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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
Name the catecholamines
dopamine noradrenaline adrenaline they can act as both neurotransmitters and hormones
26
List the monoamine neurotransmitters
serotonin dopamine noradrenaline adrenaline
27
What is the monoamine theory of depression (Schildkraut 1965)?
-suggests that depression results from funtionally deficient monoaminergic transmission in the CNS -deficient in serotonin and noradrenaline
28
What is the monoamine theory of depression (Schildkraut 1965) based on?
- ability of known antidepressant drugs (TCA and MAOI) to facilitate monoaminergic transmission -the ability to drugs such as reserpine to cause depression
29
How is reserpine thought to cause depression (MOA)?
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
30
Biochemical studies on depressed patients suggest that the monoamine theory of depression is ___________.
oversimplified
31
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 ...
secondary adaptive changes to the brain after neurochemical effects, there are secondary adaptive changes to the brain
32
What is the most successful therapeutic approach for treating depression?
Pharmacological manipulation of monoamine transmission
33
What drug evidence is there to support the monoamine theory?
TCA MAOI Reserpine a-methyltyrosine methyldopa electroconulsive therapy tryptophan (5-hydroxytryptophan) tryptophan depletion
34
What is the principal action of TCAs? What is the effect of this action in depressed patients?
block NE and 5HT reuptake increased mood
35
What is the principal action of MAOIs? What is the effect of this action in depressed patients?
increase stores of NE and 5-HT (they are not metabolised) increases mood
36
What is the principal action of Reserpine? What is the effect of this action in depressed patients?
inhibits NE and 5-HT storage decreases mood
37
What is the principal action of a-methyltyrosine? What is the effect of this action in depressed patients?
inhibits NE synthesis decreases mood- calms manic patients down
38
What is the principal action of methyldopa? What is the effect of this action in depressed patients?
inhibits NE synthesis decreases mood
39
What is the principal action of electroconvulsive therapy? What is the effect of this action in depressed patients?
?increases CNS responses to NE and 5-HT increases mood
40
What is the principal action of tryptophan (5-hydroxytryptophan)? What is the effect of this action in depressed patients
increases 5-HT synthesis increases mood in some studies
41
What is the principal action of tryptophan depletion? What is the effect of this action in depressed patients
decreases brain 5-HT synthesis induces relapse in SSRI treated patients (selective serotonin reuptake inhibitors)
42
Does serotonin cross the BBB? What is the implication of this?
no this means that serotonin produced in the periphery cannot the BBB and enter the brain it exhibits distinct functions in different locations
43
How is serotonin synthesised in the brain ?
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
44
VMAT-2 stands for...
vesicular monoamine transporter-2
45
How is serotonin (5-HT) metabolised?
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
46
Serotonin receptors are a group of ...
GPCR and ligand gated ion channels
47
Gas 5-HT receptors include
5-HT4, 5-HT6, 5-HT7
48
Gai 5-HT receptors include
5-HT1A, 5-HT1B, 5-HT1D, 5-HT1E, 5-HT1F
49
Gaq 5-HT receptors include
5-HT2A, 5-HT2B, 5-HT2C
50
5-HT3 serotonin receptors are what kind of receptors?
ligand gated ion channels
51
Where does the 5-HT molecule bind to on the 5-HT3 serotonin receptor?
binds to the A-A interface
52
5-HT is involved in what physiological processes?
sleep appetite thermoregulation and pain perception disorders such as migraines, depression, psychosis and drug abuse
53
How is noradrenaline synthesised?
L-tyrosine ---> L-DOPA ---> Dopamine ---> noradrenaline this process uses the enzyme dopamine beta hydroxylase
54
How is noradrenaline metabolised?
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
55
What are the noradrenergic receptors ?
a1 receptors a2 receptors B1, B2, B3 receptors a- alpha B- beta
56
a1 noradrenergic receptors (GPCR) are ____ linked.
Gq linked
57
What are the subtypes of the a1 noradrenergic receptors ?
1a, 1b, 1d
58
a2 noradrenergic receptors (GPCR) are ____ linked.
