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HHD 2 > Antidepressants, Anxiolytics and Antipsychotics > Flashcards

Antidepressants, Anxiolytics and Antipsychotics Flashcards

1
Q

What is the percentage of adults diagnosed with at least 1 mental health problem?

A

26%

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2
Q

Women (33%) are more likely than men (19%) to report having being diagnosed with a mental health problem. True or false

A

True

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3
Q

1 in 10 children and young people aged ____ and ____ were clinically diagnosed with a mental health disorder in 2004

A

5 and 16

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4
Q

What is the current single biggest killer of men under 45 in the UK?

A

suicide

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5
Q

What is depression?

A

low mood that lasts for a long time and affects your everyday life. Heterogenous disorder which can be associated with anxiety, eating disorders and drug addiction

Defined as a disorder of low mood that can last a long time

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6
Q

What is anxiety?

A

excessing feeling of unease, worry and fear

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7
Q

What is general anxiety disorder?

A

ongoing state of excessive anxiety lacking any clear reason

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8
Q

What is social anxiety disorder?

A

fear of being with and interacting with other people

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9
Q

What is a panic disorder ?

A

sudden attack of overwhelming fear, symptoms including sweat, tachycardia, chest pains, trembling and chocking

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10
Q

What are phobias?

A

strong fear of objects or situations e.g. snakes, flying

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11
Q

What is post traumatic stress disorder?

A

anxiety triggered by recall of past stressful experiences

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12
Q

What is obsessive compulsive disorder?

A

compulsive ritualistic behaviour driven by irrational anxiety e.g. fear of contamination

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13
Q

What is self-harm?

A

hurting ones self as a way of dealing with very difficult feelings, painful memories, overwhelming situations and experiences that feel out of control

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14
Q

What are suicidal feelings?

A

feelings associated with the act of intentionally taking your own life

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15
Q

What is a psychotic illness (schizophrenia)

A

characterised by delusions, hallucinations, thought disorder, together with social withdrawal and flattening of emotional responses and cognitive impairment

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16
Q

Depression ranges from …

A

a mild condition (bordering on normality) to severe psychotic depression (accompanied by hallucinations)

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17
Q

Depression is often associated with other psychiatric conditions including …

A

anxiety
eating disorders
drug addiction

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18
Q

Depression is a main cause of ________ and __________.

A

disability and death

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19
Q

What are the 2 distinct depressive syndromes?

A

unipolar depression
bipolar disorder

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20
Q

What is unipolar depression?

A

mood changes are always in the same direction
unipolar depression is more common

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21
Q

In bipolar disorder, depression alternates with _______

A

mania
they are either depressed or manic

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22
Q

What are the emotional symptoms of depression?

A

low mood
excessive negative thoughts
misery
apathy
pessimism
indecisiveness
loss of motivation
loss of reward and feeling pleasure (anhedonia)

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23
Q

What are the biological symptoms of depression?

A

retardation of thought (slowing)
retardation of action
loss of libido
sleep disturbances
loss of appetite

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24
Q

Depression is connected to changes in the following neurotransmitters …

A

serotonin
noradrenaline
dopamine

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25
Q

Name the catecholamines

A

dopamine
noradrenaline
adrenaline

they can act as both neurotransmitters and hormones

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26
Q

List the monoamine neurotransmitters

A

serotonin
dopamine
noradrenaline
adrenaline

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27
Q

What is the monoamine theory of depression (Schildkraut 1965)?

A

-suggests that depression results from funtionally deficient monoaminergic transmission in the CNS

-deficient in serotonin and noradrenaline

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28
Q

What is the monoamine theory of depression (Schildkraut 1965) based on?

A
  • ability of known antidepressant drugs (TCA and MAOI) to facilitate monoaminergic transmission
    -the ability to drugs such as reserpine to cause depression
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29
Q

How is reserpine thought to cause depression (MOA)?

A

Reserpine irreversibly blocks VMAT-2 pump
this results in blockage of serotonin, dopamine and NE reuptake into presynaptic storage vesicles

this action will then lead to their depletion by cytoplasmic MAO from peripheral and central synapses

so there is an increase in neuronal cytoplasmic NT however they are not repackaged in vesicles thus they cannot be released- they are then available to cytoplasmic MAO to metabolise

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30
Q

Biochemical studies on depressed patients suggest that the monoamine theory of depression is ___________.

