La homeostasis del potasio

Potasio, el catión intracelular más abundante, es esencial para la vida del organismo. El potasio se obtiene a través de la dieta, y comunes de alimentos ricos en potasio son las carnes, frijoles, frutas y papas.
La absorción gastrointestinal es completa, lo que resulta en exceso de ingesta diaria de aproximadamente 1 mEq / kg / d (60-100 mEq). El noventa por ciento de este exceso se elimina por los riñones, y el 10% se excreta a través del intestino. Homeostasis de potasio se mantuvo predominantemente a través de la regulación de la excreción renal. El sitio más importante de la regulación es el conducto colector, donde los receptores de aldosterona están presentes.
La excreción se incrementa en (1) la aldosterona, (2) la entrega de sodio de alta para el conducto de recogida (por ejemplo, diuréticos), (3) el flujo de orina alta (por ejemplo, diuresis osmótica), (4) alto nivel de potasio en suero, y (5) la entrega de iones cargados negativamente en el conducto colector (por ejemplo, bicarbonato).
La excreción se reduce a (1) la deficiencia o ausencia relativa de la aldosterona, (2) la entrega bajo contenido de sodio al conducto colector, (3) el flujo urinario bajo, (4) el bajo nivel de potasio en suero, y (5) la insuficiencia renal
Riñones adaptarse a las alteraciones agudas y crónicas en la ingesta de potasio. Cuando la ingesta de potasio es siempre alta, la excreción de potasio también se incrementa. En ausencia de la ingesta de potasio, las pérdidas renales son obligatorios 10-15 mEq / d. Así, las pérdidas crónicas se producen en ausencia de cualquier potasio ingerido. El riñón mantiene un papel central en el mantenimiento de la homeostasis del potasio, incluso en el contexto de la insuficiencia renal crónica. Renales mecanismos de adaptación permitirá a los riñones para mantener la homeostasis de potasio hasta que la tasa de filtración glomerular disminuye a menos de 15-20 ml / min. Adicionalmente, en la presencia de insuficiencia renal, la proporción de potasio excretado a través de los aumentos de la tripa. El colon es el principal sitio de regulación intestinal de la excreción de potasio. Por lo tanto, los niveles de potasio pueden permanecer relativamente normal en condiciones estables, incluso con insuficiencia renal avanzada. Sin embargo, a medida que empeora la función renal, los riñones no pueden ser capaces de manejar una carga de potasio aguda.
Nivel de potasio en suero
El potasio es un catión intracelular predominante, por lo tanto, los niveles séricos de potasio puede ser un indicador muy pobre de las reservas corporales totales. Debido a que se mueve de potasio fácilmente por las membranas celulares, los niveles de potasio en suero reflejan el movimiento de potasio entre compartimientos de fluidos intracelulares y extracelulares, así como la homeostasis corporal total de potasio.
Mecanismos para la detección de la concentración de potasio extracelular no se conocen bien. La evidencia sugiere que las células adrenales glomerulosa y células beta pancreáticas puede jugar un papel en la detección de potasio, resultando en alteraciones en la aldosterona y la secreción de insulina. [1, 2] Como ambos sistemas hormonales juegan papeles importantes en la homeostasis del potasio, estos nuevos hallazgos no son sorpresa, sin embargo, los mecanismos moleculares por los cuales estos canales de potasio señalar los cambios en la secreción de hormonas y la actividad aún no se han determinado.
Muscle contiene la mayor parte del potasio corporal, y la noción de que el músculo podría desempeñar un papel destacado en la regulación de la concentración de potasio en suero a través de alteraciones en la actividad de la bomba de sodio ha sido promovida por un número de años. La insulina estimulada por la ingesta de potasio aumenta la actividad de la bomba de sodio en las células musculares, lo que resulta en un aumento de la captación de potasio. Estudios en un modelo de privación de potasio demostrar que de forma aguda, músculo esquelético desarrolla resistencia a la insulina estimula la captación de potasio, incluso en ausencia de cambios en la expresión de células de músculo bomba de sodio. Sin embargo, los resultados a largo plazo de privación de potasio en una disminución de la célula muscular sodio-bomba de expresión, dando como resultado la captación muscular disminuida de potasio. [3, 4, 5]
Por lo tanto, parece que hay un sistema bien desarrollado para la detección de potasio por las glándulas suprarrenales y el páncreas, resultando en ajustes rápidos en la eliminación inmediata de potasio y de la homeostasis del potasio a largo plazo. Estados muy potasio estimular la captación celular a través de la insulina mediada por la estimulación de la actividad de la bomba de sodio en el músculo y estimular la secreción de potasio por el riñón a través de la aldosterona mediada por el aumento de la expresión renal distal de los canales de potasio de secreción (ROMK). Estados bajos de potasio resulta en resistencia a la insulina, impidiendo la absorción de potasio en las células musculares y causar una disminución de la liberación de aldosterona, lo que disminuye la excreción renal de potasio.
Varios factores regulan la distribución de potasio entre el espacio intracelular y extracelular, de la siguiente manera:
Hormonas Glycoregulatory: (1) La insulina aumenta la entrada de potasio en las células, y (2) glucagón deteriora entrada de potasio en las células.
Estímulos adrenérgicos: (1) El beta-adrenérgicos estímulos mejorar la entrada de potasio en las células, y (2) alfa-adrenérgicos estímulos perjudicar entrada de potasio en las células.
pH: (1) Alcalosis mejora entrada de potasio en las células, y (2) la acidosis deteriora entrada de potasio en las células.
Un aumento agudo en la osmolalidad hace que el potasio pueda salir de las células. Una aguda de células / tejidos descomposición libera potasio hacia el espacio extracelular.

