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Psychopharmacology Flashcards

1
Q

Is acetylcholine excitatory or inhibitory?

A

Excitatory

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2
Q

Is glutamate excitatory or inhibitory?

A

Excitatory

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3
Q

Is dopamine excitatory or inhibitory?

A

Excitatory

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4
Q

Is GABA excitatory or inhibitory?

A

Inhibitory

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5
Q

Is serotonin excitatory or inhibitory?

A

Inhibitory

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6
Q

Is noradrenaline excitatory or inhibitory?

A

Both, depending on the receptor

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7
Q

What is the mechanism of action for SSRIs?

A

Bind to the SERT (serotonin transporter) on the presynaptic neuron to inhibit the reuptake of serotonin, and increase the amount of serotonin in the synaptic cleft. This increases stimulation of post-synaptic neurons

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8
Q

What are the side effects of SSRIs?

A

Feeling agitated, shaky or anxious, feeling or being sick.
indigestion, diarrhoea or constipation

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9
Q

What are some examples of SSRIs?

A

Fluoxetine, paroxetine, citalopram, sertraline

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10
Q

What is the mechanism of action of SNRIs?

A

Bind to the SERT and NAT (noradrenaline transporter) on the presynaptic membrane to inhibit their uptake, and increase the amount of neurotransmitter in the synaptic cleft

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11
Q

What are the side effects of SNRIs?

A

Feeling agitated, shaky or anxious.
feeling or being sick.
indigestion, diarrhoea or constipation

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12
Q

What are some examples of SNRIs?

A

Venlafaxine, duloxetine

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13
Q

What are the side effects of TCA antidepressants?

A

Blocks muscarinic receptors too - dry mouth,
slight blurring of vision, constipation, problems passing urine, drowsiness, dizziness, weight gain

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14
Q

What is the mechanism of action of TCA anti-depressants?

A

Bind to the SERT and NAT (noradrenaline transporter) on the presynaptic membrane to inhibit their uptake, and increase the amount of neurotransmitter in the synaptic cleft

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15
Q

What are some examples of TCA antidepressants?

A

Lofepramine, amitriptyline

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16
Q

What is the mechanism of action of monoamine oxidase inhibitor anti-depressants?

A

Inhibit the action of mono-amine oxidase enzymes (MAO-A and MAO-B), to reduce the breakdown of mono-amine neurotransmitters and increase their availability for post synaptic transmission
MOA-A breaks down serotonin, dopamine, melatonin, adrenaline and noradrenaline, so these are increased

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17
Q

What are some examples of MAOI anti-depressants?

A

Phenelzine

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18
Q

What is the mechanism of action of NaSSA antidepressants? (noradrenergic and specific serotonergic)

A

Antagonises the adrenergic alpha2-autoreceptors in the presynaptic neuron membrane – these receptors inhibit exocytosis of adrenaline or noradrenaline, so antagonising them increases exocytosis of the NTs.
It also blocks 5-HT2 and 5-HT3 receptors in certain areas to prevent serotonergic transmission in unwanted areas, which can limit side effects of SSRIs

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19
Q

What are some examples of NaSSA antidepressants?

A

Mirtazapine

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20
Q

What is the mechanism of action for serotonin antagonists and reuptake inhibitors (SARIs)

A

Inhibits the reuptake of serotonin and antagonises 5-HT-2A receptors, H1 receptors, and alpha-1-adrenergic receptors.

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21
Q

What is an example of a SARI antidepressant?

A

Trazodone

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22
Q

What is the mechanism of action of anti-convulsants for anxiety?

A

Inhibits release of excess excitatory neurotransmitters like glutamate by binding to the widely distributed voltage-dependent calcium channels in the overexcited neurons of the brain and spinal cord

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23
Q

What are the side effects of anticonvulstants?

A

Drowsiness, dizziness, increased appetite and weight gain, blurred vision, headaches, dry mouth, vertigo. Because they lower nerve cell excitability, they can also affect normal activity, leading to problems with thinking, remembering, paying attention or concentrating

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24
Q

What is an example of an anti-convulsant used for anxiety?

A

Pregabalin

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25
Q

What is the mechanism of action of benzodiazepines used for anxiety?

A

Benzos enhance the activity of the inhibitory neurotransmitter GABA by facilitating it’s binding to GABA receptors, producing a sedative effect

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26
Q

What are the side effects of benzodiazepines for anxiety?

A

Drowsiness, difficulty, concentrating, headaches, vertigo, an uncontrollable shake or tremble in part of the body (tremor) , low sex drive

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27
Q

What are some examples of benzodiazepines used for anxiety?

A

Usually diazepam

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28
Q

What is the function of the mesolimbic dopaminergic pathway and where does it travel from and to?