A

oversimplified

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31
Q

The fact that direct neurochemical effects of anti-depressants is rapid (takes mins to hours) whereas the anti-depressant effects takes weeks to develop suggests …

A

secondary adaptive changes to the brain
after neurochemical effects, there are secondary adaptive changes to the brain

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32
Q

What is the most successful therapeutic approach for treating depression?

A

Pharmacological manipulation of monoamine transmission

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33
Q

What drug evidence is there to support the monoamine theory?

A

TCA
MAOI
Reserpine
a-methyltyrosine
methyldopa
electroconulsive therapy
tryptophan (5-hydroxytryptophan)
tryptophan depletion

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34
Q

What is the principal action of TCAs?
What is the effect of this action in depressed patients?

A

block NE and 5HT reuptake
increased mood

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35
Q

What is the principal action of MAOIs?
What is the effect of this action in depressed patients?

A

increase stores of NE and 5-HT (they are not metabolised)
increases mood

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36
Q

What is the principal action of Reserpine?
What is the effect of this action in depressed patients?

A

inhibits NE and 5-HT storage
decreases mood

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37
Q

What is the principal action of a-methyltyrosine?
What is the effect of this action in depressed patients?

A

inhibits NE synthesis
decreases mood- calms manic patients down

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38
Q

What is the principal action of methyldopa?
What is the effect of this action in depressed patients?

A

inhibits NE synthesis
decreases mood

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39
Q

What is the principal action of electroconvulsive therapy?
What is the effect of this action in depressed patients?

A

?increases CNS responses to NE and 5-HT
increases mood

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40
Q

What is the principal action of tryptophan (5-hydroxytryptophan)?
What is the effect of this action in depressed patients

A

increases 5-HT synthesis
increases mood in some studies

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41
Q

What is the principal action of tryptophan depletion?
What is the effect of this action in depressed patients

A

decreases brain 5-HT synthesis
induces relapse in SSRI treated patients (selective serotonin reuptake inhibitors)

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42
Q

Does serotonin cross the BBB? What is the implication of this?

A

no
this means that serotonin produced in the periphery cannot the BBB and enter the brain

it exhibits distinct functions in different locations

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43
Q

How is serotonin synthesised in the brain ?

A

synthesised from dietary tryptophan (Trp) which is transported to into the brain using a neutral amino acid carrier

Tryprophan hydroxylase (TH) converts tryptophan to 5-hydroxytryptophan (5-HTP)

Aromatic amino acid decarboxylase (AADC) subsequently converts 5-HTP to 5-hydroxytryptamine (5-HT)

5-HT is serotonin

5-HT is taken up into vesicles by VMAT-2 transporter protein

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44
Q

VMAT-2 stands for…

A

vesicular monoamine transporter-2

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45
Q

How is serotonin (5-HT) metabolised?

A

5-HT (5 hydroxytrypamine) is taken back up by SERT into nerve terminals and glia actively
5-HT can also be broken down by cellular monoamine oxidase-A

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46
Q

Serotonin receptors are a group of …

A

GPCR and ligand gated ion channels

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47
Q

Gas 5-HT receptors include

A

5-HT4, 5-HT6, 5-HT7

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48
Q

Gai 5-HT receptors include

A

5-HT1A, 5-HT1B, 5-HT1D, 5-HT1E, 5-HT1F

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49
Q

Gaq 5-HT receptors include

A

5-HT2A, 5-HT2B, 5-HT2C

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50
Q

5-HT3 serotonin receptors are what kind of receptors?

A

ligand gated ion channels

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51
Q

Where does the 5-HT molecule bind to on the 5-HT3 serotonin receptor?

A

binds to the A-A interface

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52
Q

5-HT is involved in what physiological processes?

A

sleep
appetite
thermoregulation and pain perception
disorders such as migraines, depression, psychosis and drug abuse

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53
Q

How is noradrenaline synthesised?

A

L-tyrosine —> L-DOPA —> Dopamine —> noradrenaline
this process uses the enzyme dopamine beta hydroxylase

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54
Q

How is noradrenaline metabolised?

A

noradrenaline is removed from the synaptic cleft by noradrenaline transporter (NET)

two enzymes are involved in the synthesis of noradrenaline
1.) MAO- mitochondrial location, metabolised DA, NE and 5-HT
2.) catechol-O-methyl transferase- COMT

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55
Q

What are the noradrenergic receptors ?

A

a1 receptors
a2 receptors
B1, B2, B3 receptors

a- alpha
B- beta

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56
Q

a1 noradrenergic receptors (GPCR) are ____ linked.

A

Gq linked

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57
Q

What are the subtypes of the a1 noradrenergic receptors ?

