CNS pharmacology questions.
Central nervous system drugs are where students most often resort to memorising, and where mechanism rescues them most dramatically. Almost every side effect in this topic is the intended action of the drug appearing at a receptor somewhere it was not wanted.
Commit to an answer before you reveal it. Every explanation says why the right option is right, not merely which one it is, since a reason is what transfers to the next question and a fact is not.
Q1 At GABA-A, benzodiazepines differ from barbiturates because they…
Answer: Increase how often the chloride channel opens
Benzodiazepines increase how often the channel opens, while barbiturates increase how long it stays open. Because benzodiazepines still require GABA to be present, there is a ceiling to their effect, which is the main reason they are far safer in overdose than barbiturates.
Q2 Why must a patient be observed after naloxone reversal?
Answer: Naloxone may wear off first, so sedation returns
Naloxone is a competitive antagonist with a relatively short duration, so it can wear off while a long-acting opioid is still bound and circulating. The patient wakes, appears fixed, and then re-sedates, which is why observation rather than discharge follows a successful reversal.
Q3 Codeine provides no analgesia in some patients because…
Answer: It is a prodrug needing CYP2D6 to become morphine
Codeine has little affinity for the mu receptor itself and works through the morphine it is converted into. CYP2D6 activity varies genetically, so poor metabolisers produce too little morphine to get an effect, while ultra-rapid metabolisers produce dangerously much from a standard dose.
Q4 Serotonin syndrome is most likely when an SSRI is combined with…
Answer: An MAOI, or with tramadol for pain relief
The syndrome needs serotonin raised by more than one route at once. An SSRI blocks reuptake, an MAOI blocks breakdown, and tramadol both inhibits reuptake and has opioid activity. Because MAOI effects persist after stopping, a washout period is required rather than a straight switch.
Q5 Extrapyramidal side effects from haloperidol are caused by…
Answer: D₂ blockade in the nigrostriatal pathway
The antipsychotic effect comes from D₂ blockade in the mesolimbic pathway, but the drug cannot confine itself to one pathway. The same blockade in the nigrostriatal pathway produces parkinsonian features, and in the tuberoinfundibular pathway it raises prolactin.
Q6 Clozapine requires regular blood monitoring because of the risk of…
Answer: Agranulocytosis, developing without warning signs
Clozapine can suppress neutrophil production unpredictably and without warning symptoms until infection appears, so the count has to be checked rather than waited for. It remains in use despite that burden because it works in treatment-resistant schizophrenia where others do not.
Q7 Which combination most raises the risk of lithium toxicity?
Answer: Lithium with an NSAID, ACE inhibitor or thiazide
Lithium is cleared entirely by the kidney and is handled like sodium, so anything reducing renal perfusion or increasing sodium reabsorption increases lithium retention. With a therapeutic range as narrow as lithium’s, a modest fall in clearance reaches toxic concentrations.
Q8 Carbidopa is combined with levodopa in order to…
Answer: Block decarboxylation of levodopa in the periphery
Levodopa is converted to dopamine wherever decarboxylase finds it, and conversion outside the brain causes nausea and hypotension while wasting the dose. Carbidopa does not cross the blood-brain barrier, so it blocks that conversion only in the periphery.
Q9 Tricyclic antidepressant overdose is dangerous mainly because of…
Answer: Sodium channel blockade widening the QRS
Tricyclics are promiscuous, and the receptor blockade causing dry mouth and sedation at therapeutic doses is not what kills in overdose. Sodium channel blockade in cardiac tissue slows conduction, widens the QRS and precipitates arrhythmia, which is why bicarbonate is used.
Q10 Flumazenil reverses benzodiazepine sedation because it is…
Answer: A competitive antagonist at the benzodiazepine site
Flumazenil occupies the benzodiazepine binding site without producing any effect of its own, so it displaces the drug by competition. It is used cautiously because removing benzodiazepine activity abruptly can precipitate seizures in someone dependent or co-ingesting a proconvulsant.
Pick an answer to check it. Nothing is saved, and you can reset the set at any time.
Where to take this next
A set answered once shows you where the gaps are. Closing them takes repetition spaced over weeks, with the misses returning more often than the hits, which is what spaced repetition in the app is for. In the meantime these go deeper on the mechanisms behind the questions above.
- Opioids — the mechanism these questions rest on
- Benzodiazepines — the mechanism these questions rest on
- SSRIs — the mechanism these questions rest on
- CYP450 inducers and inhibitors
- False positives on urine drug screens
- Half-life and steady state calculator — free calculator with a worked example
- Corticosteroid equivalence calculator — free calculator with a worked example
Other practice sets
Cardiovascular · Antimicrobials · Autonomic · Pharmacokinetics · Endocrine · All practice questions
If you are working towards a named licensing exam, the exam preparation hub shows which of these topics your board weights most heavily.
Study aid only. These questions are written for learning and examination practice. They are not medical advice, not clinical decision support, and must never be used to make a decision about a real patient. Always verify against your local formulary, the product literature and a qualified pharmacist. See our medical disclaimer.
Ten questions is a start. Ten a day is a pass.
The app brings cns drugs back on a schedule, and leans on whatever you keep getting wrong. Free download, no credit card.
Free to download. 7-day Pro trial. Cancel anytime.