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Psychiatry (Y4) > 6- Therapeutics commonly used in psychiatry (Pharmacological)) > Flashcards

6- Therapeutics commonly used in psychiatry (Pharmacological)) Flashcards

1
Q

The perfect medication in psychiatry

A
  • Has a very specific activity on receptors (or chemicals) and only in areas where those receptors (or chemicals) are clearly implicated in the cause of the psychiatric condition or the reduction of psychiatric symptoms
  • Therefore has less potential for side effects and we are able to predict effectiveness
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2
Q

in reality psychiatric medication have many side effects

A

Adrenergic/Noradrenergic:
– Sweating
– Tremor
– Headaches
– Nausea
– Dizziness
Muscarinic (Acetylcholine):
– Dry mouth, difficulty swallowing, thirst
– Difficulty urinating, urinary retention
– Hot and flushed skin. Dry skin
Histamine:
– Dry mouth
– Drowsiness
– Dizziness
– Nausea and vomiting

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3
Q

classes of psychiatric medication

A
  • Antidepressants
  • Antipsychotics
  • Anxiolytics
  • Hypnotics
  • Mood stabilisers
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4
Q

Antidepressants background

A
  • Most work on serotonin activity (and maybe other receptors) and aim to increase activity at post synaptic receptors
  • Most have most of their effect in two to three weeks – may take up to 6 weeks to have maximum effect
  • Only for the treatment of Severe or Moderate Depression, (they don’t work for mild depression)
  • Most commonly used anti-depressants are SSRI’s
  • Follow up after 2 weeks to screen for suicidal ideation
  • Other types include:
    – SNRIs
    – Mirtazapine
    – Tricyclics
    – MAOIs (I have started once in 20 years!)
  • Also used to treat anxiety
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5
Q

Selective serotonin reuptake inhibitors (SSRIs) examples

A

sertraline and citalopram most popular first line

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6
Q

SSRI indication

A
  • Moderate to severe depression
  • Panic disorders
  • Generalised anxiety
  • OCD
  • PTSD
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7
Q

MOA of SSRI

A

They work by inhibiting the reuptake of serotonin from the synaptic cleft into pre-synaptic neurones and therefore SSRIs increase the concentration of serotonin in the synaptic cleft.

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8
Q

side effects of SSRIs

A

Side effects

  • Sense of restlessness, agitation on initiation (countered by judicious use of benzodiazepines)
  • Nausea, GI disturbance
  • Headache
  • Weight changes
  • Sexual dysfunction
  • Less common – bleeding and suicidal ideation (age related)
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9
Q

contraindication to antidepressants

A

History of mania, epilepsy, cardiac disease (sertraline is the safest), acute angle-closure glaucoma, diabetes mellitus (monitor glycaemic control after initiation), concomitant use with drugs that cause bleeding, GI bleeding (or history of GI bleeding), hepatic/renal impairment, pregnancy and breast-feeding, young adults (possible
-> suicide risk), suicidal ideation.
Contraindications: Mania.

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10
Q

examples of noradrenaline and serotonin reuptake inhibitors (NSRIs)

A
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11
Q

Indication for SNRIs

A

Second or third-line
in the treatment of depression and anxiety disorders. SNRIs have
a more rapid onset of action and are more effective than SSRIs (for major depression).

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12
Q

MOA of SNRI

A

SNRIs work by
preventing the reuptake of noradrenaline and serotonin but do not block cholinergic receptors and therefore do not have as many anti-cholinergic side effects as TCAs.

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13
Q

Side effects of SNRIs

A
  • Similar to SSRIs but greater potential for sedation, nausea and sexual dysfunction
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14
Q

contraindication to SNRIs

A
  • Kidney or liver problems
  • Heart problems
  • Glaucoma
  • Epilepsy, manic episodes or bipolar
  • Pregnancy
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15
Q

tricyclic antidepressants examples

A
  • Newer: lofepramine (safest) and nortriptyline
  • Amitriptyline (less well tolerated)
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16
Q

indication of TCA

A
  • depression
  • nocturnal enuresis in children,
  • neuropathic pain (unlicensed),
  • migraine prophylaxis (unlicensed).
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17
Q

TCA background

A
  • Out of favour but reasonably effective and useful for those who do not respond to SSRI’s
  • Newer tricyclics (such as lofepramine and and nortriptyline) tolerated better than older tricyclics (amitriptyline)
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18
Q

MOA of TCA

A

TCAs work by inhibiting the reuptake of adrenaline and serotonin in the synaptic cleft. They also have affinity for cholinergic receptors and 5HT2 receptors and these contribute to side effects.

