lunes, 19 de diciembre de 2011
lunes, 19 de septiembre de 2011
Acute Myocardial Ischaemia Update 2011
Acute Myocardial Ischaemia Update 2011
Link
http://www.mediafire.com/?mavm1nd4yttdaxc
Murillo Santucci Cesar de Assunção
Unidade de Terapia Intensiva adulto
Disciplina de Anestesiologia, Dor e Terapia Intensiva
Escola Paulista de Medicina
Rua Napoleão de Barros,715
Vila Clementino - São Paulo - CEP: 04024-002
Tel/Fax: +55-11-55757768
Tel/Fax: +55-11- 55764069
m.assuncao@unifesp.br
murilloassuncao@gmail.com
From: Murillo Santucci Cesar de Assunção <murilloa@uol.com.br>
Date: 2011/9/19
Subject: [interno_residente_medico_PERU] Acute Myocardial Ischaemia Update 2011
To: UTI - Anestesiologia UNIFESP <uti-anestesiologia@yahoogrupos.com.br>
Acute Myocardial Ischaemia Update 2011
Acute Myocardial Ischaemia Update 2011 Link http://www.mediafire.com/?mavm1nd4yttdaxc |
jueves, 18 de agosto de 2011
BASIC LIFE SUPPORT (BLS)
Sociem Ucv Trujillo posted in cibermedicos.Sociem Ucv Trujillo5:18pm Aug 18
BASIC LIFE SUPPORT (BLS)
Acreditación Nacional e Internacional:
Certificado y Tarjeta de Acreditación Internacional BLS de American Heart Association válida por dos años (será otorgada a quienes aprueben satisfactoriamente las evaluaciones teórico-prácticas).
Certificado de asistencia al curso otorgado por el Centro de Entrenamiento Internacional - UPCH.
UPCH
www.upch.edu.pe
Dirigido a: Profesionales de la Salud y Personal Prehospitalario (Médico General y/o Especialista
View Post on Facebook
De: Sociem Ucv Trujillo <notification+yfo6tzj9@facebookmail.com>
Fecha: 18 de agosto de 2011 17:18
Asunto: [cibermedicos] BASIC LIFE SUPPORT (BLS)
Para: cibermedicos <internetymedicos@groups.facebook.com>
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domingo, 10 de julio de 2011
2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction (Updating the 2007 Guideline)
Luhttps://mail.google.com/mail/?ui=2&ik=14d8f0f8db&view=att&th=13114f5f727bf89e&attid=0.1&disp=safe&zfe=windows-1252:es&zwis Eduardo Vargas.
Especialista en Medicina de Emergencias.
relucho@gmail.com
Skype: relucho16
Twiter: @relucho
Enviado desde mi iPad
2011 ACCF_AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina_Non–ST-Elevation Myocardial Infarction (Updating the 2007 Guideline).pdf
1184 K Ver Descargar (descarga para Español)
From: Luis Vargas <relucho@gmail.com>
Date: 2011/7/10
Subject: [SALUD_LORETO] 2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction (Updating the 2007 Guideline)
To: "salud_loreto@yahoogroups.com" <salud_loreto@yahoogroups.com>
Guias de IAM, Rosana
miércoles, 29 de junio de 2011
PRASUGREL
se abre Trial con prasugrel en casimiro en colaboracion con clinica INCA de Dr Mogrovejo
Prasugrel
Systematic (IUPAC) name | |
---|---|
(RS)-5-[2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-4,5,6,7- tetrahydrothieno[3,2-c]pyridin-2-yl acetate | |
Clinical data | |
Licence data | EMA:Link, US FDA:link |
Pregnancy cat. | B(US) B |
Legal status | POM (UK) ℞-only (US) |
Routes | Oral |
Pharmacokinetic data | |
Bioavailability | ≥79% |
Protein binding | Active metabolite: ~98% |
Metabolism | Rapid intestinal and serum metabolism via esterase-mediated hydrolysis to a thiolactone (inactive), which is then converted, via CYP450-mediated (primarily CYP3A4 and CYP2B6) oxidation, to an active metabolite (R-138727) |
Half-life | ~7 hours (range 2-15 hours) |
Excretion | Urine (~68% inactive metabolites); feces (27% inactive metabolites) |
Identifiers | |
CAS number | 150322-43-3 |
ATC code | B01AC22 |
PubChem | CID 6918456 |
ChemSpider | 5293653 Y |
ChEMBL | CHEMBL1201772 N |
Chemical data | |
Formula | C20H20FNO3S |
Mol. mass | 373.442 g/mol |
SMILES | eMolecules & PubChem |
N(what is this?) [1] |
