
1. Definition
1.1. Schizophrenia is characterized by thought disorders that reflect a break between the cognitive and the emotional sides of one's personality.
2. Etiology
2.1. A consistent finding is the enlargement of the lateral and third ventricles and the widening of frontocortical fissures and sulci
2.2. abnormally high concentrations of the brain neurotransmitter dopamine cause schizophrenia.
2.3. underactivation of glutamate receptors contributes to schizophrenia
3. Risk Factors
3.1. Schizophrenia has a strong Genetic predisposition,
3.1.1. genetically programmed neural development that alter structure and function
3.2. And environmental factors
3.2.1. (e.g., viral infection, nutritional deficiencies, prenatal birth complications, urban upbringing)
4. Signs and Symptoms
4.1. Schizophrenic symptoms are classified into positive, negative, and cognitive categories.
4.1.1. Positive symptoms include hallucinations, delusions, formal thought disorder, and bizarre behavior.(Psychotic Episode)
4.1.1.1. Hallucinations can manifest in various forms, including auditory, olfactory, somatic-tactile, and visual types, such as voices commenting or conversing.
4.1.1.2. delusions of being controlled, mind reading, and reference, as well as grandiosity, guilt, persecutory, religious, somatic beliefs, thought broadcasting, thought insertion, and thought withdrawal
4.1.1.3. Positive formal thought disorder is characterized by circumstantiality, derailment, distractible speech, illogicality, incoherence, pressure of speech, and tangentiality
4.1.1.4. Bizarre behavior may include aggressive or agitated actions, unusual clothing or appearance, repetitive or stereotyped movements, and inappropriate social or sexual behavior.
4.1.2. Negative symptoms include flattened affect, alogia, anhedonia, attention deficits, and apathy.
4.1.2.1. Affective flattening is the near absence of emotional or facial expressions
4.1.2.2. anhedonia reflects an inability to feel pleasure or pain.
4.1.2.3. Alogia is characterized by reduced spontaneous speech
4.1.2.4. avolition is a lack of motivation for goal-directed actions
4.1.3. Cognitive symptoms are the inability to perform daily tasks requiring attention and planning.
5. Complications
5.1. A related side effect of conventional antipsychotics that develops in 15% to 20% of schizophrenics after several years of treatment
5.1.1. tardive dyskinesia.
5.1.2. sedation, hypotension, akathisia (motor restlessness), constipation, weight gain, amenorrhea, and, less frequently, hepatotoxicity and electrocardiographic changes.
5.1.3. Schizophrenics treated with clozapine also are at risk of developing agranulocytosis, a potentially lethal blood disorder
5.2. Chronic inflammation and oxidative stress are additional factors that may play a role in the disease's progression
5.2.1. increased severity of negative symptoms and further reductions in cognitive functioning. These results highlight the ineffectiveness of current medications for schizophrenia to attenuate or reverse the loss of frontal brain tissue.
6. Pathophysiology
6.1. Role of the hypothalamic-pituitary-adrenal (HPA) axis dysregulation. Neuroinflammatory processes and cytokine involvement. Oxidative stress and mitochondrial dysfunction.
6.1.1. Disruptions in neurotransmitter systems, brain structure, and neural connectivity.
6.1.2. Dysregulation of dopamine pathways, particularly hyperactivity in the mesolimbic system
6.1.2.1. Associated with positive symptoms such as hallucinations and delusions)
6.1.3. Hypoactivity in the mesocortical system
6.1.3.1. Linked to negative symptoms such as affective flattening and avolition
6.1.3.1.1. Changes in the dorsal prefrontal cortex (DLPFC)
6.1.4. Glutamate dysfunction, particularly involving N-methyl-D-aspartate (NMDA) receptors,
6.1.4.1. Contributes to cognitive impairments and neural circuit disruptions.
6.1.4.1.1. underactivation of glutamate receptors contributes to schizophrenia.
6.1.5. Structural brain changes,
6.1.5.1. Such as reduced gray matter volume, enlarged ventricles, and impaired prefrontal cortex function
7. Effects on Body systems
7.1. Brain structural abnormalities (e.g., enlarged ventricles, reduced gray matter).
7.2. Brain abnormalities in schizophrenia are believed to originate in the prenatal period of cell proliferation and migration.
7.2.1. Abnormal amygdala connectivity is widely reported in schizophrenia
7.2.1.1. Reported amygdala abnormalities in schizophrenia include reduced volume and abnormal functional activation patterns for social and emotion processing.
7.2.2. the induction of abnormal amygdala projections to brain regions such as the hippocampus during late adolescence and young adulthood may be linked to the onset of schizophrenia.
8. Diagnostics
8.1. DSM-5 diagnostic criteria. Imaging findings (MRI, fMRI, PET scans). Role of biomarkers in emerging diagnostic approaches.
8.2. Atleast two symptoms below(1) delusions, (2) hallucinations, (3) disorganized speech, (4) disorganized or catatonic behavior, and (5) negative symptoms
8.3. symptoms are experienced most of the time during a 1-month period with some disturbance present over 6 months.
9. Treatments/Medications
9.1. Pharmacological interventions (antipsychotics, targeting dopamine receptors). Non-pharmacological therapies (CBT, psychosocial interventions). Emerging therapies (e.g., immunomodulatory treatments, psychedelics in research).
9.1.1. First-Generation (Typical) Antipsychotics include Chlorpromazine (Thorazine), Fluphenazine (Prolixin), Haloperidol (Haldol), Perphenazine (Trilafon), Pimozide (Orap), Prochlorperazine (Compazine), Thioridazine (Mellaril), Thiothixene (Navane), and Trifluoperazine (Stelazine).
9.1.2. Second-Generation (Atypical) Antipsychotics consist of Aripiprazole (Abilify), Clozapine (Clozaril), Loxapine (Loxitane), Lurasidone (Latuda), Molindone (Moban), Olanzapine (Zyprexa), Paliperidone (Invega), Quetiapine (Seroquel), Risperidone (Risperdal), and Ziprasidone (Geodon).
9.1.3. Cognitive-behavioral therapy (CBT), a talking therapy that initiates cognitive and behavioral change
10. Referrals
10.1. a multidisciplinary approach to address the medical, psychological, and social needs of the patient
10.1.1. Psychiatrist/ APMHNP: For accurate diagnosis, medication management (e.g., antipsychotics), and ongoing mental health care
10.1.2. Psychologist/Therapist: To provide cognitive-behavioral therapy (CBT) or other psychotherapeutic interventions to address delusions, hallucinations, and social functioning.
10.1.3. Social Worker: To assist with housing, employment, disability benefits, and community resources
10.1.4. Occupational Therapist: To help the patient develop skills for daily living and improve functionality in work and social environments.
10.1.5. Neurologist: For patients with complex neurological symptoms or to rule out other neurological conditions.
10.1.6. Dietitian: To address nutritional needs, especially if medications cause weight gain or metabolic issues.
10.1.7. Support Groups or Peer Support Programs: To offer the patient social support and shared experiences with others living with schizophrenia.
10.1.8. Primary Care Provider: For routine physical health monitoring, as schizophrenia patients are at higher risk for metabolic syndrome, cardiovascular diseases, and diabetes