A

1a, 1b, 1d

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58
Q

a2 noradrenergic receptors (GPCR) are ____ linked.

A

Gi linked

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59
Q

What are the subtypes of the a2 noradrenergic receptors?

A

2a
2b
2c

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60
Q

B1, B2 and B3 noradrenergic receptors are _____ linked

A

Gs

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61
Q

Noradrenergic transmission is involved in what physiological processes?

A

arousal
mood control
blood pressure regulation

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62
Q

What are the categories for antidepressant drugs?

A

Inhibitors of monoamine uptake
monoamine oxidase inhibitors (MAIOs)
Monoamine receptor antagonists
Melatonin receptor agonist

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63
Q

What are the categories of antidepressant drugs that inhibit monoamine uptake?

A

Tricyclic antidepressants (TCAs)
Selective serotonin reuptake inhibitors (SSRI)
Serotonin- noradrenaline reuptake inhibitors (SNRIs)
Selective noradrenaline reuptake inhibitors

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64
Q

What is the MOA of TCAs?

A

they block SERT and NET (serotonin and noradrenaline transporters)
this elevates synaptic concentrations of 5-HT and NA, this leads to the enhancement of neurotransmission

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65
Q

TCAs have little/no affinity for what transporter?

A

DAT (dopamine transporter)
therefore they are not dopamine reuptake inhibitors

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66
Q

Give examples of TCAs

A

Imipramine
Amitriptyline
Nortriptyline
Lofepramine
Clomipramine

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67
Q

TCAs vary in activity and selectivity in inhibition of NA and 5-HT reuptake. True or false

A

True
some may be more selective for 5-HT or dopamine transporters

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68
Q

TCA are long acting (12-24h). True or False

A

True

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69
Q

How is the active metabolite of TCA produced?

A

Produced by hydroxylation
TCA compounds are metabolised by P450 enzymes in the liver

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70
Q

What are the clinical uses of TCAs?

A

depression
anxiety
OCD
neuropathic pain

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71
Q

What are the adverse effects of TCAs?

A

interference with autonomic control which leads to:
-dry mouth
-blurred vision
-constipation
-urinary retention

(anticholinergic effects- similar side effects to muscarinic antagonists)

-postural hypotension (head rush)
-seizures
-impotence
-sedation

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72
Q

What are the risks of a TCA overdose?

A

ventricullar dysrhythmias
high risk interaction with CNS depressants such as alcohol, MAOI

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73
Q

TCAs are first generation antidepressants. Why are newer compounds being used and developed?

A

newer compounds have fewer side effects and lower overdose risk

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74
Q

What is the MOA of SSRIs?

A

they have selectivity for blocking SERT (serotonin transporter), therefore 5-HT induced enhancement of neurotransmission

(they do not block NET; noradrenaline neurotransmitters hence selective serotonin)

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75
Q

Give examples of SSRIs

A

Fluoxetine
Fluvoxamine
Paroxetine
Setraline
citalopram
escitalopram
vilazodone

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76
Q

SSRIs are long acting (18-24h). Which SSRI has the longest half life?

A

Fluoxetine

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77
Q

SSRI are metabolised by …

A

P450 enzymes in the liver

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78
Q

What are the clinical uses of SSRIs?

A

commonly prescribed for depression (similar efficacy to TCAs
anxiety

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79
Q

What are the side effects of SSRIs?

A

fewer anti-cholinergic effects than TCAs (less interference of autonomic control)
less sedating
nausea
insomnia
sexual dysfunction

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80
Q

What are the risks of SSRI overdose?

A

less cardiotoxic effects in overdoses compared to TCAs and MAOIs

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81
Q

Use of SSRIs is contraindicated with the use of …
Why is this?

A

MAOIs
this is because there is a risk of serotonin toxicity/reaction

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82
Q

What are the consequences of a serotonin reaction?

A

neuromuscular hyperactivity (tremor, hyperreflexia, rigidity)
autonomic dysfunction- tachycardia, blood pressure changes, CV collapse, hyperthermia, diarrhoea
altered mental state- agitation, confusion, mania

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83
Q

5-HT is released from platelets. What is the effect on the CVS?

A

vasoconstriction
(increase blood pressure); stop bleeding

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84
Q

SSRIs are also contraindicated for concurrent use of NSAIDs or those with bleeding disorders. Why is this?

