Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sem 3: TI > Treatment of Psychotic Disorders > Flashcards

Treatment of Psychotic Disorders Flashcards

1
Q

What is the neurodevelopmental hypothesis of schizophrenia?

A

Schizophrenia is a consequence of damage to the prefrontal cortex in young adults with sustained brain damage before 16 months. This results in:

  • Impaired decision making
  • Behavioural disinhibition and insensitivity to punishment
  • Disrupted social communication and abnormal emption
  • Defective social and emotional reasoning
  • Impaired acquisition of complex social conventions and a sense of right and wrong
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the nigrostriatal pathway and what does it control?

A

One of several dopaminergic pathways in the brain, responsible for control of movement.

The nigrostriatal pathway consists of neurons projecting from the substantia nigra to the striatum, where dopamine is released.

This pathway degenerates in Parkinson’s disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Dopaminergic neurons of the mesocortical and mesolimbic pathways both originate where?

A

Ventral tegmental area (VTA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Dopaminergic neurons of the mesolimbic pathway project to where?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Dopamine released by the hypothalamus into the hypophyseal portal system inhibits prolactin release from the anterior pituitary by acting on which receptor?

A

D2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the dopamine theory of schizophrenia and the pharmacological evidence behind it.

A
  • Psychotic episodes are induced by hyperactivity of (only) the mesolimbic dopamine pathway.
  • Excessive release of dopamine in the amygdala, hippocampus and nucleus accumbens.
  • D2 agonists produce stereotypies - repetitive behaviours characteristic of schizophrenia.
  • Reserpine depletes DA - controls positive symptoms.
  • Strong correlation between D2 blockade and antipsychotic action.
  • Dopamine releasing agents such as amphetamine and cocaine enhance DA release and make the disease worse.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the evidence against the dopamine theory of schizophrenia.

A
  • No clear change in CSF HVA (homovanillic acid) levels - HVA is a dopamine metabolite.
  • No change in dopamine receptors in drug-free schizophrenia patients - we would expect receptor desensitisaion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the explanation for the negative sypmtoms of schizophrenia in terms of dopamine?

A
  • Hypodopaminergic activity in the mesocortical pathway
  • Inadequate release of dopamine acting on D1 receptors in the (prefrontal) cortex
  • This results in decreased cognition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the evidence for glutamate having a role in schizophrenia.

A
  • NMDA antagonists - e.g. ketamine, phencyclidine - provoke psychotic symptoms - hallucinations, thought disorder.
  • Transgenic mice with reduced NMDA receptor expression in the prefrontal cortex - stereotypies, decreased social interaction, responsive to antipsychotics.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the evidence for the involement of serotonin in schizophrenia.

A
  • LSD - partial 5-HT agonist - hallucinations
  • Many antipsychotics antagonise 5-HT receptors
  • 5-HT activates dopamine pathways
  • 5-HT2A antagonism – may contribute to antipsychotic effect and reduce movement disorder side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the generally accepted current theory about the neurotransmitters involved in schizophrenia.

A
  • Overstimulation of mesolimbic D2 receptors
  • Hypostimulation of frontal cortex D1 receptors
  • Reduced prefrontal glutaminergic activity
  • 5-HT involved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the characteristics of D1 like receptors

A
  • D1 and D5 receptors
  • Gs coupled
  • Postsynaptic activation
  • Blockade of D1 not linked to antipsychotic action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the characteristics D2 like receptors.

A
  • D3, D4, D5 receptors
  • Gi - presynaptic and postsynaptic inhibition
  • D2 in limbic system - mood and emotional stability
  • D2 receptors in basal ganglia - movement control
  • D3, D4 receptors in limbic system - cognition and emotion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the general features of antipsychotic/neuroleptic drugs.

A
  • D2 antagonists
  • Increase and then decrease activity of midbrain DAergic neurons - chronic use increases receptor sensitivity
  • Mesolimbic/mesocortical - antipsychotic, sedation
  • Substantia nigra - motor effects
  • Antipsychotics take several weeks to take effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Haloperidol is a typical antipsychotic that decreases the activity of nigrostriatal and mesolimbic neurons. Which neurons does it have a greater affect on?

A

Mesolimbic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the motor impairments caused by typical antipsychotics known as?

A
  • Caused by D2 antagonism of nigrostriatal neurons
  • Results in extrapyramidal symptoms
  • These are Parkinsonian-like symptoms such as dyskinesia, tardive dyskinesia, dystonia, tremor etc
17
Q

Describe the actions of typical antispychotics on the dopaminergic, adrenergic and muscarinic systems.

A

Sem 3: TI (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions