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Chapter Ⅵ . Calcium Homeostasis. PS Wang/2004.05. W.F.Ganong: Review of Medical Physiology 1983 12th Ed. Fig21-2 #1440. Remodeling of Bone. Bone Marrow or Fibrous Periosteum Mesenchymal Stem Cells Osteoclasts Bone Absorption Osteoblasts Bone Deposition (new bone) - PowerPoint PPT Presentation
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1
Chapter Ⅵ. Calcium Homeostasis
PS Wang/2004.
05
2W.F.Ganong: Review of Medical Physiology 1983 12th Ed. Fig21-2 #1440
3
Remodeling of Bone
Bone Marrow or Fibrous Periosteum
Mesenchymal Stem Cells
Osteoclasts Bone Absorption
Osteoblasts Bone Deposition(new bone)
Osteocytes
PS Wang/2004.0
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4Guyton & Hall : Textbook of Medical Physiology 10th ed.2000 fig.79-4 #365
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Mechanism of Bone Absorption1. Osteoclasts (lysosomes) proteolytic enzymes
organic matrix digest or dissolute
2. Osteoclasts acids (citric acid & lactic acid)
bone salts solution
3. Bone salts & collagen villi from
osteoclasts digestion
phagocytosis
PS Wang/2004.0
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6 M. Azria: The Calcitonins (Physiology and Pharmacology). 1989. fig.34a
7L.E. Mcdonald: Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-15 #38
8W.F. Ganong:Review of Medical Physiology 1983 12th Ed. #1439
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L.E. Mcdonald: Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #29
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10W.F. Ganong:Review of Medical Physiology 2003 20th Ed. fig.21-9 #187
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M. E. Hadley: Endocrinology 4th ed. 1996 fig.9.1 #1992
12W.F.Ganong: Review of Medical Physiology 2003 20th Ed. #188 fig.21-10
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Guyton & Hall : Textbook of Medical Physiology 10th ed.2000 fig.79-9
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Functional Cytology of the Parathyroid Gland
1. Chief cells---- secrete PTH
2. Oxyphil cells
(1) absent in many animals & in young human beings
(2) increase in numbers with advancing age
(3) probably age-chief cells
(4) poorly developed ER, Golgi apparatus, & secretory granules
3. Transitional oxyphil cells
PS Wang/2004.0
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Biological Effects of PTH1. blood [ Ca2+ ] ( absorption of Ca2+ & PO4
-3 from bone)
2. blood [ PO4-3 ] ( excretion of renal phosphate)
3. urine [ PO4-3 ] and urine [ Ca2+ ]
4. the rate of skeletal remodeling and the net rate of bone resorption
5. osteocytic osteolysis in bone (rapid effect) and the numbers and/or activation of osteoclasts on bone surface (slow phase)
6. urinary excretion of hydroxyproline-containing peptides7. activation of adenyl cyclase in target cells.8. formation of active vit. D metabolites by the kidney.
PS Wang/2004.0
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16M. E. Hadley: Endocrinology 2nd ed. 1988 fig.9.3 #1993
17
L.E. Mcdonald: Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-5 #32
18
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-6 #33
19Guyton & Hall : Textbook of Medical Physiology 10th ed.2000 fig.79-10 #367
20L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-12 #36 p69
21W.F.Ganong:Review of Medical Physiology 2003 20th Ed. fig.21-6 #1441
22
Christiansen, C. “New Horizon in Osteoporosis” The Parthenon Publishing Group, Lancs, UK, 1988, pp.15
23L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. Fig.4-18 #41
24L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. Fig.4-23 #42
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Calcitonin, CT• Source ---(1) in animals :parafollicular cells (C- cells) of
thyroid gland
(2) in lower animals : C-cells in ultimobranchial glands
• Chemistry --- (1) polypeptide, 32 A.A.
(2) MW = 3,000
•Effects---(1) hypocalcemia : ↓activity of osteoclasts (rapid effect)↑ osteoblastic activity(transient effect)↓ formation of new osteoclasts from the
osteoprogenitor cells (prolonged effect) (2) hypophosphatemia
•Regulation of Secretion ---- (1) blood [ Ca2+ ] ↑ → ↑ CT (2) gastrin, pacreozymin, & glucagon → ↑ CT
PS Wang/2004.0
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26
W.F.Ganong:Review of Medical Physiology 2003 20th Ed. #1442 fig.21-16
27W.F.Ganong:Review of Medical Physiology 1983 12th Ed. #1443 fig.21-13
28W.F.Ganong:Review of Medical Physiology 1983 12th Ed. #189 fig.21-11
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Comparison of Calcitonin Effects with PTH Effects
(1) PTH ---- slowly, need several hrs.
CT ----- rapidly, less than 1 hr.
(2) PTH ---- long-term regulation
CT ----- short-term regulation
PS Wang/2004.0
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L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #43 p.84
31W.F.Ganong:Review of Medical Physiology 2003 20th Ed. fig.21-7 #182
32
M. E. Hadley: Endocrinology 2nd ed. 1988 fig. 9.9 #1995
33
M. E. Hadley: Endocrinology 2nd ed. 1988 fig. 9.10 #1996
34Guyton & Hall : Textbook of Medical Physiology 10th ed.2000 fig.79-6 #366
35W.F. Ganong:Review of Medical Physiology 1983 12th Ed. Fig. 21-14 #1444
36
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #44 p.85
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L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #45 p.86
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Secondary Hyperparathyroidism• low Ca2+ diet• pregnancy• lactation blood [ Ca2+ ] [ PTH ] ric
kets• osteomalacia
•Tumors•Osteoclasts active•Blood [ Ca++ ] ↑•Broken bone (decalcification)•Cystic bone (osteoclasts tumors)•Osteoblasts active•Kidney stones (calcium phosphate) ↑
Hyperparathyroidism
PS Wang/2004.0
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L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #47 p.94
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L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #48 p.95
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L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #49 p.96
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Hypoparathyroidism• Symptoms:
blood [ Ca2+ ]↓ osteoclasts inactive no. of osteoblasts ↓ bone strongtetany ↑ death
• treatment:PTH --- expensive,
long-term effects Ab ↑Vit. D ----↑absorption of Ca2+ from GI &
bone ↓rickets (children)
PS Wang/2004.0
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Rickets• Causes ---
in children, lack of vit. D blood [ Ca2+ ]• Symptom----
blood [ PO4-3 ]↓↓↓ , blood [ Ca2+ ]↓
( Parathyroid∵ ↑ bone absorption ↑ & PO4
- 3 excretion ↑)
bone weaker
osteoblastic activity ↑, but calcification rate↓
parathyroid gland hyperplasia
tetany ↑(when blood [ Ca2+ ]↓ ) respiratory spasm death
• Treatment ---- (1)↑↑ Ca2+, PO4-3 & vit. D in diet
(2) exposed to sunlightPS
Wang/2004.05
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Adult Rickets = Osteomalacia
• Causes
(1) fat absorption ↓ vit. D ↓
↓ Ca2+ & PO4-3 absorption
Osteomalacia
(2) kidney damage 1,25-DiOH-CC ↓
PS Wang/2004.0
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