A

this is because there is an increased risk of GI adverse event such as bleeding

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85
Q

There is a risk of suicidal thoughts in children and adolescents who take SSRIs. True or false

A

true

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86
Q

What is the MOA of SNRIs (serotonin noradrenaline reuptake inhibitors) ?

A

they are a non-selective inhibitor of SERT and NET
low dose inhibitor of SERT
high dose inhibitor of NET
(higher dose required to inhibitor NET)

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87
Q

Give examples of SNRIs

A

Venlafaxine
Desvenlafaxine
duloxetine

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88
Q

SNRIs are long acting antidepressants (12-14h). What SNRI has the shortest half-life and is therefore shorter acting?

A

Venlafaxine has a shorter half life and is therefore shorter acting

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89
Q

Conversion of venlafaxine into desvenlafaxine leads to …

A

greater inhibition of NA uptake
able to inhibit NET more effectively

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90
Q

What are the clinical uses of SNRIs?

A

used second line if SSRIs fail
moderate to sever depression
general anxiety disorder (GAD)

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91
Q

What are the side effects of SNRIs?

A

due to enhanced activation of adrenoceptors
-headache
-insomnia
-sexual dysfunctio
-dry mouth
-dizziness
-sweating and decreased appetite

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92
Q

What are the risks/symptoms of SNRI overdose?

A

CNS depression
serotonin toxicity- neuromuscular hyperactivity, autonomic dysfunction (tachycardia, high blood pressure)
seizures
cardiac conduction abnormalities
hepatotoxicity

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93
Q

What SNRI is hepatotoxic?

A

duloxetine

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94
Q

SNRIS are contraindicated for use in the following situations…

A

with MAOIs- risk of serotonin reaction/toxicity
with NSAIDs or bleeding disorders (5-HT usually causes vasoconstriction when released from platelets)

95
Q

What is the MOA of selective noradrenaline reuptake inhibitors?

A

selective inhibitor of NET; enhancing NA transmission
however they can also inhibit DAT (dopamine reuptake)

96
Q

Give an example of a selective noradrenaline reuptake inhibitor

97
Q

Bupropion is metabolised by P450 enzymes in the liver. Give an example of a potent active metabolite of bupropion

A

radafaxine

98
Q

What are the clinical uses of selective noradrenaline reuptake inhibitors?

A

depression associated with anxiety
used to treat nicotine dependence (slow release formulation)

99
Q

What are the side effects of selective noradrenaline reuptake inhibitors?

A

headache
dry mouth
agitation
insomnia

100
Q

What are the symptoms associated with selective noradrenaline reuptake inhibitor overdose?

A

seizure at high doses
less risk of cardiac effects
safer in overdoses than TCAs

101
Q

MAOIs were among the first introduced antidepressants however, they were superceded by others, why is this?

A

newer compounds had less side effects

102
Q

What is the mechanism of MAOIs?

A

inhibit monoamine oxidase
leads to a reduction in the breakdown of monoamines (dopamine, 5-HT, NA)

103
Q

Give examples of MAOIs

A

phenelzine
tranylcypromine
isocarboxazid
moclobemide

104
Q

Give an example of an irreversible, long acting, non selective (between MAO-A/B) MAOI

A

Isocarboxzid

105
Q

Give an example of a reversible, short acting, MAO-A selective MAOI

A

moclobemide

106
Q

What is the clinical use of moclobemide?

A

Moclobemide is used as it has less severe actions than other long acting MAOIs

it is used for major depression and social phobias when other antidepressants fail

107
Q

What are the side effects of MAOIs ?

A

postural hypotension
anti-cholinergic side effects (as with TCAs)
weight gain
CNS stimulation
restlessness
insomnia
hepatoxicity
neurotoxicity (rare)

108
Q

What are the contraindications of MAOIs?

A

interaction with certain foods such as cheese- cheese reaction- cheese, red wine, meat
interaction with other amines (ephedrine in OTC decongestants)
pethidine (opioid) - potentially lethal

109
Q

What is the MOA of monoamine receptor antagonists?

A

block a2 adrenoceptors (Gi linked) and 5-HT 2c (Gq linked) receptors
by blocking receptors it enhances noradrenaline and 5-HT release

they have a faster onset than other antidepressants

110
Q

Give an example of monoamine receptor antagonists

A

Mirtazapine

111
Q

What are the side effects of monoamine receptor antagonists?

A

dry mouth
sedation
weight gain

112
Q

What are the contraindications of monoamine receptor antagonists?

A

no serious drug interactions

113
Q

What is melatonin?

