OSTEOMALACIA
Osteomalacia is a metabolic bone disease characterized by inadequate mineralization of bone. As a result of faulty mineralization,there is softening and weakening of the skeleton, causing pain,tenderness to touch, bowing of the bones, and pathologic fractures.
On physical examination, skeletal deformities (spinal kyphosis and bowed legs) give patients an unusual appearance and a waddling or limping gait. These patients may be uncomfortable with their appearance. As a result of calcium deficiency, muscle weakness,and unsteadiness, there is an increased risk for falls and fractures.
Pathophysiology of Osteomalacia
The primary defect in osteomalacia is a deficiency of activated vitamin D (calcitriol), which promotes calcium absorption from the gastrointestinal tract and facilitates mineralization of bone.
The supply of calcium and phosphate in the extracellular fluid is low. Without adequate vitamin D, calcium and phosphate are not moved to calcification sites in bones.
Osteomalacia may result from failed calcium absorption (eg, malabsorption syndrome) or from excessive loss of calcium celiac disease, chronic biliary tract obstruction, chronic pancreatitis, small bowel resection) in which fats are inadequately absorbed are likely to produce osteomalacia through loss of vitamin D (along with other fatsoluble vitamins) and calcium, the latter being excreted in the feces with fatty acids. In addition, liver and kidney diseases can produce a lack of vitamin D because these are the organs that convert vitamin D to its active form.
Severe renal insufficiency results in acidosis. The body uses available calcium to combat the acidosis, and PTH stimulates the release of skeletal calcium in an attempt to reestablish a physiologic pH. During this continual drain of skeletal calcium, bony fibrosis occurs and bony cysts form. Chronic glomerulonephritis,
obstructive uropathies, and heavy-metal poisoning result in a reduced serum phosphate level and demineralization of bone.
Hyperparathyroidism leads to skeletal decalcification and thus to osteomalacia by increasing phosphate excretion in the urine.
Prolonged use of antiseizure medication (eg, phenytoin, phenobarbital) poses a risk for osteomalacia, as does insufficient vitamin D (dietary, sunlight).
The malnutrition type of osteomalacia (deficiency in vitamin D often associated with poor intake of calcium) is a result of poverty,food faddism, and lack of knowledge about nutrition. It occurs most frequently in parts of the world where vitamin D is not added to food, where dietary deficiencies exist, and where sunlight is rare.
Osteomalacia is a metabolic bone disease characterized by inadequate mineralization of bone. As a result of faulty mineralization,there is softening and weakening of the skeleton, causing pain,tenderness to touch, bowing of the bones, and pathologic fractures.
On physical examination, skeletal deformities (spinal kyphosis and bowed legs) give patients an unusual appearance and a waddling or limping gait. These patients may be uncomfortable with their appearance. As a result of calcium deficiency, muscle weakness,and unsteadiness, there is an increased risk for falls and fractures.
Pathophysiology of Osteomalacia
The primary defect in osteomalacia is a deficiency of activated vitamin D (calcitriol), which promotes calcium absorption from the gastrointestinal tract and facilitates mineralization of bone.
The supply of calcium and phosphate in the extracellular fluid is low. Without adequate vitamin D, calcium and phosphate are not moved to calcification sites in bones.
Osteomalacia may result from failed calcium absorption (eg, malabsorption syndrome) or from excessive loss of calcium celiac disease, chronic biliary tract obstruction, chronic pancreatitis, small bowel resection) in which fats are inadequately absorbed are likely to produce osteomalacia through loss of vitamin D (along with other fatsoluble vitamins) and calcium, the latter being excreted in the feces with fatty acids. In addition, liver and kidney diseases can produce a lack of vitamin D because these are the organs that convert vitamin D to its active form.
Severe renal insufficiency results in acidosis. The body uses available calcium to combat the acidosis, and PTH stimulates the release of skeletal calcium in an attempt to reestablish a physiologic pH. During this continual drain of skeletal calcium, bony fibrosis occurs and bony cysts form. Chronic glomerulonephritis,
obstructive uropathies, and heavy-metal poisoning result in a reduced serum phosphate level and demineralization of bone.
Hyperparathyroidism leads to skeletal decalcification and thus to osteomalacia by increasing phosphate excretion in the urine.
Prolonged use of antiseizure medication (eg, phenytoin, phenobarbital) poses a risk for osteomalacia, as does insufficient vitamin D (dietary, sunlight).
The malnutrition type of osteomalacia (deficiency in vitamin D often associated with poor intake of calcium) is a result of poverty,food faddism, and lack of knowledge about nutrition. It occurs most frequently in parts of the world where vitamin D is not added to food, where dietary deficiencies exist, and where sunlight is rare.
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Unknown - Thursday 7 April 2011
