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CPTP 3 > CPTP 3.4 Neuropharmacology 2 (Antipsychotics) > Flashcards

CPTP 3.4 Neuropharmacology 2 (Antipsychotics) Flashcards

1
Q

When is the onset of schizophrenia?

A

Adolescence & young adulthood

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2
Q

There is a ‘spectrum of symptoms’ for schizophrenia. What does this divide the symptoms into?

A
  • Positive symptoms
  • Negative symptoms
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3
Q

What are the ‘positive’ symptoms of schizophrenia?

A
  • Disorders of thought
  • Hallucinations
  • Paranoia
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4
Q

What are the ‘negative’ symptoms of schizophrenia?

A

Catatonic Behaviour

  • Blunted emotions
  • Social withdrawal
  • Apathy
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5
Q

What is the importance of positive and negative symptoms?

A

They respond differently to different medications.

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6
Q

What brain differences are seen in those with schizophrenia?

A
  • Developmental abnormalities in the limbic system
  • Smaller temporal lobes
  • Enlarged ventricles
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7
Q

Describe a theory of schizophrenia.

A

Dopamine theory of Schizophrenia: “Schizophrenia is caused by overactive MESOLIMBIC AND MESOCORTICAL dopamine systemS in the brain”

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8
Q

What are the three main dopamine systems in the brain?

A
  • Nigrostriatal
  • Mesolimbic/Mesocortical
  • Tuberoinfundibular
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9
Q

Where does the tuberoinfundubular pathway run from and to? What does dopamine do at the destination?

A

Hypothalamus –> pituitary stalk Dopamine acts tonically as prolactin release inhibiting factor (PRIF)

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10
Q

Outline prolactin regulation

A

Stimulating:

  • Suckling
  • Hypothalamic nuclei release prolactin releasing factor (PRF)
  • PRF Stimulates anterior pituitary to release prolacin

Inhibiting:

• Dopamine from tuberoinfundibular tract inhibits anterior pituitary prolactin release

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11
Q

What does prolactin do?

A

Stimulates milk production and differentiation of mammary tissue

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12
Q

Where is prolactin released from?

A

Anterior pituitary

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13
Q

What is released from the posterior pituitary?

A

Oxytocin

Vasopressin

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14
Q

Where does the nigrostriatal pathway run from and to? What does dopamine do at the destination?

A

substantia nigra –> dorsal striatum Involved in the initiation and control of movement (extrapyramidal pathway of movement)

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15
Q

What are the diseases of the nigrostriatal pathway?

A
  • Parkinson’s disease
  • Huntington’s chorea
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16
Q

What is the relevance of the nigrostriatal pathway with schizophrenia?

A

No direct relationship, but the drugs used to treat schizophrenia have side effects which affect this pathway

17
Q

Where does the mesolimbic pathway run from and to? What does dopamine do at the destination?

A

Ventral tegmentum –> Ventral striatum & hippocampus Reward, addiction, sensory processing

18
Q

Where does the mesocortical pathway run from and to? What does dopamine do at the destination?

A

Ventral tegmentum –> frontal cortex Cognition, mood

19
Q

What causes dopamine imbalance in schizophrenia?

A

Increased synthesis of dopamine

20
Q

How do antipsychotic drugs work?

A

They block D2 receptors in limbic and cortical areas

21
Q

What were the first antipsychotic drug classes to be high-affinity D2 receptor antagonists? What are the side effects of this and why?

A

Phenothiazines and thioxanthenes Have tri-cyclic structures (like TCAs but arent) which means its not selective, and has affinity for many receptors:

H1:

  • Weight gain
  • Sedation

M1:

  • Dry mouth
  • Blurred vision
  • Constipation
  • Urinary retention

a1:

• Postural hypotension

D2 (nigrostriatal):

• Extrapyrimidal side effects

D2 (tuberoinfundibular)

  • Galactorrhoea
  • Gynaecomastea

NB: D2 for mesocortical and mesolimbic pathways is the therapeutic target

22
Q

Antipsychotics which are specific to D2 receptors may still cause side effects. What are these? Why does this occur?

A

D2 (nigrostriatal):

• Extrapyrimidal side effects

D2 (tuberoinfundibular):

  • Galactorrhoea
  • Gynaecomastia
23
Q

What does ‘tardive’ mean in tardive dyskinesia?

A

Tardive, because it begins 6 months after initiation of treatment

24
Q

Is tardive dyskinesia permanent?

A

Yes

25
Q

What are the extrapyramidal side effects?

A
  • Parkinson’s symptoms (rigidity, tremor, etc)
  • Tardive dyskinesia (repetitive involuntary movement)
26
Q

What are the side effect profiles of phenothiazines and thioxanthenes?

A

Group I: Sedation (H1)

Group II: Anticholinergic (M1)

Group III: Extrapyrimidal (D2)

27
Q

What drug class ditched the tricyclic structure, and were more selective for just D2 receptors? Give an example.

A

Butyrophenones

• Haloperidol

28
Q

What are the side effects of butyrophenones?

A

Extrapyramidal side effects remain

Prolactin side effect remain (galactorrhea and gynaecomastia)

29
Q

Summarise the 1st generation antipsychotic classes and an example of each

A

Tricyclic compounds:

  • Phenothiazines
  • Thioxanthenes

Selective:

• Butyrophenones

30
Q

What are 2nd generation antipsychotics also known as?

A

Atypical antipsychotics

31
Q

Name the 2nd generation antipsychotics. What are the benefits of these?

A
  • Clozapine
  • Olanzapine
  • Risperidone
  • Amisulpiride
  • Aripiprazole
  • Quetiapine

They have a better EPS profile, and do not have any affinity for M1, a1 or H1

32
Q

What is the main side effect of:

1) Clozapine?
2) Olanzapine?
3) Risperidone?

A

Clozapine = agranulocytosis

Olanzapine and risperidone = weight gain and insulin resistant diabetes

33
Q

Which drugs are good at treating positive and negative symptoms?

A

Treating positive symptoms –> 1st generation antipsychotics

Treating negative symptoms –> 2nd generation antipsychotics

34
Q

What are the affinities of 2nd generation antipsychotics?

A

D2: low

D3: High

D4: High

5-HT2A: High

35
Q

Recall the D1-like family

A

D1 & D5

36
Q

How do atypical (2nd generation) antipsychotics reduce their EPS side effects, while still maintaining therapeutic efficacy?

A

They have loose binding for D2 receptors, because their dissociation rate is much higher.

In the nigrostriatal pathway, dopamine is released PHASICALLY (lots released infrequently).

Here, the phasic dopamine is enough to displace the drug. (therefore less ‘distortion’ of dopamine signalling here)

However, in the cortex, from the mesocortical pathway (the target), the release of dopamine is tonic (constant, lower levels), therefore the drug is not displaced as much, and can have its antagonistic effect.

There is also a role in the 5-HT2A antagonism having antidepressant effects

37
Q

What are 1st generation antipsychotics also known as?

A

Classical, typical

38
Q

What are the practical distinctions between typical and atypical antpsychotic use?

A

Atypical have:

  • Fewer extrapyrimidal side effects
  • More efficacy in treating drug-resistant patients
  • Better at treating negative symptoms

CPTP 3 (21 decks)

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