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.
Sunday, 10 April 2011
Tuesday, 14 December 2010
Excessive consumption of cola drinks can cause muscle problems
"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,.
El consumo excesivo de bebidas cola puede generar problemas musculares
"Al respecto, tenemos cada vez más evidencias que nos permiten sugerir que el exceso de consumo de estas bebidas cola puede también dar lugar a hipopotasemia, en la que la caída los niveles de potasio en sangre, terminan provocando un efecto adverso en las funciones vitales de los músculos".
De acuerdo a la definición que se publica en la Wikipedia, la "hipopotasemia" (también conocida como hipokalemia), es un trastorno en el equilibrio hidroelectrolítico del cuerpo, que se caracteriza por un descenso en los niveles del ion potasio (K) en la sangre, con niveles por debajo de 3.5mmol/lt.
La hipokalemia tiene varias causas. Entre las más frecuentes están una ingestión disminuida, un aumento en las pérdidas de potasio (estas pueden ser renales o darse por vómitos y diarreas), el aumento de la sustancia conocida como renina (que hace que aumente la aldosterona), el Síndrome de Cushing (en el cual hay un aumento en los niveles de glucocorticorticoides, los cuales tienen también efecto mineralcorticoide como la aldosterona), la hiperglucemia (por la diuresis que provoca), etc.
Debido a que el potasio se encarga de facilitar la transmisión del impulso nervioso a través de la membrana celular, los síntomas de este trastorno son: cansancio, mialgias (dolor muscular), puede llegar a haber una debilidad progresiva con hipoventilación y posible páralisis completa.
Entre las conclusiones se comenta que la hipopotasemia puede ser causada por el consumo excesivo de tres de los ingredientes más comunes presentes en las bebidas cola: glucosa, fructosa y cafeína.
"El papel individual de cada uno de estos ingredientes en la fisiopatología de la hipopotasemia inducida por este tipo de bebida no se ha determinado y puede variar según los distintos pacientes,.
Tuesday, 9 November 2010
Symptoms of low potassium?
Potassium affects the way neuromuscular cells discharge energy (depolarize) and then regenerate (repolarize) that energy to be able to fire again. When potassium levels are low, the cells cannot repolarize and are unable to fire repeatedly, as is needed for the function of muscles and nerves. It is understandable then that the effects of low potassium include
1) muscle weakness,
2) muscle aches, and
3) muscle cramps.
( A muscle cramp is an involuntarily and forcibly contracted muscle that does not relax. When we use the muscles that can voluntarily be controlled, such as those of our arms and legs, they alternately contract and relax as we move our limbs. Muscles that support our head, neck, and trunk contract similarly in a synchronized fashion to maintain our posture. A muscle (or even a few fibers of a muscle) that involuntarily (without consciously willing it) contracts is called a "spasm." If the spasm is forceful and sustained, it becomes a cramp.)
Since the heart is also a muscle, there can be some changes in the electrocardiogram (EKG or ECG) What is an electrocardiogram (ECG, EKG)?
(the electrocardiogram (ECG or EKG) is a noninvasive test that is used to reflect underlying heart conditions by measuring the electrical activity of the heart. By positioning leads (electrical sensing devices) on the body in standardized locations, information about many heart conditions can be learned by looking for characteristic patterns on the EKG.)
that are associated with hypokalemia, especially in the repolarization section of the EKG tracing.
Palpitations ( Palpitations are the unpleasant sensations of irregular and/or forceful beating of the heart in the chest. This symptom can be caused by a change in the rate or rhythm, or by an increase in the force of the contraction of the heart muscle. In some patients with palpitations, no heart disease or abnormal heart rhythms can be found. In others, palpitations result from abnormal heart rhythms called arrhythmias. Arrhythmias are heartbeats that are too slow, too rapid, irregular, or too early.) (irregular heartbeats) may be perceived by the patient. In severe cases, hypokalemia can lead to dangerous disturbances in heart rhythm (arrhythmias).
