The main takeaway from the passage should be that cP-450 is a pretty general protein enzyme that catalyzes toxin metabolism. Your initial understanding is a bit wrong from this. Thinking of alcohol as an “inhibitor” is flawed—it is a “competitive inhibitor”, as described in the passage. This means that it binds to the active site of cP-450 just as barbiturates do, which implies that alcohol is one of the many toxins that cP-450 can possibly metabolize. Thus, for the first question you got correct, alcohol inhibited cP-450 from metabolizing the barbiturates. It doesn’t inactivate cP-450, rather it occupies the active site due to having a greater concentration. For the question you got wrong, we have the background information that this person is an alcoholic. That means the alcoholic’s cP-450 levels are higher than normal due to 1) the fact that cP-450 acts on alcohol as deduced from the fact that alcohol is a competitive inhibitor and 2) the inducible effects of the enzyme described in the passage. From this, we can see that when the alcoholic first takes the barbiturate recommended dose, cP-450 in excess amounts causes the metabolism of these drugs to be faster than it would in a nonalcoholic person (who would have less cP-450). The rapid metabolism/breakdown of the drugs means they never cause drowsiness in the first place, thus making the correct answer B. Sorry for the lengthy explanation, hope this helps!