Talk:Tetany
This article is rated C-class on Wikipedia's content assessment scale. It is of interest to the following WikiProjects: | |||||||||||
|
Ideal sources for Wikipedia's health content are defined in the guideline Wikipedia:Identifying reliable sources (medicine) and are typically review articles. Here are links to possibly useful sources of information about Tetany.
|
No longer needs expert attention?
[edit]I have made some changes that I think addressed a lot of the concerns talked about on this page. If there are no objections I will remove the help needed template in a week's time. BryonDavis (talk) 23:29, 20 November 2013 (UTC)
Needs cleanup
[edit]This article needs quite a bit of work:
- Tetany is a medical sign, and that should be made clear here.
- The article reads like a description of hypocalcemia. The two are not interchangeable. Chvostek and Trousseau signs are used primarily to diagnose hypocalcemia; they are elicited responses. This should at least be explained.
- The article linked to milk-and-alkali tetany, another stub which has no references at all. "Milk-and-alkali tetany" is not, as far as I am aware, a formally defined condition. I've deleted the link.
- The mechanism is not clear, and it describes only the case for hypocalcemia. It also lacks a citation.
The article supposedly refers to Harrison, but I have a hard time believing Harrison was actually used here.
I do not know enough about the subject to make these changes, I would only end up deleting things and making it more stubby than it already is.--Rhombus (talk) 15:09, 13 September 2013 (UTC)
Sign
[edit]The first sentence says that tetany is a medical sign. The category is symptoms. Can someone figure out which is the correct answer and make them match? WhatamIdoing (talk) 02:51, 6 December 2007 (UTC)
18:08, 28 May 2008 (UTC)dk med student
I think the section on pathophysiology really needs work.
namely,
1) how does dec low extracellular Ca result in higher Na? (is it that Na rises to balance out the equilibrium potential?0
2) how does excessive Ca influx cause sustained contractions? is it because there are too many free actin myosin-binding sites and thus excessive myosin-actin interaction?