Biopsychology of Psychiatric Disorders Flashcards
For schizophrenia diagnosis: 2 of the following for atleast 6 months
delusions: unjustifiable beliefs
-hallucinations
-disorganized speech
-disorganized behaviour
-weak or absent signs of emotions, speech, or socialization.
Prevalence: approx. 1.3%
type I schizophrenia
Positive symptoms (behavioural excesses, such as hallucinations and agitated movements);
Possibly due to a dopaminergic dysfunction associated with acute onset, good prognosis, and a favourable response to neuroleptics
type II schizophrenia
Negative symptoms (behavioural deficits, such as reduction in motivation, catatonia) and associated with chronic (stabilized) affliction, poor prognosis, poor response to neuroleptics, cognitive impairments, enlarged ventricles, and cortical atrophy, particularly in the frontal cortex
cognitive symptoms of schizophrenia
Slow processing speed
Impaired long-term memory
Difficulty perceiving others’ emotions from their facial expressions and body language
Errors in perceiving others’ intentions and beliefs.
Abnormalities in the Wernickes area, auditory areas, subcortical areas, hippocampus, and dorsolateral prefrontal cortex
the neurodevelopmental hypothesis
Abnormalities occurred in prenatal or neonatal nervous system development can produce abnormalities in the developing brain that predispose to schizophrenia.
the two-hit hypothesis
A combination of a genetic predisposition and environment in prenatal/neonatal development, later in life, or both
Dopamine hypothesis
Schizophrenia results from excess activity at dopamine synapses in certain areas of the brain.
Substance-induced psychotic disorder
Research indicates increased activity, specifically at the D2 receptor
second generation (atypical) antipsychotics
Clozapine, Amisulpride, Risperidone, Olanzapine
Weakly block D2 receptors so there are fewer Parkinson-like effects
But its atypical because it also blocks D1, D4, and serotonin 5-HT2 receptors
-5-HT is serotonin
Improves motivation and reduces agitation, but may result in weight gain
glutamate hypothesis
Deficient activity at glutamate synapses, especially in the prefrontal cortex
Dopamine inhibits glutamate release
Or, glutamate stimulates neurons that inhibit dopamine release
Increased dopamine can produce the same effects as decreased glutamate
ketamine
Has hallucinogenic properties and is used in some clinical settings (mostly by vets) as a dissociative anesthetic (i.e., you feel separate from the body, and it reduces pain)
The difference between the “correct” dose and a potentially lethal overdose is on the order of milligrams.
Date rape drug
monoamine oxidase (MAO) inhibitors
Block the enzyme MAO from degrading neurotransmitters such as dopamine, noradrenaline, and serotonin.
Thus, these drugs increase amounts of dopamine, noradrenaline, and serotonin for release
tricyclic antidepressants
First-generation antidepressants with a chemical structure characterized by three rings that block reuptake transporter proteins
Block transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after release; therefore, more norepinephrine, dopamine and serotonin are available.
E.g., Amitriptyline
second-generation antidepressants
Action is similar to first-generation antidepressants but is more selective in its action on the serotonin reuptake transporter proteins
Selective Serotonin Reuptake Inhibitors (SSRIs)
Block the reuptake of serotonin by the presynaptic terminal
E.g. Prozac (fluoxetine)- prescribed for depression
SNRIs
Serotonin and norepinephrine reuptake inhibitors
Block reuptake of serotonin and norepinephrine
E.g., desvenlafaxine (Pristiq), duloxetine (Cymbalta), levomilnaciprin (Fetzima), venlafaxine (Effexor XR),
Atypical antidepressants
Miscellaneous group of drugs with antidepressant effects and milder side effects
E.g., bupropion (Wellbutrin)
Inhibits the reuptake of dopamine and, to some extent, norepinephrine, but not serotonin