Hyperkalemia pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
==Pathophysiology==
===Physiology===
The normal physiology of [name of process] can be understood as follows:
===Pathogenesis===
*The exact pathogenesis of [disease name] is not completely understood.
OR
*It is understood 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.
* 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 potential]]s in [[nerve cell]]s. 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 amount of potassium level in the body is highly regulated mainly through renal excretion. 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 increase intake of potassium, excessive production as seen in tissue breakdown, or ineffective elimination of potassium. Ineffective elimination can be hormonal (in [[aldosterone]] deficiency) or due to abnormalities in the renal parenchyma.
* Increased extracellular potassium levels result in alteration of the membrane potentials of cells. This depolarization opens some [[sodium channel|voltage-gated sodium channel]]s, but not enough to generate an action potential. After a short while, the open sodium channels becomes inactivated and become [[refractory period|refractory]], increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, [[cardiac]], and [[gastrointestinal]] organ systems.  Increased extracellular potassium levels result in alteration of the membrane potentials of cells.
* 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.
==Pathophysiology==
==Pathophysiology==
===Physiology===
===Physiology===

Revision as of 13:59, 28 June 2018

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

Overview

Potassium is the most abundant intracellular cation and is critically important for many physiologic processes. The amount of potassium level in the body is highly regulated mainly through renal excretion. Hyperkalemia develops when there is increase intake of potassium, excessive production as seen in tissue breakdown, or ineffective elimination of potassium. Increased extracellular potassium levels result in alteration of the membrane potentials of cells. Increased extracellular potassium levels result in alteration of the membrane potentials of cells.

Pathophysiology

Pathophysiology

Physiology

The normal physiology of [name of process] can be understood as follows:

Pathogenesis

  • The exact pathogenesis of [disease name] is not completely understood.

OR

  • It is understood 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.
  • Hyperkalemia develops when there is increase intake of potassium, excessive production as seen in tissue breakdown, or ineffective elimination of potassium. Ineffective elimination can be hormonal (in aldosterone deficiency) or due to abnormalities in the renal parenchyma.
  • Increased extracellular potassium levels result in alteration 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 becomes inactivated and become refractory, increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Increased extracellular potassium levels result in alteration of the membrane potentials of cells.
  • 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.

Pathophysiology

Physiology

The normal physiology of [name of process] can be understood as follows:

Pathogenesis

  • The exact pathogenesis of [disease name] is not completely understood.

OR

  • It is understood 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.
  • Hyperkalemia develops when there is increase intake of potassium, excessive production as seen in tissue breakdown, or ineffective elimination of potassium. Ineffective elimination can be hormonal (in aldosterone deficiency) or due to abnormalities in the renal parenchyma.
  • Increased extracellular potassium levels result in alteration 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 becomes inactivated and become refractory, increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Increased extracellular potassium levels result in alteration of the membrane potentials of cells.
  • 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.

References


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