A

hormone that regulates sleep and wakefulness (circardian rhythm)

serotonin is a precursor to the production of melatonin

114
Q

What is the MOA of melatonin receptor agonists?

A

they act as agonists at MT1 and MT2 receptors and may correct disturbances in circardian rhythm often associated with depression

115
Q

What is the recommended dose of melatonin?

A

1 daily before bed

116
Q

Give an example of a melatonin receptor agonist

A

Agomelatine

117
Q

Agomelatine is ______ acting.

A

short
1-2hours

118
Q

What are the side effect of melatonin receptor agonists?

A

headache
dizziness
fatigue
sleep disturbance
anxiety
nausea
GI disturbances
sweating

119
Q

What are the contraindications for melatonin receptor agonist use?

A

liver disease (can cause hepatoxicity)
alcohol

120
Q

What does a normal fear response to a threat involve?

A

fight or flight response- physiological reaction to perceived threat
defensive behaviour
autonomic reflexes
catecholamine secretion (NA, A)
corticosteroid secretion
arousal and alertness
negative emotions

121
Q

What is anxiety?

A

anticipate and fear of a threat without reason
symptoms interfere with normal productive activities

122
Q

What are the emotional symptoms of anxiety?

A

restlessness
sense of dread
feeling constantly on edge
difficulty concentrating
irritability

123
Q

What are the biological symptoms of anxiety?

A

dizziness
tiredness
heart palpitations
muscle aches and tension
trembling and shaking
dry mouth
excessive sweating
shortness of breath
stomach ache
nausea
headache
pins and needles
insomnia

124
Q

What are anxiolytics?

A

drugs which are used to reduce anxiety symptoms

125
Q

What are sedatives?

A

these are drugs that have a calming, tranquilising, sleep-inducing effect (reduce anxiety, stress, irritability or excitement)

126
Q

What are hypnotic drugs?

A

these are drugs which induce sleep (induce hypnosis, drowsiness, onset and/or maintain sleep)

127
Q

Anxiolytic and hypnotic drugs fall into what categories ?

A

Benzodiazepines (diazepam, midazolam)
Z-drugs
Melatonin receptor agonists
Barbiturates

Others: buspirone, B-adrenoceptor antagonists, antidepressants, anti-epileptics

128
Q

What is the MOA of benzodiazepines?

A

they bind to the specific regulatory site on the GABAa receptor, thus enhancing the inhibitory effect of GABA

129
Q

What are the 2 GABA binding sites?

A

a-B interface
a-y interface

130
Q

What is the binding site for benzodiazepines on the GABAa receptor?

A

(a-y interface)

131
Q

GABAa receptor is composed of ____ subunits which are usually … (name the subunits)

A

5
2 alpha
2 Beta
1 gamma

those are the subunits usually present however they can change!

132
Q

GABAa is a ____________ permeable ion channels involved in inhibitory neurotransmission

133
Q

What are the pharmacological effects of benzodiazepines?

A

reduction of anxiety and aggression (GABAa with a2 subunit)

sedation (GABAa with a1 subunit), improves insomnia

reduction of muscle tone (relaxation) and coordination

suppression of convulsion (anti-epileptic effect)

anterograde amnesia

134
Q

What is anterograde amnesia?

A

prevents memory of events whilst under the influence of benzodiazepines

135
Q

What are the advantages of using BZDs?

A

minor surgery without unpleasant memories
midazolam

136
Q

What are the disadvantages of using BZDs?

A

date rape drug/ roofies
Rohypnol (flunitrazepam)

137
Q

How are BZDs metabolised?

A

they are directly conjugated with glucoronide and excreted in the urine

138
Q

What is the benzodiazepine antagonist, flumanezil, used for?

A

reverse effect of BZD overdose (only if there is severe respiratory depression)

reverse effects of BZD (midazolam) used for minor surgery

139
Q

What is the MOA of flumanezil ?

A

competitively inhibits the BZD binding site

140
Q

What is the active metabolite of midazolam?

A

the hydroxylated derivative

141
Q

What are the main uses of midazolam?

A

hypnotic
intravenous anaesthetic

142
Q

Lorazepam, oxazepam, temazepam, lormerazepam are mainly used as …

A

anxiolytics
hypnotics

143
Q

What is the active metabolite of alprazolam ?

A

hydroxylated derivative

144
Q

What are the main uses of alprazolam?

A

anxiolytic
antidepressant

145
Q

What is the active metabolite for both diazepam and chlordiazpoxide?

A

Nordazepam

146
Q

What is the main use of diazepam and chlordiazpoxide?

