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Block 6 PHARMACOLOGY > Mechanisms of psychotropic drug action > Flashcards

Mechanisms of psychotropic drug action Flashcards

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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
what do Antipsychotics antagonise
D2 receptors in the mesolimbic system (& other stuff, unfortunately)
26
side effects of antipsychotics
effects on other Dopamine pathways blocking other receptors metabolic, cardiac and others
27
which dopamine pathways do antipsychotics effect and now
Nigrostriatal → “Extrapyramidal side effects” -ie Parkinsonism, Akathisia, Acute Dystonias, Tardive Dyskinesia Tubuloinfundibular → excess Prolactin → Galactorrhoea, Amenorrhoea, Infertility
28
What are first genertion antipsychotics
Haloperidol
29
What are second genertion antipsychotics
Risperidone, Olanzapine
30
what is good about second genertion antipsychotics
less extra-pyramidal side effects
31
which antipsycotic do we use when others arent working
Clozapine
32
why do are we cautious when prescribing Clozapine?
agranulocytosis
33
which other receptors do antipsychotics antagonise and what does this cause
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
what is meant by the metabolic, cardiac and other things that happen as a side effect of antiphschotics
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
what is schizophrenia a result of
dopamine hyperactivity in certain areas of the brain
36
excess Dopamine in Mesolimbic tracts causes postive or negative symptoms
postive
37
inadequate Dopamine in Mesocortical tracts causes postive or negative symptoms?
negative
38
arguements for schizophrenia a result of dopamine hyperactivity in certain areas of the brain
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
arguements against schizophrenia a result of dopamine hyperactivity in certain areas of the brain
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
Hypotheses re pathophysiology of schizophrenia
Neuro-developmental Dopamine Psychological Damage from auto-antibodies
41
in a case where one twin was schizo and the other wasnt, what conclusions can be drawn from this?
its not pure genetic, there are othe rbiological factors playing a rol there are meausrealble structureal and functional abbnormalilties in a schizo brain
42
what is depression?
a collection of several symptoms occurring together
43
symptoms of depression
Persistent low mood, reduced enjoyment/interest, fatigue Sleep, appetite, weight, concentration changes Loss of confidence, guilt, hopelessness, suicidal thoughts and acts
44
what are the 4 classes of antidepressents
Tricyclic antidepressant Selective serotonin reuptake inhibitors (SSRIs) Monoamine Oxidase Inhibitors (MAOIs) Serotonin Noradrenaline reuptake inhibitors (SNRIs)
45
examples of Tricyclic antidepressioon
Amitriptyline, Lofepramine
46
whawt does Tricuclic antidepressent treat
Treat Depression (also pain, anxiety)
47
what deos the Trycyclic antedepressant do?
Block Noradrenaline and Serotonin reuptake transporters at synapses -increases availability of these monoamines
48
downside of Tricyclic
Can take a couple of weeks to take effect | Block other stuff as well, unfortunately
49
side effects of tricyclic antidepressent
``` Toxic in overdose Antagonises Histamine (H1) receptors → sedation Antagonises muscarinic receptors → dry mouth, blurred, vision, constipation, urinary retention Antagonises alpha adrenoceptors → postural hypotension ```
50
how do Selective serotinoinc reuptake inhibitors work?
Block only serotonin reuptake transporters, increasing serotonin availability at the synapse
51
down sidde of SSRI
Treats depression (also anxiety) May take a couple of weeks in take effect
52
eg of SSRI
E.g. Fluoxetine, Citalopramz
53
side effects of stimulating the various 5HT receptors
``` Nausea and vomiting Sexual dysfunction ?? increase suicidal ideation, particularly in children Withdrawal reaction Safer in overdose ```
54
what do MAOI's inhibihity
Block the action of this enzyme in the nerve terminals, increasing the availability of Noradrenaline, Serotonin, Dopamine
55
examples of Monoamine oxidase inhibitor AOIS
E.g. Phenelzine, Moclobemide
56
can a hypertensive crisis be made if people eat foods rich in Tyramine e.g. mature cheese, Bovril
yes
57
which chemical ppts NA release from the vesicles
Tyramine
58
what is the monoamine theory of depression
Depression is a result of a deficiency in brain monoamine neurotransmitters –Noradrenaline, Serotonin, Dopamine
59
arguement for the what is the monoamine theory of depression
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
arguement against the monoamine theory of depression
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
what are the theories re pathophysiology depression
Behavioural, cognitive and other psychological Monoamine Endocrine
62
Why do antidepressants take two weeks to work?
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
what are anxiety disorders and what are the symptoms
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
examples of Benzodiazepines
Diazepam (Valium), Lorazepam (Ativan), Temazepam
65
use of Benzodiazepines
Also used vs seizures and increased muscle tone (“spasticity”)
66
mechanism of action of Benzodiazepines
Bind to a site on the GABA receptor, potentiating the effects of GABA ie the GABA causes more Cl- flux and more inhibition
67
side effects of Benzodiazepines
``` Drowsiness Confusion Forgetfulness Impaired motor control Tolerance and Dependence Respiratory depression –especially with alcohol ```

Block 6 PHARMACOLOGY (20 decks)

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