tag:blogger.com,1999:blog-89733826950675018812024-03-06T12:01:27.307-08:00SYMPTOMS AND CAUSES OF HYPOKALEMIC PERIODIC PARALYSISHypokalemia- Hipopotasemia - نقص بوتاسيوم الدم - 低血鉀症 -
Hypokaliämie - 低カリウム血症 - гипокалиемия - hipokaliemia - υποκαλιαιμία - hạ kali máu - хипокалемија - ipokaliemia - хипокалиемия - هیپوکالمی - היפּאָקאַלעמיאַ
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The purpose of this blog is to collate all the key information regarding Hypokalemic Periodic Paralys, its symptoms, side effects and treatment. Information in English and Spanish. *****hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.comBlogger228125tag:blogger.com,1999:blog-8973382695067501881.post-74247873987282878902022-03-09T06:29:00.001-08:002022-03-09T06:42:01.631-08:00Si mi nivel de potasio en la sangre es normal, ¿eso prueba que no tengo parálisis periódica hipopotasémica?<p>No. Aunque tener niveles bajos de potasio en la sangre durante los ataques es típico de la parálisis periódica hipopotasémica, entre ataques, las personas con parálisis periódica hipopotasémica pueden tener un nivel normal de potasio en la sangre (con frecuencia en el rango normal bajo).</p><p>Los ataques de parálisis generalmente se desencadenan por la caída del nivel de potasio en la sangre. Tales fluctuaciones de potasio ocurren en todos, pero en personas con parálisis periódica hipopotasémica familiar, estas caídas de potasio pueden producir episodios de parálisis. Por ejemplo, una comida rica en carbohidratos da como resultado la secreción de insulina en la sangre, lo que provoca una caída del nivel de potasio en la sangre a medida que el potasio y la glucosa ingresan a las células. En personas normales, una caída de este tipo en el potasio en sangre no produce síntomas. Sin embargo, en las personas con parálisis periódica hipopotasémica familiar, la caída del potasio en la sangre a menudo desencadena un episodio de parálisis.</p><p>Los niveles de potasio en la sangre pueden permanecer bajos mientras el músculo se recupera de un ataque reciente. Durante un ataque, los músculos que se paralizan se hinchan y absorben potasio, lo que provoca una disminución del potasio en la sangre. Pero a medida que se resuelve la hinchazón, el nivel de potasio en la sangre vuelve al rango normal. En consecuencia, un nivel normal de potasio en la sangre después de tal recuperación no debe considerarse evidencia en contra de una persona que tiene parálisis periódica hipopotasémica.</p><p>Al evaluar los niveles de potasio en sangre, es importante tener en cuenta los tratamientos recientes. Haber tomado potasio recientemente o estar tomando un medicamento que reduce el potasio en la sangre, como la acetazolamida, tendrá efectos en los niveles de potasio en la sangre.</p><p>También es importante considerar otras razones por las que el potasio es bajo. Algunas personas tienen niveles bajos crónicos de potasio en la sangre, por ejemplo, debido a una enfermedad renal (p. ej., síndrome de Bartter). Pueden tener parálisis periódica "secundaria" o "sintomática" a pesar de no tener uno de los trastornos familiares del canal de parálisis periódica "primaria".</p><p><br /></p><p><span style="color: #2b00fe;">Por favor Continue aqui en Ingles</span>: <a href="https://simulconsult.com/resources/hypopp/">https://simulconsult.com/resources/hypopp/</a></p>hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-73730876013033480642022-03-09T06:26:00.000-08:002022-03-09T06:26:02.615-08:00If my blood potassium level is normal, does that prove I don’t have hypokalemic periodic paralysis?<p style="box-sizing: border-box; color: rgba(17, 19, 21, 0.6); font-family: proxima-nova, sans-serif; font-size: 15px; font-stretch: normal; line-height: 1.33; margin: 5px 0px 0px; padding: 0px; text-rendering: optimizeLegibility;">No. Although having low levels of blood potassium during attacks is typical of hypokalemic periodic paralysis, between attacks, people with hypokalemic periodic paralysis can have a normal blood potassium level (frequently in the low normal range). </p><p style="box-sizing: border-box; color: rgba(17, 19, 21, 0.6); font-family: proxima-nova, sans-serif; font-size: 15px; font-stretch: normal; line-height: 1.33; margin: 20px 0px 0px; padding: 0px; text-rendering: optimizeLegibility;">Attacks of paralysis are typically triggered by the level of potassium dropping in the blood. Such potassium fluctuations occur in everyone, but in people with familial hypokalemic periodic paralysis, these drops in potassium can produce episodes of paralysis. For example, a large carbohydrate meal results in secretion of insulin into the blood, which results in a drop of the blood potassium level as potassium and glucose enter cells. In normal people, such a drop in blood potassium produces no symptoms. In people with familial hypokalemic periodic paralysis, however, the drop in blood potassium often triggers an episode of paralysis. </p><p style="box-sizing: border-box; color: rgba(17, 19, 21, 0.6); font-family: proxima-nova, sans-serif; font-size: 15px; font-stretch: normal; line-height: 1.33; margin: 20px 0px 0px; padding: 0px; text-rendering: optimizeLegibility;">Potassium levels in the blood can remain low as muscle is recovering from a recent attack. During an attack, muscles that become paralyzed swell and take up potassium, causing a drop in potassium in the blood. But as the swelling resolves, the level of potassium in the blood returns to the normal range. Consequently, a normal blood potassium after such a recovery should not be considered evidence against a person having hypokalemic periodic paralysis.</p><p style="box-sizing: border-box; color: rgba(17, 19, 21, 0.6); font-family: proxima-nova, sans-serif; font-size: 15px; font-stretch: normal; line-height: 1.33; margin: 20px 0px 0px; padding: 0px; text-rendering: optimizeLegibility;">When evaluating blood potassium levels it is important to take into account recent treatments. Having just taken potassium or being on a drug that lowers blood potassium, such as acetazolamide, will have effects on blood potassium levels. </p><p style="box-sizing: border-box; color: rgba(17, 19, 21, 0.6); font-family: proxima-nova, sans-serif; font-size: 15px; font-stretch: normal; line-height: 1.33; margin: 20px 0px 0px; padding: 0px; text-rendering: optimizeLegibility;">It is also important to consider other reasons for potassium being low. Some people have chronic low blood potassium, for example due to kidney disease (e.g., Bartter syndrome). They can have “secondary” or “symptomatic” periodic paralysis despite not having one of the familial “primary” periodic paralysis channel disorders.</p><p style="box-sizing: border-box; color: rgba(17, 19, 21, 0.6); font-family: proxima-nova, sans-serif; font-size: 15px; font-stretch: normal; line-height: 1.33; margin: 20px 0px 0px; padding: 0px; text-rendering: optimizeLegibility;"><br /></p><p style="box-sizing: border-box; font-family: proxima-nova, sans-serif; font-size: 15px; font-stretch: normal; line-height: 1.33; margin: 20px 0px 0px; padding: 0px; text-rendering: optimizeLegibility;"><span style="color: #2b00fe;">Please Continue Here</span><span style="color: rgba(17, 19, 21, 0.6);">: <a href="https://simulconsult.com/resources/hypopp/">https://simulconsult.com/resources/hypopp/</a></span></p>hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-28438012427308756302018-09-07T21:14:00.000-07:002018-09-07T21:16:00.301-07:00Structure reveals mechanism behind periodic paralysis<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEieHV8-g7eYRfac2ItHHV-PzfiKtZ6suXs-U2OIuuo7UbpQiuN5IzFD6ArnINEc-lyTV9qccnGpgZiSc7NgTiG5ouF9J3QCnjwsbSQFNKDoVFoLrdMcqV8qLyBCL9d__pyfgicu7n6_gzw/s1600/Screen+Shot+2018-09-08+at+05.15.14.png" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="280" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEieHV8-g7eYRfac2ItHHV-PzfiKtZ6suXs-U2OIuuo7UbpQiuN5IzFD6ArnINEc-lyTV9qccnGpgZiSc7NgTiG5ouF9J3QCnjwsbSQFNKDoVFoLrdMcqV8qLyBCL9d__pyfgicu7n6_gzw/s400/Screen+Shot+2018-09-08+at+05.15.14.png" width="400" /></a>Three states of the voltage-sensing domain (VSD) of a membrane-channel protein. In the normal state, the water-accessible space (magenta) does not extend through the channel, preventing sodium (gray spheres) from passing through. In the disease state, a clear passage allows sodium to leakthrough, resulting in muscle paralysis. In the “rescued” state, the binding of guanidinium (blue and yellow spheres) effectively closes the channel and blocks sodium leakage. The red sphere represents the location of the disease-causing mutation. The side-chain sticks represent the voltage sensors of the sodium channel.</div>
