ENARM Flashcards
ALF is defined by three criteria
<div> <div> <div> <div>● Rapid development of hepatocellular dysfunction</div> <div>● Encephalopathy </div> <div>● Absence of a prior history of liver disease.<br></br> </div> </div> </div></div>
<div> <div> <div> <div>Histopathological features of autoim- mune hepatitis include portal inflammation with a {{c1::mononuclear cellular infiltrate}} including plasma cells, extending beyond the limiting plate of hepatocytes into the lobule .</div> </div> </div></div>
“<div> <div> <div> <div>V<span>arying degrees of fibrosis may be present. Fatty change, iron excess, and biliary pathology are not features</span></div> </div> </div></div>”
what are the 2 CAGE question for alcoholism
<div> <div> <div> <div> <div>Have you ever felt you should cut down on your drinking?</div><div>Have people annoyed you by criticizing your drinking?</div><div>Have you ever felt bad or guilty about your drinking?</div><div>Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover (eye-opener)?</div> </div> </div> </div></div>
Define azotemia prerenal
Un aumento en el BUN y Creatinina debido a una perfusión y presión intraglomerular inadecuada
<div> <div> <div> <div> <div>In AKI glomerular filtration can be maintained despite reduced renal blood flow by angiotensin II mediated renal {{c2::efferent}} {{c1::vasoconstriction}}</div> </div> </div> </div></div>
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<div> <div> <div> <div>A particularly poor prognosis of patient with liver disease is seen in the case of type 1 hepatorenal syndrome, in which AKI, defined as {{c1::>two- fold increase in SCr to >2.5 mg/dL, within 2 weeks without an alter- nate cause (e.g., shock and nephrotoxic drugs),}} persists despite volume administration and withholding of diuretics.</div> </div> </div></div>
<div> <div> <div> <div>AKI is a common complication in this setting, and it can be triggered by volume depletion and sponta- neous bacterial peritonitis.</div> </div> </div></div>
Mechanism by wich and NSAID causes a decrease of GFR and the glomerular capillary pressure to drop in AKI
” <div> <div> <div><div><img></img>Loss of vasodilatory prostaglandins increases afferent resistance</div> </div> </div> </div>”
Mechanism by wich ACEI and ARB cause a drop in GFR and GLomerular Capillary Pressure in AKI
“<img></img>Loss of angiotensin II action reduces efferent resistance”
<div> <div> <div> <div> <div>Pathophysiology of sepsis- induced AKI.</div> </div> </div> </div></div>
Endothelial damage. Leucocyte adhesion. Thrombosis. Increased presure. Reduction of renal flow. Acrivation of reactive oxigen species.<div><br></br></div>
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Porción basal del occipital
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Porción escamosa del occipital<div><br></br></div>
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Foramen Magno
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Condilos del occipital<div><br></br></div>
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Porción petrosa del temporal<div><br></br></div>
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Porción Escamosa<div><br></br></div>
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Proceso Mastoides<div><br></br></div>
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Arco zigomático
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Superficie para articulación temporo-mandibular
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Conducto auditivo externo<div><br></br></div>
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Proceso estiloides
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Conducto carotideo
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Foramen yugular<div>z</div>
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CONDUCTO HIPOGLOSO
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Cuerpo Vertebral
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Elevación ≥ 0,3 mg/dl
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Elevación de la creatinina sérica hasta ≥ 4 mg/dl
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Anuria durante ≥ 12 h
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El analisis de orina muestra piuria, hematuria, proteinuria leve, cilindros granulosos y epiteliales, eosinófilos
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• prolongation of the QT interval.
• widening of the QRS complex;
• suppression of the P wave;
• lengthening of the PR interval.
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severa pero también pueden verse en
microangiopatía y lesiones renales
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La fase lútea comienza en el momento de la ovulación, dura de 12 a 14 días y finaliza con la degeneración del cuerpo lúteo.
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Yuxtamedulares= Largas"