http://emedicine.medscape.com/article/242008-overview

Hypokalemia

The reference range for serum potassium level is 3.5-5 mEq/L, with total body potassium stores of approximately 50 mEq/kg (ie, approximately 3500 mEq in a 70-kg person).

Hypokalemia is defined as a potassium level less than 3.5 mEq/L.

Moderate hypokalemia is a serum level of 2.5-3 mEq/L.

Severe hypokalemia is defined as a level less than 2.5 mEq/L.

Potassium Homeostasis

Potassium, the most abundant intracellular cation, is essential for the life of the organism. Potassium is obtained through the diet, and common potassium-rich foods include meats, beans, fruits, and potatoes.

Gastrointestinal absorption is complete, resulting in daily excess intake of approximately 1 mEq/kg/d (60-100 mEq). Ninety percent of this excess is excreted through the kidneys, and 10% is excreted through the gut. Potassium homeostasis is maintained predominantly through the regulation of renal excretion. The most important site of regulation is the collecting duct, where aldosterone receptors are present.

Excretion is increased by (1) aldosterone, (2) high sodium delivery to the collecting duct (eg, diuretics), (3) high urine flow (eg, osmotic diuresis), (4) high serum potassium level, and (5) delivery of negatively charged ions to the collecting duct (eg, bicarbonate).

Excretion is decreased by (1) absence or relative deficiency of aldosterone, (2) low sodium delivery to the collecting duct, (3) low urine flow, (4) low serum potassium level, and (5) renal failure

Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is chronically high, potassium excretion likewise is increased. In the absence of potassium intake, obligatory renal losses are 10-15 mEq/d. Thus, chronic losses occur in the absence of any ingested potassium. The kidney maintains a central role in the maintenance of potassium homeostasis, even in the setting of chronic renal failure. Renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the glomerular filtration rate drops to less than 15-20 mL/min. Additionally, in the presence of renal failure, the proportion of potassium excreted through the gut increases. The colon is the major site of gut regulation of potassium excretion. Therefore, potassium levels can remain relatively normal under stable conditions, even with advanced renal insufficiency. However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load.

Serum potassium level

Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores. Because potassium moves easily across cell membranes, serum potassium levels reflect movement of potassium between intracellular and extracellular fluid compartments, as well as total body potassium homeostasis.

Mechanisms for sensing extracellular potassium concentration are not well understood. Evidence suggests that adrenal glomerulosa cells and pancreatic beta cells may play a role in potassium sensing, resulting in alterations in aldosterone and insulin secretion.^{[1, 2]} As both of these hormonal systems play important roles in potassium homeostasis, these new findings are no surprise; however, the molecular mechanisms by which these potassium channels signal changes in hormone secretion and activity have still not been determined.

Muscle contains the bulk of body potassium, and the notion that muscle could play a prominent role in the regulation of serum potassium concentration through alterations in sodium pump activity has been promoted for a number of years. Insulin stimulated by potassium ingestion increases the activity of the sodium pump in muscle cells, resulting in an increased uptake of potassium. Studies in a model of potassium deprivation demonstrate that acutely, skeletal muscle develops resistance to insulin-stimulated potassium uptake even in the absence of changes in muscle cell sodium pump expression. However, long term potassium deprivation results in a decrease in muscle cell sodium-pump expression, resulting in decreased muscle uptake of potassium.^{[3, 4, 5]}

Thus, there appears to be a well-developed system for sensing potassium by the pancreas and adrenal glands, resulting in rapid adjustments in immediate potassium disposal and for long-term potassium homeostasis. High potassium states stimulate cellular uptake via insulin-mediated stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidney via aldosterone-mediated enhancement of distal renal expression of secretory potassium channels (ROMK). Low potassium states result in insulin resistance, impairing potassium uptake into muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion.