A

Anxiolytic
muscle relaxant
diazepam is used as an anti-convulsant

147
Q

What is the active metabolite of flurazepam?

A

Desmethylflurazepam

148
Q

What is the main use of flurazepam?

A

anxiolytic

149
Q

What is the main use clonazepam?

A

anticonvulsant
anxiolytic (especially mania)

150
Q

What BZDs (benzodiazepines) are in the DPF?

A

Diazepam oral solution
Diazepam tablets
Temazepam oral solution
Temazepam tablets

151
Q

Sedation for dental procedures should be limited to ________ sedation

152
Q

When is temazepam preffered for use for dental procedures?

A

when it is important to minimise any residual effect the following day
this is because it has a short duration of action (12-18 hours)

153
Q

Midazolam has a _________ duration of action

A

ultrashort
<6 hours

154
Q

Regarding dental procedures in both adults and children, sedation should be limited to ______________ whenever possible

A

conscious sedation

155
Q

What sedatives are usually effective for many children?

A

NO
midazolam

156
Q

NO is the least potent inhalation anaesthetic therefore it is often delivered along side…

A

More potent volatile inhalation anaesthetics

157
Q

Why do TCAs cause anticholinergic effects?

A

they are referred to as “sloppy” antidepressants because they will bind to and block muscarinic receptors

158
Q

What are the unwanted effects of BZDs during normal therapeutic use?

A

drowsiness
confusion
amnesia
impaired coordination (affects manual skills, driving, job performance even day after)
enhance the depressant effect of other drugs such as alcohol (relaxing effect?)

159
Q

Acute toxicity of BZDs during overdose is described to be ________ dangerous than other anxiolytics and hypnotic drugs

160
Q

Overdose of BZDs causes…

A

prolonged sleep without serious respiratory and cardiovascular depression

161
Q

What is tolerance?

A

more and more of drug required for the same effect

162
Q

Tolerance and dependence occurs with BZDs.
True or false

163
Q

Abrupt cessation of BZD treatment can cause…

A

rebound heightened anxiety, tremor, dizziness, tinnitus, weight loss, disturbed sleep (withdrawal syndrome)

164
Q

Withdrawal syndrome has a slower onset for BZDs than opioids. When is the estimated onset of withdrawal syndrome for diazepam?

165
Q

Short acting BZDs cause more __________ withdrawal effects

166
Q

What is the difficult part of giving BZDs up?

A

physical and psychological symptoms

167
Q

What is the abuse potential for benzodiazepines?

A

widely abused in combination with opioids and alcohol

168
Q

What are Z drugs?

A

non BZDs anxiolytics
they are short acting hypnotics

169
Q

What are the clinical uses of Z drugs?

170
Q

What is the MOA of Z drugs?

A

agonist at GABAa with high affinity for a1 subunit (sedative)
they enhance the activity of GABA receptors thus facilitating GABA mediated opening of chloride channels

171
Q

Give examples of Z drugs

A

Zaleplon
Zolpidem
Zopiclone

172
Q

Anti-epileptic drugs can also be used to treat…

A

GAD
generalised anxiety disorder

173
Q

Tiagabine is an anti-epileptic drug. What is its MOA?

A

Blocks GABA transporters (GAT-1)
acts as a GABA reuptake inhibitor
facilitates inhibition of neurotransmission

174
Q

Valproate is an anti-epileptic drug. What is its MOA?

A

inhibits the GABA metabolising enzyme
GABA transaminase
More GABA available for inhibition of neurotransmission

175
Q

Phenobarbital (barbiturate) is an anti-epileptic drug. What is its MOA?

A

positive allosteric modulators of the GABAa receptor
At higher doses they act as agonists to the GABAa receptors
they lead to prolonged opening of the chloride ion channel

176
Q

Barbiturates have been long used as anxiolytics an hypnotics but today have largely been replaced by ____________.

A

Benzodiazepines

177
Q

Gabapentin and pregabalins are structurally related to ________.

178
Q

What is the effect of gabapentin and pregabalin on inhibitory neurotransmission?

A

despite structural relation to GABA, they have no effect on GABA binding, uptake or degradation

179
Q

What is the MOA of Gabapentin and Pregabalin?

A

bind to VGCC subunits reducing their trafficking to the cell membrane
(less VGCC found at the cell membrane)
this reduces calcium entry to nerve terminals and thus reduces (excitatory-the aim) neurotransmitter release

180
Q

What are the clinical uses of Buspirone?

