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Yr 2 - Pharmacology > sedatives and anxiolytics > Flashcards

sedatives and anxiolytics Flashcards

1
Q

What is a neurotransmitter?

A

A chemical substance released at the end of a nerve fibre by the arrival of a nerve impulse to another nerve fibre, muscle fibre or some other structure

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2
Q

What is an excitatory neurotransmitter?

A

Increases the probability that the target cell will fire an action potential

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3
Q

Give an example of an excitatory neurotransmitter:

A

Glutamate

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4
Q

What is an inhibitory neurotransmitter?

A

Decreases the probability that the target cell will fire and action potential

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5
Q

Give two examples of inhibitory neurotransmitters:

A

GABA (fast, found in virtually every part of the brain = short interneurones e.g. pain modulation)

Glycine (the inhibitory transmitter in the spinal cord)

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6
Q

Anxiety is a disorder of the…

A

CNS

Too few GABA = Anxiety

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7
Q

What was GABA first discovered as?

A

A product of microbial and plant metabolism

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8
Q

Which drug enhances the effects of GABA?

A

Valium

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9
Q

What causes epilepsy?

A

When GABA is lacking in certain parts of the brain

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10
Q

Where are there long GABAergic tracts to?

A

Cerebellum

Striatium

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11
Q

Which enzyme produces GABA?

A

Glutamic Acid Decarboxylase (GAD) -> found primarily in CNS

Co-enzyme = Vitamin B6

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12
Q

Which reaction produces GABA?

A

Glutamate -> GABA + CO2

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13
Q

How many isoforms of Glutamic Acid Decarboxylase are found in the brain?

A

Two

(GAD1 & GAD2 -> evolved separately but do same job!)

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14
Q

What is a glial cell?

A

A helper axillary cell = mop up and release neurotransmitter

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15
Q

What breaks GABA down?

A

GABA-Transaminase (GABA-T)

Co-factor = Vitamin B6= located in the mitochondria

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16
Q

What does GABA-T break GABA down into?

A

L-glutamate

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17
Q

Which drug is the most potent inhibitor of GABA-T?

A

Gabaculine (used more in lab than clinically)

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18
Q

What happens inside the cell after Gabaculine is given?

A
  • Lots of GABA in cleft
  • Eventually it stops vesicles containing GABA (relies on action of GAD to package produce GABA from glutamate and package into vesicle) = action potential = no release of GABA = no inhibition = Anxiety
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19
Q

Which cells express GABA receptors?

A
  • Most neurones in the CNS
  • Glial cells (astrocytes) = ANS neurones
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20
Q

When GABA binds what happens to the neurone?

A

Shift in membrane permeability to Chloride ions

postsynaptic inhibition = hyperpolarisation

presynaptic inhibition = depolarisation

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21
Q

How many types of GABA receptor are there?

What are they called?

A

Two

GABA-A & GABA-B

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22
Q

What type of receptor is GABA-A?

A

Ligand-gated ion (chloride) channel

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23
Q

What type of receptor is GABA-B?

A

GPCR

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24
Q

Which drug does GABA enhance the binding of?

A

Benzodiazepine

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25
Q

Why does GABA enhance binding of benzodiazepine?

A

GABA-A and Benzodiazepine (BDZ) receptor make up 2 separate parts of the same complex

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26
Q

Which is the most prevalent GABA receptor?

A

GABA-A

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27
Q

How many subunits does the GABA-A receptor have?

A

5 (pentameric)

N.b. subunit composition varies between brain regions and neuronal subpopulations (how we get sensitivity to specific regions)

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28
Q

Between which two subunits on the GABA-A receptor do benzodiazepines bind?

A

Alpha & Gamma

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29
Q

Which subunit of the GABA-A receptor binds GABA?

A

Alpha

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30
Q

Whats the birds eye view subunit arrangement for the GABA-A receptor?

A
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31
Q

What are the two types of allosteric modulators that act on GABA-A receptors?

A

Channel blockers (picrotoxin)

Channel modifiers (ethanol, volatile anaesthetics & neurosteroids)

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32
Q

What is the most common arrangement of subunits in GABA-A receptors?

A

1 X Alpha

2 X Beta

2 X Gamma

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33
Q

What are the different effects of benzodiazepine on GABA-A receptors with different subunits?

A

No effect = Alpha 4 & 6

Sedation and Amnesia = Alpha 1

Anxiolytic = Alpha 2 &3

For sensitivity to benzodiazepine = Gamma 2

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34
Q

Where are GABA-A receptors found?

A

Postsynaptic membrane

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35
Q

Where are GABA-B receptors found?

