This error is potentially life-threatening if the less-effective medication is sold to the public instead of the more effective one.Īs you conduct your hypothesis tests, consider the risks of making type I and type II errors. That is, the researcher concludes that the medications are the same when, in fact, they are different. However, if a type II error occurs, the researcher fails to reject the null hypothesis when it should be rejected. If the medications have the same effectiveness, the researcher may not consider this error too severe because the patients still benefit from the same level of effectiveness regardless of which medicine they take. The two medications are not equally effective.Ī type I error occurs if the researcher rejects the null hypothesis and concludes that the two medications are different when, in fact, they are not. The two medications are equally effective. This value is the power of the test.Ī medical researcher wants to compare the effectiveness of two medications. The probability of rejecting the null hypothesis when it is false is equal to 1–β. You can do this by ensuring your sample size is large enough to detect a practical difference when one truly exists. You can decrease your risk of committing a type II error by ensuring your test has enough power. The probability of making a type II error is β, which depends on the power of the test. Type II error When the null hypothesis is false and you fail to reject it, you make a type II error. However, using a lower value for alpha means that you will be less likely to detect a true difference if one really exists. To lower this risk, you must use a lower value for α. An α of 0.05 indicates that you are willing to accept a 5% chance that you are wrong when you reject the null hypothesis. The probability of making a type I error is α, which is the level of significance you set for your hypothesis test. Type I error When the null hypothesis is true and you reject it, you make a type I error. Therefore, you should determine which error has more severe consequences for your situation before you define their risks. The risks of these two errors are inversely related and determined by the level of significance and the power for the test. When you do a hypothesis test, two types of errors are possible: type I and type II. Because the test is based on probabilities, there is always a chance of making an incorrect conclusion. Different pharmacological agents have been tested, but the use of iso-osmolar or hypo-osmolar contrast agents along with continuous hydration before, during, and after the intervention are the only methods that have currently achieved adequate nephroprotection.No hypothesis test is 100% certain. As there is no specific treatment available for this condition, emphasis should be placed on prevention. It is the third leading cause of in-hospital acute kidney injuries, and it leads to an increase in morbidity and mortality of the population. Contrast-induced nephropathy is defined as an absolute (≥ 0.5 mg/dL) or relative increase (≥ 25%) of the serum creatinine within 24-72 hours post-exposure to the contrast media. It is estimated that the incidence is about 0-5% among the population with normal renal function however it can reach 12-27% among people with altered baseline renal function. The use of contrast media in the diagnostic and therapeutic medical arsenal can cause adverse effects, such as renal toxicity and acute kidney injury, known as contrast-induced nephropathy. Se han probado distintos agentes farmacológicos, sin embargo, hoy en día los únicos métodos que han logrado asegurar adecuada nefroprotección son el uso de agentes de contraste isoosmolares o de baja osmolaridad junto con hidratación continua del paciente antes, durante y después de la intervención. Por tanto, el énfasis se realiza en la prevención. No se dispone de un tratamiento específico para esta entidad. Es la tercera causa de injuria renal aguda intrahospitalaria y conlleva un aumento en la morbimortalidad de la población. La nefropatía inducida por contraste se define como un aumento absoluto (≥ 0,5 mg/dl) o relativo (≥ 25%) de la creatinina sérica en 24-72 h postexposición al medio de contraste. Se estima que en la población con función renal normal la incidencia es del 0-5% sin embargo, en personas con alteración de la función renal basal puede llegar a un 12-27%. El uso de medios de contraste dentro del arsenal diagnóstico y terapéutico médico puede ocasionar efectos adversos como toxicidad renal e injuria renal aguda, conocida como nefropatía inducida por contraste.
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