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{{CMG}}; {{AE}} {{Anmol}}
{{CMG}}; {{AE}} {{Anmol}}


== Classification ==
{| class="wikitable"
! colspan="4" |Classification of hyperparathyridism
|-
|Features
|'''Primary hyperparathyroidism'''
|'''Secondary hyperparathyroidism'''
|'''Tertiary hyperparathyroidism'''
|-
|Pathology
|Hyperfunction of parathyroid cells due to hyperplasia, adenoma or carcinoma.
|Physiological stimulation of parathyroid in response to hypocalcaemia.
|Following long term physiological stimulation leading to hyperplasia.
|-
|Cause
|
|
|
|-
|Associations
|May be associated with multiple endocrine neoplasia.
|Usually due to chronic renal failure or other causes of Vitamin D deficiency.
|Seen in chronic renal failure.
|-
|Serum calcium
|High
|Low/Normal
|High
|-
|Serum phosphate
|Low/Normal
|High
|High
|-
|Management
|Usually surgery if symptomatic. Cincacalcet can be considered in those not fit for surgery.
|Treatment of underlying cause.
|Usually cinacalcet or surgery in those that don't respond.
|}


=Epidemiology PE & DVT=
=Pathogenesis=
For causes of [[hypoparathyroidism]], [[Hypoparathyroidism causes|click here]].
GSD type 1 results due to defects in the function of microsomal enzyme glucose-6-phosphatase (G6Pase).
G6Pase catalyzes the conversion of glucose-6-phosphate to glucose during glycogenolysis and gluconeogenesis.
 
==References==
==References==
{{reflist|2}}
{{reflist|2}}

Revision as of 15:53, 30 October 2017

Hyperparathyroidism Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2]


Pathogenesis

GSD type 1 results due to defects in the function of microsomal enzyme glucose-6-phosphatase (G6Pase). G6Pase catalyzes the conversion of glucose-6-phosphate to glucose during glycogenolysis and gluconeogenesis.

References

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