<span style="color: red; font-size: large;">Please continued Here:<a href="https://als.lbl.gov/wp-content/uploads/2018/09/381.pdf" target="_blank">https://als.lbl.gov/wp-content/uploads/2018/09/381.pdf</a></span><br />
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-27476528811293306092018-09-07T20:55:00.003-07:002018-09-07T20:55:59.092-07:00Myopathy of Hypokalemic Periodic Paralysis<div dir="ltr" style="text-align: left;" trbidi="on">
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EREDITARY intermittent flaccid paralysis of skeletal muscle is at present classified into three types on the basis of the changes in the serum potassium during the paralytic attack. The hypokalemic form was the first to be clinically recognized, and is the most common of the three variants, more than 600 cases having been described in the literature by 1959.<sup style="box-sizing: inherit; line-height: 1;">1</sup> The clinical manifestations of this disease will not be detailed here as many reviews are available.<sup style="box-sizing: inherit; line-height: 1;">2-5</sup> Worthy of emphasis, however, is that permanent proximal muscle weakness may occur. This feature was first noted by Oppenheim<sup style="box-sizing: inherit; line-height: 1;">6</sup> in 1891 and was later thought to be a variant of spinal muscular atrophy occurring in conjunction with periodic paralysis.<sup style="box-sizing: inherit; line-height: 1;">7</sup> However, it has now become apparent that permanent myopathic weakness is not uncommon, and not dependent upon severe or repeated paralytic attacks.<sup style="box-sizing: inherit; line-height: 1;">8-10</sup></div>
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<span style="font-size: large;">Please Continued Here:<a href="https://jamanetwork.com/journals/jamaneurology/article-abstract/568933" target="_blank">https://jamanetwork.com/journals/jamaneurology/article-abstract/568933</a></span></div>
hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-49470194763727396712018-09-07T20:46:00.002-07:002018-09-07T20:46:41.376-07:00What is hypokalemic periodic paralysis?<div dir="ltr" style="text-align: left;" trbidi="on">
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What is hypokalemic periodic paralysis?</h2>
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Hypokalemic periodic paralysis is an inherited condition characterized by transient episodes of extreme muscle weakness and/or paralysis of the muscles in the arms and legs, along with a decreased serum potassium concentration during an attack. These episodes may last from a few hours to one day.</div>
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<span style="font-size: large;">Very interesting, please continue here:<a href="https://www.patientslikeme.com/conditions/1540-hypokalemic-periodic-paralysis" target="_blank">https://www.patientslikeme.com/conditions/1540-hypokalemic-periodic-paralysis</a></span></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-43938478394816929652018-09-07T20:19:00.004-07:002018-09-07T20:19:47.387-07:00Hyper- and Hypokalemic Periodic Paralysis Study <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: large;">Hyper- and Hypokalemic Periodic Paralysis Study </span></div>
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Periodic paralysis is a relatively rare, life-long disorder characterized by intermittent bouts of paralysis, progressive weakness, and diminished quality of life. Two drugs, acetazolamide (ACZ) and dichlorphenamide, have been prescribed to treat the disorder, however, dichlorphenamide is no longer available. In this multi-center, parallel, randomized trial researchers will compare the effects of dichlorphenamide vs. placebo in patients with hyperkalemic (HYP) and hypokalemic (HOP) periodic paralysis. The trial consists of two 9-week studies—one study will enroll persons with hyperkalemic periodic paralysis and the other study will enroll persons with hypokalemic periodic paralysis. Participants will be randomly assigned to one of two treatment groups: dichlorphenamide or placebo (an inactive substance). During the studies, participants will be asked to keep a daily diary to record the time, length, and severity of each episode of weakness (attack). The study coordinator will contact participants weekly to review the diary information. The 9-week phase will be followed by a 1-year open-label dichlorphenamide extension without placebo to determine the long-term effects of dichlorphenamide on the course of the disease and on inter-attack weakness. Duration of the trial for participants is approximately 65 weeks, including a screening phase to determine eligibility, the first 9-week treatment phase, and the one-year open-label extension phase. </div>
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<b><span style="color: red; font-size: large;">Please Continued Here:<a href="https://www.ninds.nih.gov/Disorders/Clinical-Trials/Hyper-and-Hypokalemic-Periodic-Paralysis-Study" target="_blank">https://www.ninds.nih.gov/Disorders/Clinical-Trials/Hyper-and-Hypokalemic-Periodic-Paralysis-Study</a></span></b></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-14951575567224607372018-09-07T20:14:00.000-07:002018-09-07T20:14:00.310-07:00HYPERKALEMIC PP VS HYPOKALEMIC PERODIC PARALYSIS<div dir="ltr" style="text-align: left;" trbidi="on">
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<li style="box-sizing: inherit; margin: 0px; padding: 0px;">HYPERKALEMIC PERIODIC PARALYSIS MUTATED GENE SCN4A CHROMOSOME 17q DEFECTIVE CHANNEL SODIUM MODE OF INHERITENCE AUTOSOMAL DOMINANT </li>
<li style="box-sizing: inherit; margin: 0px; padding: 0px;"><a href="https://image.slidesharecdn.com/hpp-141125075826-conversion-gate02/95/hypokalemic-periodic-paralysis-7-638.jpg?cb=1416902365" style="box-sizing: inherit; color: #008ed2; line-height: inherit; text-decoration: none;" target="_blank" title="Hyperkalemic Periodic Paralysis
• term hyperkalemic is mis..."> </a>Hyperkalemic Periodic Paralysis • term hyperkalemic is misleading since patients are often normokalemic during attacks. • Onset first decade • M : F 1:1 • Attacks are brief and mild, usually lasting 30 minutes to 4 hours. • Weakness affects proximal muscles, sparing bulbar muscles. • Attacks are precipitated by rest following exercise and fasting. </li>
<li style="box-sizing: inherit; margin: 0px; padding: 0px;"> In a variant of this disorder, the predominant symptom is myotonia without weakness (potassium-aggravated myotonia). • The symptoms are aggravated by cold, and myotonia makes the muscles stiff and painful. • Clinically apparent myotonia is seen less than 20% of patients, but electrical myotonia may be found in 50-75%. </li>
<li style="box-sizing: inherit; margin: 0px; padding: 0px;">Pathophysiology In hyperKPP, Na+ channels fail to inactivate and prolonged openings and depolarization result. Increased extracellular K+ levels worsen the inactivation of Na+ channels.</li>
