9. Action of calcitriol on the
intestine
•Increases the intestinal absorption
of calcium and phosphate
•By increased synthesis of calcium
binding protein
10. Action of calcitriol on the bone
• Mineralization of bone at low doses
• Mobilization of calcium from bone at high doses
11. Action of calcitriol on the
kidney
•Increased reabsorption of
calcium and phosphorus
•Decreased excretion of calcium
and phosphorus
14. Vitamin D resistant rickets (hypophosphatemic rickets)
Vitamin D dependent rickets (type I) D defeciency
Vitamin D dependent rickets (type II) D resistance
Rickets classification
16. CLINICAL FEATURES OF RICKET
GENERAL
Listlessness
Protruding Abdomen,UMBILICAL HERNIA
hypotonia of abdominal wall muscles
Muscle Weakness(specially proximal)
Fractures
29. VITAMIN D DEFICIENCY
ETIOLOGY
• Most commonly occur in infancy due to
poor intake and inadequate cutaneous
synthesis
• Formula fed infants- receive adequate vit
D even without cutaneous synthesis
• Breast fed infants rely on cutaneous
synthesis or vitamin d supplements
30. Cutaneous synthesis is limited
due to
Ineffectiveness of winter sun
Avoidance of sunlight
Decreased cutaneous
synthesis due to increased
skin pigmentation
31. LABORATORY FINDINGS
• Hypocalcemia – variable finding due to action of
↑PTH
• Hypophosphatemia- due to PTH induced renal
loss of phosphate and decreased intestinal
absorption
• 1,25D level-N,↑,↓- secondary to up regulation
of renal 1 α hydroxylase due to
hypophosphatemia and hyperparathyroidism
• Some patients have Metabolic acidosis
secondary to PTH induced renal bicarbonate
wasting
• Generalized aminoaciduria
32. MANAGEMENT OF VITAMIN D
DEFICIENCY
• Should receive Vitamin D and adequate
nutritional intake of calcium and phosphorus
• STROSS THERAPY- 3-6 Lakh IU of Vitamin D
oral/IM as 2-4 doses over 1 day
0R
Daily High dose Vitamin D 2000-5000 IU/day
over 4-6 weeks
or
Daily Vitamin D intake of 400 IU/day
33. Hypervitaminosis D
It may occur due to chronic ingestion of
large doses or due to increased
sensitivity of tissues to vitamin D.
Hypercalcaemia,weakness,fatigue,vomiti
ng,diarrhoea,renal stones,hypertension.
Even coma may occur.
39. In rickets seen
Increased ALP
Decreased ALP
Decreased phosphate in blood
Increased phosphate in blood
hyperphosphaturia
40. A 2yr old boy has vitamin D resistant rickets his investigation revealed
serum ca+9mg/dl, PO42.4mg%, ALP 1041iu/L ,normal PTH .Bicarbona
22meq/l (22-28)
which of the following is most probable diagnosis
Distal renal tubular acidosis
Hypophosphatemic rickets
Vitamin D dependent rickets
hypoparathyroidism
42. A 2yr old boy has vitamin d refracrory rickets
investigations shows serum calcium 9mg/dl
phosphate 2.4mg/dl (3-4.5mg/dl)ALP 1040 IU/L
(30-120iu/l).PTH & bicarbonate levels are normal
.most probable diagnosis is
distal renal tubular acidosis
Hypophosphatemic rickets
Vit D dependent rickets
Proximal renal tubular acidosis
43. True about nutritional rickets
Craniotabes
Widening of wrists
Growth retardation
Decreased phosphate in serum
Multiple fractures
44.
45. Rickets in infants present as all
except
Craniotabes
Widened fontanelle
Rachitic rosary
Bow legs
46. All of the following are seen in rickets except
Bow legs
Gun stock deformity
Pot belly
craniotabes
47.
48. Most common cause of genu valgum is
Osteoarthritis
Rickets
Pagets disease
Rheumatoid arthritis
50. True about vit d deficiency rickets
Vit d3 given at a dose of 50-100mg/day
X ray knee joint is diagnostic
Rickety rosary is tender
Increased chances of respiratory tract infections
hyponatremia
51. 6lac IU /15000ug / 15mg-------------every 2weekly
Healing started
400IU10ug every day
4-6 weeks 50-150mg/dl
2000-5000 IU / 50-126ug / 0.5-2mg /day
52. hypophosphatemic rickets is characterised by
Increased forehead sweating
Charecteristically Decreased calcium
Anterior fontanelle widened
Increased ALP