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Year 1 > Mechanism of Psychotropic Drugs > Flashcards

Mechanism of Psychotropic Drugs Flashcards

1
Q

How can mental illness be allieviated?

A

Through lifestyle changes such as diet and exercise
Social support to reduce isolation
Psychotherapy such as CBT
Medication

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2
Q

Which pathways are dopaminergic?

A

Nigrostriatal for initiating and modulating movement
Mesolimbic for reward and reinforcement
Mesocortical for planning
TUberoinfundibular for prolactin release

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3
Q

What is the tubero-infundibular pathway?

A

Dopaminergic pathway involving the arcuate nucleus of the hypothalamus. This releases dopamine which acts on the pituitary gland to reduce the release of prolactin hormone.

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4
Q

What is the role of prolactin?

A

Hormone produced in pregnant or lactating people to induce milk production. It is also plays a role in reducing stress

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5
Q

How is dopamine metabolised?

A

By MAO or COMT enzymes

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6
Q

What are the noradrenergic neurons?

A

Locus coreleus is the prinicipal noradrenergic neuron for alertness, wakefulness and regulating REM sleep. it is activated by novel stimuli.

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7
Q

How is noradrenaline metabolised?

A

Reuptake into pre-synaptic vesicles or metabolised by MAO or COMT undergoes oxidation.

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8
Q

What are the serotenergic neurons?

A

Raphe nuclei involved in mood, emotional behaviour, feeding behaviour for satiety and sleep.

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9
Q

How is serotonin metabolised?

A

By MAO or re-uptake into pre-synaptic vesicles for oxidation into 5-hydrooxyindoleacetic acid

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10
Q

What are the GABAnergic neurons?

A

Inhibitory neurons which induce influx of Cl- for hyperpolarisation

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11
Q

What is Schizophrenia?

A

It is a mental illness which typically begins in young adult life. There are periods of relapse and remission. It is characterised by positive and/or negative symptoms and theorised to be associated with levels of dopamine in the brain.

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12
Q

What are the positive symptoms of schizophrenia?

A

These occur first and it is during an episode with hallucinations, thought disorders and delusions

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13
Q

What are the negative symptoms of schizophrenia?

A

These occur over time- lack of emotion, lack of motivation, social withdrawal and reduced speech

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14
Q

What are first-degree relatives?

A

Parents, child and full siblings

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15
Q

What contributes to Schizophrenia?

A

Hereditary links with 10% increased risk if first-degree relative has condition, environmental factors such as taking specific drugs. These lead to disruption of the grey matter in neurodevelopment and cause schizophrenia.

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16
Q

What is the dopamine hypothesis?

A

Dopamine is the main neurotransmitter implicated in schizophrenia.

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17
Q

Which drugs can cause psychosis?

A

Amphetamines, levadopa and cocaine which increase levels of dopamine in the brain.

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18
Q

What is a SPECT scan?

A

Imaging of the brain by ingesting a radioactive tracer and using gamma rays to obtain 3D image.

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19
Q

How does MAO metabolise catecholamines?

A

Deamination into DOPAX or homovanillic acd

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20
Q

What is an upstream factor?

A

Social determinants of health such as the housing, neighbourhood deprivation, employment and education level

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21
Q

What is the argument for dopamine hypothesis?

A

High levels of dopamine in PET and SPECT scans of patients with schizophrenia, psychosis induced by amphetamines, cocaine or levadopa which increases dopamine levels. Antipsychotics deplete dopamine levels and reserpine disrupts dopamine transmission and are used as treatments for schizophrenia.

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22
Q

What is the dopamine focused treatment for schizophrenia?

A

Taking antipsychotics to reduce dopamine levels or reserpine to block dopamine transmission

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23
Q

What are the argumetns against dopamine’s involvement in schizophrenia?

A

Environmental influence such as upstream factors may influence this, antipsychotics have an immediate effect on the dopamine neurotransmitter levels but it takes 2 weeks to work, other neurotransmitters may be involved such as serotonin and histamine. When symptoms worsen with schizophrenia caused by more neruodegeneration, it is associated with high levels of glutamate that causes excitotoxicity.

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24
Q

What are antipsychotics?

A

They are a treatment for schizophrenia to reduce dopamine levels by primarily targeting the D2 receptor, however they cause a range of side effects due to binding to other receptor classes. It takes weeks for improvement in condition to occur.

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25
Q

What are first generation anti-pyschotics?

A

Haloperidol which binds to both D2 and D1 receptors. It can impact the nigrostriatal pathway and lead to extrapyramidal effects because it blocks the D1 receptor and the tuberoinfundibular pathway due to reduced dopamine.

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26
Q

What is the impact of first gen anti-pyschotics on the body?

A

Greater affinity for adrenergic, histamine and serotonin receptors. It can cause sedation and extrapyramidal side effects. Increases production of prolactin, causes hypothermia and hypersensitivity

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27
Q

What are second generation anti-psychotics?

A

Risperidone which binds to D2 and D1 more weakly. It can lead to weight gain which increases the cardiovascular risk of Schizophrenic patients and also cause hypotension.

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28
Q

What is the impact of second gen anti-psychotics on the body?

A

Greater affinity for adrenergic receptors and serotonin. Less extrapyramidal and sedative side effects than haloperidol

29
Q

What is an alternative medication to first and second generation antipsychotics?

A

Clozapine is a second gen anti-psychotic- this is given to 30% of all patients because they experience tolerance to the other antipsychotics. It depletes dopamine less than first and second gen medication and targets serotonin more.

30
Q

What is an extrapyramidal effect?

