Hyperparathyroidism pathophysiology: Difference between revisions

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===Tertiary Hyperparathyroidism===
===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.
[[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 and mineral homeostasis===
===Parathyroid, Vitamin D and mineral homeostasis===
 
The effect of Parathyroid hormone and Vitamin on mineral metabolism is as follows:<ref name="pmid14184232">{{cite journal |vauthors=HARRISON MT |title=INTERRELATIONSHIPS OF VITAMIN D AND PARATHYROID HORMONE IN CALCIUM HOMEOSTASIS |journal=Postgrad Med J |volume=40 |issue= |pages=497–505 |year=1964 |pmid=14184232 |pmc=2482768 |doi= |url=}}</ref><ref>{{cite book | last = Nussey | first = Stephen | title = Endocrinology : an integrated approach | publisher = Bios NCBI | location = Oxford, UK Bethesda, Md | year = 2001 | isbn = 1-85996-252-1 }}</ref>
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{{familytree | | | | | | | | | | | | A01 |A01=Parathyroid hormone}}  
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{{familytree | | | | | | | |,|-|-|-|-|^|-|-|-|-|-|-|-|-|-|-|-|.|}}
{{familytree | | | | | B01 | | | | | | | | | B02 | | |B01=Kidney|B02=Bone}}
{{familytree | | | | | | | B01 | | | | | | | | | | | | | | | B02 | | |B01=Kidney|B02=Bone}}
{{familytree | |,|-|-|-|+|-|-|-|.| | | | | | |!| }}
{{familytree | |,|-|-|-|-|-|+|-|-|-|-|v|-|-|-|-|.| | | | | | |!| }}
{{familytree | C01 | | C02 | | C03 | | | | | C04 |C01=Increase excretion of inorganic phosphate|C02=Decreased excretion of magnesium|C03=Decrease excretion of calcium|C04=Increased resorption of bone}}
{{familytree | C01 | | | | C02 | | | C03 | | | C04 | | | | | C05 |C01=Increasead conversion of inactive 25-hydroyxvitamin D to the active 1,25-dihydroyxvitamin D|C02=Increase excretion of inorganic phosphate|C03=Decreased excretion of magnesium|C04=Decrease excretion of calcium|C05=Increased resorption of bone}}
{{familytree | |!| | | |!| | | |!| | | | | | |!| |}}
{{familytree | |!| | | | | |!| | | | |!| | | | |!| | | | | | |!| |}}
{{familytree | D01 | | D02 | | |`|-|-|D03|-|'| |D01=Decreased serum concentration of inorganic phosphate|D02=Increased serum concentration of magnesium|D03=Increased serum concentration of calcium}}
{{familytree | D01 | | | | D02 | | | D03 | | | |`|-|-|D04|-|'| |D01=Increased absorption of calcium from gut|D02=Decreased serum concentration of inorganic phosphate|D03=Increased serum concentration of magnesium|D04=Increased serum concentration of calcium}}
{{familytree | |!| | | | | | | | | | |!| | | | }}
{{familytree | |!| | | | | |!| | | | | | | | | | | | |!|!| | | }}
{{familytree | |`|-|-|-|-| E01 |-|-|-|'|E01=Prevents precipitation of calcium phosphate in bones}}
{{familytree | |!| | | | | |`|-|-|-|-|-| E01 |-|-|-|-|'|!|E01=Prevents precipitation of calcium phosphate in bones}}
{{familytree | |`|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|'|}}  
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Revision as of 14:11, 14 August 2017

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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

  1. HARRISON MT (1964). "INTERRELATIONSHIPS OF VITAMIN D AND PARATHYROID HORMONE IN CALCIUM HOMEOSTASIS". Postgrad Med J. 40: 497–505. PMC 2482768. PMID 14184232.
  2. Nussey, Stephen (2001). Endocrinology : an integrated approach. Oxford, UK Bethesda, Md: Bios NCBI. ISBN 1-85996-252-1.

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