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53 Finals > IC8 Pharmacology II (Antipsychotics, Depression drugs) > Flashcards

IC8 Pharmacology II (Antipsychotics, Depression drugs) Flashcards

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1
Q

Onset of schizophrenia

A

late adolescence/ early adulthood

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2
Q

5 sx of schizophrenia

A

+‘ve, -‘ve, anxiety/depression, aggressive, cognitive

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3
Q

Examples of positive sx

A
  • Delusions (often paranoid)
  • Hallucination (bizarre ideas)
  • Thought disorders
  • Abnormal behaviours (sterotypical or aggressive behaviours)
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4
Q

Examples of negative sx

A
  • Withdrawal
  • Flattening of emotional responses
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5
Q

As disease progresses which sx is more dominant?

A

negative

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6
Q

Causes of schizophrenia

A

genetic and environmental factors (a neurodevelopmental disorder)

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7
Q

3 neurochemical theories for schizophrenia

A

dopamine, 5HT, glutamate

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8
Q

How does a linear graph shows that D2 receptor is involved in schizophrenia?

A

drugs with high Kd = low affinity for D2 receptors will have lower efficacy and need higher doses

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9
Q

4 dopamine pathways of the brain

A

Nigrostriatal, Mesolimbic, Mesocortical, Tuberoinfundibular

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10
Q

Type of dopamine receptor and the effect of antagonism at Nigrostriatal

A

(start at substantia nigra to dorsal striatum)
Dopamine (D1/D2) antagonism = less dopamine (like Parkinson) = extrapyramidal SE (EPS)

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11
Q

Type of dopamine receptor and the effect of antagonism at
Mesolimbic/ Mesocortical

A

Dopamine antagonism: antipsychotic effects

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12
Q

Type of dopamine receptor and the effect of antagonism at Tuberoinfundibular

A

Dopamine (D2/D3) antagonism → increase prolactin secretion (breast swelling, lactation, gynaecomastia)

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13
Q

Examples of FGA

A

Haloperidol, chlorpromazine

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14
Q

Major SE of FGA

A

EPSE (involuntary movements, Parkinson’s like) → eg dystonia, cogwheel rigidity and tremor at rest

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15
Q

what receptors do chlorpromazine antagonise?

A

D2, M1, H1, a1

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16
Q

what receptors do haloperidol antagonise?

A

D2, a1 (no M1, H1)

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17
Q

EPSE involves which part of the brain?

A

basal ganglia (including substantia nigra and striatum)

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18
Q

Examples of SGA

A

amisulpride, clozapine, olanzapine, risperidone

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19
Q

What properties define SGA?

A

5HT and D2 antagonism

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20
Q

Additional properties of SGA

A
  • greater affinity at 5HT2 receptors
  • greater affinity at D4 receptors
  • mixed antagonism at alpha-adrenoceptor, H1 histamine receptors, muscarinic acetylcholine receptors and 5HT2 receptors
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21
Q

SE of olanzapine and clozapine

A

M1, H1, a1 antagonism SE

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22
Q

SE of risperidone

A

a1 (no M1 and H1)