Gi linked
59
What are the subtypes of the a2 noradrenergic receptors?
2a 2b 2c
60
B1, B2 and B3 noradrenergic receptors are _____ linked
Gs
61
Noradrenergic transmission is involved in what physiological processes?
arousal mood control blood pressure regulation
62
What are the categories for antidepressant drugs?
Inhibitors of monoamine uptake monoamine oxidase inhibitors (MAIOs) Monoamine receptor antagonists Melatonin receptor agonist
63
What are the categories of antidepressant drugs that inhibit monoamine uptake?
Tricyclic antidepressants (TCAs) Selective serotonin reuptake inhibitors (SSRI) Serotonin- noradrenaline reuptake inhibitors (SNRIs) Selective noradrenaline reuptake inhibitors
64
What is the MOA of TCAs?
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
65
TCAs have little/no affinity for what transporter?
DAT (dopamine transporter) therefore they are not dopamine reuptake inhibitors
66
Give examples of TCAs
Imipramine Amitriptyline Nortriptyline Lofepramine Clomipramine
67
TCAs vary in activity and selectivity in inhibition of NA and 5-HT reuptake. True or false
True some may be more selective for 5-HT or dopamine transporters
68
TCA are long acting (12-24h). True or False
True
69
How is the active metabolite of TCA produced?
Produced by hydroxylation TCA compounds are metabolised by P450 enzymes in the liver
70
What are the clinical uses of TCAs?
depression anxiety OCD neuropathic pain
71
What are the adverse effects of TCAs?
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
72
What are the risks of a TCA overdose?
ventricullar dysrhythmias high risk interaction with CNS depressants such as alcohol, MAOI
73
TCAs are first generation antidepressants. Why are newer compounds being used and developed?
newer compounds have fewer side effects and lower overdose risk
74
What is the MOA of SSRIs?
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)
75
Give examples of SSRIs
Fluoxetine Fluvoxamine Paroxetine Setraline citalopram escitalopram vilazodone
76
SSRIs are long acting (18-24h). Which SSRI has the longest half life?
Fluoxetine
77
SSRI are metabolised by ...
P450 enzymes in the liver
78
What are the clinical uses of SSRIs?
commonly prescribed for depression (similar efficacy to TCAs anxiety
79
What are the side effects of SSRIs?
fewer anti-cholinergic effects than TCAs (less interference of autonomic control) less sedating nausea insomnia sexual dysfunction
80
What are the risks of SSRI overdose?
less cardiotoxic effects in overdoses compared to TCAs and MAOIs
81
Use of SSRIs is contraindicated with the use of ... Why is this?
MAOIs this is because there is a risk of serotonin toxicity/reaction
82
What are the consequences of a serotonin reaction?
neuromuscular hyperactivity (tremor, hyperreflexia, rigidity) autonomic dysfunction- tachycardia, blood pressure changes, CV collapse, hyperthermia, diarrhoea altered mental state- agitation, confusion, mania
83
5-HT is released from platelets. What is the effect on the CVS?
vasoconstriction (increase blood pressure); stop bleeding
84
SSRIs are also contraindicated for concurrent use of NSAIDs or those with bleeding disorders. Why is this?
this is because there is an increased risk of GI adverse event such as bleeding
85
There is a risk of suicidal thoughts in children and adolescents who take SSRIs. True or false
true
86
What is the MOA of SNRIs (serotonin noradrenaline reuptake inhibitors) ?
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)
87
Give examples of SNRIs
Venlafaxine Desvenlafaxine duloxetine
88
SNRIs are long acting antidepressants (12-14h). What SNRI has the shortest half-life and is therefore shorter acting?
Venlafaxine has a shorter half life and is therefore shorter acting
89
Conversion of venlafaxine into desvenlafaxine leads to ...
greater inhibition of NA uptake able to inhibit NET more effectively
90
What are the clinical uses of SNRIs?
used second line if SSRIs fail moderate to sever depression general anxiety disorder (GAD)
91
What are the side effects of SNRIs?
due to enhanced activation of adrenoceptors -headache -insomnia -sexual dysfunctio -dry mouth -dizziness -sweating and decreased appetite
92
What are the risks/symptoms of SNRI overdose?
