Download Free Medical Rickets and Metabolic Bone Diseases PowerPoint Presentation

Rickets and Metabolic Bone Diseases PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

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

This medical PowerPoint presentation is about rickets and metabolic bone diseases, a group of disorders that affect the bones, resulting in weakened bones and increased risk of fractures. Rickets is a childhood disorder that results from a deficiency of vitamin D, calcium, or phosphorus, which can lead to soft and weak bones. In contrast, metabolic bone diseases are a group of disorders that affect the bone metabolism, including osteoporosis, osteomalacia, and Pagets disease.

Osteoporosis is a condition that causes bones to become thin and fragile, leading to an increased risk of fractures. Osteomalacia is a disorder in which bones become soft and weak due to a deficiency of vitamin D or a problem with vitamin D metabolism. Pagets disease is a disorder that results in abnormal bone growth and remodeling, leading to weakened and deformed bones.

Treatment for rickets and metabolic bone diseases often involves addressing the underlying cause of the disorder. This may include supplementation with vitamin D, calcium, or phosphorus, as well as medications to prevent bone loss or promote bone growth. In some cases, surgery may be necessary to correct bone deformities or fractures. Prevention measures include ensuring an adequate intake of vitamin D and calcium, regular exercise, and avoidance of smoking and excessive alcohol consumption.

Tags : Rickets, Metabolic Bone Diseases, risk of fractures, bone metabolism, osteoporosis, osteomalacia, Pagets disease, Orthopaedic Surgery, Orthopaedic Surgery PowerPoint presentation

Published on : Jun 23, 2023 | Views : 1544 | Downloads : 2

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Rickets & Metabolic Bone Diseases
Slide 2-

Physiology Calcium Phosphate PTH Vitamin D Calcitonin
Slide 3-

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
Slide 4-

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
Slide 5-

Phosphate Key component of bone mineral Enzyme systems and molecular interactions 85% in bone Plasma Phosphate is mostly unbound 1000-1500 mg/day
Slide 6-

Brinker, M. R. (2000). Basic sciences. In M. D. Miller & M. R. Brinker (Eds.), Review of orthopaedics (pp. 1-40). Saunders, Philadelphia
Slide 7-

Vitamin D metabolism
Slide 8-

Secondary role Other Hormones - Estrogen - Corticosteroids - Thyroxin Non-hormonal Factors - Mechanical stress - Prostaglandin E - Acid-base balance
Slide 9-

Rickets
Slide 10-

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.
Slide 11-

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
Slide 12-

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
Slide 13-

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
Slide 14-

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.
Slide 15-

ppt slide no 15 content not found
Slide 16-

ppt slide no 16 content not found
Slide 17-

ppt slide no 17 content not found
Slide 18-

ppt slide no 18 content not found
Slide 19-

ppt slide no 19 content not found
Slide 20-

ppt slide no 20 content not found
Slide 21-

Diagnostic approach to suspected rickets
Slide 22-

Diagnostic approach to hypocalcimic rickets
Slide 23-

Diagnostic approach to hypophosphatemic rickets
Slide 24-

Biochemical findings in rickets
Slide 25-

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.
Slide 26-

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.
Slide 27-

Other Metabolic Bone Diseases
Slide 28-

ppt slide no 28 content not found
Slide 29-

ppt slide no 29 content not found
Slide 30-

*Primary hyperplasia - adenoma - carcinoma *Secondary persistent hypocalcaemia *Tertiary secondary leads to hyperplasia Hyperparathyroidism
Slide 31-

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
Slide 32-

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
Slide 33-

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
Slide 34-

ppt slide no 34 content not found
Slide 35-

X-rays - Subperiosteal bone resorption - Generalized decrease in bone density - Brown tumors - Chondrocalcinosis knee , wrist and shoulder Hyperparathyroidism
Slide 36-

ppt slide no 36 content not found
Slide 37-

ppt slide no 37 content not found
Slide 38-

ppt slide no 38 content not found
Slide 39-

ppt slide no 39 content not found
Slide 40-

ppt slide no 40 content not found
Slide 41-

ppt slide no 41 content not found
Slide 42-

Treatment Surgical excision of adenoma or hyperplastic parathyroid tissue Hungry bone syndrome Treated by vitamin D Hyperparathyroidism
Slide 43-

* Normal mineralization * Decrease bone mass (amount of bone per unit volume) * Age related * Associated or manifestation of other conditions Osteoporosis
Slide 44-

Causes * Idiopathic * Nutritional * Endocrine disorders * Drug induced * Malignant diseases * Miscellaneous Osteoporosis
Slide 45-

ppt slide no 45 content not found
Slide 46-

- 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
Slide 47-

Symptoms & Signs - Bony aches - Easy fractures spine - lower radius - femoral neck - Rib fracture , chest pain - Normal biochemistry Osteoporosis
Slide 48-

ppt slide no 48 content not found
Slide 49-

X-rays - Decrease bone density - Wedging or biconcave vertebrae - Thin cortex and deformities - Dexa Scan - Biopsy Osteoporosis
Slide 50-

ppt slide no 50 content not found
Slide 51-

ppt slide no 51 content not found
Slide 52-

ppt slide no 52 content not found
Slide 53-

ppt slide no 53 content not found
Slide 54-

ppt slide no 54 content not found
Slide 55-

ppt slide no 55 content not found
Slide 56-

Treatment - Treat underlying cause - Idiopathic , extremely difficult - Calcium and vitamin D - Fluoride and triple therapy - Calcitonin , Diphosphonate - Treat fractures Osteoporosis
Slide 57-

ppt slide no 57 content not found
Slide 58-

Prevention * Good diet * Exercise * Exposure to sun light * Ca supplement * Hormone therapy Osteoporosis
Slide 59-

Renal Osteodystrophy Diminished renal P excretion Increased Ca excretion Impaired synthesis of Vit D Toxicity e.g. Aluminum and amyloidosis
Slide 60-

Brinker, M. R. (2000). Basic sciences. In M. D. Miller & M. R. Brinker (Eds.), Review of orthopaedics (pp. 1-40). Saunders, Philadelphia
Slide 61-

Thank You