1) muscle weakness,
2) muscle aches, and
3) muscle cramps.
( A muscle cramp is an involuntarily and forcibly contracted muscle that does not relax. When we use the muscles that can voluntarily be controlled, such as those of our arms and legs, they alternately contract and relax as we move our limbs. Muscles that support our head, neck, and trunk contract similarly in a synchronized fashion to maintain our posture. A muscle (or even a few fibers of a muscle) that involuntarily (without consciously willing it) contracts is called a "spasm." If the spasm is forceful and sustained, it becomes a cramp.)
Since the heart is also a muscle, there can be some changes in the electrocardiogram (EKG or ECG) What is an electrocardiogram (ECG, EKG)?
(the electrocardiogram (ECG or EKG) is a noninvasive test that is used to reflect underlying heart conditions by measuring the electrical activity of the heart. By positioning leads (electrical sensing devices) on the body in standardized locations, information about many heart conditions can be learned by looking for characteristic patterns on the EKG.)
that are associated with hypokalemia, especially in the repolarization section of the EKG tracing.
Palpitations ( Palpitations are the unpleasant sensations of irregular and/or forceful beating of the heart in the chest. This symptom can be caused by a change in the rate or rhythm, or by an increase in the force of the contraction of the heart muscle. In some patients with palpitations, no heart disease or abnormal heart rhythms can be found. In others, palpitations result from abnormal heart rhythms called arrhythmias. Arrhythmias are heartbeats that are too slow, too rapid, irregular, or too early.) (irregular heartbeats) may be perceived by the patient. In severe cases, hypokalemia can lead to dangerous disturbances in heart rhythm (arrhythmias).
Monday, 4 October 2010
Hypokalemic periodic paralysis
Hypokalemic periodic paralysis is a condition in which a person has episodes of muscle weakness and sometimes severe paralysis.
The condition is congenital, which means it is present from birth. In most cases, it is passed down through families (inherited) as an autosomal dominant disorder. That means only one parent needs to pass the gene related to this condition on to you in order for you to be affected.
Occasionally, the condition may be the result of a genetic problem that is not inherited.
Unlike other forms of periodic paralysis, persons with congenital hypokalemic periodic paralysis have normal thyroid function and very low blood levels of potassium during episodes of weakness. This results from potassium moving from the blood into muscle cells in an abnormal way.
Risks include having other family members with periodic paralysis. The risk is slightly higher in Asian men who also have thyroid disordersthyroid disorders.
Disorders that cause intermittent episodes of paralysis as their primary effect are uncommon. Hypokalemic periodic paralysis occurs in approximately 1 out of 100,000 people.
The disorder involves attacks of muscle weakness or loss of muscle movement (paralysis) that come and go. Initially, there is normal muscle strength between attacks.
Attacks usually begin in adolescence, but they can occur before age 10. Attacks that do not begin until adulthood are rare in people with hypokalemic periodic paralysis and are usually caused by other disorders.
How often the attacks occur varies. Some people have attacks every day, while others have them once a year. Episodes of muscle weakness usually last between a few hours and a day.
The weakness or paralysisparalysis:
* Most commonly is located at the shoulders and hips
* May also affect the arms, legs, muscles of the eyes, and muscles that help you breathe and swallow
* Occurs intermittently
* Most commonly occurs on awakening
* Most commonly occurs after sleep or rest
* Is rare during exercise, but may be triggered by rest after exercise
* May be triggered by heavy, high-carbohydrate, high-salt meals or alcohol consumption
* Usually lasts 3 - 24 hours
Other symptoms may include:
* Eyelid myotonia (a condition in which after opening and closing the eyes, the patient cannot open them for a short time)
Note: The patient's thinking remains alert during attacks.
Between attacks, a physical examination shows nothing abnormal. Before an attack, there may be leg stiffness or heaviness in the legs.
During an attack of muscle weakness, the blood potassium level is low. This confirms the diagnosis. There is no decrease in total body potassium, and blood potassium levels are normal between attacks.
