Talk:Hypokalemia

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Can be Caused by Hypoglycemia[edit]

According to NCBI [1] — Preceding unsigned comment added by Hippypink (talkcontribs) 16:36, 4 September 2013 (UTC)

What[edit]

What exactly does the unit mEq mean? Simon A. 09:56, 10 Sep 2004 (UTC)

I have written a stub at milliequivalent. It is actually quite a complex concept, and I'm surprised it hasn't already been covered. -- FirstPrinciples 14:29, Sep 10, 2004 (UTC).
OK, I've expanded that article and moved it to Equivalent weight (chemistry) -- FirstPrinciples 04:07, Sep 11, 2004 (UTC)

Hypokalemia[edit]

As I understand hypokalemia, and its causes, I believe it can also be genetic.

I'm glad you understand hypokalemia! Honestly, there are a few hereditary conditions in which there is low potassium (e.g. Bartter syndrome, periodic paralysis), but the vast majority is not genetic. JFW | T@lk 06:50, 1 August 2005 (UTC)

This statement seems to contradict itself. "...potassium is needed to repolarize the cell membrane to a resting state after an action potential has passed. Decreased potassium levels in the extracellular will cause hyperpolarization of the resting membrane potential." The first part says that potassium is needed to repolarize the cell, implying that a lack of potassium would result in a depolarized cell. The next part says that the lack of potassium causes hyperpolarization. 05:33, 15 December 2005 (UTC)

Decreased extracellular potassium levels cause a greater difference between intracellular and extracellular potassium levels, thus creating hyperpolarization. Still potassium is indeed needed for repolarization. But even with low potassium levels, the cell is able to pump potassium into the cell (using NaKATPase). The repolarization will take longer though. The first place where this will be problematic is in the heart with hypokalemia leading to arrythmia's. A total lack of potassium would lead to death very quickly. --WS 11:15, 15 December 2005 (UTC)

I know that you are correct about the role of potassium in action potentials, I just think that the way that that statement is worded is confusing. When it says that potassium is needed for repolarization after the action potential, it is not talking about extracellular potassium. It is intercellular potassium that is needed for repolarization, and hypokalemia is a lack of extracellular potassium. This increases the relative concentration of intercellular potassium, which is responsible for repolarization. The two sentences are talking about different things, but it is not very clear. I also think that when you said above that repolarization will take longer with low potassium levels that is misleading, as well. Again, this is referring to low intercellular potassium, and hypokalemia results in an increased concentration of intercellular potassium, relative to the outside of the cell. It is a decrease of extracellular potassium that leads to the hyperpolarization. When this is the case, the repolarization will not take longer. 19:31, 16 December 2005 (UTC)

Relationship of Hypokalemia and Muscular Dystrophy[edit]

Noticed that User:Danieliralevy removed the Muscular Dystrophy template I placed on the page yesterday. I have no qualms with him doing so but am hoping to resolve the reasoning why others have sated on the main Muscular Dystrophy page that Hypokalemia is classified as muscular dystrophy under "Less Common Myophathies", "Periodic Paralysis". It may well be that the muscular dystrophy page is wrong and would like to correct that if so. Any thoughts/ideas/sources would be appreciated. Theflyer 04:33, 8 March 2007 (UTC)

Muscular dystrophy is an inherited disorder that causes progressive muscle weakness (myopathy) and loss of muscle mass (atrophy) due to defects in genes required for normal functioning of muscle. Severe hypokalemia (and hyperkalemia) can cause muscle weakness, but the symptoms only occur until the electrolyte disorder is corrected. A seperate set of hereditary disorders, hypokalemic & hyperkalemic periodic paralysis, are hereditary (genetic). These disorders are paroxysmal (come on as acute attacks) and are associated with defective ion channels that can either make the muscle more sensitive to the abnormal potassium concentration, and/or can cause shifts of potassium in or out of the cells which causes the electrolyte disorder. The periodic paralyses are nueromuscular disorders, but certainly not muscular dystrophies. I believe that putting that long block of muscle disorders on a hyperkalemia or hypokalemia page is not at all appropriate. However, I can certainly add a few lines to the causes and pathophysiology sections.Dan Levy 15:19, 8 March 2007 (UTC)
Dan, Thank you for the response. Please feel free to add information as you feel appropriate to the Hypokalemia page about its relationship to MD. I do not have a problem with the Hypokalemia's editors deciding against using the Muscular Dystrophy template. More importantly, it appears we may need to fix something in Wikipedia because the Muscular Dystrophy article does link Hypokalemic and Hyperkalemic, which you claim are different diseases from hypokalemia and hyperkalemia. If this is true, then we definitely need to break those redirects and make separate articles for the hereditary versions. I'm also engaging over on the Talk:Muscular dystrophy page to see if I can get better sourcing/information on why Hypokalemic and Hyperkalemia are "Generally classified as Muscular Dystrophy". Theflyer 14:15, 10 March 2007 (UTC)

