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Rickets and Metabolic Bone Diseases PowerPoint Presentation

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Description : Check out this medical titled "Rickets & Metabolic Bone Diseases".

This medical talks about rickets, a condition that affects bone development in children, resulting in weak and brittle bones. It is caused by a deficiency in vitamin D, calcium, or phosphorus, which are essential for proper bone growth. Rickets can also occur in adults, known as osteomalacia, which is also caused by a deficiency in vitamin D, calcium, or phosphorus.

Metabolic bone diseases are a group of disorders that affect the bones, such as osteoporosis, osteogenesis imperfecta, and Pagets disease. These diseases affect bone formation, remodeling, or resorption, leading to a decrease in bone mass and density. Osteoporosis is the most common metabolic bone disease and is characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to bone fragility and an increased risk of fractures.

The management of rickets and metabolic bone diseases typically involves addressing the underlying cause and providing adequate nutrition, supplementation, and physical activity. Treatment may also involve medications, such as bisphosphonates, calcitonin, and hormone replacement therapy, to improve bone health and prevent fractures. In severe cases, surgery may be necessary to correct bone deformities or fractures. Regular monitoring and follow-up are essential to ensure the effectiveness of treatment and prevent complications.

Tags : rickets, bone development in children, brittle bones, deficiency in vitamin D, deficiency in calcium, deficiency in phosphorus, Metabolic bone diseases are a group of disorders that affect the bones, osteoporosis, osteogenesis imperfecta, Pagets disease, endocrinology, endocrinology

Published on : Apr 21, 2023 | Views : 1919 | Downloads : 6

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Rickets & Metabolic Bone Diseases
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Physiology Calcium Phosphate PTH Vitamin D Calcitonin
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Calcium > 99% in bone Muscle and nerve function Clotting mechanisms Free plasma Ca = Bound plasma Ca Active transport absorption in the duodenum and passive diffusion in the jejunum 98% reabsorption in the kidney
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Calcium Requirement 600 mg/day in children 1300 mg/day in adolescents and young adults 750 mg/day in adults 1500 mg/day in pregnant women 2000 mg/day in lactating women 1500 mg/day in postmenopausal women and patients with fractures
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Phosphate Key component of bone mineral Enzyme systems and molecular interactions 85% in bone Plasma Phosphate is mostly unbound 1000-1500 mg/day
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Brinker, M. R. (2000). Basic sciences. In M. D. Miller & M. R. Brinker (Eds.), Review of orthopaedics (pp. 1-40). Saunders, Philadelphia
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Vitamin D metabolism
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Secondary role Other Hormones - Estrogen - Corticosteroids - Thyroxin Non-hormonal Factors - Mechanical stress - Prostaglandin E - Acid-base balance
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Rickets
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Introduction 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.
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Causes of Rickets 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 deficiency Low 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
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Causes of Rickets RENAL LOSSES X-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 DISTAL RENAL TUBULAR ACIDOSIS
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Clinical features of Rickets 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
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Extra skeletal findings in Rickets 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.
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Diagnostic approach to suspected rickets
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Diagnostic approach to hypocalcimic rickets
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Diagnostic approach to hypophosphatemic rickets
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Biochemical findings in rickets
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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.
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Treatment of 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.
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Other Metabolic Bone Diseases
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*Primary hyperplasia - adenoma - carcinoma *Secondary persistent hypocalcaemia *Tertiary secondary leads to hyperplasia Hyperparathyroidism
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Pathology - PTH overproduction - Increased renal tubular absorption , intestinal absorption and bone resorption of Ca - Hypercalcaemia and hypercalciuria - Suppressed phosphate tubular reabsorption - Hypophosphataemia and hyperphosphaturia Hyperparathyroidism
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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 Hyperparathyroidism
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Symptoms & Signs *Hypercalcaemia anorexia , nausea , depression and polyuria *Bone rarefaction pain , pathological fractures and deformities *Biochemistry hypercalcaemia , hypophosphataemia , high alk. Phosphatase and serum PTH Hyperparathyroidism
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X-rays - Subperiosteal bone resorption - Generalized decrease in bone density - Brown tumors - Chondrocalcinosis knee , wrist and shoulder Hyperparathyroidism
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Treatment Surgical excision of adenoma or hyperplastic parathyroid tissue Hungry bone syndrome Treated by vitamin D Hyperparathyroidism
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* Normal mineralization * Decrease bone mass (amount of bone per unit volume) * Age related * Associated or manifestation of other conditions Osteoporosis
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Causes * Idiopathic * Nutritional * Endocrine disorders * Drug induced * Malignant diseases * Miscellaneous Osteoporosis
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- 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 Osteoporosis
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Symptoms & Signs - Bony aches - Easy fractures spine - lower radius - femoral neck - Rib fracture , chest pain - Normal biochemistry Osteoporosis
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X-rays - Decrease bone density - Wedging or biconcave vertebrae - Thin cortex and deformities - Dexa Scan - Biopsy Osteoporosis
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Treatment - Treat underlying cause - Idiopathic , extremely difficult - Calcium and vitamin D - Fluoride and triple therapy - Calcitonin , Diphosphonate - Treat fractures Osteoporosis
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Prevention * Good diet * Exercise * Exposure to sun light * Ca supplement * Hormone therapy Osteoporosis
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Renal Osteodystrophy Diminished renal P excretion Increased Ca excretion Impaired synthesis of Vit D Toxicity e.g. Aluminum and amyloidosis
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Brinker, M. R. (2000). Basic sciences. In M. D. Miller & M. R. Brinker (Eds.), Review of orthopaedics (pp. 1-40). Saunders, Philadelphia
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Thank You