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<span style="font-family: Helvetica Neue, Helvetica, Roboto, Arial, sans-serif;"><span style="caret-color: rgb(59, 56, 53);"><b><span style="color: red;">Please continued Here</span></b><span style="color: #3b3835; font-size: 14px;">: <a href="https://www.slideshare.net/laxmikantjoshi2/hypokalemic-periodic-paralysishpp" target="_blank">https://www.slideshare.net/laxmikantjoshi2/hypokalemic-periodic-paralysishpp</a></span></span></span></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-9929444926869549062017-11-01T03:24:00.000-07:002017-11-01T03:24:09.194-07:00Hypokalemic Estimated.<div dir="ltr" style="text-align: left;" trbidi="on">
<span class="ghr-condition" style="box-sizing: border-box; color: #202020; font-family: Roboto, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 16px;">hypokalemic periodic paralysis</span><span style="background-color: white; color: #202020; font-family: Roboto, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 16px;"> is estimated to affect 1 in 100,000 people. Men tend to experience symptoms of this condition more often than women.</span></div>
hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-89004587343473704082017-11-01T03:18:00.003-07:002017-11-01T03:18:41.916-07:00If a genetic disorder runs in my family, what are the chances that my children will have the condition?<div dir="ltr" style="text-align: left;" trbidi="on">
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When a genetic disorder is diagnosed in a family, family members often want to know the likelihood that they or their children will develop the condition. This can be difficult to predict in some cases because many factors influence a person's chances of developing a genetic condition. One important factor is how the condition is inherited. For example:</div>
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Autosomal dominant inheritance: A person affected by an autosomal dominant disorder has a 50 percent chance of passing the mutated gene to each child. The chance that a child will not inherit the mutated gene is also 50 percent <a data-footer="U.S. National Library of Medicine" data-title="Autosomal dominant" data-toggle="lightbox" href="https://ghr.nlm.nih.gov/primer/illustrations/autodominant.jpg" style="box-sizing: border-box; color: #551a8b;">(illustration)</a>. However, in some cases an autosomal dominant disorder results from a new (de novo) mutation that occurs during the formation of egg or sperm cells or early in embryonic development. In these cases, the child's parents are unaffected, but the child may pass on the condition to his or her own children <a data-footer="U.S. National Library of Medicine" data-title="Autosomal dominant new mutation" data-toggle="lightbox" href="https://ghr.nlm.nih.gov/primer/illustrations/dominantnewmutation.jpg" style="box-sizing: border-box; color: #551a8b;">(illustration)</a>.</div>
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Autosomal recessive inheritance: Two unaffected people who each carry one copy of the mutated gene for an autosomal recessive disorder (carriers) have a 25 percent chance with each pregnancy of having a child affected by the disorder. The chance with each pregnancy of having an unaffected child who is a carrier of the disorder is 50 percent, and the chance that a child will not have the disorder and will not be a carrier is 25 percent <a data-footer="U.S. National Library of Medicine" data-title="Autosomal recessive" data-toggle="lightbox" href="https://ghr.nlm.nih.gov/primer/illustrations/autorecessive.jpg" style="box-sizing: border-box; color: #551a8b;">(illustration)</a>.</div>
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<b><span style="color: blue;">Continue Here: <a href="https://ghr.nlm.nih.gov/primer/inheritance/riskassessment" target="_blank">https://ghr.nlm.nih.gov/primer/inheritance/riskassessment</a></span></b></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-38014334594115121872017-11-01T03:08:00.000-07:002017-11-01T03:08:04.684-07:00Información sobre los niveles anormales de potasio que los pacientes tienen con (HypoKpp)<div dir="ltr" style="text-align: left;" trbidi="on">
Le doy información sobre los niveles anormales de potasio que los pacientes tienen con (HypoKpp)<br />
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La información que estoy poniendo se obtiene de muchos pacientes que tienen (HypoKpp) de todo el mundo que tienen el mismo problema con los niveles de potasio en la sangre.<br />
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Cuando obtenemos la sangre para saber el nivel de potasio y potasio sale con niveles normales como 4.0 4.5, pero tenemos ataques de parálisis, con niveles de potasio que son normales para los médicos, y que confunde a los médicos y las personas que están a nuestro alrededor.<br />
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Somos conscientes de que no todos los pacientes con (HypoKpp) responden de la misma manera a los tratamientos que realizan los médicos y que a veces los medicamentos no funcionan para todos, y que hay casos en los que los pacientes con (HypoKpp) Medicamentos lo hacen bien.<br />
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En pacientes con parálisis periódica no es necesario que el nivel de potasio caiga fuera del rango normal para que se desencadene un ataque: pacientes con HypoKpp si el nivel de potasio es normalmente alrededor de 4, entonces cualquier cambio por debajo podría causar un ataque.<br />
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3.5 está en el extremo inferior de la normalidad en todos los pacientes. Lo que es importante tener en cuenta es que, en el tipo de parálisis periódica, el potasio se desplaza fuera de la sangre, este es el nivel más bajo y, a medida que el ataque comienza a mejorar, los niveles aumentarán.<br />
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Los médicos están buscando el potasio disponible en el torrente sanguíneo. La parálisis periódica ocurre a nivel celular: puede tener gran cantidad de potasio en la sangre, pero si los canales iónicos no funcionan correctamente, los músculos seguirán débiles. Esa es una gran diferencia en el pensamiento del doctor,<br />
Los doctores asumen que dado que el potasio en la sangre no es bajo, la Parálisis Periódica no puede ser la respuesta<br />
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Un ejemplo (el tanque de gasolina puede estar lleno pero si su bomba de combustible no funciona, su vehículo no arrancará).<br />
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Los pacientes que tienen (Hypokpp) necesitan que el número de potasio sea alrededor de 4.5 *.<br />
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Los pacientes con niveles de potasio alrededor de 3.0 a 3.5 * están en parálisis total.</div>
hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-34725250971284975282017-11-01T03:04:00.000-07:002017-11-01T03:04:04.124-07:00Information about the abnormal levels of potassium that patients have with (HypoKpp) <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: large;"><span style="-webkit-text-stroke-width: initial;">I give you some information about the abnormal levels of potassium that patients have with (HypoKpp)</span><span style="-webkit-text-stroke-width: initial;"> </span></span></div>
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<span style="-webkit-text-stroke-color: rgb(0, 0, 0); -webkit-text-stroke-width: initial; font-family: Garamond; font-size: large;"><span style="-webkit-text-stroke-width: initial; text-align: left;">The information I am putting is obtained from many patients who have (HypoKpp) from around the world who are having the same problem whit levels of potassium in the </span><span style="font-kerning: none;"></span></span><span style="font-family: Garamond; font-size: large;">blood.</span></div>
