Avioli / Krane Metabolic Bone Disease

Volume II
1. Auflage 2013
ISBN: 978-1-4832-6792-0
Verlag: Elsevier Science & Techn.
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 734 Seiten, Web PDF

Metabolic Bone Disease, Volume II describes the clinical disorders of bone and mineral metabolism characterized by elevated levels of circulating parathyroid hormone. This book emphasizes the relationship between hormonal synthesis, biological activity, and abnormalities in specific clinical syndromes. The metabolism and structure-function relationships of parathyroid hormone and other revealing interactions with specific receptors in target organs are also elaborated in this publication, including a basis for some understanding of the parathyroid hormone and vitamin D-'resistant states. Other topics discussed include the fundamental considerations of the physiology and biochemistry of parathyroid hormone; pathogenesis of renal osteodystrophy; and metabolic aspects of Paget's disease. This publication also covers the effects of hypercalcemia and normocalcemic disorders of mineral metabolism. This volume is beneficial to clinicians and students concerned with metabolic bone diseases.

Autoren/Hrsg.

Avioli, Louis V.

Krane, Stephen M.

Inhaltsverzeichnis

1;Front Cover;1
2;Metabolic Bone Disease;4
3;Copyright Page;5
4;Table of Contents;6
5;List of Contributors;10
6;Preface;12
7;Contents of Other Volumes;14
8;Chapter 1. Parathyroid Physiology and Primary Hyperparathyroidism;16
8.1;I. Introduction;16
8.2;II. Fundamental Considerations of the Physiology and Biochemistry of Parathyroid Hormone;19
8.3;III. Primary Hyperparathyroidism;63
8.4;References;147
9;Chapter 2. Renal Osteodystrophy;164
9.1;I. Introduction;164
9.2;II. Pathogenesis of Renal Osteodystrophy;166
9.3;III. Clinical and Radiological Correlates;181
9.4;IV. Soft Tissue Calcification;192
9.5;V. Dialysis Bone Disease;198
9.6;VI. The Nature of the Bone Lesions;202
9.7;VII. Therapeutic Management;210
9.8;References;220
10;Chapter 3. Hypoparathyroidism;232
10.1;I. Postoperative Hypoparathyroidism;233
10.2;II. Nonsurgical Damage to the Parathyroid Glands;260
10.3;III. Functional Hypoparathyroidism of Diverse Etiology in the Newborn;266
10.4;IV. Secondary Hypoparathyroidism Due to Hypercalcemia, with Special Reference to the Newborn Infant of a Hyperparathyroid Mother;272
10.5;V. Secondary Hypoparathyroidism Due to Hypermagnesemia;273
10.6;VI. Acquired Metabolic Resistance to Parathyroid Hormone;274
10.7;VII. Hypoparathyroidism Due to the Secretion of Ineffective Parathyroid Hormone;283
10.8;VIII. Idiopathic Hypoparathyroidism;284
10.9;IX. Pseudohypoparathyroidism and Related Disorders;311
10.10;X. Signs and Symptoms of Hypocalcemia;410
10.11;XI. Biological Findings;417
10.12;XII. Treatment;420
10.13;XIII. Concluding Remarks;430
10.14;References;430
11;Chapter 4. The Thyroid Gland in Skeletal and Calcium Metabolism;462
11.1;I. Introduction;462
11.2;II. The Thyroid Hormones: T3 and T4;463
11.3;III. Calcitonin;473
11.4;IV. Recent Developments;494
11.5;References;496
12;Chapter 5. Paget's Disease of Bone;504
12.1;I. Introduction;505
12.2;II. Historical Aspects;505
12.3;III. Incidence and Epidemiology;505
12.4;IV. Histopathology;509
12.5;V. Focal Manifestations;520
12.6;VI. Complications;533
12.7;VII. Metabolic Aspects of Paget's Disease;545
12.8;VIII. Systemic Complications and Associated Diseases;560
12.9;IX. Drug Treatment;566
12.10;X. Etiology;579
12.11;References;582
13;Chapter 6. Disorders of Mineral Metabolism in Malignancy;592
13.1;I. Introduction;593
13.2;II. Effects of Hypercalcemia;593
13.3;III. Clinical Occurrence;600
13.4;IV. Pathogenesis of Tumor-Associated Hypercalcemia;605
13.5;V. Treatment of Hypercalemia;625
13.6;References;637
14;Chapter 7. Metabolic Bone Disease in Children;648
14.1;I. Growth and Development of Skeleton;649
14.2;II. Differential Diagnosis of Hypercalcemia;658
14.3;III. Differential Diagnosis of Hypocalcemia;673
14.4;IV. Normocalcemic Disorders of Mineral Metabolism;687
14.5;V. Bone Disease in Disorders of Renal Function;704
14.6;References;711
15;Index;718