Prasugrel (marketing name Effient in the US, Efient in the EU and Prasita in India) is a novel platelet inhibitor developed by Daiichi Sankyo Co. and produced by Ube and currently marketed in the United States in cooperation with Eli Lilly and Company for acute coronary syndromes planned for percutaneous coronary intervention (PCI). Prasugrel was approved for use in Europe in February 2009, and is currently available in the UK. On July 10, 2009, the US Food and Drug Administration approved the use of prasugrel for the reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with acute coronary syndrome who are to be managed with PCI.[1]
[edit] Pharmacology
Prasugrel is a member of the thienopyridine class of ADP receptor inhibitors, like ticlopidine (trade name Ticlid) and clopidogrel (trade name Plavix). These agents reduce the aggregation ("clumping") of platelets by irreversibly binding to P2Y12 receptors. Compared to clopidogrel, "prasugrel(trade name apagrel) inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel in healthy volunteers and in patients with coronary artery disease, including those undergoing PCI".[2] Clopidogrel, unlike prasugrel, was issued a black box warning from the FDA on March 12, 2010, as the estimated 2-14% of the US population that have low levels of the CYP 2C19 liver enzyme needed to activate clopidogrel may not get the full effect. Tests are available to predict if a patient would be susceptible to this problem or not.[3][4] Prasugrel has not been shown to carry those same limitations.
[edit] Pharmacodynamics
Prasugrel produces inhibition of platelet aggregation to 20 μM or 5 μM ADP, as measured by light transmission aggregometry.[5] Following a 60-mg loading dose of Effient, approximately 90% of patients had at least 50% inhibition of platelet aggregation by 1 hour. Maximum platelet inhibition was about 80% (Figure 2). Mean steady-state inhibition of platelet aggregation was about 70% following 3 to 5 days of dosing at 10 mg daily after a 60-mg loading dose of Effient. Platelet aggregation gradually returns to baseline values over 5–9 days after discontinuation of prasugrel, this time course being a reflection of new platelet production rather than pharmacokinetics of prasugrel. Discontinuing clopidogrel 75 mg and initiating prasugrel 10 mg with the next dose resulted in increased inhibition of platelet aggregation, but not greater than that typically produced by a 10 mg maintenance dose of prasugrel alone. It should also be noted that increasing platelet inhibition could increase bleeding risk. The relationship between inhibition of platelet aggregation and clinical activity has not been established. [2]
[edit] Pharmacokinetics
Prasugrel is a prodrug and is rapidly metabolized to a pharmacologically active metabolite and inactive metabolites. The active metabolite has an elimination half-life of about 7 hours (range 2–15 hours). Healthy subjects, patients with stable atherosclerosis, and patients undergoing PCI show similar pharmacokinetics.
[edit] TRITON-TIMI 38 study
As published in the New England Journal of Medicine's online edition, the TRITON-TIMI 38 study of 13,608 patients with acute coronary syndromes compared prasugrel against clopidogrel, both in combination with aspirin, and found that, as a more potent anti-platelet agent, prasugrel reduced the combined rate of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke (12.1% for clopidogrel vs. 9.9% for prasugrel). This difference in the primary endpoint was mainly driven by the reduction of non-fatal myocardial infarctions. However, an increased rate of serious bleedings (1.4%, vs. 0.9% in the clopidogrel group) and fatal bleedings (0.4% vs. 0.1%) was also observed.[6] Overall mortality did not differ between the two treatment groups.
