Hyperkalemia pathophysiology: Difference between revisions
No edit summary |
Rim Halaby (talk | contribs) No edit summary |
||
Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{| class="infobox" style="float:right;" | |||
|- | |||
| [[File:Siren.gif|30px|link=hyperkalemia resident survival guide]]|| <br> || <br> | |||
| [[Hyperkalemia resident survival guide|Resident <br> Survival <br> Guide]] | |||
|} | |||
{{Hyperkalemia}} | {{Hyperkalemia}} | ||
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com] | {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com] |
Revision as of 20:41, 23 July 2013
Resident Survival Guide |
Hyperkalemia Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Hyperkalemia pathophysiology On the Web |
American Roentgen Ray Society Images of Hyperkalemia pathophysiology |
Risk calculators and risk factors for Hyperkalemia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]
Pathophysiology
Potassium is the most abundant intracellular cation. It is critically important for many physiologic processes, including maintenance of cellular membrane potential, homeostasis of cell volume, and transmission of action potentials in nerve cells. Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana) and meat. Elimination is through the gastrointestinal tract and the kidney.
The renal elimination of potassium is passive (through the glomeruli), and resorption is active in the proximal tubule and the ascending limb of the loop of Henle. There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone.
Hyperkalemia develops when there is excessive production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (in aldosterone deficiency) or due to causes in the renal parenchyma that impair excretion.
Increased extracellular potassium levels result in depolarization of the membrane potentials of cells. This depolarization opens some voltage-gated sodium channels, but not enough to generate an action potential. After a short while, the open sodium channels inactivate and become refractory, increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.
Patients with the rare hereditary condition of hyperkalemic periodic paralysis appear to have a heightened sensitivity of muscular symptoms that are associated with transient elevation of potassium levels. Episodes of muscle weakness and spasms can be precipitated by exercise or fasting in these subjects.