During an attack, muscle reflexes may be decreased or absent, and muscles go limp rather than staying stiff. The muscle groups near the body, such as shoulders and hips, are involved more often than the arms and legs.
* An ECGECG or heart tracing may be abnormal during attacks.
* An EMGEMG or muscle tracing is usually normal between attacks and abnormal during attacks.
* A muscle biopsymuscle biopsy may show abnormalities.
Muscle weakness that involves the breathing or swallowing muscles is an emergency situation. Dangerous heart arrhythmiasarrhythmias may also occur during attacks.
The goals of treatment are relief of symptoms and prevention of further attacks.
Potassium that is given during an attack may stop the attack. It is preferred that potassium be given by mouth, but if weakness is severe, potassium may need to be given through a vein (IV). Note: Potassium, especially intravenous potassium, should be given with caution, especially in individuals with kidney disease.
Taking potassium supplements will not prevent attacks.
Avoiding alcohol and eating a low-carbohydrate diet may help.
A medicine called acetazolamide prevents attacks in many cases. If you take this medicine, your doctor may tell you to also take potassium supplements because acetazolamide may cause your body to lose potassium.
Triamterene or spironolactone may help to prevent attacks in people who do not respond to acetazolamide.
Hypokalemic periodic paralysis responds well to treatment. Treatment may prevent, and even reverse, progressive muscle weakness. Although muscle strength is initially normal between attacks, repeated attacks may eventually cause worsening and permanent muscle weakness between attacks.
Possible Complications
* Kidney stonesKidney stones (a side effect of acetazolamide)
* Heart arrhythmias during attacks
* Difficulty breathingDifficulty breathing, speaking, or swallowing during attacks (rare)
* Progressive muscle weakness
Hypokalemic periodic paralysis cannot be prevented. Because it can be inherited, genetic counseling may be advised for couples at risk for the disorder.
Treatment prevents attacks of weakness. Before an attack, there may be leg stiffness or heaviness in the legs. Performing mild exercise when these symptoms start may help prevent a full-blown attack.
The condition is congenital, which means it is present from birth. In most cases, it is passed down through families (inherited) as an autosomal dominant disorder. That means only one parent needs to pass the gene related to this condition on to you in order for you to be affected.
Occasionally, the condition may be the result of a genetic problem that is not inherited.
Unlike other forms of periodic paralysis, persons with congenital hypokalemic periodic paralysis have normal thyroid function and very low blood levels of potassium during episodes of weakness. This results from potassium moving from the blood into muscle cells in an abnormal way.
Risks include having other family members with periodic paralysis. The risk is slightly higher in Asian men who also have thyroid disordersthyroid disorders.
Disorders that cause intermittent episodes of paralysis as their primary effect are uncommon. Hypokalemic periodic paralysis occurs in approximately 1 out of 100,000 people.
The disorder involves attacks of muscle weakness or loss of muscle movement (paralysis) that come and go. Initially, there is normal muscle strength between attacks.
Attacks usually begin in adolescence, but they can occur before age 10. Attacks that do not begin until adulthood are rare in people with hypokalemic periodic paralysis and are usually caused by other disorders.
How often the attacks occur varies. Some people have attacks every day, while others have them once a year. Episodes of muscle weakness usually last between a few hours and a day.
The weakness or paralysisparalysis:
* Most commonly is located at the shoulders and hips
* May also affect the arms, legs, muscles of the eyes, and muscles that help you breathe and swallow
* Occurs intermittently
* Most commonly occurs on awakening
* Most commonly occurs after sleep or rest
* Is rare during exercise, but may be triggered by rest after exercise
* May be triggered by heavy, high-carbohydrate, high-salt meals or alcohol consumption
* Usually lasts 3 - 24 hours
Other symptoms may include:
* Eyelid myotonia (a condition in which after opening and closing the eyes, the patient cannot open them for a short time)
Note: The patient's thinking remains alert during attacks.