Several factors regulate the distribution of potassium between the intracellular and extracellular space, as follows:

• Glycoregulatory hormones: (1) Insulin enhances potassium entry into cells, and (2) glucagon impairs potassium entry into cells.
• Adrenergic stimuli: (1) Beta-adrenergic stimuli enhance potassium entry into cells, and (2) alpha-adrenergic stimuli impair potassium entry into cells.
• pH: (1) Alkalosis enhances potassium entry into cells, and (2) acidosis impairs potassium entry into cells.

An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissue breakdown releases potassium into extracellular space.

http://emedicine.medscape.com/article/242008-overview

What Are the Effects of Elevated Potassium Levels?

Please visit this website there is important information.

http://www.whatisall.com/health/what-are-the-effects-of-elevated-potassium-levels.html

Guías alimentarias para la parálisis periódica hipopotasémica

La guías alimentarias para la parálisis periódica hipopotasémica

Los cambios en su dieta puede ayudar a reducir la frecuencia de episodios de parálisis. Sin embargo,
usted todavía tendrá que tomar sus pastillas de potasio según lo prescrito por su médico.
Recomendaciones:
• Reducir el consumo de sal. No agregue sal al cocinar o en la mesa. Elige la sal
alimentos reducidos (por ejemplo, la margarina, los alimentos enlatados).
• Reducir y modificar su consumo de carbohidratos. Elija alimentos ricos en carbohidratos, que
digieren lentamente por el cuerpo. Estos incluyen panes y cereales, vegetales con almidón,
fruta y leche y el yogur.
Y Grupo de alimentos
Panes y cereales integrales, panes ™ de rollos de pan integral tostado y panecillos, los
pan de fruta, pan de pita.
™ cereales integrales / galletas multigrano, galletas dulces simples, por ejemplo, rico
El té, harina de trigo triturado.
™ de alta fibra de cereales para el desayuno egallbran, miniwheats, tostadas
muesli, special K, tutor, copos de avena, vita británicos.
™ Pasta de todo tipo, arroz de grano largo como el basmati o doongara
arroz.
Las verduras con almidón ™ camote y choclo, las papas Pontiac.
™ de leguminosas: frijoles, lentejas, garbanzos, frijoles al horno.
Frutas ™ de Apple, albaricoques secos, cerezas, naranjas, kiwis, plátanos,
melocotones (en jugo), peras, ciruelas.
La leche y el yogur de leche ™, yogur endulzado artificialmente, helados, natillas.
• Incluir un montón de alimentos ricos en potasio que son bajos en hidratos de carbono.
Por ejemplo:
o aguacate, almendras, nueces, nueces de macadamia, pacanas, queso, huevos, Bruselas
coles, coliflor, calabaza, tomates, espinacas, espárragos, repollo,
brócoli, champiñones, nueces, mantequilla de maní.
* Evite el alcohol.

Dietary guidelines for hypokalemic periodic paralysis

Dietary guidelines for hypokalemic periodic paralysis
Changes to your diet may help reduce the frequency of episodes of paralysis. However,
you will still need to take your potassium tablets as prescribed by your doctor.
Recommendations:
• Reduce your salt intake.  Do not add salt in cooking or at the table. Choose salt
reduced foods (eg margarine, canned foods).
• Reduce and modify your carbohydrate intake. Choose carbohydrate foods which are
digested slowly by the body. These include breads and cereals, starchy vegetables,
fruit and milk and yoghurt.
Food group  Choose
Breads and cereals  ™ Wholegrain breads, wholegrain bread rolls and toasting muffins,
fruit loaf, pita bread.
™ Wholegrain/multigrain crackers, plain sweet biscuits e.g. Rich
Tea, shredded wheatmeal.
™ High fibre breakfast cereals e.g.allbran, miniwheats, toasted
muesli, special K, guardian, rolled oats, vita brits.
™ Pasta of all types, long grain rice such as basmati or doongara
rice.
Starchy vegetables  ™ Sweet potato and corn, pontiac potatoes.
™ Legumes: kidney beans, lentils, chickpeas, baked beans.
Fruit  ™ Apple, dried apricots, cherries, orange, kiwifruit, bananas,
peaches (in juice), pears, plums.
Milk and yoghurt  ™ Milk, artificially sweetened yoghurt, ice-cream, custard.
• Include plenty of high potassium foods which are low in carbohydrate.
For example:
o Avocado, almonds, walnuts, macadamias, pecans, cheese, eggs, brussel
sprouts, cauliflower, pumpkin, tomatoes, spinach, asparagus, cabbage,
broccoli, mushrooms, nuts, peanut butter.
*Avoid alcohol.

