Rickets is a disease of growing bone caused by unmineralized bone matrix at the growth plates, occurring only in children before fusion of the epiphyses. It is caused by vitamin D disorders, calcium deficiency, renal losses, or phosphorous deficiency. Clinical features include failure to thrive, bowed legs, widened wrists and ankles, and bone pain. X-rays show widened growth plates and fraying and cupping of the metaphysis. Treatment involves high dose vitamin D and calcium supplementation.
INTRODUCTION â Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. ⢠Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus ď growth plate cartilage accumulates and the growth plate thickens. ⢠In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. ⢠In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
achondroplasia is genetic disorder that results in dwarfism
problem is not in forming cartilage but in converting it to bone.
This disorder usually results in the following: An average-size trunk; Short arms and legs, with particularly short upper arms and upper legs; Short fingers.
Mutation in FGFR3 on chromosome 4 is responsible for achondroplasia.
INTRODUCTION â Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. ⢠Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus ď growth plate cartilage accumulates and the growth plate thickens. ⢠In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. ⢠In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
achondroplasia is genetic disorder that results in dwarfism
problem is not in forming cartilage but in converting it to bone.
This disorder usually results in the following: An average-size trunk; Short arms and legs, with particularly short upper arms and upper legs; Short fingers.
Mutation in FGFR3 on chromosome 4 is responsible for achondroplasia.
Vitamin D deficiency remains the most common cause of Osteomalacia & rickets.
My first presentation prepared by me as a first year family medicine board resident. đ
Rickets and osteomalacia presentation for postgarduate in orthopaedics(2) (1...SumitKumar108462
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its about bones dealing with rickets and osteomalacia. useful for postgraduate student in orthopaedics . for presentation in cme. useful information for exam writting. can be used as notes. its a classic presentaion on bone softening dealing with pathophysiology , feon basics to types of rickets and osteomalsia .
should go through before exam. jkdscjkas njbsjkfbsjkf
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9. PHEX gene mutationď increases FGF-23ď inhibition of ph. reabsorb in PT
- FGF 23 -mutation
- DMP1 and EMPP1 ď increase FGF 23
- mutations in the gene encoding a chloride channel that is expressed in the kidney
- dysfunction of the renal proximal tubule
rare complication
polyostotic fibrous dysplasia, hyperpigmented macules, and polyendocrinopathy
11. HEAD
⢠Craniotabes â
- softening of the cranial bones
- can be detected by applying pressure at the occiput or over the
parietal bones. The sensation is similar to the feel of pressing into a
ping-pong ball and then releasing.
- Craniotabes may also be secondary to osteogenesis imperfecta,
hydrocephalus, and syphilis.
- It is a normal finding in many newborns, especially near the suture
lines, but it typically disappears within a few months of birth
12. HEAD
⢠Frontal and parietal bossing- box like appearance of head- hot cross
bun appearance or caput quadratum
⢠Delayed fontanel closure- anterior fontanelle remains wide open and
its closure is delayed
⢠Delayed dentition & caries
⢠Craniosynostosis
13. CHEST
Rachitic rosary
⢠Widening of the costochondral
junctions
⢠Feels like the beads of a rosary as
the examinerâs fingers move along
the costochondral junctions from
rib to rib
⢠Smooth angle
( Sharp angle in scurvy)
14. CHEST
⢠Harrison groove
- horizontal depression along the lower anterior chest
- occurs from pulling of the softened ribs by the diaphragm during
inspiration
23. History
⢠Dietary history
⢠Drug intake â
- Anticonvulsants phenobarbital and phenytoin, increase degradation
of vitamin D,
- aluminum-containing antacids interfere with the absorption of
phosphate
24. ⢠A history of renal disease (proteinuria, hematuria, urinary tract
infections)
⢠Polyuria can occur in children with chronic kidney disease or Fanconi
syndrome
⢠Fat malabsorption is often associated with diarrhea or oily stools
⢠Alopecia suggests vitamin Dâdependent rickets type 2.
25.
26. Xray findings
⢠Thickening of the growth plate
⢠Physis- Widening
⢠Metaphysis- Cupping and Fraying
⢠Rarefaction â decreased density and trabecula is prominent.
Healing rickets â provisional zone of calcification
Between shaft and epiphysis
27. Labs
⢠Serum phosphate â Decreased
⢠Serum calcium â normal or decreased
⢠Serum alkaline phosphatase - increased
29. Treatment
⢠Stoss therapy, 300,000-600,000 IU of vitamin D are administered
orally or intramuscularly as 2-4 doses over 1 day.
⢠The alternative is daily, high-dose vitamin D, with doses ranging from
2,000-5,000 IU/day over 4-6 wk.
⢠Either strategy should be followed by daily vitamin D intake of 400
IU/day if 1 yr old.
30. ⢠Rickets in infancy is characterised by the following except : ( AIIMS
May 2007)
a) Craniotabes
b) Rachitic rosary
c) Wide open fontanelles
d) Bow legs
31. NEET â pedia mcq
2.True regarding nutritional rickets is:
a)Decreased cortical bone
b)Decreased calcification of mature bone
c)Decreased calcification of growing bone
d) Decreased production of steroid
32. NEET
3) Basic pathology in rickets-
a)Defective bone matrix formation
b)Defect in mineralization
c)A defect in osteoid formation
d) All of the above
33. NEET
4) Enlarged tender epiphysis with bowing of long bones and xray
evidence of delayed carpal ossification suggest the diagnosis
a) Scurvy
b) Infantile rickets
c) Syphilis
d) Osteogenesis imperfecta
34. NEET
5) Which statement is untrue in renal rickets?
a) Results from renal insufficiency in infancy
b) Is due to deficient phosphorus excretion
c) Manifests itself by marked dwarfism
d) Causes no deformity at puberty
e) Ends fatally from uraemia at puberty
35. Renal rickets
⢠CKD + Hyperphosphatemia + secondary hyperparathyroidism
⢠Clinically â growth retardation
⢠Lower limb more involved than upper limb
⢠Rx â Diet low in phosphorus
⢠Dialysis
⢠High dose of calcitriol
36. NEET
⢠6) A 4 yr old rachitic child developed genu varum. The best line of Rx
is by â
a) Antirachitic treatment
b) Repeated moulding
c) Corrective splints
d) Tibial osteotomy
37. 7) 13 yr old boy presented for consultation bcoz his knees tend to knock
together & he tends to fall during running. Examination â Separation of
medial malleoli by 3 inches when standing with knee in contact with
each other and feet directed forwards. The correct diagnosis is?
A) Coxa vara
B) Genu valgum
C) Genu varum
D) Ctev
E) Bilateral flat foot
38. 8) Inheritance of vitamin D dependent rickets is
a) AD
b) AR
c) X linked recessive
d) X linked dominant
39. 9) Features of rickets â
a) Marfan sign
b) Laryngismus stridulus
c) Tackle deformity
d) None of the above
e) All of the above
40. ⢠10) True statements about rickets-
a) Hypotonia occurs due to hypocalcaemia
b) Green stick fractures can occur
c) Short stature
d) All of the above
e) None of the above