Between attacks, a physical examination shows nothing abnormal. Before an attack, there may be leg stiffness or heaviness in the legs.
During an attack of muscle weakness, the blood potassium level is low. This confirms the diagnosis. There is no decrease in total body potassium, and blood potassium levels are normal between attacks.
During an attack, muscle reflexes may be decreased or absent, and muscles go limp rather than staying stiff. The muscle groups near the body, such as shoulders and hips, are involved more often than the arms and legs.
* An ECGECG or heart tracing may be abnormal during attacks.
* An EMGEMG or muscle tracing is usually normal between attacks and abnormal during attacks.
* A muscle biopsymuscle biopsy may show abnormalities.
Muscle weakness that involves the breathing or swallowing muscles is an emergency situation. Dangerous heart arrhythmiasarrhythmias may also occur during attacks.
The goals of treatment are relief of symptoms and prevention of further attacks.
Potassium that is given during an attack may stop the attack. It is preferred that potassium be given by mouth, but if weakness is severe, potassium may need to be given through a vein (IV). Note: Potassium, especially intravenous potassium, should be given with caution, especially in individuals with kidney disease.
Taking potassium supplements will not prevent attacks.
Avoiding alcohol and eating a low-carbohydrate diet may help.
A medicine called acetazolamide prevents attacks in many cases. If you take this medicine, your doctor may tell you to also take potassium supplements because acetazolamide may cause your body to lose potassium.
Triamterene or spironolactone may help to prevent attacks in people who do not respond to acetazolamide.
Hypokalemic periodic paralysis responds well to treatment. Treatment may prevent, and even reverse, progressive muscle weakness. Although muscle strength is initially normal between attacks, repeated attacks may eventually cause worsening and permanent muscle weakness between attacks.
Possible Complications
* Kidney stonesKidney stones (a side effect of acetazolamide)
* Heart arrhythmias during attacks
* Difficulty breathingDifficulty breathing, speaking, or swallowing during attacks (rare)
* Progressive muscle weakness
Hypokalemic periodic paralysis cannot be prevented. Because it can be inherited, genetic counseling may be advised for couples at risk for the disorder.
Treatment prevents attacks of weakness. Before an attack, there may be leg stiffness or heaviness in the legs. Performing mild exercise when these symptoms start may help prevent a full-blown attack.
Friday, 24 September 2010
Tuesday, 10 August 2010
Hypokalemia (Hypopotassemia)
CAUSAS hipopotasemia
Causas La hipopotasemia puede ser consecuencia de una o más de las siguientes condiciones médicas:
Inadecuada ingesta de potasio
* Tal vez la causa más evidente es el consumo insuficiente de potasio (es decir, una dieta baja en potasio). Sin embargo, sin pérdida excesiva de potasio del cuerpo, esta es una causa poco frecuente de hipopotasemia.
Gastrointestinal / tegumento pérdida
* Una causa más frecuente es la pérdida excesiva de potasio, a menudo asociados con grandes pérdidas de líquido que "flush" de potasio del cuerpo. Normalmente, esto es una consecuencia de la diarrea, sudoración excesiva, o las pérdidas asociadas con los procedimientos quirúrgicos. Los vómitos pueden causar hipopotasemia, aunque no de potasio que se pierde mucho del vómito. Más bien, hay fuertes pérdidas urinarias de K + en el marco de bicarbonaturia post-emético que la excreción urinaria de potasio vigor (véase Alcalosis abajo).
la pérdida urinaria
* Algunos medicamentos pueden causar pérdida de exceso de potasio en la orina. Los diuréticos, como los diuréticos tiazídicos (por ejemplo, hidroclorotiazida) y los diuréticos de asa (por ejemplo, furosemida) son una causa frecuente de hipopotasemia. Otros medicamentos como el antifúngico, la anfotericina B, o el medicamento contra el cáncer, el cisplatino, también puede causar hipopotasemia a largo plazo.