A

Reward pathway, transmitting dopmaine from the ventral tegmental area to the ventral striatum

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29
Q

What is the function of the mesocortical dopaminergic pathway and where does it travel from and to?

A

Cognition and emotion, transmitting dopamine from the VTA to the prefrontal cortex

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30
Q

What is the function of the nigrostriatal dopaminergic pathway and where does it travel from and to?

A

Movement regulation, transmitting from the substantia nigra in the midbrain to the caudate nucleus and putamen in the dorsal striatum

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31
Q

What is the function of the tuberoinfundibular dopaminergic pathway and where does it travel from and to?

A

Regulates secretion of pituitary hormones, transmitting from the infundibular nucleus of the hypothalamus

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32
Q

What causes positive symptoms in schizophrenia?

A

Hyperactivity of dopamine D2 receptorsin the subcortical and limbic brain regions

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33
Q

What causes negative symptoms in schizophrenia?

A

Negative symptoms, such as flattened affect, are attributed to thehypoactivity of the dopamine D2 receptorsin the mesocortical pathway

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34
Q

What are the extrapyramidal side effects of antipsychotics and which type are they most common with

A

Acute Dystonia
Akathisia
Parkinsonism
Tardive dyskinesia
(ADAPT)

35
Q

What are the common signs of neuroleptic malignant syndrome?

A

Triad of fever, muscle rigidity and altered mental status (drowsiness, agitation, confusion, delirium, coma), as well as autonomic dysfunction (labile BP, tachypnoea, tachycardia, sweating and flushing)

36
Q

What are the signs of anticholinergic toxicity?

A

Flushing (from vasodilation), anhidrosis (dry mucous membranes, not sweating), mydriasis, altered mental status (delirium, hallucinations, agitation, restlessness, confusion), fever, urinary retention, tachycardia, arrhythmias

37
Q

What is the mechanism of action of first generation antipsychotics?

A

Inhibition of D2 dopaminergic receptors in the mesolimbic pathway of the brain, leading to a decrease in the incidence of positive symptoms. They also have noradrenergic, cholinergic and histaminergic blocking properties.

38
Q

What are some examples of common cholinergic side effects of typical antipsychotics?

A

Dry skin, blurred vision, tachycardia, constipation, vomiting, sedation (due to antihistamine effects),

39
Q

What are some examples of first generation antipsychotics?

A

Haloperidol, droperidol, fluphenazine, chlorpromazine, prochlorperazine, loxopine

40
Q

What is the mechanism of action of second generation antipsychotics?

A

Inhibition of D2 dopamine receptors in the mesolimbic pathway of the brain, leading to a decrease in the incidence of positive and negative symptoms. This is as well as serotonin receptor (5-HT2A) antagonist action

41
Q

Is QTc prolongation more of a concern with first or second generation antipsychotics?

A

Second generation

42
Q

Are extrapyramidal side effects more common in first or second generation antipsychotics?

A

First generation

43
Q

What are some common or dangerous side effects of clozapine?

A

Common: hypersalivation, tachycardia, hypotension, constipation
Serious: agranulocytosis and leukopenia, bowel ileus/obstruction, lower seizure threshold, myocarditis/cariomyopathy

44
Q

What are some examples of second generation antipsychotics?

A

Olanzapine, quetiapine, clozapine, risperidone, Iloperidone, aripiprazole

45
Q

What are the signs of lithium toxicity?

A
  • Nausea, vomiting, tremor, fatigue (mild)
  • Confusion, agitation, delirium, tachycardia, hypertension (moderate)
  • Coma, seizures, hyperthermia, hypotension (severe)
46
Q

What are the theorised mechanisms of action of lithium?

A

It’s not well understood, but it’s thought that it either interferes with inositol triphosphate formation or cAMP formation

47
Q

What are the types of lithium?

A

Lithium carbonate, lithium citrate

48
Q

What anticonvulsants are used as mood stabilisers?

A

Carbamazepine, lamotrigine, valproate

49
Q

What antipsychotics are used as mood stabilisers?

A

Haloperidol, olanzapine, quetiapine, risperidone

50
Q

For how long should antidepressants be continued before stopping, to reduce the risk of relapse?

A

Antidepressants should be continued for at least 6 months after remission of symptoms to decrease risk of relapse

51
Q

How long do antidepressants take to work?

A

between 3-6 weeks, but may be as quick as 1 week or as long as 3 months

52
Q

What foods should patients on MOAIs (phenelzine) avoid and why?

A

Cheese - it can cause a hypertensive crisis. Remember, MAOuses like cheese!

53
Q

Which atypical antipsychotic has the most favourable side effect profile?

A

Aripiprazole - especially for prolactin related symptoms like gynaecomastia

54
Q

What is the most common side effect of atypical antipsychotics like olanzapine?

