Seminario Dm II 2008 Complicaciones Agudas
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Este documento presenta información sobre tres complicaciones agudas de la diabetes: cetoacidosis diabética, estado hiperglucémico hiperosmolar y hipoglicemia. Describe la fisiopatología, factores precipitantes, síntomas clínicos, diagnóstico y tratamiento de cada una.
![COMPLICACIONES AGUDAS DIABETES MELLITUS ,[object Object],[object Object],[object Object],INTERNO MAXIMILIANO RIVERA NAVARRETE VI AÑO MEDICINA UA 2008](https://image.slidesharecdn.com/seminariodm2008complicacionesagudas-090916193302-phpapp02/85/Seminario-Dm-II-2008-Complicaciones-Agudas-1-320.jpg)
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Seminario Dm II 2008 Complicaciones Agudas
- 4. DISMINUCIÓN ABSOLUTA DE INSULINA AUMENTO DE HORMONAS DE CONTRARREGULACION DISMINUCIÓN UTILIZACÍÓN PERIFERICA DE GLUCOSA AUMENTO PROD HEPÁTICA DE GLUCOSA AUMENTO DE LIPÓLISIS Y PROTEOLISIS LIBERACIÓN DE AGL Y GLICEROL GLUCONEOGENESIS GLICOGENOLISIS HIPERGLICEMIA AUMENTA CETOGENESIS CETOACIDOSIS GLUCOSURIA PERDIDA DE H2O Y ELP DESHIDRATACION INSUF RENAL AG HIPEROSMOLARIDAD >GLICOGENO <BUFFERS (HCO3) AUMENTA VLDL Y TG OXIDACION AGL CAD
- 8. Wang K. N Engl J Med 2004;351:593 A 38-year-old man presented to the emergency department with nausea, vomiting, and epigastric pain. Antec: DM I, tto: Insulin; HTA, tto: lisinopril GLU: 839 mg%; K+: 7.9 mEq/L; pH: 7.21 ¿DIAGNOSTICO?
- 9. Wang K. N Engl J Med 2004;351:593 K+: 5.1 mEq/L CAD
- 11. CLÍNICA
- 12. CLÍNICA
- 19. TRATAMIENTO
- 20. TRATAMIENTO
- 21. TRATAMIENTO NOTA: PO 4 - se administra solo cuando es < 1 mg/dL (ICC, IResp); 20-30 mEq/L KPO4
- 28. DISMINUCIÓN RELATIVA DE INSULINA PROLONGADA LEVE AUMENTO DE HORMONAS DE CONTRARREGULACION DISMINUCIÓN UTILIZACÍÓN PERIFERICA DE GLUCOSA AUMENTO PROD HEPÁTICA DE GLUCOSA AUMENTO DE LIPÓLISIS Y PROTEOLISIS GLUCONEOGENESIS GLICOGENOLISIS HIPERGLICEMIA CETOSIS DIURESIS OSMOTICA PERDIDA DE H2O Y ELP DESHIDRATACION INSUF RENAL AG HIPEROSMOLARIDAD LIBERACIÓN DE AGL Y GLICEROL FACTOR DESENCADENANTE BAJA INGESTA HIDRICA EHH
- 31. FACTORES PRECIPITANTES PARA LA APARICION DE EHH
- 33. CLÍNICA
- 34. CLÍNICA
- 38. TRATAMIENTO 4-6 litros en 8-10 h Osm > 360 Na > 160 IC o IRenal
- 39. TRATAMIENTO
- 42. HIPOGLICEMIA
- 45. CLÍNICA
Hinweis der Redaktion
- A 38-year-old man presented to the emergency department with nausea, vomiting, and epigastric pain. The patient had type 1 diabetes mellitus and was being treated with insulin. He was also taking lisinopril for the treatment of hypertension. The initial electrocardiogram (Panel A) revealed sinus tachycardia and ST-segment elevation in leads V1 to V3 -- findings highly suggestive of acute anteroseptal myocardial infarction. Peaked T waves were noted in leads II, III, aVF, and V3 to V6. The serum glucose concentration was 839 mg per deciliter (46.6 mmol per liter), the arterial blood pH was 7.21, and the serum potassium concentration was 7.9 mmol per liter. The diagnosis of diabetic ketoacidosis was made. When the electrocardiogram was repeated several hours later, after the potassium concentration was lowered to 5.1 mmol per liter with treatment (Panel B [lead V5 is not placed]), the ST-segment elevation disappeared completely, as did the peaked T waves. This case is an example of hyperkalemia causing a &quot;pseudoinfarction&quot; pattern. The clue to the correct diagnosis is the T wave in V4, which is tall, narrow, and pointed, with a short QT interval. The tall T waves that are characteristic of hyperacute ischemic changes tend to be associated with a long QT interval, and the T waves are broad rather than narrow and pointed.