Osteomalacia and rickets
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Osteomalacia and rickets
Pathology
Pediatric musculoskeletal conditions
Radial head subluxation (Nursemaid elbow)
Developmental dysplasia of the hip
Legg-Calve-Perthes disease
Slipped capital femoral epiphysis
Transient synovitis
Osgood-Schlatter disease (traction apophysitis)
Musculoskeletal injuries and trauma
Rotator cuff tear
Dislocated shoulder
Radial head subluxation (Nursemaid elbow)
Winged scapula
Thoracic outlet syndrome
Carpal tunnel syndrome
Ulnar claw
Erb-Duchenne palsy
Klumpke paralysis
Iliotibial band syndrome
Unhappy triad
Anterior cruciate ligament injury
Patellar tendon rupture
Meniscus tear
Patellofemoral pain syndrome
Sprained ankle
Achilles tendon rupture
Spondylolysis
Spondylolisthesis
Degenerative disc disease
Spinal disc herniation
Sciatica
Compartment syndrome
Rhabdomyolysis
Bone disorders
Osteogenesis imperfecta
Craniosynostosis
Pectus excavatum
Arthrogryposis
Genu valgum
Genu varum
Pigeon toe
Flat feet
Club foot
Cleidocranial dysplasia
Achondroplasia
Osteomyelitis
Bone tumors
Osteochondroma
Chondrosarcoma
Osteoporosis
Osteomalacia and rickets
Osteopetrosis
Paget disease of bone
Osteosclerosis
Lordosis, kyphosis, and scoliosis
Joint disorders
Osteoarthritis
Spondylosis
Spinal stenosis
Rheumatoid arthritis
Juvenile idiopathic arthritis
Gout
Calcium pyrophosphate deposition disease (pseudogout)
Psoriatic arthritis
Ankylosing spondylitis
Reactive arthritis
Spondylitis
Septic arthritis
Bursitis
Baker cyst
Muscular disorders
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Polymyositis
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Inclusion body myopathy
Polymyalgia rheumatica
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Other autoimmune disorders
Sjogren syndrome
Systemic lupus erythematosus
Mixed connective tissue disease
Antiphospholipid syndrome
Raynaud phenomenon
Scleroderma
Limited systemic sclerosis (CREST syndrome)
Musculoskeletal system pathology review
Back pain: Pathology review
Rheumatoid arthritis and osteoarthritis: Pathology review
Seronegative and septic arthritis: Pathology review
Gout and pseudogout: Pathology review
Systemic lupus erythematosus (SLE): Pathology review
Scleroderma: Pathology review
Sjogren syndrome: Pathology review
Bone disorders: Pathology review
Bone tumors: Pathology review
Myalgias and myositis: Pathology review
Neuromuscular junction disorders: Pathology review
Muscular dystrophies and mitochondrial myopathies: Pathology review
Pediatric musculoskeletal disorders: Pathology review
Assessments
Osteomalacia and rickets
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High Yield Notes
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Osteomalacia and rickets
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USMLE® Step 1 style questions USMLE
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Which of the following set of laboratory findings will be most likely present in this patient?
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Calcium
in osteomalacia/rickets p. 473
Hypophosphatemic rickets p. 57
Osteomalacia/rickets p. 473
Parathyroid hormone (PTH) p. 336
osteomalacia/rickets p. 473
Rachitic rosary p. 473
Rickets p. 473
Fanconi syndrome p. 719
hypophosphatemic p. 617, 617
inheritance p. 57
lab values in p. 474
vitamin D deficiency p. 68
Vitamin D deficiency p. 350
osteomalacia/rickets p. 473, 473
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Transcript
Content Reviewers
Bone softening caused by a faulty process of bone mineralization manifests as either rickets in children or osteomalacia in adults.
Inadequate bone mineralization could be due to a deficient or impaired metabolism of vitamin D, phosphate or calcium.
But first, a bit about bones. Now, long bones, like the femur, are made up of two epiphyses, which are its ends, and the diaphysis, which is the shaft.
Between each epiphysis and the diaphysis, there’s a region called the metaphysis.
And the metaphysis contains the epiphyseal plate, or the growth plate, which is the part of the bone that grows during childhood.
Once growth stops, the growth plate is replaced by an epiphyseal line, and this is known as epiphyseal closure.
Now, for bones to grow and develop properly, special bone cells, called osteoblasts, are hard at work.
To build bone, osteoblasts secrete osteoid, which is an organic matrix made of type 1 collagen.
These collagen fibers are the framework for the osteoblasts' work.
Osteoblasts then deposit calcium and phosphate crystals into the framework.
This process is called bone mineralization, and it confers strength to the growing bones.
Bone mineralization is dependent on an enzyme called alkaline phosphatase - which increases in response to osteoblast activity.
So, at the end of the day, bones are like a storage warehouse for calcium and phosphate.
Now, the levels of calcium and phosphate in the bone, but also in the blood, are regulated by vitamin D and parathyroid hormone, or PTH.
Vitamin D-wise, two steps are necessary for optimal metabolism: first, there must be enough vitamin D in the body, either from food, or created in the skin in response to sunlight exposure.
Summary
Rickets and osteomalacia are conditions characterized by bone softening due to a calcium deficiency or lack of vitamin D. The main difference between the two is the age at which they occur. Osteomalacia affects adults, whereas rickets affects children.
The key symptoms are diffuse bone and joint pain, proximal muscle weakness, bone fragility, and increased risk of fractures with minimal trauma. For rickets, there may also be craniotabes( softening and thinning of skull bones). The treatment typically involves vitamin D supplementation and treating the underlying cause.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
- "The Developmental Basis of Skeletal Cell Differentiation and the Molecular Basis of Major Skeletal Defects" Biological Reviews (2008)
- "Triradiate deformity of the pelvis in Paget's disease of bone." Postgraduate Medical Journal (1980)
- "Vitamin D supplementation in pregnancy: a systematic review" Health Technology Assessment (2014)
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