"Psychopharmacology" — Practice

Question 1

A young man given haloperidol develops sustained upward deviation of the eyes four hours later. This is

Accepted Answer

B

Question 2

Galactorrhoea in a patient on an antipsychotic results from blockade in which pathway?

Accepted Answer

D

Question 3

A patient on an antipsychotic feels unable to sit still and appears agitated. The team increases the dose. What has gone wrong?

Accepted Answer

The team has treated akathisia as worsening psychosis, and increasing the dose will make it worse.

Akathisia is a subjective sense of inner restlessness with an inability to remain still, appearing within days to weeks of starting or increasing an antipsychotic. It is regularly mistaken for agitation, anxiety or psychotic deterioration because it looks like all three from the outside.

The distinction rests on asking the patient: akathisia is experienced as an unpleasant compulsion to move, not as fear or as a response to hallucinations. It matters because it is strongly associated with distress, treatment refusal and suicide.

Management is to reduce the dose or switch, with propranolol or a benzodiazepine symptomatically. Anticholinergics are relatively ineffective here, unlike in dystonia and parkinsonism.

Question 4

A patient started on clozapine three weeks ago develops fever, tachycardia and malaise. Which two diagnoses must be excluded urgently?

Accepted Answer

Agranulocytosis and myocarditis. Both occur characteristically in the early weeks of clozapine treatment and both can be fatal.

An urgent full blood count is required for agranulocytosis, which is the reason clozapine is dispensed under mandatory haematological monitoring through a registry.

Myocarditis is the diagnosis more often missed, because fever, tachycardia and malaise in the first weeks are readily attributed to infection or to the drug's ordinary effects. Troponin, C-reactive protein, electrocardiography and echocardiography are indicated.

Neither should be dismissed as a simple febrile illness, and clozapine is withheld while they are being investigated.

Question 5

Which withdrawal states are potentially fatal, and what is the pharmacological reason?

Accepted Answer

Alcohol and benzodiazepine withdrawal are potentially fatal; opioid withdrawal, though intensely unpleasant, usually is not.

Both alcohol and benzodiazepines are positive modulators at the GABA-A receptor, the principal inhibitory system in the brain. Chronic exposure downregulates GABA-A signalling and upregulates excitatory glutamatergic transmission as a compensation. Abrupt withdrawal removes the inhibitory input while the compensatory excitation persists, producing a hyperexcitable state with tremor, autonomic instability, seizures and delirium tremens.

Opioid withdrawal, by contrast, arises from loss of mu receptor agonism with noradrenergic rebound from the locus coeruleus. It causes severe distress with sweating, cramps, diarrhoea and piloerection, but it does not produce the seizures or cardiovascular collapse that make the GABAergic withdrawals dangerous.

The practical consequence is that alcohol and benzodiazepine detoxification require medically supervised tapering, whereas opioid withdrawal is managed for comfort and retention in treatment.

Question 6

A patient on an SSRI is given tramadol for back pain. Within hours he is agitated and febrile with dilated pupils, hyperreflexia and clonus in the legs. Diagnose and distinguish from the syndrome it resembles.

Accepted Answer

Serotonin syndrome, precipitated by adding tramadol, which has serotonergic activity, to an SSRI.

It is distinguished from neuroleptic malignant syndrome principally by hyperreflexia and clonus, which are decisive and do not occur in neuroleptic malignant syndrome. Other separating features are onset within 24 hours rather than over days to weeks, dilated pupils, increased bowel sounds, and rigidity greatest in the lower limbs rather than the generalised lead-pipe rigidity of neuroleptic malignant syndrome.

Management is to stop all serotonergic agents, provide supportive care with cooling, fluids and benzodiazepines for agitation, and give cyproheptadine in moderate to severe cases. Resolution is usually rapid once the drugs are withdrawn, which is itself a diagnostic feature, in contrast to the slow resolution of neuroleptic malignant syndrome.

Question 7

An 80-year-old on amitriptyline, an antipsychotic and trihexyphenidyl becomes confused with urinary retention and a dry mouth. Explain and manage.

Accepted Answer

This is anticholinergic toxicity from cumulative antimuscarinic burden rather than from any single drug.

Amitriptyline is strongly antimuscarinic, many antipsychotics have antimuscarinic activity particularly the low-potency typicals, and trihexyphenidyl is a pure anticholinergic. The effects add together and the total burden is what matters.

Older adults are especially vulnerable because of reduced cholinergic reserve, greater blood-brain barrier permeability and reduced clearance, which is why central effects such as confusion appear at doses tolerated by younger patients.

Management is to review the whole prescription rather than treat the confusion symptomatically: withdraw or substitute the anticholinergic agents where possible, choose alternatives with lower antimuscarinic activity, and reassess whether each drug is still needed. Adding another drug to treat the confusion would be the wrong direction entirely.

Question 8

A patient on valproate is started on lamotrigine at the standard monotherapy titration rate. Ten days later she develops a widespread rash with mucosal involvement. Explain.

Accepted Answer

This is a severe cutaneous adverse reaction, likely Stevens-Johnson syndrome, precipitated by lamotrigine escalated too quickly in the presence of valproate.

Lamotrigine carries a dose- and titration-rate-dependent risk of serious rash, which is why monotherapy is started at a low dose and increased slowly over weeks rather than days.

Valproate inhibits lamotrigine glucuronidation, roughly doubling its plasma concentration for a given dose. A standard monotherapy titration therefore delivers approximately double the intended exposure, and the titration schedule must be halved when the two are combined.

Management is immediate and permanent discontinuation of lamotrigine, supportive care in an appropriate setting given the mucosal involvement, and clear documentation so that it is never restarted. The drug is not rechallenged after a serious rash even at a lower dose.

Question 9

A 60-year-old with Parkinson disease on levodopa and a dopamine agonist develops visual hallucinations and has begun gambling heavily. How is this understood and managed?

Accepted Answer

Both features are dopaminergic adverse effects rather than a primary psychiatric illness, and they arise from the same pharmacology acting in different pathways.

Visual hallucinations reflect excess dopaminergic stimulation in mesolimbic and visual association pathways, and they are commoner with advancing disease, cognitive impairment and higher total dopaminergic load. Impulse control disorders, including pathological gambling, hypersexuality and compulsive shopping, are specifically associated with dopamine agonists more than with levodopa, reflecting D3 receptor stimulation in reward circuitry.

Management begins with the drug rather than with an added antipsychotic. Reduce or withdraw the dopamine agonist first, since it contributes disproportionately to both problems and is more expendable than levodopa. Review anticholinergics and other contributors, and exclude infection and metabolic causes of delirium.

If an antipsychotic is unavoidable, conventional agents worsen parkinsonism through nigrostriatal D2 blockade, so quetiapine or clozapine are preferred. The gambling must also be asked about explicitly, since patients rarely volunteer it and the financial consequences can be catastrophic.

Practice — "Psychopharmacology"

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