A

GAD (general anxiety disorder) but not phobias

181
Q

What is the MOA of buspirone?

A

potent agonist of 5-HT1A receptors (Gi linked, inhibitory autoreceptors)

182
Q

What are the side effects of buspirone?

A

less troublesome than BZD
dizziness
nausea
headache
not sedation or loss of coordination

183
Q

What are the clinical uses of propanolol?

A

treat symptoms of anxiety (sweating, tremor, tachycardia)

184
Q

What is the MOA of propanolol?

A

B-adrenoceptor antagonists (beta blockers)
block peripheral sympathetic responses rather than central effects

185
Q

Schizophrenia is a psychotic illness which affects __% of the population, links to both genetic and environmental factors

186
Q

What are the symptoms of schizophrenia?

A

positive features
negative features
cognitive clinical features
anxiety
guilt
depression
self punishment
attempted suicide

187
Q

What do positive features (add on) of schizophrenia refer to?

A

change in behaviour and thoughts

delusions- often paranoid in nature
hallucinations-often inciting voices
thought disorder-wild trains of thought, delusions of grandeur, garbled sentences and irrational conclusions
abnormal, disorganised behaviour -stereotyped movements, disorientation and occasionally aggressive behaviours
catatonia- can be apparent as immobility or purposeless motor activity

188
Q

What are the negative symptoms of schizophrenia?

A

withdrawal from social contacts
flattening of emotional responses
Anhedonia
reluctance to perform everyday tasks

189
Q

What is Anhedonia?

A

this is an inability to experience pleasure

190
Q

What are the cognitive symptoms of schizophrenia?

A

Deficits in cognitive function- attention, memory
Selective attention- inability to discriminate between significant and insignificant stimuli e.g. words of a companion vs a ticking clock (would focus more on a ticking clock)

191
Q

What determines the efficacy of antipsychotic drugs?

A

the clinical phenotype of schizophrenia
(positive, negative or cognitive symptoms)

192
Q

How does schizophrenia present in younger patients ?

A

more dramatically with predominantly positive symptoms (chronic, severe, disabling)

193
Q

How does schizophrenia present in older patients?

A

presents more gradually with negative symptoms
there is a worse prognosis

194
Q

Positive symptoms of schizophrenia result from…

A

overactivity in the mesolimbic (emotion and motivation) dopaminergic pathway; leading to activation of the D2 receptors

195
Q

Negative and cognitive symptoms of schizophrenia may result from…

A

decreased activity in the mesocortical (cognitive control, motivation and emotional response) dopaminergic pathway (via D1 receptors)

196
Q

Antipsychotic drugs owe their therapeutic effects mainly to …

A

blockade of D2 receptors

197
Q

What dopaminergic pathways seem to appear normally in schizophrenia?

A

Nigrostriatal pathway (controlling motor movements via D2 receptors)

Tuberoinfundibular (inhibits prolactin release) via D2 receptors

198
Q

The treatment of schizophrenia with D2 receptor antagonists can lead to …

A

drug-induced extrapyramidal motor symptoms
increased prolactin release

(interferes with the prior unaffected dopaminergic pathways)

199
Q

A side effect of anti-psychotic drugs is …
(why does this occur)

A

parkinsonim
extrapyramidal effects

this is because of the interferance of D2 antagonists in the nigrostriatal pathway

200
Q

What are the dopaminergic pathways related to schizophrenia (state the symptoms observed)?

A

Mesolimbic pathway (related to positive symptoms)
Mesocortical pathway (related to negative symptoms)
Nigrostriatal pathway (related to extrapyradimal symptoms)
Tuberoinfundibular pathway (related to hyperprolactinaemia)

201
Q

The nigrostriatal pathway contains around ___% of the brains dopamine

202
Q

The nigrostriatal pathway originates from the _____________ of the substantia nigra and sends projections to the ___________ and __________.

A

par compacta region of the substantia nigra
it sends projections to the caudate and putamen (striatum)

substantia nigra (part of the basal ganglia) projects to other structures in the basal ganglia- the caudate and putamen

203
Q

The substantia nigra pars compacta contains majority of the dopaminergic neurons whilst the substantia nigra reticulata contains ___________ neurons

A

GABAergic neurons

204
Q

Caudate and putamen together are referred to as the …

205
Q

What are the two pathways of the basal ganglia?

A

Direct and indirect pathway

206
Q

The direct pathway is …

A

excitatory

207
Q

The indirect pathway is …

A

inhibitory
prevents unwanted muscle contractions from competing with voluntary movements

208
Q

What is the effect of dopamine in the nigrostriatal pathway?

