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In pharmacokinetics, steady state refers to the situation where the overall intake of a drug is fairly in dynamic equilibrium with its elimination. In practice, it is generally considered that steady state is reached when a time of 4 to 5 times the half-life for a drug after regular dosing is started.
The time to reach steady state is defined by the elimination half-life of the drug. So in a patient with renal dysfunction, the plasma half-life is going to be prolonged and the time to reach steady state will increase proportionally.
loading dose is independent of the concentration of the drug in the plasma and the dose frequency...this is why you give a patient who is seizing a huge dose of anti-seizure meds in order to reach a theraputic range on the first dose despite the high risk of toxicity and side effects...primary objective when seizing is stoping the seizure so you want to increase the dose response curve with a massive load
loading dose is independent of DOSE (should have said dose, not concentration in plasma) & FREQUENCY
aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child?
Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything.
There is a Uworld qx that explain this in detail> ID: 863
I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina.
wouldn't she have any possibility of developing osteosarcoma as well? :(
did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation
But how can a 5 year old get two mutations to get retinoblastoma? In 5 years?! Obviously doctor is probably wrong LOL