Topic 8

What is the primary goal of antipsychotic medications?

Reduce psychotic symptoms, improve functioning, and prevent relapse; they control symptoms but do not cure schizophrenia.

How do first-generation antipsychotics (FGAs) work?

Strongly block dopamine (D2) receptors.

How do second-generation antipsychotics (SGAs) work?

Block dopamine and serotonin (5-HT2A) receptors.

How do third-generation antipsychotics (TGAs) work?

Act as dopamine partial agonists that stabilize dopamine activity.

Which antipsychotic generation primarily treats positive symptoms?

First-generation antipsychotics (FGAs).

Which antipsychotic generation treats both positive and negative symptoms?

Second-generation antipsychotics (SGAs).

Which antipsychotic generation generally has the lowest risk of EPS?

Third-generation antipsychotics (TGAs).

What dopamine pathway is responsible for positive symptoms?

Mesolimbic pathway.

Blocking dopamine in the mesolimbic pathway causes what effect?

Decreases hallucinations and delusions.

What dopamine pathway is associated with negative symptoms?

Mesocortical pathway.

Blocking dopamine in the nigrostriatal pathway causes what complication?

Extrapyramidal symptoms (EPS).

Blocking dopamine in the tuberoinfundibular pathway causes what adverse effect?

Increased prolactin causing galactorrhea, gynecomastia, and sexual dysfunction.

Examples of first-generation antipsychotics

Haloperidol, Chlorpromazine, Fluphenazine, Thioridazine, Trifluoperazine.

Examples of second-generation antipsychotics

Clozapine, Risperidone, Olanzapine, Quetiapine, Ziprasidone.

Examples of third-generation antipsychotics

Aripiprazole, Brexpiprazole, Cariprazine.

What are the four extrapyramidal symptoms (EPS)?

Acute dystonia, Parkinsonism, Akathisia, Tardive dyskinesia.

Which EPS is an emergency that develops within hours to days?

Acute dystonia.

Signs of acute dystonia

Torticollis, tongue protrusion, jaw spasms, oculogyric crisis, laryngospasm.

What is the priority nursing assessment during acute dystonia?

Assess airway and swallowing immediately.

First-line treatment for acute dystonia

IM/IV Benztropine (Cogentin).

Alternative treatment for acute dystonia

IM/IV Diphenhydramine (Benadryl).

Which EPS causes pacing and inability to sit still?

Akathisia.

How is akathisia treated?

Propranolol or Lorazepam.

Which EPS resembles Parkinson's disease?

Pseudoparkinsonism.

Signs of pseudoparkinsonism

Tremor, rigidity, mask-like face, shuffling gait, bradykinesia.

Treatment for pseudoparkinsonism

Benztropine or Diphenhydramine.

Which EPS develops months to years after therapy?

Tardive dyskinesia.

Signs of tardive dyskinesia

Lip smacking, tongue protrusion, chewing movements, involuntary facial/body movements.

Can tardive dyskinesia become permanent?

Yes, if not recognized early.

What assessment tool is used to monitor tardive dyskinesia?

AIMS (Abnormal Involuntary Movement Scale).

When should the AIMS assessment be performed?

At baseline and regularly throughout antipsychotic therapy.

What is Neuroleptic Malignant Syndrome (NMS)?

A life-threatening reaction to antipsychotics characterized by fever, rigidity, altered mental status, and autonomic instability.

Classic signs of NMS

Fever, lead-pipe rigidity, confusion, diaphoresis, tachycardia, unstable blood pressure, elevated CK.

Priority nursing intervention for suspected NMS

Stop the antipsychotic immediately and notify the provider.

Treatment for NMS

IV fluids, cooling measures, dantrolene, bromocriptine or amantadine, benzodiazepines.

Why are IV fluids important during NMS?

Prevent kidney injury from rhabdomyolysis.

What urine finding may indicate rhabdomyolysis?

Dark or tea-colored urine.

Which antipsychotics have the highest risk for QT prolongation?

Haloperidol, Ziprasidone, Iloperidone, Thioridazine.

What life-threatening dysrhythmia can QT prolongation cause?

Torsades de Pointes.

What labs should be monitored in clients at risk for QT prolongation?

Potassium and magnesium.

What assessment is required before and during therapy with QT-prolonging antipsychotics?

ECG monitoring.

High-potency FGAs produce what side effect profile?

More EPS, less sedation.

Low-potency FGAs produce what side effect profile?

Less EPS, more sedation, more anticholinergic effects, more orthostatic hypotension.

Major adverse effects of chlorpromazine

Sedation, hypotension, dry mouth, constipation, photosensitivity.

Patient teaching for chlorpromazine

Rise slowly, wear sunscreen, avoid abrupt discontinuation.

Why are SGAs considered first-line treatment?

Lower risk of EPS while treating both positive and negative symptoms.

Major disadvantage of SGAs

Metabolic syndrome.

Components of metabolic syndrome

Weight gain, hyperglycemia, dyslipidemia, hypertension.

What should be monitored for clients taking SGAs?

Weight, BMI, waist circumference, fasting glucose/A1C, lipid panel, blood pressure.

Which SGAs have the highest metabolic risk?

Clozapine and Olanzapine.

Which SGAs have the lowest metabolic risk?

Ziprasidone, Lurasidone, Aripiprazole.

Which SGA commonly causes hyperprolactinemia?

Risperidone.

Which SGA is associated with QT prolongation?

Ziprasidone.

Which antipsychotic is reserved for treatment-resistant schizophrenia?

Clozapine.

Major adverse effect of clozapine

Agranulocytosis.

What laboratory value must be monitored with clozapine?

Absolute Neutrophil Count (ANC).

How often is ANC monitored?

Weekly → Biweekly → Monthly if stable.

Early signs of agranulocytosis

Fever, sore throat, infection.

Other serious clozapine adverse effects

Myocarditis, seizures, severe constipation, weight gain.