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19
Q

TCA side effects

A

Anticholinergic: dry mouth, constipation, urinary retention, blurred vision, confusion.
Cardiovascular: arrhythmias, postural hypotension, tachycardia, syncope, sweating. Hypersensitivity reactions: urticarial, photosensitivity.
Psychiatric: hypomania/mania, confusion or delirium (especially in elderly).
Metabolic: appetite and weight gain, changes in blood glucose levels. Endocrine: testicular enlargement, gynaecomastia, galactorrhoea.
Neurological: convulsions, movement disorders and dyskinesias, dysarthria, paraesthesia, taste disturbances, tinnitus.
Others: headache, sexual dysfunction and tremor.

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20
Q

TCA and overdose

A

causes QTc prolongation and arrhythmias

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21
Q

TCA complications

A

Cautions : cardiac disease, history of epilepsy, pregnancy, breast-feeding, elderly, hepatic impairment, thyroid disease, phaeochromocytoma, history of mania, psychoses (may aggravate psychotic symptoms), susceptibility to angle-closure glaucoma, history of urinary retention,

Contraindications: recent myocardial infarction, arrhythmias (particularly heart block), mania, severe liver disease, agranulocytosis.

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22
Q

Monoamine oxidase inhibitors (MAOIs) background

A
  • If changing to another antidepressant need a washout period (up to 6 weeks)
  • Should only be started by psychiatrists (in my opinion)
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23
Q

Monoamine oxidase inhibitors (MAOIs) examples

A
  • Irreversible – more dangerous: Phenelzine; Isocarboxazid
  • Reversible – less dangerous: Moclobamide; Tranylcypromine
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24
Q

Monoamine oxidase inhibitors indication

A

Third-line for depression: atypical or treatment-resistant depression. NOTE: Its use is substantially limited by toxicity, interaction with food and inferior efficacy compared to SSRIs and TCAs (see Key facts 2).
􏰀 Social phobia.

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25
Q

MOA of MOAi

A
  • MAOIs inactivate monoamine oxidase enzymes that oxidize the monoamine neurotransmitters dopamine, noradrenaline, serotonin (5-HT), and tyramine.
  • There are two main forms of MAO enzymes: MAO-A and MAO-B. Moclobemide is comparatively recent compared with the other MAOIs and binds selectively to MAO-A, therefore nullifying the need for dietary restrictions.
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26
Q

side effects of MOAis

A
  • Dry mouth.
  • Nausea, diarrhea or constipation.
  • Headache.
  • Drowsiness.
  • hypotension
  • Insomnia.
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27
Q

MAOi contraindication

A

Contraindications 􏰆 acute confusional states, phaeochromocytoma.

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28
Q

Mirtazapine background

A
  • Used to be called a NaSSA (Noradrenergic and Specific Serotonergic Antidepressant)
  • Now recognised as a class of its own
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29
Q

indication of mirtazapine

A

Often used second-line for depressed patients who would benefit from weight gain and who suffer from insomnia e.g. patients with co-morbid physical conditions.

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30
Q

mirtazapine MOA

A
  • Unique class. Acts as a 5HT-2 and 5HT-3 antagonist
  • Strong H1 (histamine) activity – hence sedation
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31
Q

Side effects of mirtazapine

A
  • Major side-effects are sedation and weight gain
  • “Side-effects” can be used to therapeutic advantage
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32
Q

Contraindication of mirtazapine

A
  • Diabetes as can make blood sugar unstable
  • Glaucoma
  • Epilepsy
  • Pregnancy
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33
Q

