Chapter Ⅵ . Calcium Homeostasis

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Chapter Ⅵ. Calcium Homeostasis

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2W.F.Ganong: Review of Medical Physiology 1983 12th Ed. Fig21-2 #1440

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Remodeling of Bone

Bone Marrow or Fibrous Periosteum

Mesenchymal Stem Cells

Osteoclasts Bone Absorption

Osteoblasts Bone Deposition(new bone)

Osteocytes

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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

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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

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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.

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16M. E. Hadley: Endocrinology 2nd ed. 1988 fig.9.3 #1993

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L.E. Mcdonald: Veterinary Endocrinology and Reproduction. 1976 2nd Ed. fig.4-5 #32

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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

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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

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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

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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

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M. E. Hadley: Endocrinology 2nd ed. 1988 fig. 9.9 #1995

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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

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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

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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)

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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

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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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