Free PMHNP practice questions

1. A. NSAID-induced reduction in renal prostaglandins decreases lithium clearance, raising the serum levelCorrect

   Correct. Lithium is cleared almost entirely by the kidney and is reabsorbed alongside sodium in the proximal tubule. NSAIDs inhibit prostaglandin synthesis, which reduces renal blood flow and increases proximal reabsorption — so lithium clearance falls and the level rises. Coarse tremor, GI upset and cognitive dulling are classic early toxicity. Check a level now.

2. B. Ibuprofen displaces lithium from plasma protein binding sites, raising the free fraction

   Incorrect. Protein-binding displacement is a real interaction mechanism for highly protein-bound drugs such as warfarin or phenytoin. Lithium is an ion that is essentially not protein bound, so there is nothing to displace.

3. C. Ibuprofen induces hepatic enzymes, accelerating lithium metabolism and causing withdrawal symptoms

   Incorrect on two counts. Lithium is not hepatically metabolised at all — it is excreted unchanged by the kidney — and the symptoms described are toxicity, not withdrawal.

4. D. The symptoms represent a breakthrough mood episode rather than a drug interaction

   Incorrect. Coarse tremor with nausea and cognitive slowing, appearing two weeks after starting an interacting drug, points to a pharmacokinetic cause. Anchoring on a mood episode here risks missing rising toxicity — obtain the level before reaching that conclusion.

Educational objective: NSAIDs, thiazide diuretics, ACE inhibitors and ARBs all reduce renal lithium clearance and can precipitate toxicity in a previously stable patient.

1. A. Clonus and hyperreflexiaCorrect

   Correct. Neuromuscular hyperexcitability — clonus, hyperreflexia, myoclonus, ocular clonus — is the signature of serotonin syndrome and is the single most useful discriminator. NMS produces the opposite motor picture: generalised "lead-pipe" rigidity with hyporeflexia. The rapid onset after a serotonergic addition supports it further.

2. B. Fever above 38.5°C

   Incorrect. Hyperthermia occurs in both syndromes and cannot separate them. It signals severity, not aetiology.

3. C. Autonomic instability with diaphoresis and hypertension

   Incorrect. Autonomic instability is a feature of both. It tells you the patient is unwell and needs monitoring, not which syndrome is present.

4. D. Altered mental status

   Incorrect. Confusion and agitation appear in both, and in several other causes of hyperthermic encephalopathy. It is a non-discriminating finding.

Educational objective: Serotonin syndrome presents with hyperreflexia and clonus and evolves over hours; NMS presents with lead-pipe rigidity and hyporeflexia and evolves over days.

1. A. A mood stabiliser or an antipsychotic with evidence in bipolar depression, rather than antidepressant monotherapyCorrect

   Correct. The prior four-day episode of decreased sleep need, pressured speech and impulsivity meets the duration threshold for hypomania, which makes this bipolar depression rather than a unipolar episode. Treatment should begin with an agent that has evidence in bipolar depression; antidepressant monotherapy risks a switch into hypomania or mania and can accelerate cycling.

2. B. An SSRI alone, titrated to full dose

   Incorrect, and the central trap in this item. The presenting complaint is depression, but the history establishes bipolarity. Unopposed antidepressant monotherapy in bipolar depression risks a manic switch — which is why taking a hypomania history before prescribing is standard.

3. C. An SNRI alone, since the depressive symptoms are the current problem

   Incorrect, for the same reason as SSRI monotherapy. Treating only what is in front of you, without accounting for the documented hypomanic episode, is the error being tested.

4. D. A stimulant to address the hypersomnia and low energy

   Incorrect. Stimulants do not treat bipolar depression and carry their own risk of destabilisation. Hypersomnia here is a symptom of the depressive episode, not a primary sleep disorder to be countered.

Educational objective: Screen every depressive presentation for past hypomania: a qualifying episode reclassifies the illness as bipolar and changes first-line treatment away from antidepressant monotherapy.