Vortioxetine

A

Novel antidepressant

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34
Q

vortioxetine MOA

A

Indication
- Depression with difficult to treat cognitive symptoms

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35
Q

MOA vortioexetine

A
  • All sorts of serotonergic activity
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36
Q

side effect of vortioxetine

A
  • Well tolerated
  • Most common side effect is nausea
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37
Q

syndromes associated with antidepressants

A

discontinuation syndrome
serotoin syndrome

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38
Q

discontinuation syndrome

A
  • Antidepressants are not addictive but they can be difficult to stop
    Which antidepressants to look out for:
  • Paroxetine
  • Venlafaxine
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39
Q

prevention of discontinuation syndrome

A
  • Reduce dose slowly
  • Can alternate days or snap tablets in half
  • Can sometimes switch to fluoxetine (very long half-life) and then reducing fluoxetine
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40
Q

cause of discontunation syndrome

A
  • This is influenced by half-life
  • The shorter the half-life the bigger the problem
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41
Q

presentation of discontinuation syndrome

A
  • Shakes
  • Agitation
  • Insomnia
  • Headaches
  • Irritability
  • Nausea and vomiting
  • Paraesthesia
  • Clonus
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42
Q

prognosis of discontinuation syndrome

A
  • It is very unpleasant but not life-threatening
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43
Q

Serotonin syndrome

A

Serotonin syndrome is a potentially life-threatening condition that occurs when you take medications that affect serotonin levels e.g. antidepressants

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44
Q

serotoin syndrome presentation

A
  • Very vague
  • Cognitive – headaches, agitation, hypomania, confusions, coma
  • Autonomic – shivering, sweating, hyperthermia, tachycardia, nausea and diarrhoea
  • Somatic – myoclonus, hyper-reflexia and tremor
  • Treatment usually supportive: fluids and monitoring
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45
Q

management of serotonin syndrome

A

Management
- Fluids
- Monitoring

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46
Q

things to think about when prescribing antidepressants

A
  • What has been used before?
    – If something has worked before try that one again
  • Was it effective and/or tolerated?
  • Are there particular symptoms or comorbidities you may want to address
    – Weight loss- mirtazapine
    – Insomnia- mirtazapine
    – Neuropathic pain- SNRI
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47
Q

scenarios: 1) New cases of depression with no previous treatment:

A

SSRI
- Unless major weight loss or major sleep difficulty.. in which case consider Mirtazapine
- Unless comorbid neuropathic pain.. in which case consider SNRI

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48
Q

scenarios: 2) If no effect after starting SSRI switch to a different SSRI, if still not effect switch to

A

SNRI venlafaxine or mirtazapine
- NICE would suggest that GPs should trial at least 2 antidepressants, for the minimum effective period, (usually seen as 6 weeks), unless patient needs an urgent referral to psychiatry services, (based on risk).

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49
Q

increasing the dose or switching antidepressants

A
  • Should take effect within 3 weeks -> however should wait 4 weeks before making final decision
  • NICE would suggest that GPs should trial at least 2 antidepressants, for the minimum effective period, (usually seen as 6 weeks), unless patient needs an urgent referral to psychiatry services, (based on risk).
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50
Q

dopamine theory of schizophrenia

A

The dopamine hypothesis of schizophrenia postulates that hyperactivity of dopamine D2 receptor neurotransmission in subcortical and limbic brain regions contributes to positive symptoms of schizophrenia, whereas negative and cognitive symptoms of the disorder can be attributed to hypofunctionality of dopamine D1 receptor neurotransmission in the prefrontal cortex

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51
Q

indications for antipsychotics

A
  • Treatment of schizophrenia
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52
Q

MOA of antipsychotics

A

All current antipsychotics reduce the level of dopamine activity at D2 receptors

- Target pathways
o Mesocortical
o Mesolimbic
- Unwanted affected pathways
o Nigrostriatal (movement)
o Tuberoinfundibular (HPA axis)

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53
Q

general side effects of antipsychotics

A

One of the main properties of antipsychotics is that they block dopamine receptors, in particular
D2 receptors. However, they also have an affinity for muscarinic, 5HT, histaminergic and adrenergic receptors, which explains their side effect profile:

  • Extrapyramidal side effects are more common in typical antipsychotics
  • Anti-muscarinic (‘can’t see, can’t wee, can’t spit, can’t st’) – blurred vision (can’t see), urinary retention (can’t wee), dry mouth (can’t spit), constipation (can’t st).
  • Anti-histaminergic: sedation and weight gain.
  • Anti-adrenergic: postural hypotension, tachycardia and ejaculatory failure.
  • Endocrine/metabolic -> prolactin (sexual dysfunction, reduced bone mineral density, menstrual disturbances, breast enlargement, and galactorrhoea), impaired glucose tolerance, hypercholesterolaemia
  • Neuroleptic malignant syndrome
  • Prolonged QT interval: QT interval prolongation is a particular concern with pimozide and haloperidol. There is a higher probability in any antipsychotic drug (or combination of drugs) with doses exceeding the recommended maximum. Cases of sudden death have occurred through fatal arrhythmias (e.g. torsades de pointes).
  • Clozapine has the specific side effects of hypersalivation (patients may wake up with their pillows soaking with saliva), agranulocytosis requiring special monitoring and constipation
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54
Q

severe complication of psychotics

A
  • Acute dystonia – oculogyric crisis
  • Agranulocytosis
  • Neuroleptic malignant syndrome
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55
Q

why do antipsychotics require monitoring of specific parameters

A

Important due to side effects of weight gain and dyslipidaemia

  • Baseline: FBC; Lipids; LFT; HbA1C. Weight. ECG. Blood pressure and pulse
  • Weekly: Weight in an ideal world
  • Three months: FBC; Lipids; LFT; HbA1C. Weight. ECG. Blood pressure and pulse
  • Yearly: FBC; Lipids; LFT; HbA1C. Weight. ECG. Blood pressure and pulse
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56
Q

Typical vs atypical antipsychotics

A
  • Typical older and more likely to cause extra-pyramidal side effects – remember this difference if you only remember one difference
    – Typical tend to bind more to muscarinic and histaminic receptors
  • Atypical tend to have more serotonergic activity.
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57
Q

example typical antipsychotics

A

– Haloperidol
– Chlorpromazine

58
Q

examples of atypical antipsychotics

A

(also called Second Generation Antipsychotics: SGAs):
– Clozapine –Treatment Resistant Schizophrenia
– Olanzapine
– Risperidone
– Quetiapine
– Amisulpride
– Aripiprazole – note a D2 partial agonist (not antagonist) – fewer side effects

59
Q

side effects of typical antipsychotics

A

(more likely to cause):
– Extra-Pyramidal Side Effects (EPSE’s) Including: bradykinesia, muscle stiffness and tremor; tardive dyskinesia; akathisia
– Dizziness
– Sexual dysfunction

60
Q

side effects of atypical antipsychotics

A

– Weight gain
– Dyslipidaemia and diabetes

61
Q

clozapine

A
  • First atypical antipsychotic (synthesised in 1958) used for patients in late 1960s; withdrawn by manufacturer in 1975 and not used for a decade.
  • Most efficacious antipsychotic ever!
  • Improvements can continue for several months
62
Q

extrapyramidal side effects

A

parkinsonian features

63
Q

clozapine indication

A
  • Should be used in schizophrenia after two other antipsychotics have not been effective (Treatment Resistant Schizophrenia)
64
Q

MOA of clozapine

A
  • D2 antagonist; 5HT-2 antagonist.
65
Q

MOA of clozapine

A
  • D2 antagonist; 5HT-2 antagonist.
66
Q

side effects of clozapine

A
  • Significant potential for agranulocytosis (severe leukopenia – especially neutrophils): therefore close monitoring of FBC: weekly for first 18 weeks, then fortnightly for up to a year, then monthly
  • Significant potential for gastrointestinal hypo-mobility: constipation, potentially fatal bowel obstruction
  • Other side-effects include hypersalivation and urinary incontinence.
67
Q

how to reduce risk of side effects from clozapine

A
  • Dose titrated slowly upward over two weeks and vital signs monitored due to potential for autonomic dysregulation
    treatment
68
Q

agranulocytosis

A

a deficiency of granulocytes in the blood, causing increased vulnerability to infection.
- esp neutrophils

69
Q

prevention of agranulocytosis when using clozapine

A
  • FBC checked before clozapine can be prescribed
  • to look at neutrophil count
70
Q

presentation of clozapine induced agranulocytosis

A
  • may be asymptomatic, or may clinically present with sudden fever, rigors and sore throat.
  • Infection of any organ may be rapidly progressive (e.g., pneumonia, urinary tract infection).
  • Sepsis may also progress rapidly.
71
Q

