Plenaries Are Ace

Aren't they?

Monday, January 08, 2007

The Grandmother's Fall CPC

8.1.07

Vitamin D
• Sources:
-From 7-dehydrocholesterol in skin.
§Up to 80% requirements → D3.
-From diet (D2).
§Fish, plants etc.
§Fortified.
• Metabolism:
-Converted to 25(OH)D in liver.
-Then to 1,25(OH)2D in kidney.
-Renal feedback control of 1,25 form to maintain both:
§Itself.
§Ca2+ and PO43- levels.
• Functions:
-More like steroid hormone:
§Absorption of calcium and phosphorus.
§If Ca2+ low, works with parathyroid hormone to increase release.
§Normally required for mineralisation of bones.
§Renal resorption of Ca2+ (?exact mechanism).
§? Differentiation of osteoclasts.

Osteomalacia
• Blood test.
-Reduced Ca2+.
-Mildly reduced PO43-.
-Raised alkaline phosphatase.
• X-ray.
-Bone rarefaction.
-Looser's zones (linear rarefaction) in femoral cortex.

Osteoporosis
• Average 0.7% bone loss per year (normal).
• Peak bone mass.
• Physical activity.
• Ageing effects on osteoblasts.
• Genetic factors (vitamin D receptor affinity).
• Hormonal environment.

Paget's disease of bone
• Blood tests.
-FBC normal for age.
-Marked rise in alkaline phosphatase.
• Features.

Osteopetrosis
• Marble bone disease.
• Inherited osteoclast defect.
• Brittle bones even though dense and heavy.
-Autosomal recessive malignant type.
§Fatal early in life.
-Dominant benign form.
§Fractures in adolescence.

Healing of bone
• Fracture → haemorrhage.
-Inflammation.
-Necrosis locally.
-Granulation tissue - small blood vessels growing into necrosed tissue.
• Provisional callus.
-Woven bone with cartilage islands.
• External callus.
• Remodelling.
-Possible sources of failure.

Sadly, no notes for the second plenary due to sodding comm skills.

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