* Un caso especial de la pérdida de potasio se produce con cetoacidosis diabética. Además de las pérdidas urinarias de poliuria y contracción de volumen, también existe pérdida obligada de potasio de los túbulos renales como socio catiónica de la cetona con carga negativa, β-hidroxibutirato.
* La hipomagnesemia puede causar hipopotasemia. El magnesio es necesario para la tramitación adecuada de potasio. Esto puede ser evidente cuando hipocalemia persiste a pesar de suplementos de potasio. Otras anomalías en los electrolitos pueden también estar presentes.
* Alcalosis puede causar hipopotasemia transitoria por dos mecanismos. En primer lugar, la alcalosis provoca un desplazamiento de potasio del plasma y los líquidos intersticiales en las células, quizá mediado por la estimulación de Na +-H + y un cambio subsiguiente activación de la actividad Na + / K +-ATPasa. En segundo lugar, un aumento agudo de plasma HCO3-concentración (causada por el vómito, por ejemplo) deberá exceder la capacidad del túbulo proximal renal para reabsorber este anión, y el potasio se excreta en forma de un socio ción obliga al bicarbonato. La alcalosis metabólica suele estar presente en los estados de depleción de volumen, por lo que también se pierde potasio a través de mecanismos mediados por la aldosterona.
* Los estados de enfermedad que llevan a niveles anormalmente altos de aldosterona puede causar hipertensión y el exceso de pérdidas urinarias de potasio. Estos incluyen estenosis de la arteria renal y tumores (en general, no maligno) de las glándulas suprarrenales. La hipertensión y la hipocaliemia también puede ser visto con una deficiencia de la deshidrogenasa tipo 11-beta-hidroxiesteroide 2 enzima que permite cortisol para estimular los receptores de aldosterona. Esta deficiencia - conocido como el síndrome de exceso aparente de mineralocorticoides - bien pueden ser congénitas o causadas por el consumo de glicirricina, que figura en el extracto de regaliz, a veces se encuentra en los suplementos a base de hierbas, dulces y tabaco de mascar.
* Defectos hereditarios raros de los transportadores de sal renal, como el síndrome de Bartter o el síndrome de Gitelman, puede causar hipopotasemia, de manera similar a la de los diuréticos. A diferencia de los estados de la enfermedad primaria de los excesos de la aldosterona, la presión arterial normal o baja en Bartter o de Gitelman.
Distribución fuera de la LEC
* Además de la alcalosis, otros factores pueden causar transitorios desplazamiento del potasio hacia las células, presumiblemente por la estimulación de la Na-K-ATPasa. Estas hormonas y medicamentos incluyen la insulina, la adrenalina y otros agonistas beta (por ejemplo, albuterol o salmeterol) y xantinas (por ejemplo, teofilina).
* Raras hereditarias defectos de los canales iónicos y transportadores musculares que causan parálisis periódica hipopotasémica puede precipitar ataques ocasionales de hipocalemia severa y debilidad muscular. Estos defectos causan una mayor sensibilidad a los cambios normales de potasio producido por catecoles y / o insulina y / o de la hormona tiroidea, que dan lugar al movimiento de potasio del líquido extracelular en las células musculares.
Otros / no agrupados
* Ha habido un puñado de informes publicados que describen las personas con hipopotasemia grave relacionada con el consumo crónico extrema (4-10 L / día) de las colas. La hipopotasemia se piensa que es de la combinación del efecto diurético de la cafeína y el consumo de líquidos abundantes, aunque también puede estar relacionada con la diarrea causada por la ingestión de fructosa pesados.
Pseudohypokalemia
* Pseudohypokalemia es una disminución en la cantidad de potasio que se produce debido a la absorción excesiva de potasio por las células metabólicamente activas después de la sangre se ha elaborado. Es un artefacto de laboratorio que pueden ocurrir cuando las muestras sanguíneas permanecen en condiciones de calor durante varias horas antes de su transformación.