management. ofclozapine induced agranulocytosis

A
  • Stop Clozapine
  • Stop any other potentially marrow supressing drugs – e.g. Sodium Valproate
  • Avoid other antipsychotics for a couple of weeks where possible, though if needed Aripiprazole has less potential for bone marrow suppression
  • Contact Consultant Haematologist as an emergency
  • Avoid sources of infection. Consider prophylactic broad-spectrum antibiotics
  • Sometimes lithium is used to increased WCC and neutrophil count
  • Granulocyte colony-stimulating factor (G-CSF) has been used
72
Q

contraindication to antipsychotics

A

Cautions: Cardiovascular disease (an ECG may be required), Parkinson’s disease (may be exacerbated by antipsychotics), epilepsy (and other conditions predisposing to seizures), depression, myasthenia gravis, prostatic hypertrophy, susceptibility to angle-closure glaucoma, severe respiratory disease, history of jaundice, blood dyscrasias (perform blood counts if unexplained infection or fever develops).
Contraindications: Comatose states, CNS depression, phaeochromocytoma.

73
Q

Neuroleptic malignant syndrome

A

is a rare but life-threatening condition seen in patients taking antipsychotic medications. It may also occur with dopaminergic drugs (such as levodopa) for Parkinson’s disease, usually when the drug is suddenly stopped or the dose reduced.

74
Q

NMS presentation

A

Onset usually in first 10 days of treatment or after increasing dose.
Presents with pyrexia, muscular rigidity, confusion, fluctuating consciousness and autonomic
instability (e.g. tachycardia, fluctuating blood pressure). May have delirium.

75
Q

NMS death usually due to

A

o Rhabdomyolysis, renal failure, seizures
o So CK levels shoot up (blood test investigation)

76
Q

management of
NMS

A

o Emergency referral to A&E
o Stop antipsychotics
o Give benzodiazepine for acute behavioural disturbance
o Fluid resuscitation
o Reduce temperature (cooling blankets)
o Oxygen if necessary
o Rhabdomyolsis – fluids and sodium bicarbonate – alkalise the urine
o Relax muscles – first line: dantrolene or lorazepam; second line bromocriptine
o Sometimes requires an ITU bed

77
Q

NMS investigations

A

Investigations: CK (􏰁 creatinine kinase is usual), FBC (leucocytosis may be seen), LFTs
(deranged).

78
Q

complications of NMS

A

Pulmonary embolism, renal failure, shock.

79
Q

acute dystonia due to antipsychotics

A
  • Sustained, often painful, muscular spasms, producing twisted abnormal postures.
  • 50% cases in first 48 hours; 90% in first 5 days
80
Q

presentation of acute dystonia

A
  • Most common: neck; tongue; jaw; oculogyric crisis (neck arched and eyes rolled back)
81
Q

acute dystonia: oculogyric crisis

A

spasmodic movements of the eyeballs into a fixed position, usually upwards

82
Q

management of acute dystona

A
  • Stop antipsychotic
  • Administer IM or IV anticholinergics – first line is Procyclidine
  • Continue for 1 to 2 days after dystonia and consider long-term prophylactic
83
Q

what is used to treat extra pyraidal side effects (EPSEs)

A

anticholinergics

84
Q

Anticholinergics –used to treat extra pyramidal side effects (EPSEs)
x

A

Pathophysiology
* Ratio of dopamine: acetylcholine in nigrostriatal pathway more important than absolute quantities
* If there is too much acetylcholine in relation to dopamine and you cannot increase dopamine activity then — reduce acetylcholine activity by antagonising acetylcholine receptors
* Not effective for (and may exacerbate) tardive dyskinesia

Example anticholinergics
– Procyclidine – by far the most commonly used drug for EPSE. Potential for misuse
– Benzatropine
– Trihexphenidyl

85
Q

Tardive dyskinesia (TD)

A

is a condition where your face, body or both make sudden, irregular movements which you cannot control. It can develop as a side effect of medication, most commonly antipsychotic drugs.

86
Q

Tardive dyskinesia (TD)

A

is a condition where your face, body or both make sudden, irregular movements which you cannot control. It can develop as a side effect of medication, most commonly antipsychotic drugs.