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23
Q

Antagonism of M1 causes

A

dry mouth, blurred vision, constipation

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24
Q

Antagonism of H1 causes

A

sedation, weight gain

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25
Antagonism of a1 causes
postural hypotension, reflex tachycardia
26
What is the major SE with clozapine
agranulocytosis
27
Amisulpride MOA and SE
Selective for D2/D3 receptors → fewer SE (does not block alpha-1, H1 and M1 receptors) SE: more hyperprolactinemia (breast swelling, pain, lactation, gynaecomastia)
28
Which antipsychotics cause diabetes (and the mechanism)
clozapine, olanzapine, risperidone (less) - likely due to 5HT antagonism
29
Which antipsychotics cause weight gain (and the mechanism)
clozapine, olanzapine, risperidone (less) - likely due to H1 antagonism, a1/5HT receptor antagonism (but chlorpromazine does not induce weight gain)
30
Why do SGA produce less EPSE?
1. Potent 5HT2A receptor antagonism more than weak D2 antagonism 2. High D3 to D2 antagonism ratio (eg amisulpride) 3. High D4 to D2 antagonism ratio (eg clozapine) 4. High D2 to D1 antagonism ratio (eg amisulpride, risperidone)
31
Why do D1 antagonism cause more SE than D2 antagonism?
- blocking of postsynaptic D2 receptor → EPS - blocking of presynaptic D2 autoreceptors → prevent feedback inhibition → more dopamine released (counter the postsynaptic D2 receptor antagonism a little) - Hence: high D2 to D1 antagonism ration confer less complete blockade of dopaminergic function in the striatum
32
Additional benefits of SGA
- Some are more effective against negative sx (eg clozapine, olanzapine, risperidone) - Some may alleviate cognitive dysfunction better than FGA/ typical antipsychotics (eg clozapine, risperidone) - Some are better mood stabilisation than FGA/ typical antipsychotics (eg clozapine, olanzapine, risperidone)
33
Sx of depression
emotional (In.SAD.CAGES), loss of libido
34
Reactive depression
non-genetics, a/w life events, sx of anxiety and agitation
35
Endogenous depression
genetics involved, not directly related to external stress
36
Monoamine Theory
deficits in monoamine NT (NA, 5HT) cause depression (depression can be caused by NA, 5HT or both)
37
MOA of MAOI
inhibit MAO → prevent breakdown of monoamine → increase availability of monoamines (dopamine, NA, 5HT)
38
MAO-A vs MAO-B
- MAO-A: breakdown 5HT (less effect on NA and dopamine) - MAO-B: 5HT (less), NA, dopamine
39
Phenelzine
non-selective, irreversible MAOI
40
AE of MAOIs
1. Postural hypotension 2. Restlessness and insomnia 3. Serotonin syndrome
41
Explain cause of postural hypotension due to MAOI
due to sympathetic block produced by accumulation of dopamine in cervical neck ganglia (dopamine is an inhibitory transmitter for adrenaline)
42
Explain cause of restlessness and insomnia due to MAOI
more noradrenaline to stimulate CNS
43
Explain cause of serotonin syndrome due to MAOI
when combined with other drugs enhancing serotoninergic function (eg TCA, SSRI)
44
Sx of serotonin syndrome
hyperexcitability, increased muscle tone, myoclonus (jerking, involuntary movements), loss of consciousness
45
“cheese reaction” sx
acute HTN, severe throbbing headache, intracranial haemorrhage
46
causes of “cheese reaction”
Amines (eg tyramine) in cheese usually broken down by MAO. MAOI lead to accumulation of tyramine → sympathomimetic effect (tyramine displace NA from vesicles, increase release of NA into synapse)
47
“cheese reaction” are less likely to occur with
reversible, MAO-A inhibitor (moclobemide)
48
TCA MOA
monoamine reuptake inhibitors
49
Eg of TCA non-selective for serotonin transporter (SERT)/ NA transporter (NET)
- imipramine, amitriptyline - Second gen TCA: nortriptyline (milder SE improved compliance)
50
Eg of TCA selective for NET
desipramine
51
AE of TCA
- H1 histamine antagonism: sedation, weight gain - a1 blockade: postural hypotension (different mechanism of causing AE from MAOI) - Muscarinic antagonism (inhibit parasympathetic NS): dry mouth, blurred vision, constipation
52
Why is SSRI better than TCA?
- Greater 5HT reuptake receptor selectivity than TCA - More selective for 5HT than NA - Fewer SE than TCA (less M1, H1, a1 antagonism) → better compliance
53
Eg of SSRI
fluoxetine, citalopram
54
AE of SSRI
- nausea, insomnia, sexual dysfunction - citalopram have some histamine antagonism (sedation) - Serotonin syndrome when taken with other drugs that increase serotoninergic activity (eg MAOI) - Stronger withdrawal effects for SSRI than TCA
55
SNRI MOA
5HT and NA reuptake inhibition (similar to non-selective TCA)
56
Eg of SNRI
venlafaxine, desvenlafaxine, duloxetine
57
Advantages of SNRI
fewer AE than TCA, work slightly faster, work better in tx resistant patients
58
AE of SNRI
similar to SSRI
59
Mirtazapine MOA
NA and specific serotonin antidepressant (NaSSA) -> increase NA, 5HT
60
Bupropion MOA
norepinephrine-dopamine reuptake inhibitor (NDRI)
61
Agomelatine MOA
agonist of melatonin (also helps in sleep disorders)
62
Ketamine MOA
glutamate NMDA receptor agonists (rapid onset of antidepressant effects) - not used long term
63
Vortioxetine MOA
multimodal serotonergic antidepressants

53 Finals (10 decks)

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