Fisiopatología El potasio es esencial para muchas funciones del cuerpo, incluyendo el músculo y el nervio actividad. El gradiente electroquímico de potasio entre el espacio intracelular y extracelular es esencial para la función nerviosa, en particular, el potasio es necesario para repolarizar la membrana de la célula a un estado de reposo después de un potencial de acción ha pasado. Disminución de los niveles de potasio en el espacio extracelular causará hiperpolarización del potencial de membrana en reposo. Esta hiperpolarización es causada por el efecto del gradiente de potasio alterado en reposo potencial de membrana tal como se define por la ecuación de Goldman. Como resultado, un mayor estímulo normal se requiere para la despolarización de la membrana con el fin de iniciar un potencial de acción. En ciertas condiciones, esto hará que las células menos excitable. Sin embargo, en el corazón, hace que los miocitos de convertirse hiperexcitables. Bajo los potenciales de membrana en la aurícula puede causar arritmias, debido a una recuperación más completa de la inactivación de sodio canales, haciendo que el disparo de un potencial de acción más probable. Además, el potasio extracelular reducida (paradójicamente) inhibe la actividad del potasio IKr actuales y los retrasos repolarización ventricular. Este retraso en la repolarización puede promover arritmias por reentrada.
Inadecuada ingesta de potasio
* Tal vez la causa más evidente es el consumo insuficiente de potasio (es decir, una dieta baja en potasio). Sin embargo, sin pérdida excesiva de potasio del cuerpo, esta es una causa poco frecuente de hipopotasemia.
Gastrointestinal / tegumento pérdida
* Una causa más frecuente es la pérdida excesiva de potasio, a menudo asociados con grandes pérdidas de líquido que "flush" de potasio del cuerpo. Normalmente, esto es una consecuencia de la diarrea, sudoración excesiva, o las pérdidas asociadas con los procedimientos quirúrgicos. Los vómitos pueden causar hipopotasemia, aunque no de potasio que se pierde mucho del vómito. Más bien, hay fuertes pérdidas urinarias de K + en el marco de bicarbonaturia post-emético que la excreción urinaria de potasio vigor (véase Alcalosis abajo).
la pérdida urinaria
* Algunos medicamentos pueden causar pérdida de exceso de potasio en la orina. Los diuréticos, como los diuréticos tiazídicos (por ejemplo, hidroclorotiazida) y los diuréticos de asa (por ejemplo, furosemida) son una causa frecuente de hipopotasemia. Otros medicamentos como el antifúngico, la anfotericina B, o el medicamento contra el cáncer, el cisplatino, también puede causar hipopotasemia a largo plazo.
* Un caso especial de la pérdida de potasio se produce con cetoacidosis diabética. Además de las pérdidas urinarias de poliuria y contracción de volumen, también existe pérdida obligada de potasio de los túbulos renales como socio catiónica de la cetona con carga negativa, β-hidroxibutirato.
* La hipomagnesemia puede causar hipopotasemia. El magnesio es necesario para la tramitación adecuada de potasio. Esto puede ser evidente cuando hipocalemia persiste a pesar de suplementos de potasio. Otras anomalías en los electrolitos pueden también estar presentes.
* Alcalosis puede causar hipopotasemia transitoria por dos mecanismos. En primer lugar, la alcalosis provoca un desplazamiento de potasio del plasma y los líquidos intersticiales en las células, quizá mediado por la estimulación de Na +-H + y un cambio subsiguiente activación de la actividad Na + / K +-ATPasa. En segundo lugar, un aumento agudo de plasma HCO3-concentración (causada por el vómito, por ejemplo) deberá exceder la capacidad del túbulo proximal renal para reabsorber este anión, y el potasio se excreta en forma de un socio ción obliga al bicarbonato. La alcalosis metabólica suele estar presente en los estados de depleción de volumen, por lo que también se pierde potasio a través de mecanismos mediados por la aldosterona.