CNS depression serotonin toxicity- neuromuscular hyperactivity, autonomic dysfunction (tachycardia, high blood pressure) seizures cardiac conduction abnormalities hepatotoxicity
93
What SNRI is hepatotoxic?
duloxetine
94
SNRIS are contraindicated for use in the following situations...
with MAOIs- risk of serotonin reaction/toxicity with NSAIDs or bleeding disorders (5-HT usually causes vasoconstriction when released from platelets)
95
What is the MOA of selective noradrenaline reuptake inhibitors?
selective inhibitor of NET; enhancing NA transmission however they can also inhibit DAT (dopamine reuptake)
96
Give an example of a selective noradrenaline reuptake inhibitor
Bupropion
97
Bupropion is metabolised by P450 enzymes in the liver. Give an example of a potent active metabolite of bupropion
radafaxine
98
What are the clinical uses of selective noradrenaline reuptake inhibitors?
depression associated with anxiety used to treat nicotine dependence (slow release formulation)
99
What are the side effects of selective noradrenaline reuptake inhibitors?
headache dry mouth agitation insomnia
100
What are the symptoms associated with selective noradrenaline reuptake inhibitor overdose?
seizure at high doses less risk of cardiac effects safer in overdoses than TCAs
101
MAOIs were among the first introduced antidepressants however, they were superceded by others, why is this?
newer compounds had less side effects
102
What is the mechanism of MAOIs?
inhibit monoamine oxidase leads to a reduction in the breakdown of monoamines (dopamine, 5-HT, NA)
103
Give examples of MAOIs
phenelzine tranylcypromine isocarboxazid moclobemide
104
Give an example of an irreversible, long acting, non selective (between MAO-A/B) MAOI
Isocarboxzid
105
Give an example of a reversible, short acting, MAO-A selective MAOI
moclobemide
106
What is the clinical use of moclobemide?
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
What are the side effects of MAOIs ?
postural hypotension anti-cholinergic side effects (as with TCAs) weight gain CNS stimulation restlessness insomnia hepatoxicity neurotoxicity (rare)
108
What are the contraindications of MAOIs?
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
What is the MOA of monoamine receptor antagonists?
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
Give an example of monoamine receptor antagonists
Mirtazapine
111
What are the side effects of monoamine receptor antagonists?
dry mouth sedation weight gain
112
What are the contraindications of monoamine receptor antagonists?
no serious drug interactions
113
What is melatonin?
hormone that regulates sleep and wakefulness (circardian rhythm) serotonin is a precursor to the production of melatonin
114
What is the MOA of melatonin receptor agonists?
they act as agonists at MT1 and MT2 receptors and may correct disturbances in circardian rhythm often associated with depression
115
What is the recommended dose of melatonin?
1 daily before bed
116
Give an example of a melatonin receptor agonist
Agomelatine
117
Agomelatine is ______ acting.
short 1-2hours
118
What are the side effect of melatonin receptor agonists?
headache dizziness fatigue sleep disturbance anxiety nausea GI disturbances sweating
119
What are the contraindications for melatonin receptor agonist use?
liver disease (can cause hepatoxicity) alcohol
120
What does a normal fear response to a threat involve?
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
What is anxiety?
anticipate and fear of a threat without reason symptoms interfere with normal productive activities
122
What are the emotional symptoms of anxiety?
restlessness sense of dread feeling constantly on edge difficulty concentrating irritability
123
What are the biological symptoms of anxiety?
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
What are anxiolytics?
drugs which are used to reduce anxiety symptoms
125
What are sedatives?
these are drugs that have a calming, tranquilising, sleep-inducing effect (reduce anxiety, stress, irritability or excitement)
126
What are hypnotic drugs?
these are drugs which induce sleep (induce hypnosis, drowsiness, onset and/or maintain sleep)
127
Anxiolytic and hypnotic drugs fall into what categories ?