From the editorial in the NEJM, "In TRITON–TIMI 38, for each death from cardiovascular causes prevented by the use of prasugrel as compared with clopidogrel, approximately one additional episode of fatal bleeding was caused by prasugrel".[7]
In patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI), prasugrel was associated with a significantly lower incidence of ischemic events than clopidogrel, and was particularly effective in specific subgroups of patients, such as those with diabetes mellitus. In this sub-group there is a 30% relative risk reduction (4.2% ARR for unstable angina/NSTEMI and 5% AAR for STEMI) compared to the clopidogrel group without significant increased risk for major bleeding(2.2% vs. 2.3%). However, the efficacy of prasugrel was offset by a higher risk of bleeding than clopidogrel, with patients aged ≥75 years, those weighing <60 kg and those with a history of stroke or transient ischemic attack at the greatest risk. A lower dose of prasugrel in patients aged ≥75 years and those weighing <60 kg may help to minimize the bleeding risk, although more data are needed to establish this; prasugrel is contraindicated in patients with a history of stroke or transient ischemic attack.[8] The estimated number of patients needed to be treated with prasugrel at the dosage studied, as compared with standard-dose clopidogrel, to prevent one primary efficacy end point during a 15-month period was 46. The number of patients who would have to be treated to result in an excess non–CABG-related TIMI major hemorrhage was 167.[9]
Furthermore, data from a pharmacodynamic study suggests that acute coronary syndrome (ACS) patients can be safely switched from clopidogrel to prasugrel and that doing so results in a further reduction in platelet function after one week.[10] When patients receive a loading dose of prasugrel prior to switching from clopidogrel, the reduction in platelet function occurs within two hours.[11]
[edit] Adverse Effects
Cardiovascular: Hypertension (8%), hypotension (4%), atrial fibrillation (3%), bradycardia (3%), noncardiac chest pain (3%), peripheral edema (3%) Central nervous system: Headache (6%), dizziness (4%), fatigue (4%), fever (3%), extremity pain (3%) Dermatologic: Rash (3%) Endocrine & metabolic: Hypercholesterolemia/hyperlipidemia (7%) Gastrointestinal: Nausea (5%), diarrhea (2%), gastrointestinal hemorrhage (2%) Hematologic: Leukopenia (3%), anemia (2%) Neuromuscular & skeletal: Back pain (5%) Respiratory: Epistaxis (6%), dyspnea (5%), cough (4%)
[edit] References
- ^ Baker WL, White CM. Role of Prasugrel, a Novel P2Y12 Receptor Antagonist, in the Management of Acute Coronary Syndromes. American Journal of Cardiovascular Drugs Aug 1, 2009; 9 (4): 213-229. Link text
- ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482.
- ^ Food and Drug Administration (United States) (March 12, 2010). "FDA Announces New Boxed Warning on Plavix: Alerts patients, health care professionals to potential for reduced effectiveness". Press release. http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm204253.htm. Retrieved March 13, 2010.
- ^ "FDA Drug Safety Communication: Reduced effectiveness of Plavix (clopidogrel) in patients who are poor metabolizers of the drug". Drug Safety and Availability. Food and Drug Administration (United States). March 12, 2010. http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm203888.htm. Retrieved March 13, 2010.
- ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function" (in English). http://www.theheart.org. http://www.theheart.org/article/1123367.do. Retrieved 1 April 2011.
- ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482.
- ^ Bhatt DL (2007). "Intensifying Platelet Inhibition — Navigating between Scylla and Charybdis". N Engl J Med 357 (20): 2078–81. doi:10.1056/NEJMe0706859. PMID 17982183. http://content.nejm.org/cgi/content/full/NEJMe0706859?query=TOC.
- ^ Duggan ST, Keating GM. Prasugrel: A Review of its Use in Patients with Acute Coronary Syndromes Undergoing Percutaneous Coronary Intervention. Drugs Aug 20, 2009; 69 (12): 1707-26 Link text
- ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482.
- ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function". 1.Angiolillo DJ, Saucedo JF, DeRaad R, et al. Increased platelet inhibition after switching from maintenance clopidogrel to prasugrel in patients with acute coronary syndromes. J Am Coll Cardiol 2010; 56: 1017-23.. http://www.theheart.org. http://www.theheart.org/article/1123367.do. Retrieved 1 April 2011.
- ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function". http://www.theheart.org. http://www.theheart.org/article/1123367.do#bib_1. Retrieved 1 April 2011.
[edit] External links
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lunes, 27 de junio de 2011
: FEOCROMOCITOMA2
FeocromocitomaPozo Román, Jesús
Publicado en An Pediatr (Barc). 2006;64(Supl 2):92-9. - vol.64 núm Supl.2
Descargar PDF en: Español
Tumores de la médula suprarrenal. Feocromocitoma
Montanya Mias, E; Mena Ribas, E
Publicado en Medicine. 2004;09:937-45. - vol.09 núm 15
pulse sobre visualizar documento
Emergencia hipertensiva en el contexto de feocromocitoma
http://www.jano.es/ficheros/sumarios/1/0/1613/64/1v0n1613a13090293pdf001.pdf
Feocromocitoma como causa de hemoptisis masiva
García-Ferrer, Luis; Calvo, Regina; Broch, María Jesús
Publicado en Arch Bronconeumol. 2008;44:396. - vol.44 núm 07
pulse sobre visualizar documento.
Metanefrinas plasmáticas: mayor eficacia en el diagnóstico bioquímico del feocromocitoma
Publicado en Endocrinol Nutr. 2005;52:551-5. - vol.52 núm 10 Leer en: English
Descargar PDF en: Español
Protocolo diagnóstico de feocromocitoma
Beato Víbora, P; González-Albarrán, O; García Robles, R
Publicado en Medicine. 2000;08:1174-6. - vol.08 núm 22
pulse sobre visualizar documento
Feocromocitoma
Medicine. 2000;08:1153-9. -- pulse sobre visualizar documento
Atte.Dr.Máximo Cuadros Chávez
Celular 99199698
rpm #800515
http://es.groups.yahoo.com/group/interno_residente_medico_PERU/
http://es.groups.yahoo.com/group/SANFERNANDOPERU/
http://www.facebook.com/home.php?sk=group_150017968368005&ap=1
http://medicalia.ning.com/profiles/blog/list?user=1nezbq9ucojf4
UNYK: 245 HRP
Skype: maximocuadrosFeocromocitoma
Publicado en An Pediatr (Barc). 2006;64(Supl 2):92-9. - vol.64 núm Supl.2Descargar PDF en: Español
Tumores de la médula suprarrenal. Feocromocitoma
Publicado en Medicine. 2004;09:937-45. - vol.09 núm 15pulse sobre visualizar documento
Emergencia hipertensiva en el contexto de feocromocitoma
http://www.jano.es/ficheros/sumarios/1/0/1613/64/1v0n1613a13090293pdf001.pdfFeocromocitoma como causa de hemoptisis masiva
Publicado en Arch Bronconeumol. 2008;44:396. - vol.44 núm 07pulse sobre visualizar documento.
Metanefrinas plasmáticas: mayor eficacia en el diagnóstico bioquímico del feocromocitoma
Publicado en Endocrinol Nutr. 2005;52:551-5. - vol.52 núm 10Feocromocitoma
Medicine. 2000;08:1153-9. -- pulse sobre visualizar documento
Atte.rpm #800515
De: Máximo Cuadros <maximocuadros@yahoo.es>
Para: interno_residente_medico_PERU@yahoogroups.com
Enviado: dom,26 junio, 2011 10:08
Asunto: FEOCROMOCITOMA
FJ Tébar Massó. JM Rodríguez González.
Medicine. 2008;10:997-1005.
PUNTOS CLAVE:- Concepto. El feocromocitoma es un tumor poco frecuente, pero su malignidad funcional y su 10% de malignidad histológica obligan a pensar en él. Debemos tener en cuenta que el 15-20% es de localización extraadrenal.
