Hyperparathyroidism pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief:
Overview
- The exact pathogenesis of [disease name] is not fully understood.
OR
- It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathohysiology
Primary Hyperparathyroidism
- The most common cause is a benign parathyroid adenoma that loses its sensitivity to circulating calcium levels. Usually, only one of the four parathyroid glands is affected.
- A less common cause is from multiple endocrine neoplasia (MEN).
Secondary Hyperparathyroidism
Secondary hyperparathyroidism is due to resistance to the actions of PTH, usually due to chronic renal failure. The bone disease in secondary parathyroidism along with renal failure is termed renal osteodystrophy.
Tertiary Hyperparathyroidism
Tertiary hyperparathyroidism, quartary and quintary hyperparathyroidism are rare forms that are caused by long lasting disorders of the calcium feedback control system. When the hyperparathyroidism can not be corrected by medication one calls it tertiary hyperparathyroidism.
Parathyroid, Vitamin D and mineral homeostasis
The effect of Parathyroid hormone and Vitamin on mineral metabolism is as follows:[1][2]
Parathyroid hormone | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
Kidney | Bone | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Increasead conversion of inactive 25-hydroyxvitamin D to the active 1,25-dihydroyxvitamin D | Increase excretion of inorganic phosphate | Decreased excretion of magnesium | Decrease excretion of calcium | Increased resorption of bone | |||||||||||||||||||||||||||||||||||||||||||||||||||
Increased absorption of calcium from gut | Decreased serum concentration of inorganic phosphate | Increased serum concentration of magnesium | Increased serum concentration of calcium | ||||||||||||||||||||||||||||||||||||||||||||||||||||
Prevents precipitation of calcium phosphate in bones | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
Pathogenesis
- The exact pathogenesis of [disease name] is not fully understood.
OR
- It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ HARRISON MT (1964). "INTERRELATIONSHIPS OF VITAMIN D AND PARATHYROID HORMONE IN CALCIUM HOMEOSTASIS". Postgrad Med J. 40: 497–505. PMC 2482768. PMID 14184232.
- ↑ Nussey, Stephen (2001). Endocrinology : an integrated approach. Oxford, UK Bethesda, Md: Bios NCBI. ISBN 1-85996-252-1.