Benzodiazepines (diazepam, midazolam) Z-drugs Melatonin receptor agonists Barbiturates Others: buspirone, B-adrenoceptor antagonists, antidepressants, anti-epileptics
128
What is the MOA of benzodiazepines?
they bind to the specific regulatory site on the GABAa receptor, thus enhancing the inhibitory effect of GABA
129
What are the 2 GABA binding sites?
a-B interface a-y interface
130
What is the binding site for benzodiazepines on the GABAa receptor?
(a-y interface)
131
GABAa receptor is composed of ____ subunits which are usually ... (name the subunits)
5 2 alpha 2 Beta 1 gamma those are the subunits usually present however they can change!
132
GABAa is a ____________ permeable ion channels involved in inhibitory neurotransmission
chloride
133
What are the pharmacological effects of benzodiazepines?
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
What is anterograde amnesia?
prevents memory of events whilst under the influence of benzodiazepines
135
What are the advantages of using BZDs?
minor surgery without unpleasant memories midazolam
136
What are the disadvantages of using BZDs?
date rape drug/ roofies Rohypnol (flunitrazepam)
137
How are BZDs metabolised?
they are directly conjugated with glucoronide and excreted in the urine
138
What is the benzodiazepine antagonist, flumanezil, used for?
reverse effect of BZD overdose (only if there is severe respiratory depression) reverse effects of BZD (midazolam) used for minor surgery
139
What is the MOA of flumanezil ?
competitively inhibits the BZD binding site
140
What is the active metabolite of midazolam?
the hydroxylated derivative
141
What are the main uses of midazolam?
hypnotic intravenous anaesthetic
142
Lorazepam, oxazepam, temazepam, lormerazepam are mainly used as ...
anxiolytics hypnotics
143
What is the active metabolite of alprazolam ?
hydroxylated derivative
144
What are the main uses of alprazolam?
anxiolytic antidepressant
145
What is the active metabolite for both diazepam and chlordiazpoxide?
Nordazepam
146
What is the main use of diazepam and chlordiazpoxide?
Anxiolytic muscle relaxant diazepam is used as an anti-convulsant
147
What is the active metabolite of flurazepam?
Desmethylflurazepam
148
What is the main use of flurazepam?
anxiolytic
149
What is the main use clonazepam?
anticonvulsant anxiolytic (especially mania)
150
What BZDs (benzodiazepines) are in the DPF?
Diazepam oral solution Diazepam tablets Temazepam oral solution Temazepam tablets
151
Sedation for dental procedures should be limited to ________ sedation
conscious
152
When is temazepam preffered for use for dental procedures?
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
Midazolam has a _________ duration of action
ultrashort <6 hours
154
Regarding dental procedures in both adults and children, sedation should be limited to ______________ whenever possible
conscious sedation
155
What sedatives are usually effective for many children?
NO midazolam
156
NO is the least potent inhalation anaesthetic therefore it is often delivered along side...
More potent volatile inhalation anaesthetics
157
Why do TCAs cause anticholinergic effects?
they are referred to as "sloppy" antidepressants because they will bind to and block muscarinic receptors
158
What are the unwanted effects of BZDs during normal therapeutic use?
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
Acute toxicity of BZDs during overdose is described to be ________ dangerous than other anxiolytics and hypnotic drugs
less
160
Overdose of BZDs causes...
prolonged sleep without serious respiratory and cardiovascular depression
161
What is tolerance?
more and more of drug required for the same effect
162
Tolerance and dependence occurs with BZDs. True or false
True
163
Abrupt cessation of BZD treatment can cause...
rebound heightened anxiety, tremor, dizziness, tinnitus, weight loss, disturbed sleep (withdrawal syndrome)
164
Withdrawal syndrome has a slower onset for BZDs than opioids. When is the estimated onset of withdrawal syndrome for diazepam?
