Osteomalacia Flashcards

1
Q

Pathophysiology of OM

A

a metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix (osteoid) following growth plate closure in adults.
Sequential hydroxylation of vitamin D is required to produce the metabolically active form of vitamin D. Hydroxylation occurs first in the liver and then in the kidneys and produces 1,25-dihydroxyvitamin D.

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1
Q

What is rickets / osteomalacia

A

a condition that affects bone development in children. It causes bone pain, poor growth and soft, weak bones that can lead to bone deformities.

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2
Q

RF of OM

A
  • suboptimal UV-B sunlight exposure and the use of sunscreen
  • insufficient dietary supplementation, and/or
  • the inability of the small intestine to absorb adequate amounts of dietary sources of vitamin D.
  • Old age
  • Fractures
  • Hypophosphatasia
  • Anticonvulsant therapy
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3
Q

Acquired factors that affect OM

A
  • Nutritional deficiencies: vitamin D, phosphorus, and calcium deficiency related to dietary deficiency, malabsorption, or lack of UV-B light exposure
  • Drug-induced: anticonvulsants
  • Renal osteodystrophy
  • Mineralisation inhibitors
  • Tumour-induced
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4
Q

How do anticonvulsants cause OM

A

increase the catabolism of vitamin D and reduce intestinal calcium absorption

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5
Q

How can CKD MBD cause OM

A

Hyperphosphataemia in chronic kidney disease-mineral bone disorder directly induces hypocalcaemia and decreases the efficacy of 1-alpha-hydroxylase in the kidney. This, in turn, decreases active vitamin D metabolites and thus the ability of the gut to absorb calcium. Subsequently, secondary hyperparathyroidism develops.

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6
Q

How can OM be tumour acquired

A

an acquired paraneoplastic syndrome of renal phosphate wasting that resembles genetic forms of hypophosphataemic rickets.

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7
Q

Symptoms of OM

A
  • Diffuse bone pain and tenderness
  • Fractures
  • Malabsorption syndromes
  • Proximal muscle weakness
  • Waddling gait.
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8
Q

PE for OM

A

The physical examination is remarkable for bone tenderness to percussion, poorly localised bony tenderness, and proximal muscle weakness. Pain in the hips may result in a waddling gait.

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9
Q

Ix for OM

A
  • Serum calcium - low
  • Serum 25-hydroxyvitaminD levels - low
  • Serum phosphate - low
  • Serum urea and creatinine - ratio is elevated.
  • Intact PTH - High
  • ALP - high except in those with hypophosphatasia
  • 24-hour urinary calcium - low
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10
Q

Definitive Ix for OM

A

Iliac crest biopsy using double tetracycline labelling is the definitive diagnostic test; however, due to the invasive nature, it is rarely performed.

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11
Q

Treatment OM

A

Calcium + Vit D - Ergocalciferol or cholecalciferol AND calcium carbonate or calcium citrate.

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12
Q

Lifestyle factors to treat OM

A

Ensuring adequate sunlight exposure and dietary intake of fortified foods containing vitamin D, calcium, and phosphorus may help avoid osteomalacia.

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13
Q

Ddx OM

A
  • Osteoporosis
  • Pagets
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14
Q

Difference between OM and OP on Xray

A

Indistinguishable

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15
Q

Monitoring of treatment of OM

A

A patient’s 25-hydroxyvitamin D levels should be checked approximately 2 to 3 months after initiating therapy. If undergoing long-term treatment, adults require ongoing annual monitoring for signs and symptoms of osteomalacia and over-treatment with vitamin D.

16
Q

Complications of OM

A

Fractures and fragility.