickets
Treatment
3. Vit – D resistant
Vit – D 20,000- 60,000 IU/day
Or dihydrotachysterol (dose 1/3 of vit D)
Neutral phosphate-1.5- 6 g/ day (4-5 dose)
Calcium – 1 g / day
45. Rickets
Treatment
5. Vit – Dependent type – II
Respond with high dose of
1, 25 Vit – D
1,000- 20,000 IU /day for 3-6 mth
Calcium - - 1-3 g / day
i/v Ca with oral
supplement
46. Evaluation of treatment
Serum and urinary Ca measurement
Most efficacious method to monitor t/t resolution of Vit –
D deficiency
Normal 24 hr urinary Ca excretion = 100 – 250 mg
When serum alkaline Ph3ase Inorganic phosphate
comes normal
– X- ray show sign of healing
47. Evaluation hazards
●
Serum Ca > 11mg/dl
●
Urinary Ca excretion > 250 mg / 24 hr
increase chance of
soft tissue calcification & nephrocalcinosis
49. Vitamin D Toxicity
Calcification of soft tissue
Lungs, heart, blood vessels
Hardening of arteries (calcification)
Hypercalcemia
Normal is ~ 10 mg/dl
Excess blood calcium leads to stone formation in
kidneys
Lack of appetite
Excessive thirst and urination