3 weeks
165
Short acting BZDs cause more __________ withdrawal effects
abrupt
166
What is the difficult part of giving BZDs up?
physical and psychological symptoms
167
What is the abuse potential for benzodiazepines?
widely abused in combination with opioids and alcohol
168
What are Z drugs?
non BZDs anxiolytics they are short acting hypnotics
169
What are the clinical uses of Z drugs?
insomnia
170
What is the MOA of Z drugs?
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
Give examples of Z drugs
Zaleplon Zolpidem Zopiclone
172
Anti-epileptic drugs can also be used to treat...
GAD generalised anxiety disorder
173
Tiagabine is an anti-epileptic drug. What is its MOA?
Blocks GABA transporters (GAT-1) acts as a GABA reuptake inhibitor facilitates inhibition of neurotransmission
174
Valproate is an anti-epileptic drug. What is its MOA?
inhibits the GABA metabolising enzyme GABA transaminase More GABA available for inhibition of neurotransmission
175
Phenobarbital (barbiturate) is an anti-epileptic drug. What is its MOA?
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
Barbiturates have been long used as anxiolytics an hypnotics but today have largely been replaced by ____________.
Benzodiazepines
177
Gabapentin and pregabalins are structurally related to ________.
GABA
178
What is the effect of gabapentin and pregabalin on inhibitory neurotransmission?
despite structural relation to GABA, they have no effect on GABA binding, uptake or degradation
179
What is the MOA of Gabapentin and Pregabalin?
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
What are the clinical uses of Buspirone?
GAD (general anxiety disorder) but not phobias
181
What is the MOA of buspirone?
potent agonist of 5-HT1A receptors (Gi linked, inhibitory autoreceptors)
182
What are the side effects of buspirone?
less troublesome than BZD dizziness nausea headache not sedation or loss of coordination
183
What are the clinical uses of propanolol?
treat symptoms of anxiety (sweating, tremor, tachycardia)
184
What is the MOA of propanolol?
B-adrenoceptor antagonists (beta blockers) block peripheral sympathetic responses rather than central effects
185
Schizophrenia is a psychotic illness which affects __% of the population, links to both genetic and environmental factors
1
186
What are the symptoms of schizophrenia?
positive features negative features cognitive clinical features anxiety guilt depression self punishment attempted suicide
187
What do positive features (add on) of schizophrenia refer to?
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
What are the negative symptoms of schizophrenia?
withdrawal from social contacts flattening of emotional responses Anhedonia reluctance to perform everyday tasks
189
What is Anhedonia?
this is an inability to experience pleasure
190
What are the cognitive symptoms of schizophrenia?
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
What determines the efficacy of antipsychotic drugs?
the clinical phenotype of schizophrenia (positive, negative or cognitive symptoms)
192
How does schizophrenia present in younger patients ?
more dramatically with predominantly positive symptoms (chronic, severe, disabling)
193
How does schizophrenia present in older patients?
presents more gradually with negative symptoms there is a worse prognosis
194
Positive symptoms of schizophrenia result from...
overactivity in the mesolimbic (emotion and motivation) dopaminergic pathway; leading to activation of the D2 receptors
195
Negative and cognitive symptoms of schizophrenia may result from...
decreased activity in the mesocortical (cognitive control, motivation and emotional response) dopaminergic pathway (via D1 receptors)
196
Antipsychotic drugs owe their therapeutic effects mainly to ...
blockade of D2 receptors
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What dopaminergic pathways seem to appear normally in schizophrenia?
Nigrostriatal pathway (controlling motor movements via D2 receptors) Tuberoinfundibular (inhibits prolactin release) via D2 receptors
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The treatment of schizophrenia with D2 receptor antagonists can lead to ...
drug-induced extrapyramidal motor symptoms increased prolactin release (interferes with the prior unaffected dopaminergic pathways)
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A side effect of anti-psychotic drugs is ... (why does this occur)
parkinsonim extrapyramidal effects this is because of the interferance of D2 antagonists in the nigrostriatal pathway
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What are the dopaminergic pathways related to schizophrenia (state the symptoms observed)?
