Chapter Ⅵ. Calcium Homeostasis
PS Wang/2004.05
1
2
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
Osteoblasts
Bone Absorption
Bone Deposition
(new bone)
Osteocytes
3
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Guyton & Hall : Textbook of Medical Physiology 10th ed.2000 fig.79-4 #365
4
Mechanism of Bone Absorption
1.
Osteoclasts (lysosomes)
organic matrix
2.
Osteoclasts
acids (citric acid & lactic acid)
bone salts
solution
3.
Bone salts & collagen
osteoclasts
proteolytic enzymes
digest or dissolute
phagocytosis
villi from
digestion
5
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M. Azria: The Calcitonins (Physiology and Pharmacology). 1989. fig.34a
6
L.E. Mcdonald: Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-15 #38
7
8
W.F. Ganong:Review of Medical Physiology 1983 12th Ed. #1439
99
L.E. Mcdonald: Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #29
10
W.F. Ganong:Review of Medical Physiology 2003 20th Ed. fig.21-9 #187
M. E. Hadley: Endocrinology 4th ed. 1996 fig.9.1 #1992
11
W.F.Ganong: Review of Medical Physiology 2003 20th Ed. #188 fig.21-10
12
Guyton & Hall : Textbook of Medical Physiology 10th ed.2000 fig.79-9
13
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
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Biological Effects of PTH
1.
2.
3.
4.
5.
6.
7.
8.
blood ［Ca2+］( absorption of Ca2+ & PO4-3 from
bone)
blood ［PO4-3］( excretion of renal phosphate)
urine ［PO4-3］and urine ［Ca2+］
the rate of skeletal remodeling and the net rate of bone
resorption
osteocytic osteolysis in bone (rapid effect) and the
numbers and/or activation of osteoclasts on bone
surface (slow phase)
urinary excretion of hydroxyproline-containing peptides
activation of adenyl cyclase in target cells.
formation of active vit. D metabolites by the kidney.
15
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M. E. Hadley: Endocrinology 2nd ed. 1988 fig.9.3 #1993
16
17
L.E. Mcdonald: Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-5 #32
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-6 #33
18
Guyton & Hall : Textbook of Medical Physiology 10th ed.2000 fig.79-10 #367
19
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-12 #36 p69
20
W.F.Ganong:Review of Medical Physiology 2003 20th Ed. fig.21-6 #1441
21
22
Christiansen, C. “New Horizon in Osteoporosis” The Parthenon Publishing Group, Lancs, UK, 1988, pp.15
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. Fig.4-18 #41
23
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. Fig.4-23 #42
24
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
25
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W.F.Ganong:Review of Medical Physiology 2003 20th Ed. #1442 fig.21-16
26
W.F.Ganong:Review of Medical Physiology 1983 12th Ed. #1443 fig.21-13
27
W.F.Ganong:Review of Medical Physiology 1983 12th Ed. #189 fig.21-11
28
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
29
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30
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #43 p.84
W.F.Ganong:Review of Medical Physiology 2003 20th Ed. fig.21-7 #182
31
32
M. E. Hadley: Endocrinology 2nd ed. 1988 fig. 9.9 #1995
33
M. E. Hadley: Endocrinology 2nd ed. 1988 fig. 9.10 #1996
Guyton & Hall : Textbook of Medical Physiology 10th ed.2000 fig.79-6 #366
34
W.F. Ganong:Review of Medical Physiology 1983 12th Ed. Fig. 21-14 #1444
35
36
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #44 p.85
37
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #45 p.86
Hyperparathyroidism
•Tumors
•Osteoclasts
active
•Blood ［Ca++］ ↑
•Broken bone (decalcification)
•Cystic bone (osteoclasts
tumors)
•Osteoblasts
active
•Kidney stones (calcium phosphate) ↑
Secondary Hyperparathyroidism
• low Ca2+ diet
• pregnancy
• lactation
rickets
• osteomalacia
blood［Ca2+］
［PTH］
38
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L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #47 p.94
40
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #48 p.95
41
L.E. Mcdonald:Veterinary Endocrinology and Reproduction. 1976 2nd Ed. #49 p.96
Hypoparathyroidism
• Symptoms:
blood［Ca2+］↓
osteoclasts
inactive
no. of osteoblasts ↓
bone
strong
tetany ↑
death
• treatment:
PTH --- expensive,
long-term effects
Ab ↑
Vit. D ----↑absorption of Ca2+ from GI &
bone
↓rickets (children)
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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 sunlight
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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 ↓
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