- Clínica. La clínica está marcada por la hipertensión arterial, frecuentemente paroxística, en la que puede haber graves complicaciones: infarto de miocardio, accidente vascular cerebral, etc. ¿ Es imprescindible establecer el tratamiento quirúrgico lo antes posible.
- Preparación preoperatoria. El paciente debe llegar a la cirugía con bloqueo alfa-adrenérgico. ¿ El anestesista debe conocer el manejo de estos tumores, tanto para la inducción de la anestesia como para solventar los problemas que surjan en el acto quirúrgico.
Feocromocitoma: actualización diagnóstica y terapéutica
AMELIA OLEAGA. FERNANDO GOÑI.
Endocrinol Nutr. 2008;55:202-16.
pulse sobre visualizar documento
rpm #800515
http://es.groups.yahoo.com/group/SANFERNANDOPERU/
http://medicalia.ning.com/profiles/blog/list?user=1nezbq9ucojf4
UNYK: 245 HRP
Skype: maximocuadros
De: Julio César Castillejo Correa <julcast2000@yahoo.es>
Para: maximocuadros@yahoo.es
Enviado: dom,26 junio, 2011 05:55
Asunto: FEOCROMOCITOMA
saludos colega soy anestesiologo de Perú y trabajo en el Hospital Nacional Guillermo Almenara I-Essalud a proposito del tema en cuestion tendra ud algun protocolo De manejo perioperatorio de FEOCROMOCITOMA tanto en cirugia general como laparoscopica??o disculpe la confianza, en su experiencia tendra algunos Tips o cuidados que debemos tener con estos pacientes?. Soy anestesiólogo asistente desde hace 9 años aprox y en mi experiencia he tenido 3 casos sin mayor complicaciones (gracias a Dios!!!), pero puede ser que alguna vez me toque un caso complicado y me gustaria tener toda la informacion posible para enfrentar este caso....... gracias de anetmano JULIO CESAR CASTILLEJO CORREA MEDICO ANESTESIOLOGO CMP 30031 - RNE 15539 HNGAI-EsSALUD Clínica Ricardo Palma |
Feocromocitoma
Cuadros Chavez posted in cibermedicos.Maximo Cuadros Chavez10:07am Jun 26
Feocromocitoma
http://www.facebook.com/l/338ffmF_D4jZcTuKUtQ1Hnnl8Eg/www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13125936&pident_usuario=0&pident_revista=62&fichero=62v10n15a13125936pdf001.pdf&ty=147&accion=L&origen=medicine&web=www.medicineonline.es&lan=es
Medicine. 2008;10:997-1005.
PUNTOS CLAVE:
Concepto. El feocromocitoma es un tumor poco frecuente, pero su malignidad funcional y su 10% de malignidad histológica obligan a pensar en él. Debemos tener en cuenta que el 15-20% es de localización extraadrenal.
Clínica. La clínica está marcada por la hipertensión arterial, frecuentemente paroxística, en la que puede haber graves complicaciones: infarto de miocardio, accidente vascular cerebral, etc. ¿ Es imprescindible establecer el tratamiento quirúrgico lo antes posible.
Preparación preoperatoria. El paciente debe llegar a la cirugía con bloqueo alfa-adrenérgico. ¿ El anestesista debe conocer el manejo de estos tumores, tanto para la inducción de la anestesia como para solventar los problemas que surjan en el acto quirúrgico.
Feocromocitoma: actualización diagnóstica y terapéutica
http://www.facebook.com/l/338ffgVppqwxv9qOUEFcGQ-GJYw/www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13120617&pident_usuario=0&pident_revista=12&fichero=12v55n05a13120617pdf001.pdf&ty=129&accion=L&origen=medicine&web=www.medicineonline.es&lan=es
Endocrinol Nutr. 2008;55:202-16.
http://www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13120617&pident_usuario=0&pident_
apps.elsevier.es
De: Maximo Cuadros Chavez <notification+yfo6tzj9@facebookmail.com>
Fecha: 26 de junio de 2011 10:07
Asunto: [cibermedicos] Feocromocitoma
Para: cibermedicos <internetymedicos@groups.facebook.com>
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