Mesolimbic pathway (related to positive symptoms) Mesocortical pathway (related to negative symptoms) Nigrostriatal pathway (related to extrapyradimal symptoms) Tuberoinfundibular pathway (related to hyperprolactinaemia)
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The nigrostriatal pathway contains around ___% of the brains dopamine
80%
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The nigrostriatal pathway originates from the _____________ of the substantia nigra and sends projections to the ___________ and __________.
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
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The substantia nigra pars compacta contains majority of the dopaminergic neurons whilst the substantia nigra reticulata contains ___________ neurons
GABAergic neurons
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Caudate and putamen together are referred to as the ...
striatum
205
What are the two pathways of the basal ganglia?
Direct and indirect pathway
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The direct pathway is ...
excitatory
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The indirect pathway is ...
inhibitory prevents unwanted muscle contractions from competing with voluntary movements
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What is the effect of dopamine in the nigrostriatal pathway?
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
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What is the effect of dopamine antagonists in the nigrostriatal pathway?
loss of dopamine modulation/inhibition on cholinergic interneurons leads to enhanced release of ACh and extrapyramidal symptoms
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What are extrapyramidal effects?
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
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What are first generation antipsychotics?
typical, classical or conventional antipsychotics they have relatively high selectivity for the dopamine D2 receptor (highly selective D2 antagonist)
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Give examples of first generation anti-psychotics
chlorpromaxine haloperidol fluphenaxine flupenitixol clopenixol
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Second generation anti-psychotics are referred to as ...
atypical
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The incidence of extrapyramidal side effects is less in what generation anti-psychotics?
second generation anti-psychotics
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Second generation anti-psychotics are equally effective at reducing the positive symptoms of schizophrenia as first generation anti-psychotics. True or false
True
216
There have been claims to the increased efficacy of atypical antipsychotics for treating negative symptoms compared to typical anti-psychotics. True or False
True
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Atypical anti-psychotics are effective at treating "treatment-resistant" patients. True or false
True
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Atypical anti-psychotics have different ________ for blocking diverse receptor subtypes.
profiles
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Give examples of second generation antipsychotics
clozapine riseperidone sertindole quetiapine amisulpride aripiprazole zotepine ziprasidone
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A wide spectrum of side effects is caused by most anti-psychotic drugs. Why is this ?
this is because multiple receptor types are blocked by anti-psychotic drugs hence they are not selective to dopamine receptors
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Blockade of serotonin receptors by ant-psychotic drugs contributes to ...
weight gain and ejaculation side effects
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Blockade of histamine receptors by ant-psychotic drugs contributes to ...
sedation anti-emetic effects weight gain
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Blockade of alpha adrenergic receptors by ant-psychotic drugs contributes to ...
hypotension reflex tachycardia hypersalivation incontinence
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Antimuscarinic effects of antipsychotic drugs causes
dry mouth blurred vision constipation difficulty with urination sinus tachycardia episodes of narrow angle glaucoma (ipatropium)
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What first generation antipsychotic drug increases the risk of extrapyramidal effects the most ?
haloperidol
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What are the side effects of chlorpromazine?
increased prolactin (gynaecomastia) hypothermia anticholinergic effects obstructive jaundice hypersensitivity reactions hypotension
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What are the side effects of haloperidol?
increased prolactin (gynaecomastia) hypothermia anticholinergic effects -less anticholinergic effects hypersensitivity reactions hypotension (no jaundice)
228
What are the side effects of flupentixol?
increased prolactin (gynaecomastia) restlessness
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What is gynaecomastia?
overdevelopment of breast tissue in men or boys
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What are the side effects sulpriride ?
increased prolactin (gynaecomastia)
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What are the side effects of clozapine?
risk of agranulocytosis (1%)- deficiency of granulocytes in blood seizures salivation anticholinergic side effects weight gain
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What are the side effects of risperidone?
weight gain extrapyramidal side effects with a high dose hypotension
233
What are the side effects of quetiapine ?
tachycardia drowsiness dry mouth constipation weight gain
234
What are the side effects of ziprasidone?
tiredness nausea

HHD 2 (37 decks)

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