1. A. Continue clozapine at the current dose and increase the frequency of ANC monitoringCorrect

   Correct. An ANC of 1,000–1,499/µL is mild neutropenia. Guidance is to confirm with a repeat draw and continue clozapine with more frequent ANC checks — roughly three times weekly — until the count recovers above 1,500/µL. Clozapine is often the only agent controlling a treatment-resistant illness, and the thresholds for interrupting it sit lower: moderate neutropenia is 500–999/µL and severe is below 500/µL.

2. B. Discontinue clozapine immediately and never rechallenge

   Incorrect, and costly. Reflexively stopping clozapine for mild neutropenia removes the one medication controlling a treatment-resistant illness. Permanent non-rechallenge is a consideration in severe neutropenia — an ANC below 500/µL — and even then only after specialist review.

3. C. Add filgrastim prophylactically and continue routine monthly monitoring

   Incorrect. Granulocyte colony-stimulating factor has a role in managing severe clozapine-induced neutropenia in consultation with haematology, not as prophylaxis for a mild count — and reverting to routine monthly monitoring after an abnormal result is the wrong direction of travel.

4. D. Withhold clozapine for one week, then resume at half the dose without repeating the ANC

   Incorrect. Interrupting clozapine for more than about two days requires re-titration to avoid orthostatic hypotension and seizure risk, and resuming without a repeat ANC abandons the monitoring that makes the drug safe to use.

Educational objective: Clozapine ANC monitoring is tiered: mild neutropenia calls for increased monitoring frequency rather than automatic discontinuation, and interruptions longer than two days require re-titration.

1. A. Take protective steps that may include warning the identified person and notifying law enforcement, in accordance with jurisdictional lawCorrect

   Correct. A credible, specific threat against an identifiable person triggers a duty to protect in most jurisdictions. Confidentiality yields to safety here, and appropriate steps may include warning the potential victim, notifying police, and pursuing involuntary evaluation. Because statutes differ by state — some mandate, some permit — the clinician must act according to their own jurisdiction and document the reasoning.

2. B. Maintain absolute confidentiality, as disclosure would breach the therapeutic relationship

   Incorrect. Confidentiality is a strong obligation, not an absolute one. A specific threat to an identifiable third party is the textbook exception, and treating privilege as absolute here exposes both the potential victim and the clinician.

3. C. Document the threat and address it at the next scheduled appointment

   Incorrect. Documentation is necessary but not sufficient, and deferring action to a future visit leaves an articulated, specific plan unaddressed in the interim. The duty is triggered now.

4. D. Ask the patient to sign a no-harm contract and continue outpatient treatment unchanged

   Incorrect. Written contracts of this kind have no demonstrated protective effect and no legal standing, and relying on one in place of protective action misreads the obligation.

Educational objective: A credible threat to an identifiable third party creates a duty to protect that overrides confidentiality; the specific steps required are set by state law, so know your jurisdiction.

1. A. Cognitive restructuring — examining the evidence for an automatic thoughtCorrect

   Correct. The clinician has identified an automatic thought containing catastrophising and mind reading, and is guiding the patient to weigh evidence for and against it. Testing the accuracy of a specific cognition against real experience is cognitive restructuring, a core CBT technique.

2. B. Systematic desensitisation

   Incorrect. Systematic desensitisation pairs graded exposure to feared stimuli with relaxation. Nothing in this exchange involves exposure or relaxation training — the work is on the thought, not the situation.

3. C. Interpretation of transference

   Incorrect. Transference interpretation is a psychodynamic technique addressing feelings displaced onto the therapist. The exchange concerns a workplace prediction, not the therapeutic relationship.

4. D. Motivational interviewing using a decisional balance

   Incorrect. A decisional balance weighs the pros and cons of *changing a behaviour* to resolve ambivalence. Here the clinician is testing the truth of a belief, which is a different target.

Educational objective: Recognise psychotherapy techniques from dialogue: cognitive restructuring targets the accuracy of a specific automatic thought, distinct from exposure, transference work and motivational interviewing.