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Neuropharmacology > Anxiety Disorders And Their Treatment(+FXS) > Flashcards

Anxiety Disorders And Their Treatment(+FXS) Flashcards

(52 cards)

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0
Q

What is FXS?

A

It’s a mental condition which is hereditary and arises on chromosome x

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1
Q

What are prominent characteristics of FXS?

A

Elongated face
Large or protruding ears
Low muscle tone- particularly in the face

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2
Q

What causes FXS?

A

Expansion of the CGG trinucleotide repeat affecting the fragile x mental retardation 1 gene -FMR1
Prevents the expression of the fragile x mental retardation protein FMRP- this is needed for normal development

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3
Q

Which sex is more affected with FXS ?

A

Males

The mutation occurs on the X chromosome and the males only have one X chromosomes

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4
Q

What is the “full mutation” for FXS?

A

> 200 CGG
This mutation occurs in the promoter region of the FMR1 gene and causes a methylated promoter region - this shuts down the gene so little or no mRNA is produced so no protein available

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5
Q

What is the mGluR theory ?

A

Used to explain many aspects of the clinical symptoms present in patients with FXS and in FMR1 KO mouse

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6
Q

What are the clinical symptoms found in FXS patients and FmR1 KO mice ?

A
  • higher density of spines and more immature spines compared to normal
  • electrophysiological deficits in FmR1 mice
  • exaggerated dendritic protein in FmR1 KO nice after activation of mGluR5
  • behavioural phenotype in patients with FXS and FmR1 KO mice
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7
Q

What does the mGluR theory state ?

A

That AMPA receptor internalisation triggered by group 1 mGluR stimulation is exaggerated in FXS

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8
Q

What are AMPA receptors do ?

A

Essential for long term synaptic plasticity

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9
Q

What does FMRP do ?

A

It negatively regulates transcription and reduces internalisation of AMPA receptors

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10
Q

what is characteristic of neurones from patients with FXS?

A

they have increased internalisation of AMPA receptors in the absence of FMRP - this reduces long term synaptic plasticity

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11
Q

what happens when mGluR5 is activated ?

A

they signal through protein kinase c

leads to activation of SRC family tyrosine kinases

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12
Q

what happens when group 1 mGluRs are activated ?

A

causes the up regulation of protein synthesis and this has been implicated in playing a role in FRMP dependent synaptic plasticity

it is thought that using these receptors as a target, could be a treatment for FXS

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13
Q

what are therapeutic substances for FXS?

A

negative modulators of mGluR5

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14
Q

what is MPEP and what does it do ?

A

1st negative modulator of mGluR5 - classed as an mGluR5 antagonist
interacts with transmembrane domain 7

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15
Q

why is MPEP not used in clinical trials?

A

causes toxicity and had a short half life

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16
Q

what beneficial effects did MPEP have ?

A

suppressed audiogenic seizures and rescued deficits in prepulse inhibition of acoustic startle in FRM1 KO mice

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17
Q

what is anxiety ?

A

normal biological process

- apprehension, tension and fearfulness

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18
Q

what is the difference between normal anxiety and chronic anxiety ?

A

chronic anxiety is debilitating

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19
Q

how common are anxiety disorders and what are some different types ?

A 
18% of population in USA have anxiety disorders
general anxiety disorder 
social anxiety disorder 
obsessive compulsive disorder 
panic disorder
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20
Q

what are the types of symptoms of anxiety disorders ?

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A

psychological and somatic (physical)

21
Q

what do the symptoms of anxiety disorders depend on ?

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A

depends on the particular anxiety disorder

depends on the individual

22
Q

what are the causes of anxiety disorders ?

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A

most often the causes are unknown

PTSD is often a cause though

23
Q

what are some examples of somatic symptoms of anxiety disorders ?