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<span style="font-kerning: none;"><span style="font-size: large;">When we get the blood to know the level of potassium and potassium comes out with normal levels like 4.0 4.5, but we have paralysis attacks, with potassium levels that are normal for doctors, and that confuses the doctors and the people who are around us.</span></span></div>
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<span style="font-kerning: none;"><span style="font-size: large;">We are aware that not all patients with (HypoKpp) respond in the same way to treatments that are given by doctors and that sometimes medicines do not work for everyone, and that there are cases that patients with (HypoKpp) Medicines are doing well,</span></span></div>
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<span style="font-kerning: none;"><span style="font-size: large;">In patients with periodic paralysis the potassium level does not need to drop outside the normal range for an attack to be triggered – Patients whit ( HypoKpp ) if the potassium is normally level around 4 then any change below that could cause an attack. </span></span></div>
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<span style="font-kerning: none;"><span style="font-size: large;">3.5 is at the low end of normal in all patients. What is important to note is that in the type of periodic paralysis the potassium shifts out of the blood, this is the lower level, and then as the attack starts to improve the levels will increase.</span></span></div>
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<span style="font-kerning: none;"><span style="font-size: large;">The doctor’s are looking at the available potassium in your bloodstream. Periodic Paralysis happens at the cellular level - you can have lots of potassium in the blood but if the ion channels aren’t working correctly, the muscles will still be weak. That’s a big difference in doctor’s thinking ,</span></span></div>
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<span style="font-kerning: none;"><span style="font-size: large;">The doctors assume that since the blood potassium isn’t low, Periodic Paralysis can’t be the answer</span></span></div>
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<span style="font-kerning: none;"><span style="font-size: large;">Like ( Your gas tank can be full but if your fuel pump isn’t working, your vehicle Still isn’t going to start. )</span></span></div>
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<span style="font-kerning: none;"><span style="font-size: large;">Patients whit ( Hypokpp ) needs potassium number to be around 4.5*. </span></span></div>
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<span style="-webkit-font-kerning: none;"><span style="font-size: large;">Patients whit Potassium levels around 3.0- 3.5* is in full paralysis.</span></span></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-59452686410520515402017-11-01T02:56:00.003-07:002017-11-01T02:56:37.791-07:00New Update in Hypokalemic periodic paralysis Wikipedia<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://upload.wikimedia.org/wikipedia/commons/thumb/4/4e/Autosomal_dominant_-_en.svg/738px-Autosomal_dominant_-_en.svg.png" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img alt="Autosomal dominant - en.svg" border="0" class="mw-mmv-final-image svg" crossorigin="anonymous" height="653" src="https://upload.wikimedia.org/wikipedia/commons/thumb/4/4e/Autosomal_dominant_-_en.svg/738px-Autosomal_dominant_-_en.svg.png" width="375" /></a><b>Hypokalemic periodic paralysis</b> (hypoKPP) is a rare, <a class="mw-redirect" href="https://en.wikipedia.org/wiki/Autosomal_dominant" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Autosomal dominant">autosomal dominant</a> <a href="https://en.wikipedia.org/wiki/Channelopathy" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Channelopathy">channelopathy</a> characterized by muscle weakness or paralysis when there is a fall in <a href="https://en.wikipedia.org/wiki/Potassium" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Potassium">potassium</a> levels in the <a href="https://en.wikipedia.org/wiki/Blood" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Blood">blood</a>. In individuals with this mutation, attacks often begin in <a href="https://en.wikipedia.org/wiki/Adolescence" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Adolescence">adolescence</a> and most commonly occur on awakening or after sleep or rest following strenuous exercise (attacks during exercise are rare), high <a href="https://en.wikipedia.org/wiki/Carbohydrate" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Carbohydrate">carbohydrate</a> meals, meals with high <a href="https://en.wikipedia.org/wiki/Sodium" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Sodium">sodium</a> content, sudden changes in temperature, and even excitement, noise, flashing lights and cold temperatures. Weakness may be mild and limited to certain muscle groups, or more severe full-body paralysis. During an attack reflexes may be decreased or absent. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life.</div>
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Some people only develop symptoms of periodic paralysis due to <a href="https://en.wikipedia.org/wiki/Hyperthyroidism" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Hyperthyroidism">hyperthyroidism</a> (overactive <a href="https://en.wikipedia.org/wiki/Thyroid" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Thyroid">thyroid</a>). This entity is distinguished with <a class="mw-redirect" href="https://en.wikipedia.org/wiki/Thyroid_function_test" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Thyroid function test">thyroid function tests</a>, and the diagnosis is instead called <a href="https://en.wikipedia.org/wiki/Thyrotoxic_periodic_paralysis" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;" title="Thyrotoxic periodic paralysis">thyrotoxic periodic paralysis</a>.<sup class="reference" id="cite_ref-1" style="font-size: 11.199999809265137px; line-height: 1; unicode-bidi: isolate; white-space: nowrap;"><a href="https://en.wikipedia.org/wiki/Hypokalemic_periodic_paralysis#cite_note-1" style="background-image: none; background-position: initial initial; background-repeat: initial initial; color: #0b0080; text-decoration: none;">[</a></sup></div>
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<b><span style="color: blue;">Please Continue Here: </span></b><a href="https://en.wikipedia.org/wiki/Hypokalemic_periodic_paralysis" style="color: #222222;">https://en.wikipedia.org/wiki/Hypokalemic_periodic_paralysis</a></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-38598091338054922262017-02-22T13:55:00.000-08:002017-02-22T13:55:48.900-08:00Hypokalemic periodic paralysis<div dir="ltr" style="text-align: left;" trbidi="on">
<strong style="box-sizing: border-box; color: #333333; font-family: Roboto, Verdana, Geneva, Tahoma, sans-serif; font-size: 16px;">Hypokalemic periodic paralysis</strong><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;"> (HOKPP) is a condition that causes episodes of muscle </span>paralysis<span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">associated with a fall in blood potassium levels (</span>hypokalaemia<span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">).</span><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 12px;"> </span><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">Episodes typically involve a temporary inability to move muscles in the arms and legs.</span><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;"> The first attack usually occurs in childhood or adolescence. Attacks can last for hours or days, and the frequency of attacks varies among affected people. The frequency is usually highest between the ages of 15 and 35, and then decreases with age. Some people with HOKPP also develop late-onset proximal </span>myopathy<span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">.</span><br />
