LMP301H1 Lecture Notes - Lecture 15: Bone Pain, Autocrine Signalling, Hypocalcaemia
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14 Sep 2016
School
Department
Course
Professor
LMP301
Introduction to the Biochemistry of Human Disease
Lecture 15 – Calcium
Homeostasis
o Net gain at intestine = net loss at kidney (150 mg/d)
o No net change at bone formation/resorption (500 mg/d)
Hormones
o PTH
Produced by the parathyroid glands behind the thyroid
Stimulated by low serum Ca2+ and inhibited by high Ca2+
Bone: ↑ bone resorption
Kidney: ↑ Ca2+ reabsorption, ↓ PO4- reabsorption
Stimulate 1,25 (OH)2 vitD
o 1,25 (OH)2 vitD
Plants: from vitD2; Animals: from vitD3
ProvitD3 vitD3 25-OH D3 1,25(OH)2D3 (active)
Side products: 24,25(OH)2D3 and 1,24,25(OH)3D3 (inactive)
1st step: UV
2nd step: 25-hydroxylase (liver)
3rd step: 1α-hydroxylase (kidney, pancreas, etc.)
Inactivation: 24-hydroxylase
Autocrine: regulation of cell growth
Paracrine: immune modulation
Endocrine: calcium homeostasis, muscle and bone health
Intestine: ↑ Ca2+ and PO4- absorption
Bone: ↑ bone resorption
Feedback: inhibit PTH
Bound to vitD-binding protein in circulation and targets nuclear vitD
receptor
o Calcitonin
From the parafollicular/C cells of the thyroid
Stimulated by high Ca2+, gastrin, and pentagastrin
Inhibit bone resorption by osteoclasts and ↓ Ca2+ and PO4- (clinically
insignificant)
Treatment of osteoporosis
Marker of medullary thyroid carcinoma (C cells)
Bone
o Osteoclasts (resorption) and osteoblasts (formation)
Resorption markers: deoxypyridinoline
Formation markers: alkaline phosphatase, osteocalcin
Diseases
Name
Causes
Characteristics
Diagnosis
Treatments
Hypocalcemia
Idiopathic
Post-surgical
Pseudohypoparathyroidism
Neuro-
hyperexcitability
(tetany,
↓ serum Ca2+