A

release of dopamine causes an inhibitory effect on interneurons

they essentially modify activity of cholinergic interneurons
Maintains normal ACh release and therefore normal motor activity

209
Q

What is the effect of dopamine antagonists in the nigrostriatal pathway?

A

loss of dopamine modulation/inhibition on cholinergic interneurons
leads to enhanced release of ACh and extrapyramidal symptoms

210
Q

What are extrapyramidal effects?

A

Pseudoparkinsonism
-stooped posture
-shuffling gait
-rigidity
-bradykinesia
-tremors at rest
-pill rolling motion of the hand

Akathisia
-restless
-trouble standing still
-paces the floor
-feet in constant motion, rocking back and forth

Acute dystonia
-facial grimacing
-involuntary upward eye movement
-muscle spasms of the tongue, face, neck, and back (back muscle spasms cause trunk to arch forward)
-laryngeal spasms

Tardive dyskinesia
-protrusion and rolling of tongue
-sucking and smacking movements of the lips
-chewing mition
-facial dyskinesia
-involuntary movements of the body and extremeties

211
Q

What are first generation antipsychotics?

A

typical, classical or conventional antipsychotics
they have relatively high selectivity for the dopamine D2 receptor

(highly selective D2 antagonist)

212
Q

Give examples of first generation anti-psychotics

A

chlorpromaxine
haloperidol
fluphenaxine
flupenitixol
clopenixol

213
Q

Second generation anti-psychotics are referred to as …

214
Q

The incidence of extrapyramidal side effects is less in what generation anti-psychotics?

A

second generation anti-psychotics

215
Q

Second generation anti-psychotics are equally effective at reducing the positive symptoms of schizophrenia as first generation anti-psychotics. True or false

216
Q

There have been claims to the increased efficacy of atypical antipsychotics for treating negative symptoms compared to typical anti-psychotics. True or False

217
Q

Atypical anti-psychotics are effective at treating “treatment-resistant” patients. True or false

218
Q

Atypical anti-psychotics have different ________ for blocking diverse receptor subtypes.

219
Q

Give examples of second generation antipsychotics

A

clozapine
riseperidone
sertindole
quetiapine
amisulpride
aripiprazole
zotepine
ziprasidone

220
Q

A wide spectrum of side effects is caused by most anti-psychotic drugs. Why is this ?

A

this is because multiple receptor types are blocked by anti-psychotic drugs hence they are not selective to dopamine receptors

221
Q

Blockade of serotonin receptors by ant-psychotic drugs contributes to …

A

weight gain and ejaculation side effects

222
Q

Blockade of histamine receptors by ant-psychotic drugs contributes to …

A

sedation
anti-emetic effects
weight gain

223
Q

Blockade of alpha adrenergic receptors by ant-psychotic drugs contributes to …

A

hypotension
reflex tachycardia
hypersalivation
incontinence

224
Q

Antimuscarinic effects of antipsychotic drugs causes

A

dry mouth
blurred vision
constipation
difficulty with urination
sinus tachycardia
episodes of narrow angle glaucoma (ipatropium)

225
Q

What first generation antipsychotic drug increases the risk of extrapyramidal effects the most ?

A

haloperidol

226
Q

What are the side effects of chlorpromazine?

A

increased prolactin (gynaecomastia)
hypothermia
anticholinergic effects
obstructive jaundice
hypersensitivity reactions
hypotension

227
Q

What are the side effects of haloperidol?

A

increased prolactin (gynaecomastia)
hypothermia
anticholinergic effects -less anticholinergic effects
hypersensitivity reactions
hypotension

(no jaundice)

228
Q

What are the side effects of flupentixol?

A

increased prolactin (gynaecomastia)
restlessness

229
Q

What is gynaecomastia?

A

overdevelopment of breast tissue in men or boys

230
Q

What are the side effects sulpriride ?

A

increased prolactin (gynaecomastia)

231
Q

What are the side effects of clozapine?

A

risk of agranulocytosis (1%)- deficiency of granulocytes in blood
seizures
salivation
anticholinergic side effects
weight gain

232
Q

What are the side effects of risperidone?

A

weight gain
extrapyramidal side effects with a high dose
hypotension

233
Q

What are the side effects of quetiapine ?

A

tachycardia
drowsiness
dry mouth
constipation
weight gain

234
Q

What are the side effects of ziprasidone?

A

tiredness
nausea

HHD 2 (37 decks)

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