A

Presynaptic terminals

(many sites in brain & periphery)

36
Q

When GABA binds to GABA-B receptors what happens?

A
  • inhibition of voltage sensitive Ca channels
  • inhibition of transmitter release
37
Q

What type of receptor is the Glycine receptor?

A

Ligand gated Cl channel

38
Q

What is the role of Glycine in interneurones?

A

High in ventral horn

Low in ventral root fibres= associated with inhibitory interneurones

N.B. inhibitory effect of glycine is restricted to spinal cord, lower brain stem and retina

39
Q

What is the role of Glycine in the CNS?

A

inhibitory hyperpolarisation

N.B. inhibitory effect of glycine is restricted to spinal cord, lower brain stem and retina

40
Q

What type of neurotransmitter is Glycine?

A

Inhibitory

41
Q

Name 3 amino acids that activate the glycine receptor:

A

Glycine

Beta alanine

Taurine

42
Q

Name two competitive agonists of the Glycine receptor:

A

Strychnine (high affinity)

Caffiene= block the receptor

43
Q

Which receptors mediate the excitatory responses facilitated by Glycine?

A

NMDA receptors

44
Q

What effects do glycine/NMDA receptor antagonists have?

A

Anxiolytic

45
Q

What 4 features characterise anxiety disorders?

A
  • Excessive rumination
  • Worrying
  • Apprehension
  • Fear
46
Q

Which four aspects of experiences does “anxiety” cover?

A
  • mental apprehension
  • physical tension
  • physical symptoms
  • dissociative anxiety
47
Q

What are the (5) somatic and autonomic clinical manifestations of anxiety?

A
  • Restlessness and agitation
  • Tachycardia
  • Increased sweating
  • Weeping
  • GI disorders
48
Q

Which three disorders can anxiety disorder be divided into?

A
  • Generalised anxiety disorder
  • Phobic disorder
  • Panic disorder(characterised by own symptoms and have own treatment)
49
Q

What are the 6 clinically recognised anxiety disorders?

A
  1. generalised anxiety disorder = ongoing anxiety lacking any clear reason or focus
  2. social anxiety disorder = fear of being with/interacting with other people
  3. Panic disorder = sudden attacks of overwhelming fear
  4. Phobias = song fears of specific objects/ situations
  5. Post traumatic stress disorder = anxiety triggered by recall of past stressful experiences
  6. Obsessive compulsive disorder = compulsive ritualistic behaviour driven by irrational anxiety
50
Q

Which types of drugs are used to treat anxiety disorders?

A

Anxiolytics -> anxiety

Sedatives -> sedation (calming effect)

Hypnotics -> insomnia (induce sleep)

51
Q

How does dose effect anti-anxiety drugs?

A

Effect can be dose dependent

= same drug can be classified as anxiolytic/sedative/hypnotic at different dose

52
Q

Too much anti-anxiety drugs =

A

seizures/ anxiety

53
Q

What are the two possible mechanisms for anxiety?

A
  1. over activation of brain neurotransmission and neuronal firing (too much excitation e.g. excess glutamate & calcium)
  2. under-inhibition of brain neurotransmission and neuronal firing (insufficient inhibition e.g. insufficient GABA, GABA-A receptor function or enhancement of GABA)
54
Q

How do many sedative/tranquillising drugs work?

A

Enhance the effects of GABA:

  • increased GABA = blocks repute & increased GABA release
  • increased GABA signalling = Benzodiazepine agonist (partial/total) or blocking benzodiazepine inverse agonists
55
Q

Name 4 groups of anxiolytic drugs:

A
  • Phenobarbitone :
    • Barbiturate
    • Benzodiazepines
  • Older Tricyclic antidepressants (TCAs)
    • imipramine
    • doxepin
    • amitryptiline
    • trazodone
  • Monoamine Oxidase inhibitors (MAOIs)
    • phenezine
    • tranylcypromine
  • Selective serotonin reuptake inhibitors (SSRIs)
    • sertraline
    • fluoxetine
    • citalopram
    • paroxetine
56
Q

Which receptor do barbiturates bind to?

A

Beta subunit of GABA-A

(ligand gated Cl channel) = increased duration of Cl channel opening

57
Q

What are the 4 actions of barbiturates?

A
  • potentiate GABA (increased duration of Cl opening)
  • block AMPA receptor (glutamate receptor subtype)
  • inhibit Ca dependent release of neurotramsmitters
  • Binds entire superfamily of ligand gated ion channels
58
Q

What are the 2 side effects of Barbiturates?

A

Sedation and hypnotic (too much inhibition)

Risk of abuse and addiction is high (rarely used anymore)

59
Q

When are Barbiturates used clinically?

