psychosis Flashcards
Which of the following best describes a “negative symptom” of schizophrenia?
A) Hallucinations and delusions
B) Increased dopamine activity in the mesolimbic pathway
C) Impaired working memory and disorganized thinking
D) Social withdrawal and decreased motivation
D (Negative symptoms refer to a loss of normal function, such as social withdrawal and lack of motivation, whereas cognitive symptoms involve memory and thinking issues.)
what is considered to be a positive symptom of schizophrenia?
a. hallucinations and delusions
b. social withdrawal
c. disorganized thinking
hallucinations in withdrawal
b- is negative symptoms
c- is for cognitive symptoms
how is schizophrenia described as?
a. a person has 3 symptoms of psychosis for 6 months
b. a person with 3 or more symptoms of psychosis for 6 motnhs
c. a person with 2 or more symptoms of psychosis for 6 months
d. a person with 2 symptoms of psychosis for 6 months
if a person has 2 or more symptoms of psychosis for 6 months. these effects can be positive, negative, or cognitive (cognitive decline, disorganized thinking, poor memory, etc)
catecholinergic receptors are catecholamine nuerons, these nuerons contain the nuerons ___ , ___, and __.
monoamines contain ___, ___, and ___.
options: noradrenaline, dopamine, adrenaline, serotonin
- dopamine, noradrenaline, adrenaline
- dopamine, noradrenaline, serotonin
. Which of the following best describes the Dopamine Hypothesis of Schizophrenia?
A) Reduced dopamine signaling in the prefrontal cortex leads to negative symptoms, while excessive dopamine activity in the mesolimbic pathway leads to positive symptoms.
B) Excessive dopamine transmission in the nigrostriatal pathway is responsible for both positive and negative symptoms of schizophrenia.
C) Increased dopamine signaling in the mesocortical pathway leads to cognitive deficits and social withdrawal.
D) The Dopamine Hypothesis is based solely on genetic studies and has no pharmacological evidence.
A
schizos refers to hyperactive dopamine transmission (esp in mesolimbis), leads to positive symptoms
(Schizophrenia is linked to excessive dopamine activity in the mesolimbic pathway (causing hallucinations/delusions) and reduced dopamine in the mesocortical pathway (causing cognitive and negative symptoms
What is the key mechanism proposed by the Glutamate Hypothesis of Schizophrenia?
A) Overactivation of NMDA receptors on GABAergic interneurons, leading to excess inhibition of dopamine release.
B) Underactivation of NMDA receptors on GABAergic interneurons, causing dysregulated dopamine and glutamate signaling.
C) Increased glutamate release in the prefrontal cortex, leading to overstimulation of serotonin receptors.
D) Direct inhibition of dopamine release by excessive glutamate in the mesolimbic system.
B
schizo’s associated with the hypofunction on GABA interneurons in cortex, leading to dopamine downstream dysregulation
and defficiences in glutamare signalling in the cortex
(The Glutamate Hypothesis suggests NMDA receptor hypofunction on GABAergic interneurons, which disrupts inhibition, leading to abnormal dopamine signaling and schizophrenia symptoms.)
abnormal function leads to downregulation of glutamate signalling
hypothesis: deficiencies in glutamate signalling
The Serotonin Hypothesis of Schizophrenia is supported by evidence that…
A) Drugs that enhance serotonin signaling, such as LSD, can produce hallucinations similar to schizophrenia.
B) Blocking serotonin receptors, particularly 5-HT1A, is effective in treating schizophrenia.
C) Reduced serotonin levels in the mesolimbic pathway are directly responsible for positive symptoms.
D) Serotonin transmission has no interaction with dopamine pathways and plays a minor role in schizophrenia.
A
schizos increase serotonin signalling and overreaction of %-HT2A receptors
(The Serotonin Hypothesis is supported by the fact that hallucinogens like LSD (which act on 5-HT2A receptors) can induce schizophrenia-like symptoms. This suggests that serotonin plays a role in positive symptoms, likely through interactions with glutamate and dopamine pathways.)
how does dopamine normally work?
dopamine is mainly in the midbrain in the VTA (ventral tegmental area and substantial nigra)
the mesolimbic/mesocortical pathway (where dopamine nuerons are located) manage memory, learning, organization
what type of receptors are dopamine receptors?
dopamine receptors are GPCR’s
D1 receptors are Gs
D2 are gi receptors
how are D1 and D2 dopamine receptors different?