A

Reduced activity of the D1 receptor leads to the reduced nigrostriatal direct pathway for modulating and repressing movement. This includes acute dystonia, akithisia and tardive dyskinesia.

31
Q

What is akithisia?

A

Restless movement

32
Q

What is acute dystonia?

A

Irregular muscle contraction, such as randomly sticking out your tongue.

33
Q

What is tardive dyskinesia?

A

Abnormal, repetitive and involuntary movements. This can persist for years after stopping medication.

34
Q

What is galactorrhoea?

A

Swelling of the mamillary gland and milk production, even when not pregnant or nursing.

35
Q

What is amenorrhoea?

A

Loss of menstruation.

36
Q

What are the side effects of anti-psychotics on the tubuloinfundibular pathway?

A

Causes infertility, galactorrhea or amenorrhoea.

37
Q

What are the metabolic side effects of antipsychotics?

A

Leads to increased weight gain, disturbances in cholesterol and disrupted glucose homeostasis leading to diabetes

38
Q

What are the cardiac side effects of anti-psychotics?

A

Increased risk of cardiovascular disease such as atherosclerosis, which is already a higher risk in schizophrenic patients

39
Q

What is neuroleptic malignant syndrome?

A

Anti-psychotic drugs causes fever and muscle stiffness.

40
Q

What is a syndrome?

A

A group of symptoms

41
Q

What is depression?

A

A syndrome characterised by a range of symptoms such as anhedonia, low activity, changes in appetite

42
Q

What is the monoamine theory of the cause of depression?

A

Depression is caused by a low availability of the monoamines catecholeamines and serotonin. Noradrenaline is responsible for sleep, food behaviour, attention and wakefullness. Serotonin is important for mood and emotion.

43
Q

Which medication can lead to depression?

A

Reserpine depletes monoamine transmission which causes depression.

44
Q

What do antidepressants do?

A

Increases the availability of monoamines

45
Q

What are the arguments for monoamine as the cause of depression?

A

Reserpine causes depression by reducing monoamine availability, antidepressants work to increase monamine availability, people with depression have lower levels of monoamines in their CSF and the blood

46
Q

What are the arguments against monoamine as the cause of depression?

A

Cocaine and amphetamine mimic the action of noradrenaline and histamine but don’t allieviate depression. Antidepressants take weeks to alleviate symptoms. Inprindole is an antidepressant that has no impact on noradrenaline or histamine uptake.

47
Q

What is inprindole?

A

An antidepressant which is a serotonin 5HT-2 antagonist. It has no effect on noradrenaline or serotonin 5-HT.

48
Q

What are the alternative theories for depression?

A

Neuronal plasticity, glutamate levels, stress and opioid misuse which increases anhedonia.

49
Q

What are the antidepressants?

A

The antidepressants increase the availability of monoamines such as serotonin and the catecholeamines.

50
Q

What is an SNRI?

A

Serotonin noradrenaline reuptake inhibitor to increase its availability.

51
Q

What are TCA drugs?

A

Tricyclic antidepressants which the availability of serotonin and noradrenaline by inhibiting the transporters for reuptake. It also acts to antagonise muscarinic and adrenergic receptors and histamine receptors.

52
Q

What is the effect of histamine antagonism?

A

Sedation

53
Q

What are the side effects of tricyclic drugs?

A

Dry mouth, hypotension and lead to drug interactions which rely on hepatic metabolism via CYP450. It potentiates the effect of alcohol and anaesthetics.

54
Q

What are the SSRIS?

A

Fluoxetine and Citalopram

55
Q

What are the side effects of SSRIS?

A

Nausea and vomiting, sexual dysfunction, interferes with drug metabolism

56
Q

What is phenelzine?

A

Non-selective irreversible MAO inhibitor

57
Q

What is moclobemide?

A

Non-selective reversible MAO inhibitor

58
Q

What is segelinine?

A

Selective inhibitor of MAO-B

59
Q

What are important considerations with MAO inhibitors?

A

Patient eating foods rich in tyramine such as cheese and dairy which can magnify the impact of catecholamines and lead to hypertensive crisis. It can interact with TCA and pethidine.

60
Q

What are the side effect of MAOS?

A

Weight gain, insomnia and hypertension.

61
Q

What is an autoreceptor?

A

Receptor on the membrane of a neuron which causes negative feedback effect when there is excessively high neurotransmitter.

62
Q

Why do anti-depressants take time to work?

A

Increased levels of serotonin or catecholeamines lead to increased activity of autoreceptors which counteract these effects. However, these become desensitised and lead to levels of serotonin and catecholeamines increasing after a few weeks.

63
Q

What is anxiety disorder?

A

Manifestation of psychological fear as physical symptoms like bowel irritation or constipation and increased heart rate and panic attacks

64
Q

How is anxiety treated?

A

Benzodiazepam, using antidepressants such as SSRIs and SNRIs

65
Q

What is benzodiazepine indicated for?

A

Anxiety and it works as a GABA agonist by binding to B-subunit

66
Q

What are the side effects of benzodiazepine?

A

Confusion, forgetfulness, impaired motor control

67
Q

What are the sleep hypnotics?

A

GABA agonists which are Z-drugs like Zoplicone and Zolpidem and benzodiazepines

68
Q

What is the effect of cocaine, amphetamines and levadopa?

A

Increases levels of dopamine and can induce psychosis. Increases levels of serotonin and noradrenaline but does not treat depression.

69
Q

What is the effect of riseperine?

A

Inhibits dopamine transmission and used as an anti-psychotic drug. Decreases levels of serotonin and noradrenaline and can be a cause of depression.

Year 1 (191 decks)

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