A

Short-term treatment of severe insomnia

(when benzodiazepines or non-benzodiazepines have failed)

60
Q

What are the 5 clinical uses of benzodiazepines?

A
  • anti anxiety
  • sedative
  • hypnotic
  • anticonvulsant
  • muscle relaxant
61
Q

What are the 6 side effects of benzodiazepines?

A
  • Drowsiness
  • Confusion
  • Amnesia
  • Impaired motor co-ordination
  • Lack of depth perception
  • Reduced REM (rapid eye movement) sleep
62
Q

In which two treatments are benzodiazepines often used?

A

As a premedication for medical or dental procedures

63
Q

What are the three different categories of benzodiazepines?

A

Short-acting

Intermediate-acting

Long-acting

64
Q

Which two categories of benzodiazepines are preferred for insomnia?

A

Short & intermediate-acting

65
Q

Which category of benzodiazepines is preferred for anxiety?

A

Long-acting

66
Q

What happens following longer term use of benzodiazepines?

A

Tolerance, dependence & withdrawal

Psychological & physical effects

67
Q

Which receptor interactions with benzodiazepines may contribute to their addictive properties?

A

inhibits NMDA & nACh receptors

68
Q

Overall which is less toxic… barbiturates or benzodiazepines?

A

Benzodiazepines

BUT… combination with other CNS depressants (alcohol & opiates) = increased toxicity and potential of fatal overdose

69
Q

Why do we rarely use the older tricyclic antidepressants (TCAs)?

A

Severe side effects

70
Q

Name 4 different older tricyclic antidepressants (TCAs):

A
  • imipramine
  • doxepin
  • amitryptiline
  • trazodone
71
Q

Name 2 different Monoamine oxidase inhibitors (MAOs):

A
  • phenelzine
  • tranylcpromine

very effective for anxiety but lots of drug dangers so rarely prescribed

72
Q

What is the main problem with selective serotonin reuptake inhibitors (SSRIs)?

A

Early in treatment they can produce anxiety due to negative feedback through serotonergic auto receptors

(reduced by combined with a low dose of benzodiazepine)

73
Q

Name a 5HT-1A receptor partial agonist used as an anxiolytic drug:

A

Buspirone

74
Q

What are the 4 side effects for Buspirone?

A

Nausea

Dizziness

Headache

Restlessness

(less than benzodiazepines)

75
Q

What are the 3 key let downs for Buspirone?

A
  • Takes days/weeks to develop action
  • Ineffective against panic attacks
  • Prolonged use = adaptive changes/ desensitisation
76
Q

What are the 3 key benefits of Buspirone?

A
  • No reports of tolerance and physical dependence
  • Less sedation
  • Less motor incoordination
77
Q

Name two hypnotics used to treat insomnia:

A
  • Zopiclone (non BDZ hypnotic)
  • Zolpidem (non BDZ hypnotic imidazopyridine)
78
Q

Name three antihistamines used for sedation:

A

Chloral hydrate

Diphenhydramine (nytol)

Promethazine

n.b. Drowsiness = side effect due to H1 antagonism in CNS

79
Q

What are the 2 benefits of antihistamines over other sedatives?

A

Fewer side effects

Safer

80
Q

Name a beta adrenoreceptor antagonist used to remove the peripheral symptoms of anxiety:

A

Propanalol

81
Q

Why are anxiolytics often used in general dental practice?

A

As a premedication

82
Q

What are the 6 indications of using anxiolytics in general dental practice?

A

If individual is:

  • fearful
  • anxious
  • longer appointments
  • especially invasive procedures
  • pronounced gag reflex
  • may help achieve profound local anaesthesia
83
Q

What are the 5 contraindications of using anxiolytics in general dental practice?

A
  • pregnancy
  • elderly
  • medically unstable (angina/diabetes)
  • medically complex (sever systemic disease)
  • patients already presenting adverse reactions to medications
84
Q

Which anxiolytics are often used in general dental practice?

A

Chloral hydrate (now replaced with Midazolam)

Barbituates = phentobarbital

Benzodiazepines = Diazepam (valium), Lorazepam (ativan) & Triazolam

Antihistamine H1 - hydroxyzine (vistoril)

Serotonin 5-HT-1A partial antagonists = Buspirone

85
Q

What is the mechanism of action for Benzodiazepines?

A

Increase the PROBABILITY of channel opening

86
Q

What is the mechanism of action for phenobarbitone (barbiturates)?

A

Low conc = PROLONG channel opening High conc = open channel in absence of GABA

Yr 2 - Pharmacology (18 decks)

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