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A hypertensive crisis may occur with such abrupt withdrawal of the drug.Hypertensive crisis is mainly linked to monoamine oxidase inhibitors (MAOIs), not antipsychotics, so it is not the primary concern.

Significant muscle twitching may occur, increasing fall risk.Muscle twitching is not a common withdrawal effect of antipsychotics and is less urgent than psychosis relapse.

EPS symptoms such as pseudo-parkinsonism are likely to occur.
Extrapyramidal symptoms are usually a side effect during ongoing therapy, not after discontinuation.

The client may experience withdrawal and slowed activity.Phenothiazines more commonly cause sedation, not withdrawal-like symptoms, and this is not the most urgent teaching point before discharge.

Tardive dyskinesia is likely early in therapy.Tardive dyskinesia usually develops after months to years of therapy, not in the early stages.

Medications should be taken as prescribed to prevent adverse effects.
While adherence is important, this statement does not address a specific high-priority side effect for early treatment.

Restful sleep, elevated mood, and coping abilities.These outcomes are more associated with treatment of mood disorders such as depression or bipolar disorder, not the primary therapeutic goal for acute schizophrenia.

Orthostatic hypotension, reflex tachycardia, and sedation.These are adverse effects, not therapeutic outcomes. While important to monitor, they do not reflect whether the drug is achieving its intended purpose.

Relief of anxiety and improved sleep and dietary habits.
These effects may occur secondarily but are not primary indicators of antipsychotic therapeutic effectiveness.

Diazepam (Valium) – This benzodiazepine is primarily used for anxiety, muscle relaxation, and seizure control, not for preventing EPS. While it may reduce anxiety related to symptoms, it does not address the underlying neurotransmitter imbalance that causes acute dystonia.

Haloperidol (Haldol) – Another first-generation antipsychotic, haloperidol can actually increase the risk of EPS, making it inappropriate for prevention. Administering it alongside fluphenazine could worsen movement-related side effects.

Lorazepam (Ativan) – This benzodiazepine can help relieve agitation or anxiety in psychotic patients, but it does not prevent acute dystonia because it does not correct the dopamine-acetylcholine imbalance in the basal ganglia.

Pacing, squirming, or difficulty with gait such as bradykinesia – These are signs of akathisia or drug-induced parkinsonism, which are types of extrapyramidal symptoms (EPS). While uncomfortable and requiring prompt treatment, they are not typically life-threatening emergencies.

Severe spasms of the muscles of the tongue, face, neck, or back – This describes acute dystonia, an early-onset EPS that can be distressing and potentially dangerous if airway muscles are involved, but it is generally managed quickly with anticholinergic medications like benztropine or diphenhydramine.

Sexual dysfunction or gynecomastia – These are related to endocrine side effects from increased prolactin levels. They are bothersome and may affect adherence but are not medical emergencies.

Take the medication in the morning to prevent insomnia – Fluphenazine is more likely to cause sedation than insomnia. Adjusting the time of administration does not address anticholinergic effects such as dry mouth.

Use cooling measures to decrease fever – While anticholinergic drugs can reduce sweating and theoretically contribute to heat intolerance, fever is not the most common issue. Cooling measures are not a primary intervention for typical anticholinergic effects in this context.

Take an antacid to relieve nausea – Antacids are not indicated for anticholinergic effects. In addition, they can interfere with the absorption of some oral medications, including certain antipsychotics.

Shuffling gait – This finding indicates parkinsonism, an EPS that can occur with haloperidol. While it requires intervention, it does not pose an immediate threat to life like acute dystonia does.

Drowsiness – Sedation is a common side effect of haloperidol but is not life-threatening. Monitoring and dose adjustments can address this over time.

Impotence – Sexual side effects are possible with haloperidol but are not urgent or dangerous. They can be addressed during routine follow-up.

“You should have a high-carbohydrate snack between meals and at bedtime.” – Clozapine can cause weight gain and metabolic changes, so increased carbohydrate intake would worsen these effects rather than help. Dietary guidance should focus on balanced nutrition and weight control.

“You are likely to develop hand tremors if you take this medication for a long period of time.” – Tremors are more commonly linked to first-generation antipsychotics and some atypicals, but they are not a hallmark risk of clozapine. EPS incidence is generally lower with clozapine compared to conventional antipsychotics.

“You may experience temporary numbness of your mouth after each dose.” – Oral numbness is not a typical side effect of clozapine. Notable adverse effects include sedation, weight gain, hypersalivation, seizures, myocarditis, and agranulocytosis.

Parkinsonism – Typically presents with rigidity, bradykinesia, and tremors, resembling Parkinson’s disease. These symptoms usually appear early in treatment, not after long-term use.

Anticholinergic effects – These include dry mouth, blurred vision, constipation, and urinary retention. They do not explain the involuntary facial and tongue movements observed in this client.

Akathisia – Characterized by inner restlessness, inability to sit still, and pacing, typically occurring shortly after starting or increasing antipsychotic therapy. The client’s symptoms are distinctly involuntary movements, not restlessness.

Akathisia – Akathisia presents as restlessness, pacing, or an inability to sit still. It does not involve sustained muscle contractions or abnormal postures, making it distinct from acute dystonia.

Tardive dyskinesia – Tardive dyskinesia typically develops after months to years of antipsychotic therapy and involves slow, repetitive, involuntary movements, most commonly of the face and mouth, unlike the sudden onset seen in acute dystonia.

Pseudo-parkinsonism – This EPS mimics Parkinson’s disease, presenting with tremors, bradykinesia, rigidity, and shuffling gait, but does not include the acute, sustained muscle contractions seen in dystonia.

Blocking actions of epinephrine – Epinephrine is involved in the fight-or-flight response and does not play a central role in psychotic symptom development. Blocking epinephrine would not relieve hallucinations or delusions.

Promoting prostaglandin synthesis – Prostaglandins are mediators of inflammation and pain, unrelated to the mechanism of antipsychotic drugs.

Enhancing the action of gamma-aminobutyric acid (GABA) – GABA enhancement is the mechanism of benzodiazepines and some sedative-hypnotics, not antipsychotics. It primarily produces CNS depression rather than antipsychotic effects.

Quetiapine (Seroquel) – This atypical antipsychotic has a lower risk of EPS and is not used to treat EPS caused by other antipsychotics. It primarily targets positive and negative symptoms of psychosis without reversing motor side effects.

Aripiprazole (Abilify) – Another second-generation antipsychotic, aripiprazole is not indicated for managing EPS. Its mechanism is a partial dopamine agonist, which does not reverse EPS caused by dopamine antagonists.

Chlorpromazine (Thorazine) – This is a typical antipsychotic that can also cause EPS. Using it would worsen extrapyramidal symptoms, making it inappropriate for treatment.