Hypokalemic periodic paralysis Definition:

Hypokalemic periodic paralysis is a condition of intermittent episodes of muscle weakness and sometimes severe paralysis. It is one of a group of genetic disorders that includes hyperkalemic periodic paralysis and thyrotoxic periodic paralysis.
This disorder is distinguished from other forms of periodic paralysis in that people with this disorder have normal thyroid function and very low blood levels of potassium during episodes of weakness.
Hypokalemic periodic paralysis is a congenital (present from birth) condition. It can be inherited but occasionally occurs as a result of a non-inherited genetic mutation that affects just the sperm or the egg cell. In most cases, it is inherited as an autosomal dominant disorder (only one parent must transmit the gene for the baby to be affected).
The disorder involves attacks of muscle weakness or paralysis alternating with periods of normal muscle function. Attacks usually begin in adolescence, but they can occur before age 10. Attacks of intermittent weakness that do not begin until adulthood are rare and are usually caused by other disorders.
The frequency of attacks varies from daily to yearly. Episodes of muscle weakness usually last between a few hours and one day. Other forms of periodic paralysis may last longer.
During an attack of muscle weakness, there is a low level of potassium in the bloodstream. Serum potassium levels are normal between attacks. There is no decrease in total body potassium, however. Potassium flows from the bloodstream into muscle cells during attacks.
Insulin levels may affect the course of the disorder in some people because insulin increases the flow of potassium into cells.
Weakness most commonly affects the muscles of the arms and legs, but it may occasionally affect the eye muscles or the muscles involved in breathing and swallowing (which can be fatal).
Although muscle strength is initially normal between attacks, repeated attacks may eventually cause worsening and permanent muscle weakness between attacks.
Attacks may be triggered by eating meals high in carbohydrate or salt, or by consuming alcohol. Attacks most commonly occur after sleep or rest and are rare during exercise, but rest after an exercise period may trigger an attack. The risk is slightly higher in Asian men who also have thyroid disorders (thyrotoxic periodic paralysis).
Risks include having other family members with periodic paralysis.

Hypokalemic periodic paralysis occurs in approximately 1 out of 100,000 people.
Men are affected more often than women and usually have more severe symptoms.

Excessive consumption of cola drinks can cause muscle problems

Society is more and more, consuming cola soft drinks and this type or is starting to generate a series of health problems. We are consuming more soft drinks than ever before and a number of issues of health and related problems have been identified in dentures including bone demineralization, and the development of metabolic syndrome and diabetes, "says Dr. Moses Elisaf working in the Department of Internal Medicine University of Ioannina, Greece.
"In this regard, there is growing evidence that allow us to suggest that excess consumption of these drinks tail may also result in hypokalemia, which drop the blood potassium levels, end up causing an adverse effect on vital functions of muscles. "
According to the definition posted on Wikipedia, the "hypokalemia" (also known as hypokalemia) is a disorder in body fluid balance, characterized by decreased levels of potassium ion (K) blood, with levels below 3.5mmol/lt.
Hypokalemia has several causes. The most common are decreased intake, increased potassium losses (which can be taken for kidney or vomiting and diarrhea), increased substance called renin (which increases aldosterone), Cushing Syndrome (where there is an increase in the levels of glucocorticorticoides, which also have mineralocorticoid effect as aldosterone), hyperglycemia (by causing diuresis, etc.).
Because potassium is responsible for facilitating the transmission of nerve impulses across the cell membrane, the symptoms of this disorder include fatigue, myalgia (muscle pain), you can get to be a progressive weakness and possible paralysis hypoventilation.
DIFFERENT EFFECTS
The research conducted by Dr. Elisaf and colleagues has shown that the symptoms found can vary from very mild to profound weakness or partial paralysis.
Fortunately, all the patients studied achieved a rapid and complete recovery after having stopped drinking these beverages or receive oral or intravenous potassium supplements.
In the studies analyzed patients had daily intakes that ranged from two to nine liters of cola per day. Even, there were two cases of pregnant women were admitted to hospital consultation exhibiting low levels of potassium.
The first 21 years of age, admitted drinking three liters of cola per day and complained of symptoms of fatigue, loss of appetite and vomiting. An electrocardiogram also revealed that he had a heart blockage, while blood tests showed they had low levels of potassium.
The second also had low levels of potassium and suffering of the growing weakness. It turned out he had been drinking up to seven liters of cola per day for the past 10 months.

Among the findings is discussed that the hypokalemia may be caused by excessive consumption of three of the most common ingredients found in colas: glucose, fructose and caffeine.

"The individual role of each of these ingredients in the pathophysiology of hypokalemia induced by this type of beverage has not been determined and can vary in different patients,.