* Los estados de enfermedad que llevan a niveles anormalmente altos de aldosterona puede causar hipertensión y el exceso de pérdidas urinarias de potasio. Estos incluyen estenosis de la arteria renal y tumores (en general, no maligno) de las glándulas suprarrenales. La hipertensión y la hipocaliemia también puede ser visto con una deficiencia de la deshidrogenasa tipo 11-beta-hidroxiesteroide 2 enzima que permite cortisol para estimular los receptores de aldosterona. Esta deficiencia - conocido como el síndrome de exceso aparente de mineralocorticoides - bien pueden ser congénitas o causadas por el consumo de glicirricina, que figura en el extracto de regaliz, a veces se encuentra en los suplementos a base de hierbas, dulces y tabaco de mascar.
* Defectos hereditarios raros de los transportadores de sal renal, como el síndrome de Bartter o el síndrome de Gitelman, puede causar hipopotasemia, de manera similar a la de los diuréticos. A diferencia de los estados de la enfermedad primaria de los excesos de la aldosterona, la presión arterial normal o baja en Bartter o de Gitelman.
Distribución fuera de la LEC
* Además de la alcalosis, otros factores pueden causar transitorios desplazamiento del potasio hacia las células, presumiblemente por la estimulación de la Na-K-ATPasa. Estas hormonas y medicamentos incluyen la insulina, la adrenalina y otros agonistas beta (por ejemplo, albuterol o salmeterol) y xantinas (por ejemplo, teofilina).
* Raras hereditarias defectos de los canales iónicos y transportadores musculares que causan parálisis periódica hipopotasémica puede precipitar ataques ocasionales de hipocalemia severa y debilidad muscular. Estos defectos causan una mayor sensibilidad a los cambios normales de potasio producido por catecoles y / o insulina y / o de la hormona tiroidea, que dan lugar al movimiento de potasio del líquido extracelular en las células musculares.
Otros / no agrupados
* Ha habido un puñado de informes publicados que describen las personas con hipopotasemia grave relacionada con el consumo crónico extrema (4-10 L / día) de las colas. La hipopotasemia se piensa que es de la combinación del efecto diurético de la cafeína y el consumo de líquidos abundantes, aunque también puede estar relacionada con la diarrea causada por la ingestión de fructosa pesados.
Pseudohypokalemia
* Pseudohypokalemia es una disminución en la cantidad de potasio que se produce debido a la absorción excesiva de potasio por las células metabólicamente activas después de la sangre se ha elaborado. Es un artefacto de laboratorio que pueden ocurrir cuando las muestras sanguíneas permanecen en condiciones de calor durante varias horas antes de su transformación.
Fisiopatología El potasio es esencial para muchas funciones del cuerpo, incluyendo el músculo y el nervio actividad. El gradiente electroquímico de potasio entre el espacio intracelular y extracelular es esencial para la función nerviosa, en particular, el potasio es necesario para repolarizar la membrana de la célula a un estado de reposo después de un potencial de acción ha pasado. Disminución de los niveles de potasio en el espacio extracelular causará hiperpolarización del potencial de membrana en reposo. Esta hiperpolarización es causada por el efecto del gradiente de potasio alterado en reposo potencial de membrana tal como se define por la ecuación de Goldman. Como resultado, un mayor estímulo normal se requiere para la despolarización de la membrana con el fin de iniciar un potencial de acción. En ciertas condiciones, esto hará que las células menos excitable. Sin embargo, en el corazón, hace que los miocitos de convertirse hiperexcitables. Bajo los potenciales de membrana en la aurícula puede causar arritmias, debido a una recuperación más completa de la inactivación de sodio canales, haciendo que el disparo de un potencial de acción más probable. Además, el potasio extracelular reducida (paradójicamente) inhibe la actividad del potasio IKr actuales y los retrasos repolarización ventricular. Este retraso en la repolarización puede promover arritmias por reentrada.
CAUSES HYPOKALEMIA
Causes
Hypokalemia can result from one or more of the following medical conditions:Inadequate potassium intake
- Perhaps the most obvious cause is insufficient consumption of potassium (that is, a low-potassium diet). However, without excessive potassium loss from the body, this is a rare cause of hypokalemia.
