By Alberto J. Machado
ABC en emergencias fue pensado como una herramienta de trabajo. Un ayuda memoria, o una guía rápida acerca de cómo enfrentamos, y que puntos relevantes no dejar de considerar, en distintas situaciones frecuentes en Emergencias.
Emergencias es los angeles especialidad médica que estudia los hechos y situaciones patológicas de aparición súbita que ponen en riesgo o comprometen los angeles salud.
En Emergencias el tiempo nos corre, y el momento en que tomamos diferentes conductas, durante los angeles evolución del paciente, inftuye directamente en el pronóstico.
En ninguna otra especialidad, se pone en juego los angeles capacidad de decisión tiempo dependiente.
La acción organizada y sistematizada frente a una emergencia, es los angeles que redundará en mayores beneficios, permitiéndonos valorar que "es" y que "no es" de riesgo very important. Un manejo desorganizado, transforma l. a. situación, que de por sí ya es crítica, en un caos con el perjuicio directo sobre el paciente.
ABC en emergencias es un educational de consulta rápida, cuando tenemos poco tiempo para consultar.
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22. Abadie JM, Bankson DD. Assessment of serum free light chain assays for plasma cell disorder screening in a veterans affairs population. Ann Clin Lab Sci. 2006;36:157–62. 23. Nowrousian MR, Brandhorst D, Sammet C, Kellert M, Daniels R, Schiett P, Poser M, Mueller S, Ebeling P, Welt A, Bradwell AR, Buttkereit U, Opalka B, Flasshove M, Moritz T, Seeber S. Serum free light chain analysis and urine immunofixation electrophoresis in patients with multiple myeloma. Clin Cancer Res. 2005;11(24):8706–14.
Hence, increased MYC expression seems to be responsible for progression from MGUS to MM. Complex translocations involving MYC (c-MYC≫N-MYC>L-MYC) appear to be secondary progression events that often do not involve Ig loci [32]. They are rare or absent in MGUS, but occur in 15 % of newly diagnosed tumors, 50 % of advanced tumors, and 90 % of HMCLs [11, 33]. A recent report suggests that a small molecule inhibitor of BRD4 can inhibit MYC RNA expression in MM, with therapeutic effect [34]. , in t(11;14) tumors) [35].
5) [43] and most likely contributing to extramedullary spread of the disease. Interestingly, the NFKB negative regulator TRAF3 located on 14q32 is inactivated in >10 % MM tumors, suggesting that at least in the presence of RAS/BRAF compensating mutation there may be an advantage for t(4;14) MM to lose the der(14) containing FGFR3 in favor of activating the NFKB pathway. Fc, IKKβ, and NIK (MAP3K14)) are being developed as potential therapeutic agents [47, 48]. There is also some evidence suggesting that cells addicted to constitutive NFKB activation may be particularly sensitive to proteasome inhibition [46].