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Antipsychotic and Treatment of Psychotic Disorders

Antipsychotic and Treatment of Psychotic Disorders

The efficacy of second-generation antipsychotics, which have FGAs and are accompanied by a new age of treating psychosis, has revolutionized the use of antipsychotics in the treatment of psychotic diseases compared to first-generation antipsychotics (Preston et al., 2013). The postoperative sedative “Chlorpromazine” (Thorazine), which has a low potency, was first used in 1952, according to Preston, O’Neal, et al. (2013). Later, psychiatric patients took it as a sedative until it was discovered to have antipsychotic effects. More “phenothiazines” would develop in the future (Preston et al., 2013). Although the drugs’ mechanism of action was unknown when they were initially administered in a therapeutic context, they were successful in reducing the symptoms of psychosis. Subsequent studies revealed that antipsychotic drugs acted by chemically blocking dopamine (D2) postsynaptic receptors, and their clinical effectiveness was correlated with the extent of this blockage, giving rise to the dopamine theory of schizophrenia (Preston et al., 2013). Later, other potent dopamine blockers that are chemically distinct were industrialized (such as thiothixene, haloperidol, loxapine, molindone, and pimozide). These neuroleptics were collectively known as “typical” or first-generation antipsychotics (FGAs) due to the unintentional cause of neurological side effects (Preston et al., 2013).

Stronger 5-HT2A and 5-HT2C serotonin blockers in second-generation antipsychotics (SGAs) compared to first-generation antipsychotics (FGAs) result in varying degrees of dopamine D2 blockage (Preston et al., 2013). Both positive and negative symptoms can be effectively treated by the standard medication known as clozapine. Contrary to conventional FGAs, research indicates that 40% of patients who did not respond to haloperidol and chlorpromazine do so when given clozapine. Moreover, there are relatively few incidences of tardive dyskinesia and extrapyramidal adverse effects.

Effects, Alternate Therapies, and Altered Neurotransmitters

Extrapyramidal side effects, such as dystonia, tremors, and tardive dyskinesia, are three of the “typical” or FGAs’ most severe adverse effects, according to Preston et al. (2013). The most serious side effects of “atypical” or SGAs include weight gain, diabetes, and changes in lipid metabolism (Perry et al., 2007). Both Preston et al. (2013) and Perry et al. (2007) contend that SGAs are a superior option to FGAs as a treatment for schizophrenia. This is so because SGAs are thought to be more sophisticated and effective.

The most effective molecule for changing behaviour, mood, and emotions is dopamine, which also works to influence the effects of serotonin, noradrenaline, and acetylcholine in the brain (Wasti & Siddiqui, 2010).

Problems and Treatment Strategy

With a schizophrenia diagnosis, Jerry has been hearing voices for the past five months that tell him his life is meaningless. He works at a video store and thinks his boss has hidden cameras all over the place to watch him in case he makes a mistake. Jerry becomes angry and starts speaking to the clients in an odd way when things are busy at work. For instance, he might inform the client that the tape is unavailable because the FBI is analyzing it for possible use in surveillance. Jerry thinks he can’t take the humiliation of having his employer watch him in person or on camera. Jerry visits his psychiatrist, who prescribes him a medication called Thorazine. However, this caused tremors and muscle spasms, so the medication was changed to Haldol, which had fewer side effects. Jerry tells his psychiatrist that although he would like to acquire a better job, a car, and perhaps go on a date with a female, he is concerned that it might be too much for him to handle. He also says that he does not think that another drug will assist him.

Getting Jerry to take his medication consistently will be one of the difficulties a counsellor would have in this situation. According to Haddad, Brain, and Scott (2014), this might be brought on by cognitive impairment, social exclusion, stigma, positive and negative symptoms, and a lack of understanding. Also, the physician and the patient should agree on adherence and dependability.

Psychotherapy and the use of an additional antipsychotic medication would be part of Jerry’s treatment plan, but Jerry would ethically have the option to learn about the advantages and disadvantages of doing so. Contrarily, compliance suggests an unfavourable balance of power between the patient and the doctor. A social worker can also be involved in the further intervention.


Haddad, P. M., Brain, C., & Scott, J. (2014). Nonadherence with antipsychotic medication in schizophrenia: challenges and management strategies. Patient-Related Outcome Measures, 5, 43–62.

Perry, P. J., Alexander, B, Liskow, B. I., & DeVane, C. L. (2007). Psychotropic drug handbook (8th ed.). Baltimore, MD: Lippincott Williams & Wilkins.

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: Talaga New Harbinger Publications

Wasti, A., & Siddiqui, N. A. (2010). Alterations in the level of neurotransmitters associated with the chronic treatment of antipsychotic drugs. JPMA. The Journal of the Pakistan Medical Association, 60 (8), 628.


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Case Discussion on Psychosis:

There are several antipsychotics available for patients with psychotic disorders:

  1. Select an antipsychotic medication from your readings and discuss its use, potential side effects, dosing, mechanism of action, and the receptors it affects in the brain.

    Antipsychotic and Treatment of Psychotic Disorders

    Antipsychotic and Treatment of Psychotic Disorders

  2. Compare and contrast the following conditions: Tardive Dyskinesia, Acute Dystonia, Athetosis, and Tics.

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