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Block 6 PHARMACOLOGY > Mechanisms of psychotropic drug action > Flashcards

Mechanisms of psychotropic drug action Flashcards

1
Q

Tardive Dyskinesia

A

results in involuntary, repetitive body movements

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2
Q

Antipsychotics antagonise Dopamine receptors and help treat what mental illness

A

Schizophrenia

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3
Q

what do Tricyclic antidepressants block

A

reuptake transporters of Noradrenaline and Serotonin at synapses

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4
Q

SSRI antidepressants block what?

A

reuptake transporters of Serotonin

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5
Q

what do Benzodiazepines do?

A

enhance the action of GABA and ease anxiety or send you to sleep (“hypnotics”)

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6
Q

what are the drugs for anxiety

A

antidepressants –e.g. Sertraline (SSRI) or Venlafaxine (SNRI) and other e.g. Pregabalin

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7
Q

what are the drugs for sleep

A

hypnotics” -“Z –drugs” (Zopiclone, Zolpidem) and short acting benzodiazepines (Temazepam). All potentiate GABA transmission.

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8
Q

what are the 4 dopamine pathways

A

Nigrostriatal
Mesolimbic
Mesocortical
Tubero-infundibular”

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9
Q

briefly describe the Nigrostriatal dopamine pathway

A

initiation and control of movement

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10
Q

Mesolimbic

A

reward, reinforcement

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11
Q

Mesocortical

A

cognition, planning, motivation

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12
Q

Tubero-infundibular”

A

(hypothalamus to pituitary) -inhibits the release of prolactin hormone from the pituitary gland

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13
Q

what is NA released by

A

Particularly released by neurones originating from the locus coeruleus in the brainstem

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14
Q

what does NA i nfluence

A

Project widely influencing sleep, wakefulness, attention, feeding behaviour

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15
Q

what inactivates the NA

A

by reuptake into the pre-synaptic neurone (and oxidation)

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16
Q

where is 5HT released

A

Particularly released by neurones originating from the Raphe nuclei in the brainstem

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17
Q

what does 5HT influence

A

mood, emotional behaviour, satiety and sleep

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18
Q

what is 5HT inhibited by

A

reuptake into the pre-synaptic neurone (and oxidation)

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19
Q

what releases GABA

A

Released by inhibitory neurones throughout the CNS

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20
Q

what happens once GABA receptors are stimulated

A

GABA receptors allow a flux of Chloride ions across the post-synaptic membrane. This hyperpolarises (stabilises) the neurone

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21
Q

characteristics of schizophrenia positive and negative

A

Characterised by “positive” symptoms during episodes -hallucinations, delusions, thought disorder
An accumulation of “negative” symptoms over time -lack of motivation, reduced speech, reduced emotion, social withdrawal

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22
Q

eg of Antipsychotics

A

Olanzapine, Risperidone, Haloperidol

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23
Q

how long do Antipsychotics take to work

A

few weeks to have full effect

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24
Q

what do Antipsychotics treat?

A

Treat schizophrenia, particularly delusions, hallucinations, thought disorder
(also mania, depression with hallucinations/delusions, delirium etc)

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25
Q

what do Antipsychotics antagonise

A

D2 receptors in the mesolimbic system (& other stuff, unfortunately)

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26
Q

side effects of antipsychotics

A

effects on other Dopamine pathways
blocking other receptors
metabolic, cardiac and others

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27
Q

which dopamine pathways do antipsychotics effect and now

A

Nigrostriatal → “Extrapyramidal side effects” -ie Parkinsonism, Akathisia, Acute Dystonias, Tardive Dyskinesia
Tubuloinfundibular → excess Prolactin → Galactorrhoea, Amenorrhoea, Infertility

28
Q

What are first genertion antipsychotics

A

Haloperidol

29
Q

What are second genertion antipsychotics

A

Risperidone, Olanzapine

30
Q

what is good about second genertion antipsychotics

A

less extra-pyramidal side effects

31
Q

which antipsycotic do we use when others arent working

A

Clozapine

32
Q

why do are we cautious when prescribing Clozapine?

A

agranulocytosis

33
Q

which other receptors do antipsychotics antagonise and what does this cause

A

Antagonises Histamine (H1) receptors → sedation
Antagonises muscarinic receptors → dry mouth, blurred, vision, constipation, urinary retention
Antagonises alpha1 adrenoceptors → postural hypotension
Antagonising 5-HT2c receptors → hunger & weight gain

34
Q

what is meant by the metabolic, cardiac and other things that happen as a side effect of antiphschotics

A

Weight gain, Diabetes, Raised Cholesterol
Particularly second generation
Important as people with Schizophrenia may loose 15-20 years of life because of increased cardiovascular risk
Arrhythmias
Also, rare idiosyncratic “neuroleptic malignant syndrome”

35
Q

what is schizophrenia a result of

A

dopamine hyperactivity in certain areas of the brain

36
Q

excess Dopamine in Mesolimbic tracts causes postive or negative symptoms

A

postive

37
Q

inadequate Dopamine in Mesocortical tracts causes postive or negative symptoms?

