Psychosis and Affective Disorders Quiz

Study Notes

Psychosis is a profound disconnect from reality, characterized by delusions and hallucinations.
Dopamine hyperactivity in the mesolimbic pathway is linked to positive symptoms.
Antipsychotic medications target D2 receptors to reduce dopamine hyperactivity.
Affective disorders (mood disorders) involve disruptions in the cortico-limbic network, impacting emotional regulation.

Psychotic disorders include schizophrenia and schizoaffective disorder.
Positive symptoms are linked to dopamine hyperactivity (hallucinations, delusions, disorganized thoughts).
Negative symptoms are linked to dopamine hypoactivity in the mesocortical pathway (social withdrawal, anhedonia, alogia).
Mood disorders include Bipolar I/II and Major Depressive Disorder (MDD).

High heritability (~80%) is a key genetic factor.
Key genes include DISC1, DTNBP1, and GRIN2A, related to synaptic plasticity and NMDA receptor function.
NMDA hypofunction may impair synaptic plasticity and cognitive processes.

Brain structures like the thalamus, hippocampus, and prefrontal cortex play roles.
Reduced volume and network modularity in the hippocampus can impair memory.
Dopamine dysregulation in the mesolimbic and mesocortical pathways is central to symptoms.
GABA and glutamate systems are also involved in cognitive function.

Structural imaging (MRI) reveals reduced gray matter in specific brain areas.
Functional imaging (fMRI) shows disrupted network connections (Default Mode Network, white matter).
Metabolic profiling (MRS) helps investigate glutamate and GABA levels.
PET scans can target specific molecular structures, like GABA-A receptors.

Characterized by alternating mania and depression.
High suicide risk and substance abuse are common comorbidities.
Subtypes include Bipolar I (mania dominating, may include psychosis), and Bipolar II (hypomania alternating with depression).
Circadian rhythm dysfunction and ventral PFC/limbic system dysregulation are involved.
Genetics plays a role (genes like CACNA1C and BDNF).

The monoamine hypothesis suggests imbalances in serotonin, norepinephrine, and dopamine underlie depression.
Antidepressant medications take time due to neuroplastic changes.
Stress reduces hippocampal neurogenesis, and antidepressants can reverse this effect.
Reduced hippocampal volume correlates with cognitive deficits.

Animal models like the 22q11.2 deletion mouse model offer insights into neuronal dysfunction and gamma oscillations.
Ketamine can model NMDA hypofunction effects.
Emerging therapies target muscarinic receptors (e.g., KarXT) for cognitive and negative symptoms.

Connect symptoms to underlying mechanisms (e.g., positive symptoms to dopaminergic hyperactivity).
Understand imaging techniques and their applications (e.g., PET for molecular changes, MRI for structural).
Consider interventions and their targets in specific pathways (e.g., D2 antagonists for positive symptoms, lithium for mood stabilization).
Understand the impact of negative symptoms on dopaminergic hypoactivity and the role of GABAergic and glutamatergic dysfunction on cognitive symptoms.