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A

tachycardia
sweating
trembling

24
what are some examples of psychological symptoms of anxiety disorders ?
worry panic exaggerated fear
25
how are anxiety disorders diagnosed?
diagnostic and statistical manual of mental disorders, 4th edition
26
what is the pathophysiology underlying anxiety disorders ?
unknown however stress is thought to be involved and the levels of catecholamines
27
how does stress contribute to anxiety disorders ?
causes a heightened physiological response - normally emotional stress - increases catecholamine levels - thought that the hypothalamic-pituitary-adrenal axis is implicated because its involved in the release of catecholamines
28
which neurotransmitters are influence the HPA axis and/or involved in the pharmacological treatment of anxiety disorders ?
serotonin GABA noradrenaline
29
what regions of the brain have been hypothesized to have implications in anxiety disorders ?
disturbances in the cerebral cortex - especially the limbic system including the amygdala
30
what are the types of anxiolytics ?
benzodiazepines- GABAergic Beta blockers- noradrenergic SSRIs/buspirone- Serotonin SNRIs- serotonin and noradrenaline
31
what do benzodiazepines do ?
bind to GABAa receptors they have a specific binding site on these receptors it enhances the influx of chloride ions when GABA binds
32
what do GABAa receptors look like ?
mutlisubunit receptors - 19 different types | pentameric - combination of alpha beta and gamma subunits- combinations are different in different brain regions
33
where does benzodiazepine bind on GABAa receptors ?
binds at the interface between alpha and gamma subunits
34
what happens to the electrophysiological recordings in GABA receptors when a mutation is induced ?
the mutation caused the receptor to become insensitive to diazepam the alpha-2,3,and 5 receptors were rendered insensitive to diazepam when histidine is replaced by arginine at 101
35
what are the actions of benzodiazepines ?
``` sedative hypnotic anxiolytic anticonvulsant muscle relaxant amnesic ```
36
what are some other examples of benzodiazepines ?
alprazolam chlordiazepoxide lorazepam oxazepam
37
why are lorazepam and oxazepam useful ?
they have a shorter action | good for patients with hepatic impairment
38
what are the pharmacokinetics of benzodiazepines ?
normally taken orally rapidly absorbed peak concentration after one hour highly protein bound and highly lipid soluble so sequestered into body fat
39
how are benzodiazepines metabolised?
mainly by N-desmethylation - can lead to an active metabolite- desmethyldiazepam - 70 hour half life phase 2 by glucuronide- the shorting acting ones goes straight to this phase
40
what happens if you overdose on benzodiazepines?
generally safe | not lethal- prolonged sleep
41
when can benzodiazepine administration be dangerous ?
if they are taken with other CNS depressants | if they are taken with ethanol- respiratory depression
42
what is used to treat a benzodiazepine overdose?
flumazenil | - benzodiazepine site antagonist
43
what are the unwanted effects of benzodiazepines ?
drowsiness confusion amnesia poor coordination
44
do people suffer from tolerance when taking benzodiazepines?
tolerance to anxiolytic effects have been seen in animals but not humans - more pronounced tolerance to anticonvulsant and sedative effects
45
why are benzodiazepines not used for chronic administration ?
dependence there are marked withdrawal symptoms - anxiety, tremor and dizziness it is difficult to wean patients off them if they have been used for a long time withdrawal has to be slow and tapering
46
how do beta blockers work and what do they do ?
antagonist of beta-1 and 2 adrenoreceptors act on autonomic system they are used to treat the somatic symptoms they have no effect on psychological effects however the reduction in the somatic symptoms may reduce worry and fear
47
what is buspirone ?
serotonin 1a agonist
48
how does buspirone work ?
it is a partial agonist stimulates serotonin 1a receptors at low serotonin levels inhibits serotonin 1a receptors at high serotonin levels also binds to D2 and 5HT 2a receptors they are presumed to alter serotonergic transmission
49
what anxiety disorders can busprione be used to treat and which can it not treat ?
used to treat generalised anxiety disorder cant treat panic disorder or OCD not thought to show tolerance to therapeutic effects but it does show tolerance to adverse effects only for acute treatment
50
how do SNRIs work ?
they have combined selectively for both serotonergic and noradrenergic uptake mechanisms e,g venlafaxine
51
when are SSRIs and SNRIs used ?
for the management of chronic anxiety - 4or more weeks can sometimes initally worsen the effects can be taken with benzodiazepines to relieve the initial worsening of symptoms

Neuropharmacology (15 decks)

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