Psychotic and Affective Disorders Study Guide PDF

Study Guide: Psychotic and Affective Disorders 1. Psychosis and Affective Disorders - Psychosis: A profound disconnection from reality. Symptoms include delusions (fixed false beliefs) and hallucinations (sensory perceptions without stimuli). - Mechanism: Dopamine hyperactivity in the mesolimbi...

Study Guide: Psychotic and Affective Disorders 1. Psychosis and Affective Disorders - Psychosis: A profound disconnection from reality. Symptoms include delusions (fixed false beliefs) and hallucinations (sensory perceptions without stimuli). - Mechanism: Dopamine hyperactivity in the mesolimbic pathway drives positive symptoms. - Treatment Connection: Antipsychotics target D2 receptors to reduce hyperactivity. - Affective Disorders: Mood disorders, including mania, depression, or both. - Include disruptions in the cortico-limbic network, affecting emotional regulation. 2. DSM-5 Metrics - Psychotic Disorders: - Schizophrenia, schizoaffective disorder, etc. - Positive Symptoms: Hallucinations, delusions, disorganized thoughts (linked to dopamine hyperactivity). - Negative Symptoms: Social withdrawal, anhedonia, alogia (linked to dopamine hypoactivity in the mesocortical pathway). - Mood Disorders: - Bipolar I/II, major depressive disorder (MDD). Neurotransmitter dysregulation in serotonin (5-HT), GABA, and glutamate systems. 3. Risk Factors for Schizophrenia - Genetics: - High heritability (~80%). Key genes: DISC1 (synaptic plasticity), DTNBP1 (dysbindin), GRIN2A (NMDA receptor subunit). - Connection: NMDA hypofunction impairs synaptic plasticity and cognitive processes. - Environmental Factors: Prenatal infections, paternal age, urban living, and cannabis use. - Connection: Environmental stressors dysregulate the HPA axis, exacerbating neurotransmitter imbalance. 4. Neurobiology of Schizophrenia - Brain Structures: - Thalamus: Sensory relay; abnormalities affect sensory gating. - Hippocampus: Memory; reduced volume and network modularity impair episodic memory. - Prefrontal Cortex: Executive function; dopamine hypoactivity linked to negative symptoms. - Superior Temporal Gyrus: Auditory processing; dysfunction causes auditory hallucinations. - Neurotransmitters: - Dopamine: Mesolimbic hyperactivity drives positive symptoms; mesocortical hypoactivity drives negative symptoms. - GABA: Reduced PV interneurons disrupt gamma oscillations (30-80 Hz), critical for cognition. - Glutamate: NMDA hypofunction impairs synaptic activity and gamma synchrony. 5. Imaging and Findings in Schizophrenia - Structural Findings: Reduced gray matter in the hippocampus, thalamus, and PFC. - Functional Findings: Disrupted Default Mode Network (DMN) and white matter connectivity. - Imaging Techniques: - MRI: Structural volume changes. - fMRI: Functional connectivity and blood flow. - MRS: Metabolic profiling of glutamate and GABA. - PET: Molecular targets like GABA-A receptors. 6. Bipolar Disorders (BD) - Core Features: Alternating mania and depression; high suicide risk and substance abuse comorbidity. - Subtypes: - Bipolar I: Mania dominates; may include psychosis. - Bipolar II: Hypomania alternates with depression. - Neurobiology: - Ventral PFC and limbic system dysregulation cause emotional instability. - Circadian rhythm dysfunction is a hallmark feature. - Genetics: Genes like CACNA1C and BDNF affect neuroplasticity. 7. Depression and Major Depressive Disorder (MDD) - Monoamine Hypothesis: Imbalances in serotonin, norepinephrine, and dopamine. - Antidepressants restore serotonin but take time due to neuroplastic changes. - Neuroplasticity Hypothesis: Stress reduces hippocampal neurogenesis; antidepressants reverse this. - Imaging: Reduced hippocampal volume explains cognitive deficits. 8. Schizophrenia Models and Emerging Treatments - Models: - 22q11.2 Deletion Mouse Model: Mimics PV interneuron dysfunction and gamma oscillation deficits. - Ketamine Model: Supports NMDA hypofunction effects. - Emerging Therapies: Target muscarinic acetylcholine receptors (e.g., KarXT) for cognitive and negative symptoms. 9. Exam Tips - Connect Mechanisms to Symptoms: - Positive symptoms -> Dopaminergic hyperactivity.  - Negative symptoms -> Dopaminergic hypoactivity. - Cognitive symptoms -> GABAergic and glutamatergic dysfunction. - Imaging Techniques: Understand their use (e.g., PET for molecular changes, MRI for structural abnormalities). - Interventions: Know why specific treatments target pathways (e.g., D2 antagonists for positive symptoms, lithium for mood stabilization).