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<span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">HOKPP can be caused by </span><glossary class="glossarizer_replaced" glossaryid="1439" group="readSpeaker_Summary" parent="312" style="border-bottom-color: rgb(119, 119, 119); border-bottom-style: dotted; border-bottom-width: 2px; box-sizing: border-box;" term="Mutation">mutations</glossary><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;"> in the </span><em style="box-sizing: border-box; color: #333333; font-family: Roboto, Verdana, Geneva, Tahoma, sans-serif; font-size: 16px;">CACNA1S</em><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">, </span><em style="box-sizing: border-box; color: #333333; font-family: Roboto, Verdana, Geneva, Tahoma, sans-serif; font-size: 16px;">SCN4A</em><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">, or </span><em style="box-sizing: border-box; color: #333333; font-family: Roboto, Verdana, Geneva, Tahoma, sans-serif; font-size: 16px;">KCNJ18</em><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;"> </span><glossary class="glossarizer_replaced" glossaryid="167" group="readSpeaker_Summary" parent="0" style="border-bottom-color: rgb(119, 119, 119); border-bottom-style: dotted; border-bottom-width: 2px; box-sizing: border-box; color: #333333; font-family: Roboto, Verdana, Geneva, Tahoma, sans-serif; font-size: 16px;" term="Gene">gene</glossary><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">. Inheritance is </span><glossary class="glossarizer_replaced" glossaryid="33" group="readSpeaker_Summary" parent="0" style="border-bottom-color: rgb(119, 119, 119); border-bottom-style: dotted; border-bottom-width: 2px; box-sizing: border-box;" term="Autosomal Dominant">autosomal dominant</glossary><span style="background-color: white; color: #333333; font-family: "roboto" , "verdana" , "geneva" , "tahoma" , sans-serif; font-size: 16px;">. Treatment varies depending on the intensity and duration of attacks. Minor attacks may resolve spontaneously, while treatment for moderate or severe attacks may involve ingesting oral potassium salts or intravenous potassium infusion.</span><br />
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<span style="background-color: white; color: #63316e; font-family: "trebuchet ms"; font-size: 22px;">Symptoms......Continued Here:</span><br />
<span style="background-color: white; color: #63316e; font-family: "trebuchet ms"; font-size: 22px;"><a href="https://rarediseases.info.nih.gov/diseases/6729/hypokalemic-periodic-paralysis" target="_blank">https://rarediseases.info.nih.gov/diseases/6729/hypokalemic-periodic-paralysis</a></span></div>
hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-37069482504437920862016-04-26T13:41:00.004-07:002016-04-26T13:43:39.853-07:00Why Do I Use a Power Wheelchair When I Can Walk?<div dir="ltr" style="text-align: left;" trbidi="on">
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<span class="s1" style="box-sizing: border-box; font-family: "lato";">Someone asked me recently why I use a power wheelchair when I have the </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">ability to walk. Why don’t I force myself to walk? Why have I given up?</span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgg0VpFLDiToI0iKfhuG00HjsyGtuhu-vK9aMn1GcoNCAen7Y0br7qbs10JfODqXeLIgw7SBz-d3zrpVLNCE6moxl0NHv3RbLBYsiCNTPREKGkXfhP7ZyBEpWTrRavw8swK9G-6d57QxK8/s1600/Screen-Shot-2016-04-26-at-8.45.16-AM.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="260" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgg0VpFLDiToI0iKfhuG00HjsyGtuhu-vK9aMn1GcoNCAen7Y0br7qbs10JfODqXeLIgw7SBz-d3zrpVLNCE6moxl0NHv3RbLBYsiCNTPREKGkXfhP7ZyBEpWTrRavw8swK9G-6d57QxK8/s320/Screen-Shot-2016-04-26-at-8.45.16-AM.png" width="320" /></a></div>
<span style="box-sizing: border-box; font-weight: 700; line-height: inherit;"><span class="s1" style="box-sizing: border-box; font-family: "lato";">The following was my answer:</span></span></div>
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<span class="s1" style="box-sizing: border-box; font-family: "lato";">Please do not judge me until you live a day in my life and understand the </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">disabling medical condition I endure daily. </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">I am able to walk a few steps with the assistance of a walker or cane, but due to a </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">rare, invisible, chronic, hereditary, debilitating mineral metabolic disorder </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">called periodic paralysis, my skeletal and breathing muscles are weak </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">and progressively getting weaker, permanently. </span></div>
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<span class="s1" style="box-sizing: border-box; font-family: "lato";">I have developed exercise intolerance. This means I am unable to do physical </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">exercise or exertion on a level those others my age can. This condition also </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">causes extreme pain and fatigue after exercising or exertion and other debilitating </span><span class="s1" style="box-sizing: border-box; font-family: "lato";">symptoms such as a feeling of heaviness in the muscle groups. </span></div>
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Please Continued Here: <a href="http://themighty.com/2016/04/using-a-power-wheelchair-when-i-can-walk/" target="_blank">http://themighty.com/2016/04/using-a-power-wheelchair-when-i-can-walk/</a></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-84977582657737066772016-02-23T14:41:00.000-08:002016-02-23T14:41:11.275-08:00Meet Jodie: Hypokalemic Periodic Paralysis<div dir="ltr" style="text-align: left;" trbidi="on">
<span style="background-color: white; color: #333333; font-family: Roboto, arial, sans-serif; font-size: 13px;">Jodie was diagnosed with hypokalemic periodic paralysis, a rare disorder that affects about one in 100,000 people. Despite adversity, he finds that life is good. He is a husband. A father. He knows the Diplomat Difference.</span><br />
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-90656951877749464412016-02-23T14:37:00.003-08:002016-02-23T14:37:26.271-08:00The Fight Against Hypokalemic Periodic Paralysis<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: small;">20 Things Not to Say or Do to Someone in a Wheelchair</span></h1>
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<span style="background-color: white; color: #666666; font-family: 'Trebuchet MS', Trebuchet, sans-serif; font-size: 13px;">I don't necessarily agree with all of the responses, but I can relate to some of them and I really can't blame her for being frustrated.................</span></div>
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<span style="color: red;">Please continue Here:</span><span style="color: blue;"> <a href="http://fightinghkpp.blogspot.co.uk/" target="_blank">http://fightinghkpp.blogspot.co.uk</a></span></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-14779426396396302962016-02-23T14:04:00.005-08:002016-02-23T14:04:59.666-08:00Myopathy of Hypokalemic Periodic Paralysis An Electron Microscopic Study<div dir="ltr" style="text-align: left;" trbidi="on">