Cushing's[edit]

Removed explicit mention of Cohn's syndrome as that's covered under adrenal tumors a few words later. Some cases of Cushing's syndrome (mostly ectopic ACTH-producing tumors) are thought to overwhelm the 11-β hydroxylase enzyme of the renal tubules. This gives an effect like glycyrrhizin and can cause hypokalemia. Dan Levy 19:08, 9 March 2007 (UTC)

  • Rose, B.D. and T.W. Post, Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed. 2001, pages 836-887. ISBN 0-07-134682-1

Hair Loss[edit]

Does potassium deficiency cause hair loss. I am going through chemo which shouldn't be causing hair loss, but am losing some, not all. Thought maybe due to my postassium deficiency?

No relationship between the two. I'll elaborate more on the TALK page for 72.47.38.162 Dan Levy 21:17, 15 June 2007 (UTC)

U waves[edit]

It would be nice to add WHY hypokalemia causes U waves on EKG. I can't find that answer anywhere. 71.234.109.192 20:43, 15 October 2007 (UTC)rhetoric

The Hypokalemia page may not be the place for this explanation (read: this user is not willing to commit -- at this moment -- the time needed to initiate a section on cardiac electrophysiology related to hypokalemia). However, I would use this TALK forum to note that the etiology of the U waves is unclear and may be related to ventricular early afterdepolarizations or perhaps the repolarization of the Purkinje system. (See Yan et al. J Am Coll Cardiology, 42(3):401-9, 2003). To me, it seems unlikely that the Purkinje system could create a large wave, given its relatively small tissue mass.

Tetany?[edit]

I've heard of tetany as a symptom of hypocalcaemia before , but not hypokalaemia; is there a source for this? —Preceding unsigned comment added by Heyeyya (talkcontribs) 14:22, 24 October 2010 (UTC)

Agreed. I see tetany in a textbook, but it doesn't seem to be reported in the primary literature. D.I.L. (talk) 13:50, 25 October 2010 (UTC)

Hypokalaemia in hyperemetic alkalosis[edit]

I'm not sure I get the physiological mechanism behind K+ excretion in the kidney in alkalosis following excessive vomiting.

The article states that "an acute rise of plasma HCO3- concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate."

Am I right in thinking the following:

The rise in serum bicarbonate results from Henderson-Hasselbalch style buffering of the lost H+ from the vomit via carbonic acid?

I gather that bicarb reabsorption occurs after dissociation by carbonic anhydrase to CO2 and OH-, which, combined with H+, cross into the luminal cell, where they reform HCO3-. With an excess of serum and thus filtrate bicarb, there is an insufficient amount of H+ to permit transport of HCO3- back into the cell. I presume this is what is meant by exceeding the capacity to reabsorb this anion.

I'm not quite sure where potassium fits in, however. I had read that there is an H+/K+ antiporter in alpha intercalated cells of the cortical collecting tubule. Would minimal H+ as possible inactivate the antiporter and prevent reabsorption of potassium from the urine?

I'm not quite sure what is meant by K+ being the obligate cation. What exactly does this mean, and how is this borne out physiologically? Are there more channels involved than what I've mentioned?

You'll excuse me if I've missed the point, I'm just trying to get my head round this one as a student studying some of the unpleasant consequences that can occur in bulimia.

Ultimatebeej (talk) 23:14, 10 February 2011 (UTC)

External links modified[edit]

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Carbonated beverages and acidosis[edit]

Currently the article claims the following

The hypokalemia is thought to be from the combination of the diuretic effect of caffeine[2] and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.[3][4] A physiological response to hypercapnia, blood potassium (as well as calcium) helps offset acidosis, which is consistent with chronic, extreme consumption of carbonated beverages.

AFAIK, not much of any CO2 present in carbonated drinks makes it into the circulatory system - so I find this highly dubious. Maybe someone more knowledgeable can shed some light here? Tony Mach (talk) 11:28, 3 November 2016 (UTC)

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  1. ^ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769974/
  2. ^ Shirley DG, Walter SJ, Noormohamed FH (November 2002). "Natriuretic effect of caffeine: assessment of segmental sodium reabsorption in humans". Clin. Sci. 103 (5): 461–6. doi:10.1042/CS20020055. PMID 12401118. 
  3. ^ Packer, C.D. (June 2009). "Cola-induced hypokalaemia: a super-sized problem". International Journal of Clinical Practice. 63 (6): 833–5. doi:10.1111/j.1742-1241.2009.02066.x. PMID 19490191. 
  4. ^ HealthGuru (2012-03-01). "Health.yahoo.com". Health.yahoo.com. Retrieved 2012-03-10.