00:00 / 00:00
Osteomalacia and rickets
0 / 19 complete
0 / 4 complete
in osteomalacia/rickets p. 473
osteomalacia/rickets p. 473
Fanconi syndrome p. 719
hypophosphatemic p. 617, 617
inheritance p. 57
lab values in p. 474
vitamin D deficiency p. 68
osteomalacia/rickets p. 473, 473
Inadequate bone mineralization could be due to a deficient or impaired metabolism of vitamin D, phosphate or calcium.
And the metaphysis contains the epiphyseal plate, or the growth plate, which is the part of the bone that grows during childhood.
Once growth stops, the growth plate is replaced by an epiphyseal line, and this is known as epiphyseal closure.
Now, for bones to grow and develop properly, special bone cells, called osteoblasts, are hard at work.
To build bone, osteoblasts secrete osteoid, which is an organic matrix made of type 1 collagen.
These collagen fibers are the framework for the osteoblasts' work.
Osteoblasts then deposit calcium and phosphate crystals into the framework.
This process is called bone mineralization, and it confers strength to the growing bones.
Bone mineralization is dependent on an enzyme called alkaline phosphatase - which increases in response to osteoblast activity.
So, at the end of the day, bones are like a storage warehouse for calcium and phosphate.
Rickets and osteomalacia are conditions characterized by bone softening due to a calcium deficiency or lack of vitamin D. The main difference between the two is the age at which they occur. Osteomalacia affects adults, whereas rickets affects children.
The key symptoms are diffuse bone and joint pain, proximal muscle weakness, bone fragility, and increased risk of fractures with minimal trauma. For rickets, there may also be craniotabes( softening and thinning of skull bones). The treatment typically involves vitamin D supplementation and treating the underlying cause.
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