Hyperkalemia pathophysiology: Difference between revisions

	Hyperkalemia Microchapters
Home
Patient information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Hyperkalemia from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural history, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Hyperkalemia pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Hyperkalemia pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Hyperkalemia pathophysiology
CDC on Hyperkalemia pathophysiology
Hyperkalemia pathophysiology in the news
Blogs on Hyperkalemia pathophysiology
Directions to Hospitals Treating Hyperkalemia
Risk calculators and risk factors for Hyperkalemia pathophysiology

VisualWikitext

Revision as of 14:02, 2 July 2018

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 normal range of potassium in blood is 3.5-5.1meq/L .Hyperkalemia develops when the level of potassium exceeds 5.5 meq/L in blood which can be due to an increase in intake of potassium, excessive production as seen in tissue breakdown, ineffective elimination of potassium or some drugs. The potassium levels in the body are highly regulated mainly by renal excretion.The gut excretes a minimal amount of dietary potassium (approximately 10%). Hyperkalemia is very common in patients with chronic kidney disease as potassium is not effectively excreted from the body.Potassium is involved in maintaining transmembrane potentials of cells,so imbalance in potassium levels can lead to disruption of cell membrane potentials and can cause hyperexcitablity leading to fatal cardiac arrhythmias and effecting nervous system.

Pathophysiology

Physiological role of potassium

Potassium is the major intracellular cation and sodium is the major extracellular cation.Almost all cells possess an Na+-K+-ATPase, which pumps Na+ out of the cell and K+ into the cell and leads to a K+ gradient across the cell membrane (K⁺in>K+out) that is partially responsible for maintaining the potential difference across the membrane.This potential difference called the transmembrane potential is responsible for the excitability of the cells.

Factors affecting transcellular shift of potassium

The distribution of potaasium inside and outside the cells is maintained by various pumps,osmolarity,ph and the hormones insulin, aldosterone, beta 2-catecholamines, alpha-catecholamines, and prostaglandins.

Insulin regulates potassium uptake into the cells through GLUT receptors on the cell membranes by increasing the activity of Na+-K+-ATPase pump.
Catecholamines regulate potassium uptake into the cells through β2-Receptor–induced stimulation of Na+-K+-ATPase pump.
Increased osmolarity as in hyperglycemia causes water efflux from the cells that drags potassium along.
In acidosis,the decreased extracellular ph decreases the rate of Na+-H+ exchange (NHE1) and inhibit the inward rate of Na+-3HCO3 cotransport,thus decreasing intracellular Na+ levels which in turn decreases the activity of Na+-K+-ATPase pump and decreasing intracellular K+ levels.
In alkalosis,the increased extracellular ph increases the rate of Na+-H+ exchange (NHE1) and increases the inward rate of Na+-3HCO3 cotransport,thus increasing intracellular Na+ levels which in turn increases the activity of Na+-K+-ATPase pump and increasing intracellular K+ levels.

Role of kidneys

The source of potassium to the body is diet.The potassium levels in the body are dependent on dietary intake,tissue breakdown,gastrointestinal absorption and losses and most important is renal regulation via absorption and secretion.Kidney play a important role in keeping the balance of potassium. At the glomerulus, potassium is freely filtered and then largely reabsorbed in the proximal tubule and thick ascending loop of Henle (>60 % of filtered potassium). The cortical collecting duct receives 10–15% of filtered potassium and constitutes the kidney’s major site of potassium excretion. Potassium excretion at the cortical collecting duct depends on the amount of sodium delivered there and the activity of aldosterone.It does so by the following ways.

increases intracellular K+ concentration by stimulating the activity of the Na+-K+-ATPase in the basolateral membrane.
stimulates Na+ reabsorption across the luminal membrane, which increases the electronegativity of the lumen, thereby increasing the electrical gradient favoring K+ secretion.If the rate of delivery of sodium and water is very high in the distal tubules then it will cause more Na+ reabsorption and more K+ secretion.
has a direct effect on the luminal membrane to increase K+ permeability.

Aleration in the levels of potassium occur due to disruption in the above mentioned mechanisms that regulate potassium homeostasis. Hyperkalemia is the increased levels of potassium (>5.1 meq/L) in blood.It can be caused by increase in transcellular shift of potassium,impaired excretion from the kidneys or excessive intake.

Pathogenesis

Template:WikiDoc Sources

@@ Line 37: / Line 37: @@
 Hyperkalemia is the increased levels of potassium (>5.1 meq/L) in blood.It can be caused by increase in transcellular shift of potassium,impaired excretion from the kidneys or excessive intake.
 ===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==
-===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.
-==References==
 {{reflist|2}}
 [[Category:Potassium]]