Gastrointestinal/integument loss
- A more common cause is excessive loss of potassium, often associated with heavy fluid losses that "flush" potassium out of the body. Typically, this is a consequence of diarrhea, excessive perspiration, or losses associated with surgical procedures. Vomiting can also cause hypokalemia, although not much potassium is lost from the vomitus. Rather, there are heavy urinary losses of K+ in the setting of post-emetic bicarbonaturia that force urinary potassium excretion (see Alkalosis below).
Urinary loss
- Certain medications can cause excess potassium loss in the urine. Diuretics, including thiazide diuretics (e.g. hydrochlorothiazide) and loop diuretics (e.g. furosemide) are a common cause of hypokalemia. Other medications such as the antifungal, amphotericin B, or the cancer drug, cisplatin, can also cause long-term hypokalemia.
- A special case of potassium loss occurs with diabetic ketoacidosis. In addition to urinary losses from polyuria and volume contraction, there is also obligate loss of potassium from kidney tubules as a cationic partner to the negatively charged ketone, β-hydroxybutyrate.
- Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.
- Alkalosis can cause transient hypokalemia by two mechanisms. First, the alkalosis causes a shift of potassium from the plasma and interstitial fluids into cells; perhaps mediated by stimulation of Na+-H+ exchange and a subsequent activation of Na+/K+-ATPase activity. Second, 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. Metabolic alkalosis is often present in states of volume depletion, so potassium is also lost via aldosterone-mediated mechanisms.
- Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium. These include renal artery stenosis and tumors (generally non-malignant) of the adrenal glands. Hypertension and hypokalemia can also be seen with a deficiency of the 11-beta-hydroxysteroid dehydrogenase type 2 enzyme which allows cortisols to stimulate aldosterone receptors. This deficiency -- known as apparent mineralocorticoid excess syndrome -- can either be congenital or caused by consumption of glycyrrhizin, which is contained in extract of licorice, sometimes found in herbal supplements, candies and chewing tobacco.
- Rare hereditary defects of renal salt transporters, such as Bartter syndrome or Gitelman syndrome, can cause hypokalemia, in a manner similar to that of diuretics. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartter's or Gitelman's.
Distribution away from ECF
- In addition to alkalosis, other factors can cause transient shifting of potassium into cells, presumably by stimulation of the Na-K-ATPase. These hormones and medications include insulin, epinephrine, and other beta agonists (e.g. albuterol or salmeterol), and xanthines (e.g. Theophylline).
- Rare hereditary defects of muscular ion channels and transporters that cause hypokalemic periodic paralysis can precipitate occasional attacks of severe hypokalemia and muscle weakness. These defects cause a heightened sensitivity to the normal changes in potassium produced by catechols and/or insulin and/or thyroid hormone, which lead to movement of potassium from the extracellular fluid into the muscle cells.
Other/ungrouped
- There have been a handful of published reports describing individuals with severe hypokalemia related to chronic extreme consumption (4-10 L/day) of colas. The hypokalemia is thought to be from the combination of the diuretic effect of caffeine and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.
Pseudohypokalemia
- Pseudohypokalemia is a decrease in the amount of potassium that occurs due to excessive uptake of potassium by metabolically active cells after blood has been drawn. It is a laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing.
Pathophysiology
Potassium is essential for many body functions, including muscle and nerve activity. The electrochemical gradient of potassium between the intracellular and extracellular space is essential for nerve function; in particular, potassium is needed to repolarize the cell membrane to a resting state after an action potential has passed. Decreased potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. This hyperpolarization is caused by the effect of the altered potassium gradient on resting membrane potential as defined by the Goldman equation. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential.In certain conditions, this will make cells less excitable. However, in the heart, it causes myocytes to become hyperexcitable. Lower membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential more likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the IKr potassium current and delays ventricular repolarization. This delayed repolarization may promote reentrant arrythmias.
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