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

IC8 Pharmacology II (Antipsychotics, Depression drugs) Flashcards

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
Q

Antagonism of a1 causes

A

postural hypotension, reflex tachycardia

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26
Q

What is the major SE with clozapine

A

agranulocytosis

27
Q

Amisulpride MOA and SE

A

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
Q

Which antipsychotics cause diabetes (and the mechanism)

A

clozapine, olanzapine, risperidone (less)
- likely due to 5HT antagonism

29
Q

Which antipsychotics cause weight gain (and the mechanism)

A

clozapine, olanzapine, risperidone (less)
- likely due to H1 antagonism, a1/5HT receptor antagonism
(but chlorpromazine does not induce weight gain)

30
Q

Why do SGA produce less EPSE?

A
  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
Q

Why do D1 antagonism cause more SE than D2 antagonism?

A
  • 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
Q

Additional benefits of SGA

A
  • 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
Q

Sx of depression

A

emotional (In.SAD.CAGES), loss of libido

34
Q

Reactive depression

A

non-genetics, a/w life events, sx of anxiety and agitation

35
Q

Endogenous depression

A

genetics involved, not directly related to external stress

36
Q

Monoamine Theory

A

deficits in monoamine NT (NA, 5HT) cause depression (depression can be caused by NA, 5HT or both)

37
Q

MOA of MAOI

A

inhibit MAO → prevent breakdown of monoamine → increase availability of monoamines (dopamine, NA, 5HT)

38
Q

MAO-A vs MAO-B

A
  • MAO-A: breakdown 5HT (less effect on NA and dopamine)
  • MAO-B: 5HT (less), NA, dopamine
39
Q

Phenelzine

A

non-selective, irreversible MAOI

40
Q

AE of MAOIs

A
  1. Postural hypotension
  2. Restlessness and insomnia
  3. Serotonin syndrome
41
Q

Explain cause of postural hypotension due to MAOI

A

due to sympathetic block produced by accumulation of dopamine in cervical neck ganglia (dopamine is an inhibitory transmitter for adrenaline)

42
Q

Explain cause of restlessness and insomnia due to MAOI

A

more noradrenaline to stimulate CNS

43
Q

Explain cause of serotonin syndrome due to MAOI

A

when combined with other drugs enhancing serotoninergic function (eg TCA, SSRI)

44
Q

Sx of serotonin syndrome

A

hyperexcitability, increased muscle tone, myoclonus (jerking, involuntary movements), loss of consciousness

45
Q

“cheese reaction” sx

A

acute HTN, severe throbbing headache, intracranial haemorrhage

46
Q

causes of “cheese reaction”

A

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
Q

“cheese reaction” are less likely to occur with

A

reversible, MAO-A inhibitor (moclobemide)

48
Q

TCA MOA

A

monoamine reuptake inhibitors

49
Q

Eg of TCA non-selective for serotonin transporter (SERT)/ NA transporter (NET)

A
  • imipramine, amitriptyline
  • Second gen TCA: nortriptyline (milder SE improved compliance)
50
Q

Eg of TCA selective for NET

A

desipramine

51
Q

AE of TCA

A
  • 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
Q

Why is SSRI better than TCA?

A
  • 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
Q

Eg of SSRI

A

fluoxetine, citalopram

54
Q

AE of SSRI

A
  • 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
Q

SNRI MOA

A

5HT and NA reuptake inhibition (similar to non-selective TCA)

56
Q

Eg of SNRI

A

venlafaxine, desvenlafaxine, duloxetine

57
Q

Advantages of SNRI

A

fewer AE than TCA, work slightly faster, work better in tx resistant patients

58
Q

AE of SNRI

A

similar to SSRI

59
Q

Mirtazapine MOA

A

NA and specific serotonin antidepressant (NaSSA) -> increase NA, 5HT

60
Q

Bupropion MOA

A

norepinephrine-dopamine reuptake inhibitor (NDRI)

61
Q

Agomelatine MOA

A

agonist of melatonin (also helps in sleep disorders)

62
Q

Ketamine MOA

A

glutamate NMDA receptor agonists (rapid onset of antidepressant effects) - not used long term

63
Q

Vortioxetine MOA

A

multimodal serotonergic antidepressants

53 Finals (10 decks)

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