A

negative

38
Q

arguements for schizophrenia a result of dopamine hyperactivity in certain areas of the brain

A

Antipsychotics block dopamine receptors
Drugs that increase dopamine cause psychosis –amphetamine, cocaine, L-dopa
Reserpine depletes Dopamine transmission and has an antipsychotic effect (stops MOAs getting into vesicles)
PET and SPECT scans show increased brain Dopamine activity when people have Schizophrenia

39
Q

arguements against schizophrenia a result of dopamine hyperactivity in certain areas of the brain

A

Neurotransmitter effects are immediate but antipsychotics take 2+ weeks to work on symptoms
Other transmitters appear to be involved with psychosis –Glutamate, 5HT2, 5HT1A
The cause of Schizophrenia may be upstream

40
Q

Hypotheses re pathophysiology of schizophrenia

A

Neuro-developmental
Dopamine
Psychological
Damage from auto-antibodies

41
Q

in a case where one twin was schizo and the other wasnt, what conclusions can be drawn from this?

A

its not pure genetic, there are othe rbiological factors playing a rol
there are meausrealble structureal and functional abbnormalilties in a schizo brain

42
Q

what is depression?

A

a collection of several symptoms occurring together

43
Q

symptoms of depression

A

Persistent low mood, reduced enjoyment/interest, fatigue
Sleep, appetite, weight, concentration changes
Loss of confidence, guilt, hopelessness, suicidal thoughts and acts

44
Q

what are the 4 classes of antidepressents

A

Tricyclic antidepressant
Selective serotonin reuptake inhibitors (SSRIs)
Monoamine Oxidase Inhibitors (MAOIs)
Serotonin Noradrenaline reuptake inhibitors (SNRIs)

45
Q

examples of Tricyclic antidepressioon

A

Amitriptyline, Lofepramine

46
Q

whawt does Tricuclic antidepressent treat

A

Treat Depression (also pain, anxiety)

47
Q

what deos the Trycyclic antedepressant do?

A

Block Noradrenaline and Serotonin reuptake transporters at synapses -increases availability of these monoamines

48
Q

downside of Tricyclic

A

Can take a couple of weeks to take effect

Block other stuff as well, unfortunately

49
Q

side effects of tricyclic antidepressent

A 
Toxic in overdose
Antagonises Histamine (H1) receptors → sedation
Antagonises muscarinic receptors → dry mouth, blurred, vision, constipation, urinary retention
Antagonises alpha adrenoceptors → postural hypotension
50
Q

how do Selective serotinoinc reuptake inhibitors work?

A

Block only serotonin reuptake transporters, increasing serotonin availability at the synapse

51
Q

down sidde of SSRI

A

Treats depression (also anxiety)

May take a couple of weeks in take effect

52
Q

eg of SSRI

A

E.g. Fluoxetine, Citalopramz

53
Q

side effects of stimulating the various 5HT receptors

A 
Nausea and vomiting
Sexual dysfunction
?? increase suicidal ideation, particularly in children
Withdrawal reaction
Safer in overdose
54
Q

what do MAOI’s inhibihity

A

Block the action of this enzyme in the nerve terminals, increasing the availability of Noradrenaline, Serotonin, Dopamine

55
Q

examples of Monoamine oxidase inhibitor AOIS

A

E.g. Phenelzine, Moclobemide

56
Q

can a hypertensive crisis be made if people eat foods rich in Tyramine e.g. mature cheese, Bovril

A

yes

57
Q

which chemical ppts NA release from the vesicles

A

Tyramine

58
Q

what is the monoamine theory of depression

A

Depression is a result of a deficiency in brain monoamine neurotransmitters –Noradrenaline, Serotonin, Dopamine

59
Q

arguement for the what is the monoamine theory of depression

A

Antidepressants increase the availability of monoamines at synapses
Reserpine which depletes monoamine transmission causes depression (stops monoamines getting into vesicles)
People with depression can have lower levels of monoamine precursors/metabolites in their CSF or blood

60
Q

arguement against the monoamine theory of depression

A

Neurotransmitter effects of antidepressants are immediate but they take 2+ weeks to work on symptoms
Cocaine and amphetamine mimic NA and 5-HT but do not act as antidepressants
Inprindole is an antidepressant which does not effect NA or 5-HT reuptake (5HT2 antagonist

61
Q

what are the theories re pathophysiology depression

A

Behavioural, cognitive and other psychological
Monoamine
Endocrine

62
Q

Why do antidepressants take two weeks to work?

A

Theory that initially the increased 5HT in synapses is cancelled out by auto-receptors reducing 5HT release and more reuptake of the extra 5HT in the synapses
But after a couple of weeks, the auto-receptors desensitise and the blocked reuptake transporters get internalised
So eventually there really is increased 5HT in the synapses

63
Q

what are anxiety disorders and what are the symptoms

A

A collection of illness
Common thread is excessive fear and associated physical responses
Nervousness, foreboding, agitation, palpitations, sweating, bowel upset
Generalised Anxiety, Panic Disorder (episodic), Specific Phobias

64
Q

examples of Benzodiazepines

A

Diazepam (Valium), Lorazepam (Ativan), Temazepam

65
Q

use of Benzodiazepines

A

Also used vs seizures and increased muscle tone (“spasticity”)

66
Q

mechanism of action of Benzodiazepines

A

Bind to a site on the GABA receptor, potentiating the effects of GABA ie the GABA causes more Cl- flux and more inhibition

67
Q

side effects of Benzodiazepines

A 
Drowsiness
Confusion
Forgetfulness 
Impaired motor control
Tolerance and Dependence
Respiratory depression –especially with alcohol

Block 6 PHARMACOLOGY (20 decks)

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