<span style="background-color: white; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 13px;">EREDITARY intermittent flaccid paralysis of skeletal muscle is at present classified into three types on the basis of the changes in the serum potassium during the paralytic attack. The hypokalemic form was the first to be clinically recognized, and is the most common of the three variants, more than 600 cases having been described in the literature by 1959.</span><span style="border: 0px; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 0.846em; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">1</span><span style="background-color: white; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 13px;"> The clinical manifestations of this disease will not be detailed here as many reviews are available.</span><span style="border: 0px; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 0.846em; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">2-5</span><span style="background-color: white; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 13px;"> Worthy of emphasis, however, is that permanent proximal muscle weakness may occur. This feature was first noted by Oppenheim</span><span style="border: 0px; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 0.846em; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">6</span><span style="background-color: white; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 13px;"> in 1891 and was later thought to be a variant of spinal muscular atrophy occurring in conjunction with periodic paralysis.</span><span style="border: 0px; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 0.846em; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">7</span><span style="background-color: white; color: #333333; font-family: Georgia, Cambria, Times, 'Times New Roman', serif; font-size: 13px;"> However, it has now become apparent that permanent myopathic weakness is not uncommon, and not dependent upon severe or repeated paralytic attacks.</span><br />
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<span style="background-color: white;"><span style="color: blue; font-family: Georgia, Cambria, Times, Times New Roman, serif;"><u>Please continue Here: <a href="http://archneur.jamanetwork.com/article.aspx?articleid=568933" target="_blank">http://archneur.jamanetwork.com/article.aspx?articleid=568933</a></u></span></span></div>
hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-49267688652724964852016-02-23T13:44:00.000-08:002016-02-23T13:44:07.126-08:00¿Cuál es el nombre oficial del gen SCN4A?<div dir="ltr" style="text-align: left;" trbidi="on">
El nombre oficial de este gen es "sodio dependientes de voltaje canal subunidad alfa 4."<br />
SCN4A es símbolo oficial del gen. El gen SCN4A es también conocido por otros nombres, que se enumeran a continuación.<br />
Más información acerca de los nombres de genes y símbolos en la página Acerca de.<br />
¿Cuál es la función normal del gen SCN4A?<br />
El gen SCN4A pertenece a una familia de genes que proporcionan instrucciones para hacer canales de sodio. Estos canales, que transporte cargados positivamente átomos de sodio (iones de sodio) en las células, juegan un papel clave en la capacidad de una célula para generar y transmitir señales eléctricas.<br />
El gen SCN4A proporciona instrucciones para hacer una parte crítica (la subunidad alfa) de los canales de sodio que son abundantes en los músculos utilizados para el movimiento (músculos esqueléticos). Para que el cuerpo se mueve normalmente, estos músculos deben tensa (contrato) y relajarse de manera coordinada. Uno de los cambios que ayuda a las contracciones musculares de disparo es el flujo de átomos cargados positivamente (iones), incluyendo sodio, en las células musculares. Canales creados con la proteína SCN4A controlan el flujo de iones de sodio en estas células.<br />
¿Tiene las características comparten genes con otros genes SCN4A?<br />
El gen SCN4A pertenece a una familia de genes llamados SC (los canales de sodio).<br />
Una familia de genes es un grupo de genes que comparten características importantes. La clasificación de los genes individuales en familias ayuda a los investigadores describen cómo los genes están relacionados entre sí. Para obtener más información, consulte ¿Qué son las familias de genes? en el Manual.<br />
¿Cómo son los cambios en el gen SCN4A relacionada con las condiciones de salud?<br />
hipercaliémica parálisis periódica - causado por mutaciones en el gen SCN4A<br />
Se han encontrado más de 10 mutaciones en el gen SCN4A para causar parálisis periódica hiperpotasemia, una condición que causa episodios de debilidad muscular extrema que a menudo se asocian con altos niveles de potasio en la sangre (hiperpotasemia) .Las mutaciones cambian bloques de construcción individuales (amino ácidos) en la proteína SCN4A, lo que altera la estructura y función de los canales de sodio en las células del músculo esquelético. Estos cambios retrasar el cierre de los canales hechos con la proteína SCN4A o prevenir los canales de permanecer cerrada. Como resultado, los iones de sodio siguen fluyendo en células de músculo anormal. Este aumento de los iones de sodio provoca la liberación de potasio de las células musculares, lo que hace más canales de sodio para abrir y estimula el flujo de incluso más iones de sodio en estas células. Estos cambios en el transporte de iones reducen la capacidad de los músculos esqueléticos se contraiga, lo que conduce a episodios de debilidad muscular o parálisis.<br />
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Hipocaliémica parálisis periódica - causado por mutaciones en el gen SCN4A<br />
Al menos siete mutaciones en el gen SCN4A se han identificado en las personas con parálisis periódica hipopotasémica, una condición que causa episodios de debilidad muscular extrema que están asociados con niveles bajos de potasio en la sangre (hipopotasemia). Las mutaciones en el gen SCN4A representa aproximadamente el 10 por ciento de todos los casos de esta enfermedad. Cada una de las mutaciones conocidas cambia un único aminoácido en la proteína SCN4A, lo que altera la estructura y función de los canales de sodio en las células del músculo esquelético. Los canales anormales cambian el flujo normal de los iones de sodio, lo que impide músculos se contraigan normalmente. Los niveles bajos de potasio también contribuyen a este problema. Debido a que es necesaria la contracción muscular para el movimiento, estos cambios en el transporte de iones de plomo a los episodios de larga duración de debilidad muscular severa.<br />
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Paramiotonía congénita - causada por mutaciones en el gen SCN4A<br />
Al menos 18 mutaciones en el gen SCN4A se sabe que causan paramiotonía congénita, una enfermedad muscular caracterizada por episodios de tensado muscular sostenida (miotonía) que impiden los músculos se relajen normalmente. Las mutaciones del gen SCN4A que causan esta condición de cada cambio de un solo aminoácido en la proteína SCN4A, lo que altera la estructura y función de los canales de sodio en las células del músculo esquelético. Los cambios genéticos más comunes reemplazar el aminoácido arginina con uno de varios otros aminoácidos en la posición proteína 1448.<br />
Las mutaciones retrasar el cierre de los canales hechos con la proteína SCN4A y, una vez que los canales están cerrados, causa que se abran de nuevo demasiado rápido. Estos cambios aumentan el flujo de iones de sodio en las células del músculo esquelético. Un flujo de iones de sodio en exceso provoca contracciones musculares prolongadas, que son la base de los episodios característicos de la miotonía congénita paramiotonía. Los músculos con altos niveles sostenidos de iones de sodio pueden convertirse en condiciones de contrato en absoluto, lo que resulta en ataques de debilidad muscular.<br />
Los efectos de las mutaciones del gen SCN4A sobre los canales iónicos alterados pueden incrementarse por las bajas temperaturas, que pueden ayudar a explicar por qué signos y síntomas pueden ser provocados por la exposición al frío.<br />
potasio-agravado miotonía - causada por mutaciones en el gen SCN4A<br />
Varias mutaciones en el gen SCN4A en miotonía agravada potasio, una condición que causa episodios de miotonía que impiden que los músculos se relajen normalmente. La rigidez muscular resultante puede ser agravada por el consumo de alimentos ricos en potasio. Los cambios genéticos más comunes asociados con la miotonía de potasio-agravado reemplazar el aminoácido glicina con uno de varios otros aminoácidos en la posición proteína 1306. Estas mutaciones retrasar el cierre de los canales hechos con la proteína SCN4A, lo que aumenta el flujo de iones de sodio en esquelético células musculares. La presencia de exceso de potasio estimula el flujo de incluso más iones de sodio en estas células. Estos cambios en el transporte de iones de activación prolongada contracciones musculares, subyacentes en la característica rigidez muscular de la miotonía agravada potasio.<br />
otros trastornos - causadas por mutaciones en el gen SCN4A<br />
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Una mutación en el gen SCN4A también es responsable de una forma de síndrome miasténico congénito, un trastorno muscular que aparece poco después del nacimiento. Las personas con esta afección tienen debilidad muscular general y ataques recurrentes de parálisis que afecta específicamente músculos que se usan para hablar y respirar. La mutación del gen SCN4A asociada con esta afección reemplaza el aminoácido valina con el ácido glutámico aminoácido en la posición 1442 de proteína (escrito como Val1442Glu o V1442E). Este cambio genético altera la estructura y función de los canales de sodio en las células del músculo esquelético. La estancia canales cerrados anormalmente después de repetidas contracciones musculares, reduciendo el flujo de iones de sodio en las células musculares. Esta interrupción en el transporte de iones reduce aún más la contracción muscular, lo que lleva a la debilidad muscular y episodios de parálisis.<br />
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<span style="color: blue;">Obtenido Y Traducido Gracias a:</span> <a href="http://topics.sciencedirect.com/topics/page/Hypokalemic_periodic_paralysis" target="_blank">http://topics.sciencedirect.com/topics/page/Hypokalemic_periodic_paralysis</a></div>
hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-27606332525829943662016-02-23T13:39:00.001-08:002016-02-23T13:39:23.100-08:00Myotonic Muscle Disorders And Periodic Paralysis<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: blue;">Hypokalemic Periodic Paralysis </span></h3>
<a class="heading-link" href="http://www.sciencedirect.com/science/article/pii/B9781455726721000362#s0140" style="font-family: Arial, Helvetica, 'Lucida Sans Unicode', 'Microsoft Sans Serif', 'Segoe UI Symbol', STIXGeneral, 'Cambria Math', 'Arial Unicode MS', sans-serif; text-decoration: none;"></a><br />
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Hypokalemic periodic paralysis is not a myotonic disorder. However, the clinical features of periodic attacks of flaccid weakness and the development of fixed proximal weakness later in life resemble the sodiumchannel disorders discussed earlier. This is an autosomal dominant inherited disorder associated with a defect in the α subunit of a voltage-sensitive muscle <a class="term-link" href="http://topics.sciencedirect.com/topics/page/Calcium" style="color: #840084; text-decoration: none;">calcium</a> channel (<i>CACNA1S</i>) gene on chromosome 1q (hypokalemic periodic paralysis type 1). More recently, mutations were identified in the α subunit of the sodium channel gene (<i>SCN4A</i>) on chromosome 17q, and the term hypokalemic periodic paralysis type 2 was used to designate this small group of patients, who are clinically indistinguishable from those with hypokalemic periodic paralysis type 1. Both types result from missense mutations in the voltage-sensor domains of their respective channel. This similarity suggests a common functional defect produced by these voltage-sensor mutations, and may explain why different mutations on two different channels result in hypokalemic periodic paralysis. </div>
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<span style="color: blue;">Please Continue Here:</span></div>
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<a href="http://topics.sciencedirect.com/topics/page/Hypokalemic_periodic_paralysis" target="_blank">http://topics.sciencedirect.com/topics/page/Hypokalemic_periodic_paralysis</a></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-27593378346918440852016-02-22T13:54:00.001-08:002016-02-22T14:05:46.477-08:00What is the official name of the SCN4A gene?<div dir="ltr" style="text-align: left;" trbidi="on">
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What is the official name of the <span class="geneSymbol" style="font-style: italic;">SCN4A</span> gene?</h2>
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The official name of this gene is “sodium voltage-gated channel alpha subunit 4.”</div>
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<span class="geneSymbol" style="font-style: italic;">SCN4A</span> is the gene's official symbol. The <span class="geneSymbol" style="font-style: italic;">SCN4A</span> gene is also known by other names, listed below.</div>
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Read more about gene names and symbols on the <a href="http://ghr.nlm.nih.gov/about#gene_naming" style="color: #551a8b;">About</a> page.</div>
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What is the normal function of the <span class="geneSymbol" style="font-style: italic;">SCN4A</span> gene?</h2>
<a href="https://www.blogger.com/blogger.g?blogID=8973382695067501881" name="normalfunction" style="color: #000066; text-decoration: underline;"></a><span style="background-color: white; color: #000066;"></span><br />
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The <span class="geneSymbol" style="font-style: italic;">SCN4A</span> gene belongs to a family of genes that provide instructions for making sodium channels. These channels, which transport positively charged sodium atoms (sodium ions) into cells, play a key role in a cell's ability to generate and transmit electrical signals.</div>
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The <span class="geneSymbol" style="font-style: italic;">SCN4A</span> gene provides instructions for making a critical part (the alpha subunit) of sodium channels that are abundant in muscles used for movement (skeletal muscles). For the body to move normally, these muscles must tense (contract) and relax in a coordinated way. One of the changes that helps trigger muscle contractions is the flow of positively charged atoms (ions), including sodium, into muscle cells. Channels made with the SCN4A protein control the flow of sodium ions into these cells.</div>
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<b><span style="color: red; font-size: large;">Thanks to: <a href="http://ghr.nlm.nih.gov/gene/SCN4A" target="_blank">http://ghr.nlm.nih.gov/gene/SCN4A</a></span></b></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-70435569365359055242015-10-29T08:49:00.001-07:002015-10-29T08:49:38.223-07:00Parálisis Periódicas asociación Hispana De afectados por parálisis Periódica.<div dir="ltr" style="text-align: left;" trbidi="on">
