Bone deformities

Foals fed 29 or 250 mg Zn/kg diets had normal serum copper and zinc concentrations. Those fed 1000 or 2000 mg Zn/kg diet became hypocupremic in 5 to 6 weeks and developed lameness owing to cartilaginous disease similar to osteochondritis dessicous. Foals fed high zinc diets became lame when serum copper fell to 0.3 mg/L for >1 week at end of study arthritic foals had <0.2 mg copper/L serum. Serum zinc concentrations rose to >2 mg/L within 2 weeks at 1000 or 2000 mg Zn/kg diet liver zinc was <333 mg/kg DW at diets of <250 mg Zn/kg, 2728-3511 mg/kg DW at 1000 mg Zn/kg diet, and 4364-4524 mg/kg DW at the highest dietary loading of 2000 mg Zn/kg in 15 weeks Decreased growth, lameness, bone deformities, death. 

IV Mild-to-moderate bone deformity and variable short stature hearing loss occurs in some families ... 

Vitamin D is really a small family of closely related molecnles that prevent the bone disease rickets in children and osteomalacia in adnlts. In both cases, inadeqnate mineralization of bone results in bone deformation and weakness. Calcinm, Ca +, homeostasis is one goal of vitamin D activity, a goal it shares with parathyroid hormone and calcitonin. Calcium is intimately involved in bone mineralization and distnrbances of calcium levels in the blood can resnlt in inadeqnate bone mineralization or excessive calcification of other tissues. 

Other symptoms of 01 include blue sclerae, bone deformities, short stature (types III and IV only), and hearing loss. 

In poultry, manganese deficiency causes a different clinical picture when it affects the egg than when it affects the hatched bird In the case of the egg, the embryo become swollen and deformed, and their skeletons become defective and fragile [ chondrodystrophy"). Adult birds develop perosis (slipped tendon) which is an enlargement and malfunction of the libiiil metatarsal joint, followed hy slipping of the Achilles tendon from the condyles. The bone deformities seen in poultry also can be induced in mammals. 

II Lethal in the perinatal period minimal calvarial mineralization thin beaded ribs marked long bone deformity platyspondyly AD (new mutations) with parental mosaicism... 

IV Mild-to-moderate bone deformity variable short stature white or blue sclerae common dentinogenesis imperfecta hearing loss in some patients AD with parental mosaicism... 

The site and type of bone deformity seen in rickets depend on the age of the child. In a small infant, deformities of the forearms and anterior bowing of the distal tibias are more common. Clinical features such as craniotabes (areas of thinning and softening in the bones of the skull), hypotonia, and tetany are common in vitamin D-deficiency rickets, which occurs more frequently in infants 1 year old or younger. These features may be absent in calcium-deficiency rickets, which usually presents after the age of 1 year or after the child has been... 

Some hip bone deformities can be due to this problem and in some communities it is noticed that older Asian women now living in the UK have a pronounced roll in their walking and movement due to this deformity. For such communities a vitamin supplement is often suggested. 

An overstimulation of osteoclastic activity in bone, which increases release of calcium from the matrix into the bloodstream. Continuation of this process leads to bone deformities. 

Osteogenesis imperfecta also encompasses more than one disorder. At least four biochemically and chnically distingnishable maladies have been identified as osteogenesis imperfecta, aU of which are characterised by mnltiple fractures and resnltant bone deformities. 

Bone deformities (rickets) tetany (spasms of extremities). 

Fluorosis is a chronic public health problem in many parts of the world. Exposures to fluoride in concentrations greater that 1 ppm result in bone deformities, spinal compressions, and restricted movements of joints. These symptoms are easily prevented by decreasing exposure to fluoride. 

In children, bone deformities, soft flexible bones (rickets), and stunted growth result from calcium deficiency (or vitamin D or phosphorus deficiency). Early signs of adult deficiency are... 

Rickets was first reported in the mid-seventeenth century. It could be lethal, but bone deformation was more common. In the United States, rickets continued to be a problem into the 1930s until vitamin D-fortified milk became common. Older adults show bowlegs characteristic of childhood rickets. There were many attempts at giving calcium and/or phosphorous supplements. Finally, it was realized that rickets was not found in sunny climates, and populations whose main source of protein was fish did not have rickets. In 1924, Professor Henry Steenbock, University of Wisconsin, demonstrated that irradiation of foods, including milk, produced food that was antirachitic (16,17). 

Takeuchi, T., J. Dedi, Y. Haga, T. Seikai and T. Watanabe. Effect of vitamin A compounds on bone deformity in larval Japanese flounder (Paralichthys olivaceus). Aquaculture 169 155-165, 1998. 

Calcium Bone deformities, tetany Cataract gall stones atherosclerosis... 

Growth depression bone deformities pancreatic j3-cell degeneration. 

Osteomalacia is a deficiency disease. Insufficient vitamin D leads to low plasma calcium levels. This stimulates the secretion of PTH, which causes release of calcium from bone and failure to mineralize new bone. Characteristic bone deformities result in children and bone pain and tenderness in affected adults. Treatment is by vitamin D replacement. 

Dog 11 wk Gavage - not specif Musc/skel, nn-r w Bodansky et al. 1932 337 (Bone deformity and softening) NH4CL ... 

Osteogenesis Decrease in Type I Blue sclerae multiple fractures and bone deformities... 

Induced mutations in both choline kinase genes have been reported (Table 1). Targeted deletion of Chka results in embryonic lethality around day 4 (G. Wu, 2008). A natural mutation in choline kinase P was described in the rmd mouse that has hindlimb muscular dystrophy and neonatal bone deformity [6]. Although choline kinase P appears to be the major isoform in muscle, the levels of PC are only slightly decreased in the hindlimb muscles of rmd mice. 

The influence of high molybdenum concentrations in the ration can lead to bone deformities in cattle, sheep, rabbits, and rats. This skeletal damage occurs in ruminants in areas where molybdenosis is prevalent (Anke and Groppel 1987), but can also be produced experimentally. The reason for its occurrence is secondary Cu deficiency, which leads to such skeletal damage, as was shown in cattle. 

The middle-aged client with a pituitary tumor has enlarged viscera and bone deformities. Which medication would the nurse administer ... 

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