Nutritional Secondary Hyperparathyroidism in the Horse

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28 The Anatomy of the Parathyroid Glands in the Horse cytoplasm to nucleus ratio, and the nuclear size of the epithelial cells increased with age, but this was not significant. These values were also independent of sex, but they varied significantly between horses. The material does not therefore indicate any changes in parathyroid function in the horse due to sex or age. Parenchymal fat was present in the equine parathyroid glands of horses aged 4 months or more. The majority of horses up to 8 years of age showed a little fat in restricted areas of light chief cells. Only 1 of 11 horses 10 to 24 years of age had parenchymal fat. This is exactly opposite to the condition in man and the dog. In a review article BARGMANN (1939) stated that parenchymal fat makes its appearance in the human parathyroid at the latest during the 20th year of life (in rare cases as earIy as the fourth month) and that the fat content then increases continuously. In the dog parenchymal fat in the parathyroids starts to appear at the age of 3 years and, as in man, increases with increasing age. The presence of stainable fat in epithelial cells of the parathyroids is variously interpreted. BOBEAU (1 91 1) hypothesized that this fat represented degenerated and conglomerated mitochondria (fat phanerosis in Virchow’s sense) whereas WEIL [(1921), quoted from BARGMANN (1 93591 believed that the fat-positive granules in the epithelial cells were hormone precursors. These theories have not been substantiated. The fat content of the parathyroid cells is not related to the nutritional condition of the individual [BARGMANN (1 939)]. Downloaded from vet.sagepub.com by guest on April 14, 2010
11. Nutritional Secondary Hyperparathyroidism in the Horse : Review of the Literature 1. The Nature of the Osteopathy Metabolic bone diseases characterized by “too little mineralized bone” can occur, pathogenetically, for three reasons [ALBRIGHT and REIFENSTEIN (1948)] : A. Bone formation too little a) Defect in matrix formation: Osteoporosis. b) Defect in mineralization of matrix: Rickets in young individuals, osteomalacia in adults. B. Bone resorption too much a) Generalized osteitis fibrosa. Bone as a tissue [in the sense of WEINMANN and SICHER (1955)] is formed in only one way, that is, by apposition of osteoid by osteoblasts. POMMER (1885) defined osteoporosis as an osteoblastic deficiency. Osteoporosis is, accordingly, a metabolic bone disease due to too little matrix formation. The catabolic processes are not influenced, and the net result over a long period of time is loss of bone. Although POMMER’S view has been violently debated, nothing has appeared to disprove him. Etiologically, however, the nature of osteoporosis remains obscure in most cases [MCLEAN and URIST (1961)]. In rickets and its adult counterpart, osteomalacia, “too little mineralized bone” results from too low ion product of calcium and phosphorus in the blood serum [IVERSEN and LENSTRUP (1919)l. This lowered ion concentration may be due to a decrease in serum calcium or phosphorus or both. With regard to the pathogenesis we recognize a low-calcium rickets and a low-phosphorus rickets. The causes for lowered serum calcium and/or phosphorus are numerous. They have been reviewed by FOLLIS (1958). Generalized osteitis fibrosa as a separate entity was described in 1891 by VON RECKLINGHAUSEN. The cause of this generalized bone Downloaded from vet.sagepub.com by guest on April 14, 2010
Page 1 and 2: Pathologia Veterinaria Online http:
Page 3 and 4: Supplementum ad Vol. 1 (1964) Patho
Page 5 and 6: V . Experimental Nritritional Secon
Page 7 and 8: Introduction and Object of Investig
Page 9 and 10: I. The Anatomy of the Parathyroid G
Page 11 and 12: Comparative Aspects of the Embryolo
Page 13 and 14: The Aracroscopic Anatomy of the Equ
Page 15 and 16: The Microscopic Anatomy of the Equi
Page 17 and 18: 'I'hc hlicroscopic Anatomy of the E
Page 19 and 20: ’The I\licroscopic Anatomy of the
Page 21 and 22: 10 . 9 . a . 7 0 + 6 . 5 . 0 ’I
Page 23 and 24: ‘The hl icroscopic Anatomy of the
Page 25 and 26: ’I’hc hlicroscopic Anatomy of t
Page 27 and 28: ‘I’lic ihlrcroscopic Anatomy of
Page 29 and 30: ‘I’hc Alicroscopic Anatomy of t
Page 31 and 32: Discussion 25 7bbic 1 .. Avcragc si
Page 33: Discussion 27 Table VZZ. Nuclear si
Page 37 and 38: The Nature of the Osteopathy 31 Fig
Page 39 and 40: ’The Nature of the Osteopathy 33
Page 41 and 42: Etiology 35 Experiments and clinica
Page 43 and 44: Clinical Pathology 37 Table X. Seru
Page 45 and 46: 111. Experimental Nutritional Secon
Page 47 and 48: Ration 41 Table XI/. Calcium and ph
Page 49 and 50: Necrops y 43 6. Necropsy The animal
Page 51 and 52: Clinical Observations 45 During wee
Page 53 and 54: Clinico-pathologic Determinations 4
Page 55 and 56: 90. *. 90. 90. 70. / . Clinico-path
Page 57 and 58: (:linico-pathologic Determinations
Page 59 and 60: Rocntgencilogic Observations 53 Fie
Page 61 and 62: lioentgcnologic Ohscrvntions 55 I,'
Page 63 and 64: Pathologic Anatomy 57 7bb/e XIS. Si
Page 65 and 66: Pathologic Anatomy 59 fhb/c. A’X.
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Page 71 and 72: Pathologic Anatoiny Downloaded from
Page 73 and 74: Pathologic Anatomy 67 Downloaded fr
Page 75 and 76: Pathologic Anatomy 69 Fiq. 37. Cont
Page 77 and 78: V. Experimental Nutritional Seconda
Page 79 and 80: Scruin Phosphorus, Calciiiiii, and
Page 81 and 82: Serum Phosphorus, Calcium, and Alka
Page 83 and 84: Serum Phosphorus, Calcium, and Alka
Page 85 and 86:
The Parathyroid Glands 79 should be
Page 87 and 88:
The Skeleton 81 5. The Skeleton The
Page 89 and 90:
The Skeleton 83 ary hyperparathyroi
Page 91 and 92:
Summary and Conclusions The thesis
Page 93 and 94:
Siimmary and Conclusions 87 Rocntgc
Page 95 and 96:
References 89 COILIP, J. B.: 'I'hc
Page 97 and 98:
Refereiices 91 ~~CILAN, F. C. and U
Page 99 and 100:
Appendix Tables and Statistical Ana
Page 101 and 102:
Tables and Statistical Analyses 95
Page 103 and 104:
’Tablcs and Statistical Analyscs
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Nutritional Secondary Hyperparathyroidism in the Horse

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