D1- is a GS protein (activates cAMP dependant protein kinases)
this activates nuerons
D2 - is a Gi protein (inhibitory, inhibits AC), related to antipsychotic potency (stronger blockade=more potency/more drug concentration needed to produce an effect)
Which of the following best describes dopamine’s role in the nigrostriatal pathway?
A) Dopamine in this pathway inhibits voluntary movement, and blocking D2 receptors enhances motor function.
B) Dopamine in this pathway facilitates movement, and blocking D2 receptors can cause motor impairments.
C) The nigrostriatal system primarily regulates cognitive function, and dopamine has little effect on movement.
D) Dopamine in the nigrostriatal system controls hormonal release, and blocking D2 receptors increases prolactin secretion.
(Dopamine in the nigrostriatal pathway is crucial for initiating and regulating movement. Blocking D2 receptors in this pathway, as seen with some antipsychotics, can lead to extrapyramidal side effects such as tremors, rigidity, and tardive dyskinesia.)
b
how does dopamine affect the tuberionfundibular system?
- dopamine controls hormone release in the pituitary
- dopamine released in this system inhibits secretion of prolactin and growth hormone
how do antiphsychotics cause hyperprolactinemia?
because inhibiting dopamine release increase prolactin
remember: in normal conditions, dopamine inhibits secreting prolactin
inhibition of dopamine signals cause absence of menstraul cycles (amenorrhea)
Why do first-generation antipsychotics cause movement-related side effects?
A) They inhibit dopamine transmission in the mesolimbic pathway
B) They block D2 receptors in the nigrostriatal pathway
C) They increase serotonin release in the prefrontal cortex
D) They enhance glutamate signaling in the cerebral cortex
(First-generation antipsychotics block D2 receptors indiscriminately, including in the nigrostriatal pathway, which controls movement.)
What would likely happen if an antipsychotic excessively blocks dopamine in the tuberoinfundibular pathway?
A) Extrapyramidal symptoms such as tardive dyskinesia
B) Hyperprolactinemia leading to hormonal imbalances
C) Increased positive symptoms of schizophrenia
D) Overactivation of NMDA receptors causing psychosis
(Dopamine normally inhibits prolactin release; blocking D2 receptors in this pathway increases prolactin, leading to hormonal side effects.)
Hyperprolactinemia leading to hormonal imbalances
Which neurotransmitter imbalance is most associated with the glutamate hypothesis of schizophrenia?
A) Excessive glutamate activity in the mesolimbic pathway
B) Reduced NMDA receptor function on GABAergic interneurons
C) Increased serotonin signaling in the prefrontal cortex
D) Overactivation of dopamine receptors in the basal ganglia
B (Hypofunction of NMDA receptors on inhibitory GABA neurons leads to dysregulated glutamate transmission, contributing to schizophrenia symptoms.)
why is the 60-80% and 80% occupancy for D2 receptors different?
60-80%: is the required D2 recceptor occupation required to produce an antipsychotic effect
80%: D2 receptors give side effects like extrapyrimidal disease and tardive disease (cant move jaw or face), and elevated prolactin
how are first generation antipsychotics/typical antipsychotics different from 2nd gen/atypical antipsychotics?
1st gen: targets D1 and D2, effective with D2 antagonism
2nd gen: bind to 5HT and D2 receptors
bind with looser affinity to dopamine receptors compared to first gen antipsychotics and produce less dopamine
what is the difference of the mesolimbic pathway and tuberoinfundibular dor dopamine side effects?
mesolimbic: the synapse is small, mincreasing the likelyhood of receptor binding
tuberoinfundubular pathway: dopamine is released in the bloodstream abd carried across BBB (through hypophysial portal system) to the pituitary gland
this increases dopamine clearance
what is/are a drug(s) that is considered to be a first gen antipsychotic?
haloperidol and chlorpromazine
what is/are a drug(s) that is considered to be a 2nd gen antipsychotic?
clozapine and risperidone
describe the kinetics of haloperidol
- fast on, slow off
- fast on: high receptor binding potential at D2 in pituitary and striatum
this means high extrapyramidal side effects and increased prolactin release (hyperprolactinemia)
how does the kinetics of chloropromazine work (1st gen)
fast rates lead to high extrapyramidal symptoms (inhibits dopamine)
fast off=prolactin levels stay normal
how do the kinetics of clozapine and rispiradone (2nd gen antipsy’s) work?
has a slow on, fast off mechanism
- slow rates: lower rebinding potential and low extrapyramidal symptoms
- fast rates give normal prolactin levels
