Secondary Hyperparathyroidism921107

Secondary Hyperparathyroidism921107 - Secondary...

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Secondary Hyperparathyroidism Chou Chien Wen M.D. Endocrine and Metabolism Section Chi-Mei Medical Center 7 Nov 2003
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Case Report Name: 許許 x Chart No: 14117599 Sex: female Age:6 Jan 1994 (49 y/o) Cause of Renal failure: Polycystic kidney Duration of HD: 5 yrs
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Clinical Course 88-6 89-8 90-7 91-7 92-7 92-10 Ca 10.3 11.7 10.7 11.6 11.4 11.9 P 5.9 4.9 9 6 5.1 5.8 i-PTH (12-72 pg/ml) 528 771.8 1111.5
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Medication History Before 92-6-30 FA 1# qd Vit BC 1# qd Calcium Carbonate 1# tid AH 2# tid EPREX 2000 IU/0.5 cc IM stat Lopid 1# tid for CH 237 TG 869 After then D C Calcium Carbonate
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Image Study Parathyroid echo 92-10-16 Parathyroid hyperplasia, both lower pole CT scan of neck 92-10-30 Bilateral parathyroid hyperplasia or adenoma, lower pole RT 1 cm; LT 0.6 cm
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Stage of Chronic Kidney Disease Stage Description GFR 1 Kidney damage with normal or increase GFR >= 90 2 Kidney damage with mild decrease GFR 60-89 3 Moderate decrease GFR 30-59 4 Severe decrease GFR 15-29 5 Kidney failure < 15 or dialysis
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Major Features of Abnormalities in Mineral Metabolism in Kidney Failure Hypoclacemia Secondary hyperparathyroidism Hyperphosphatemia Defective intestinal absorption of calcium Altered vitamin D metabolism Bone disease Soft-tissue calcification including coronary arteries and cardiac valves calcification Altered handling of phosphate, calcium and magnesium by the kidney Pruritus Proximal myopathy Skin ulceration and soft-tissue necrosis
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Three factors are central to its development The first, reduced renal synthesis of 1,25- dihydroxyvitamin D (calcitriol) As the disease progresses, renal phosphate clearance and net calcium balance become inadequate to maintain serum phosphorus and ionized calcium levels within an optimal range. The synthesis and release of PTH are stimulated by a low serum calcium level, reduced inhibitory activity of calcitriol, and an elevated serum phosphate level. progressive increase in the mass of the parathyroid gland and, often, a benign, tumor-like growth. In its extreme form, severe hyperparathyroidism becomes unresponsive to medical treatment, and necessitates parathyroidectomy
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Biological Consequences of Vitamin D Deficiency and its Metabolism Shift in set-point of calcium for the parathyroid gland Secondary hyperparathyroidism Skeletal resistance to the calcemic action of PTH Impaired mineralization of osteoid Abnormalities in formation and maturation of collagen
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