A

Weight gain

55
Q

What is the potential risk of an SSRI+NSAID?

A

GI bleed - prevented with a PPI

56
Q

When should lithium levels be checked?

A

7 days after initiation/change, the sample should be taken 12 hours post-dose

57
Q

How is alcohol withdrawal managed in people with liver cirrhosis/hepatic impairment?

A

Lorazepam - chlordiazepoxide is metabolised extensively by the liver and has a longer half-life than lorazepam

58
Q
A
59
Q

How do ACh inhibitors like donezapil and rivastigmine help in dementia?

A

Acetylcholinesterase inhibitors inhibit breakdown of ACh in synapses to boost ACh in the synpase, which stabilises deterioration for a year or 18 months (but doesn’t slow progression)

60
Q

What is a side effect of TCAs?

A

Urinary retention, dry mouth, blurred vision, drowsiness, constipation etc. due to antimuscarinic effects

61
Q

What are the metabolic side effects of antipsychotics?

A

Metabolic side effects of antipsychotics include dysglycaemia, dyslipidaemia, and diabetes mellitus

62
Q

What medications should be avoided in patients taking an SSRI?

A

Triptans (or anything that increases serotonin)

63
Q

Which psychiatric drug causes hyperparathyroidism?

A

Long-term lithium use can result in hyperparathyroidism and resultant hypercalcaemia

64
Q

Which SSRI is most likely to lead to QT prolongation

A

Citalopram

65
Q

What is the mechanism of action of methadone and buprenorphine in supporting opioid addicts?

A

Binds and agonises opioid receptors to reduce side effects and prevent cravings

66
Q

What is the mechanism of action of naltrexone in supporting opioid addicts?

A

It binds and antagonises opioid receptors, blocking the effect of opioids and preventing intoxication in former opioid addicts

67
Q

How is acute dystonia managed?

A

Procyclidine

68
Q

What medication should SSRIs not be prescribed with, and why?

A

Triptans, increases risk of serotonin syndrome

69
Q

When should patients <25 be reviewed after starting an SSRI and why?

A

Patients ≤ 25 years who have been started on an SSRI should be reviewed after 1 week

70
Q

What are some side effects of NaSSA antidepressants?

A

Sedation, increased appetite (this is why mirtazapine is good for people who can’t sleep or who are losing weight)

71
Q

Which SSRI is preferred in children and adolescents?

A

Fluoxetine is the SSRI of choice in children and adolescents

72
Q

Which SSRI is most likely to lead to QT prolongation and Torsades de pointes?

A

Citalopram

73
Q

Which antipsychotic has the most tolerable side effect profile?

A

Aripiprazole (especially for prolactin elevation-related side effects)

74
Q

How is tardive dyskinesia managed?

A

Tetrabenazine

75
Q

Which 2 antidepressants should never be prescribed together, and why?

A

SSRIs and MAOIs should never be combined as there is a risk of serotonin syndrome

76
Q

What are the side effects of TCAs?

A

Dry mouth, constipation, blurred vision (anticholinergic) and weight gain and drowsiness (antihistaminic) are side effects of TCAs

77
Q

What is the MOA of TCAs?

A

Serotonin (5-HT): This neurotransmitter has a pivotal role in mood regulation. Inhibition of its reuptake leads to increased concentrations in the synaptic cleft, enhancing serotonergic neurotransmission.
Noradrenaline (NA): Similar to 5-HT, blocking the reuptake of NA increases its synaptic cleft concentration, intensifying noradrenergic neurotransmission.

78
Q

What monitoring do SNRIs need?

A

BP - NICE recommend that all patients have their blood pressure monitored at initiation and each dose titration of venlafaxine.

79
Q

What monitoring does citalopram need?

A

ECG as it can cause QT prolongation

80
Q

What are the side effects of lithium?

A

Leucocytosis
Increased urine output
Tremor (fine)
Hypothyroid
Increased weight gain
Upset stomach (diarrhoea)
Mum’s beware (Ebstein anomaly)

81
Q

What are the symptoms of neuroleptic malignant syndrome?

A

Fever
Autonomic dysfunction
Rigidity (lead pipe rigidity)
Mental status altered

82
Q

What is the acronym to remember the symptoms of serotonin syndrome?

A

MAN
Mental status changes
Autonomic hyperactivity (hyperthermia, hypertension, tachy)
Neuromuscular abnormalities (clonus)
GI symptoms (diarrhoea, N/V, abdominal pain)

83
Q

What blood results are seen in neuroleptic malignant syndrome

A

Elevated CK, elevated WCC

84
Q

How is NMS managed?

A

Stop the offending antipsychotic, correct electrolyte imbalances and volume deficits, give dopamine agonists (bromocriptine)

Drugs (5 decks)

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