<span style="font-size: large;"><u>Parálisis Periódicas asociación Hispana De afectados por parálisis Periódica.</u></span><div>
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<span style="font-size: large;">información importante en Español De Parálisis Periódicas </span></div>
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<span style="font-size: large;">Por favor Visiten esta pagina:</span></div>
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<span style="font-size: large;"><a href="http://www.paralisis-periodicas.es/" target="_blank">http://www.paralisis-periodicas.es</a></span></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-68403568134439825252015-06-13T11:40:00.002-07:002015-06-13T11:40:54.340-07:00¿Cuáles son los desencadenantes Parálisis Periódica? "`Como Evitar a toda costa"<div dir="ltr" style="text-align: left;" trbidi="on">
<span style="font-size: large;">H</span>ay muchos factores desencadenantes que marcan la parálisis parcial y total en movimiento. Es importante descubrir estos disparadores, porque necesitamos parar los episodios, de ser posible, con el fin de recuperar la calidad de nuestras vidas y prevenir el daño está haciendo a nuestros órganos como los turnos de potasio y agota en nuestros cuerpos. Este daño puede conducir a debilidad permanente y la discapacidad.<br />
En el caso de las personas con síndrome de Andersen-Tawil, la parálisis conduce a taquicardia y arritmias graves, incluyendo largos intervalos QT, que puede conducir a un paro cardíaco. Evitar la parálisis es absolutamente necesario, debido a estos efectos que amenazan la vida.<br />
Los disparadores pueden incluir:<br />
dieta:........<br />
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<span style="color: red;"><b>Por favor Continúen Aqui</b></span>:<a href="http://www.periodicparalysisnetwork.com/pdf/What%20are%20the%20Periodic%20Paralysis%20Triggers.pdf" target="_blank">http://www.periodicparalysisnetwork.com/pdf/What%20are%20the%20Periodic%20Paralysis%20Triggers.pdf</a></div>
hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-37613746921468897972015-06-13T11:29:00.000-07:002015-06-13T11:29:52.413-07:00What are the Periodic Paralysis Triggers? “AVOID AT ALL COST”<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: 12pt; font-weight: 700;">What are the Periodic Paralysis Triggers?
“AVOID AT ALL COST” </span></div>
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<span style="font-size: 12pt;">There are many triggers that set the partial and total paralysis into motion. It is
important to discover these triggers because we need to stop the episodes, if
possible, in order to regain the quality of our lives and to prevent the damage
being done to our organs as the potassium shifts and depletes in our bodies.
This damage can lead to permanent weakness and disability.
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<span style="font-size: 12pt;">In the case of people with Andersen-Tawil Syndrome, the paralysis leads to
tachycardia and serious arrythmias, including long QT intervals, which can
lead to cardiac arrest. Avoiding paralysis is absolutely necessary, due to these
life-threatening effects.
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<span style="font-size: 12pt;">Triggers can include:
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<span style="font-size: 12pt; font-weight: 700;">Diet: .......</span><br />
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<span style="color: red;"><span style="font-size: small;"><span style="font-weight: 700;">Please </span></span><b>Continued</b></span><span style="font-size: small;"><span style="font-weight: 700;"><span style="color: red;">Here: </span><a href="http://www.periodicparalysisnetwork.com/pdf/What%20are%20the%20Periodic%20Paralysis%20Triggers.pdf" target="_blank">http://www.periodicparalysisnetwork.com/pdf/What%20are%20the%20Periodic%20Paralysis%20Triggers.pdf</a></span></span></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-16942668655667706932015-06-06T17:20:00.002-07:002015-06-07T05:26:53.812-07:00Nuevas Noticias De Wikipedia Hypokalemic Periodic paralices<div dir="ltr" style="text-align: left;" trbidi="on">
La parálisis periódica hipocaliémica es una rara canalopatía dominante, autosómica caracterizada por debilidad muscular o parálisis con una caída correspondiente en los niveles de potasio en la sangre (principalmente debido a un defecto en un canal de calcio dependiente de voltaje). En las personas con esta mutación, los ataques a menudo comienzan en la adolescencia y son provocados por el ejercicio vigoroso seguido de descanso, comidas ricas en hidratos de carbono, las comidas con alto contenido de sodio, los cambios bruscos de temperatura, e incluso emoción, ruido, luces intermitentes y inducida por las bajas temperaturas. La debilidad puede ser leve y limitado a ciertos grupos musculares, o más grave parálisis de todo el cuerpo. Los ataques pueden durar unas horas o persistir durante varios días. La recuperación suele ser repentina cuando se produce, debido a la liberación de potasio de músculos hinchados mientras se recuperan. Algunos pacientes pueden caer en un ataque fallido o desarrollar debilidad muscular crónica más tarde en la vida. Para diferenciarlo de síndrome Gullian Barre, reflejos tendinosos profundos son nervio craneal normal y séptimo se salva.<br />
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Algunas personas sólo desarrollan síntomas de parálisis periódica debido a hipertiroidismo (tiroides hiperactiva). Esta entidad se distingue con las pruebas de función tiroidea, y el diagnóstico se llama en lugar parálisis periódica tirotóxica.<br />
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<b><span style="color: red;">Traducido Y Editado Gracias a </span></b>: <a href="http://en.wikipedia.org/wiki/Hypokalemic_periodic_paralysis" target="_blank">http://en.wikipedia.org/wiki/Hypokalemic_periodic_paralysis</a></div>
hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0tag:blogger.com,1999:blog-8973382695067501881.post-49859223265811055922015-06-06T02:53:00.004-07:002015-06-06T02:53:33.033-07:00Wikipedia Update: Hypokalemic Periodic Paralisis <div dir="ltr" style="text-align: left;" trbidi="on">
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<b>Hypokalemic periodic paralysis</b> is a rare, autosomal dominant channelopathycharacterized by muscle weakness or paralysis with a matching fall in potassium levels in the blood (primarily due to defect in a voltage-gated calcium channel). In individuals with this mutation, attacks often begin in adolescence and are triggered by strenuous exercise followed by rest, high carbohydrate meals, meals with high sodium content, sudden changes in temperature, and even excitement, noise, flashing lights and induced by cold temperatures. Weakness may be mild and limited to certain muscle groups, or more severe full body paralysis. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life. To differentiate it from Gullian Barre syndrome, deep tendon reflexes are normal and 7th cranial nerve is spared.</div>
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Some people only develop symptoms of periodic paralysis due to hyperthyroidism (overactive thyroid). This entity is distinguished with thyroid function tests, and the diagnosis is instead called thyrotoxic periodic paralysis.</div>
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<b><span style="color: red;">Continued Here: <a href="http://en.wikipedia.org/wiki/Hypokalemic_periodic_paralysis" target="_blank">http://en.wikipedia.org/wiki/Hypokalemic_periodic_paralysis</a></span></b></div>
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hypokalemiahttp://www.blogger.com/profile/08550025601933675164noreply@blogger.com0