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Calcium Phosphate PTH Vitamin D Calcitonin.

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  • CalciumPhosphatePTHVitamin DCalcitonin

  • > 99% in boneMuscle and nerve functionClotting mechanismsFree plasma Ca = Bound plasma CaActive transport absorption in the duodenum and passive diffusion in the jejunum98% reabsorption in the kidney

  • 600 mg/day in children1300 mg/day in adolescents and young adults750 mg/day in adults1500 mg/day in pregnant women2000 mg/day in lactating women1500 mg/day in postmenopausal women and patients with fractures

  • Key component of bone mineralEnzyme systems and molecular interactions85% in bonePlasma Phosphate is mostly unbound1000-1500 mg/day

  • Vitamin D metabolism

  • Secondary roleOther Hormones- Estrogen- Corticosteroids- Thyroxin

    Non-hormonal Factors- Mechanical stress- Prostaglandin E- Acid-base balance

  • Normal bone growth & mineralization require adequate availability of calcium & phosphate.

    Deficient mineralization can result in rickets and/or osteomalacia.

    Rickets refers to the changes caused by deficient mineralization at the growth plate.

    Osteomalacia refers to impaired mineralization of the bone matrix.

    Rickets & osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.

  • Vitamin D disorders Nutritional vitamin D deficiency; Congenital vitamin D deficiency; Secondary vitamin D deficiency;Malabsorption;Increased degradation;Decreased liver 25-hydroxylase; Vitamin D-dependent rickets type 1; Vitamin D-dependent rickets type 2; Chronic renal failure.

    Calcium deficiencyLow intake,Calcium deficient Diet,Premature infants (rickets of prematurity), Malabsorption,Dietary inhibitors of calcium absorption

    Phosphorus deficiency Inadequate intake,Premature infants (rickets of prematurity),Aluminum-containing antacids

  • RENAL LOSSESX-linked hypophosphatemic rickets; Autosomal dominant hypophosphatemic rickets; Hereditary hypophosphatemic rickets with hypercalciuria; Overproduction of phosphatonin(Tumor-induced rickets,McCune-Albright syndrome,Epidermal nevus syndrome,Neurofibromatosis), Fanconi syndrome, Dent disease


  • GENERAL Failure to thrive; Listlessness; Protuding abdomen; Muscle weakness (especially proximal); Fractures.

    HEAD Craniotabes; Frontal bossing; Delayed fontanelle closure; Delayed dentition; caries; Craniosynostosis

    CHEST Rachitic rosary; Harrison groove; Respiratory infections and atelectasis

    BACK Scoliosis ,Kyphosis ,Lordosis

    EXTREMITIES Enlargement of wrists and ankles; Valgus or varus deformities Windswept deformity (combination of valgus deformity of 1 leg with varus deformity of the other leg); Anterior bowing of the tibia and femur; Coxa vara; Leg pain.

    HYPOCALCEMIC SYMPTOMS Tetany ; Seizures; Stridor due to laryngeal spasm

  • Extraskeletal manifestation of rickets vary depending upon the mineral deficiency.

    Hypoplasia of the dental enamel is typical for hypocalcemic rickets, whereas abscesses of the teeth occur more often in phosphopenic rickets.

    Hypocalcemic seizures, decreased muscle tone leading to delayed motor milestones, recurrent infections, increased sweating.

  • Diagnostic approach to suspected rickets

  • Diagnostic approach to hypocalcimic rickets

  • Diagnostic approach to hypophosphatemic rickets

  • Biochemical findings in rickets

  • Alkaline phosphatase usually is in all forms of rickets.

    Serum phosphorus concentrations usually are in both hypocalcemic and hypophosphatemic rickets.

    Serum Ca is only in hypocalcemic rickets.

    Serum parathyroid hormone typically is in hypocalcemic rickets, in contrast it is N in hypophosphatemic rickets.

    25-OH vitamin D reflect the amount of vitamin D stored in the body, and is in vit D deficiency.

    1,25-OH2 vitamin D can be, N or in hypocalcemic rickets and usually is N or slightly in hypophosphatemic rickets.

  • Vitamin D. Stoss therapy: 300,000-600,000 IU orally or IM in 2-4 divided doses over one day.

    High dose vit D 2000-5000 IU orally for 4-6wks followed by 400 IU daily orally as maintenance.

    Adequate dietary Calcium & phosphorus provided by milk, formula & other dairy products.

    Symptomatic hypocalcaemia need IV Cacl as 20mg/kg or Ca gluconate as 100mg/kg as a bolus, followed by oral calcium tapered over 2-6 weeks.

  • *Primary hyperplasia - adenoma - carcinoma*Secondary persistent hypocalcaemia*Tertiary secondary leads to hyperplasia

  • Pathology- PTH overproduction- Increased renal tubular absorption , intestinal absorption and bone resorption of Ca- Hypercalcaemia and hypercalciuria- Suppressed phosphate tubular reabsorption- Hypophosphataemia and hyperphosphaturia

  • Pathology*Hypercalcaemia calcinosis , stone formation , recurrent infection and soft tissue calcification*Bone resorption loss of bone substance , subperiosteal erosion osteitis fibrosa cystica and brown tumors

  • Symptoms & Signs*Hypercalcaemia anorexia , nausea , depression and polyuria*Bone rarefaction pain , pathological fractures and deformities*Biochemistry hypercalcaemia , hypophosphataemia , high alk. Phosphatase and serum PTH

  • X-rays- Subperiosteal bone resorption- Generalized decrease in bone density- Brown tumors- Chondrocalcinosis knee , wrist and shoulder

  • TreatmentSurgical excision of adenoma or hyperplastic parathyroid tissueHungry bone syndromeTreated by vitamin D

  • * Normal mineralization* Decrease bone mass(amount of bone per unit volume)* Age related* Associated or manifestation of other conditions

  • Causes* Idiopathic* Nutritional* Endocrine disorders* Drug induced* Malignant diseases* Miscellaneous

  • - Idiopathic osteoporosis - normal investigations- In old patients we have to role out malignancy and multiple myeloma- Younger patients must be fully investigated- Several causes may be involved- Osteoporosis can be associated with osteomalacia

  • Symptoms & Signs- Bony aches- Easy fractures spine - lower radius - femoral neck- Rib fracture , chest pain- Normal biochemistry

  • X-rays- Decrease bone density- Wedging or biconcave vertebrae- Thin cortex and deformities- Dexa Scan- Biopsy

  • Treatment- Treat underlying cause- Idiopathic , extremely difficult- Calcium and vitamin D- Fluoride and triple therapy- Calcitonin , Diphosphonate- Treat fractures

  • Prevention* Good diet* Exercise* Exposure to sun light* Ca supplement* Hormone therapy

  • Diminished renal P excretionIncreased Ca excretionImpaired synthesis of Vit DToxicity e.g. Aluminum and amyloidosis

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