87
Q

Dos and donts of antipsychotics

A
88
Q

Anxiolytics

A
  • Beta-blockers
  • Benzodiazepines
  • Pregabalin
  • Antidepressants
89
Q

Benzodiazepines indication

A

anxiety disorders, insomnia, acute status epilepticus, i

90
Q

benzos examples

A
  • Most typically used are diazepam (long half-life) and lorazepam (shorter half-life)
91
Q

MOA of benzos

A
  • Bind to GABA receptors to potentiate the effect of GABA and therefore reduce the excitability of neurones.
  • Therefore they are positive allosteric modulators of GABA receptor
92
Q

Side effects of benzodiazepines

A
  • Significant potential for tolerance and dependence
  • Significant potential for misuse
  • Use very cautiously and for no more than six weeks
  • Occasionally cause paradoxical disinhibition
93
Q

contraindications for benzos

A

myasthenia gravis, sleep apnea, bronchitis, and COPD.

94
Q

beta blockers and anxiety

A
  • Limited effectiveness for enduring anxiety disorders
  • Not often prescribed in secondary care
    usually used for symptom control e.g. palpitations
95
Q

beta blocker example

A
  • Most often used in psychiatry is Propranolol – dangerous in overdose
96
Q

MOA of beta blockers

A
  • Act by reducing autonomic nervous system activation
  • Bio-psycho-feedback
  • Often misused by performers (professional musicians, actors) and the drug of choice of snooker players
97
Q

side effects of beta blockers

A
  • cold hands and feet
  • fatigue
  • erectile dysfunction
98
Q

beta blocker contraindication

A

asthma

99
Q

pregablin

A
  • Less potential for misuse and dependence (and tolerance) than benzodiazepines – but still misused – nickname “Budweisers”
100
Q

indication of pregablin

A
  • Used in anxiety, neuropathic pain and epilepsy
101
Q

MOA of pregabalin

A

Pregabalin does not act directly on GABA-A, but rather is an inhibitor of glutamate, noradrenaline and substance-P. It is an anticonvulsant and is licensed to be used in GAD, and is also used for neuropathic pain.

102
Q

side effects of pregabalin

A
  • BNF says short term use – often used indefinitely
  • Causes sedation and can cause weight gain

Side effects include dizziness, drowsiness, blurred vision, diplopia, confusion and vivid dreams.

103
Q

hypnotics (sleeping tablets) can be

A

benzodiazepines and non benzodiazepines

104
Q

benzos used as hypnotics

A
  • Temazepam, Lormatazepam, Nitrazepam
105
Q

nonbenzos used as hypnotics

A
  • Act in a very similar way (positive allosteric modulators) but are structurally different to benzodiazepines
  • Also called Z drugs
  • Zopiclone, Zolpidem
106
Q

Z drugs

A

Include zopiclone, zolpidem and zaleplon.

They work like benzos by enhancing GABA transmission but are mainly used as hypnotics as they have shorter half-lives, reduced risk of tolerance and dependence and reduced psychomotor and hangover effects as compared to BZDs.

107
Q

hynotics signif potnetial for

A

for misuse, dependence, rebound insomnia.

108
Q

how are hypnotics taken to reduce potential for tolerance

A
  • Use for only two weeks and take for only 5 out of 7 days each week to reduce potential for tolerance
109
Q

mood stabilisers

A

Mood stabilizers are drugs that are used to prevent depression and mania in bipolar affective disorder and schizoaffective disorder.
- Lithium was the first to be discovered in the early 1950s.
- Other mood stabilizers were initially introduced as anti-epileptic drugs but later found to have therapeutic effects in patients with bipolar disorder (sodium valproate, carbamazepine and lamotrigine).

110
Q

classes of mood stabilisers

A

Used to treat treatment resistant depression and bipolar mood disorder

Come from one of the following groups
– Lithium
– Anticonvulsants
– Second Generation (Atypical) Antipsychotics

111
Q

lithium indication

A
  • Bipolar
  • Significant evidence that lithium reduces suicide – and it has a licence for reduction of self-harm
  • Also used to augment antidepressants
112
Q

MOA of lithium

A
  • Mechanism of action unknown – does all sorts of things in the brain, notably lowering noradrenaline release and increasing serotonin synthesis
113
Q

pharmacodynamics/kinetics of lithium

A
  • Narrow therapeutic window (gap between effective dose and toxic dose) so a requirement for regular serum lithium levels – weekly after dose change until level stable then 3 monthly once stable
  • Excreted by kidneys
114
Q

side effects of lithium

A

Short term

  • GI disturbance (especially on initiation), metallic taste and/or dry mouth, fine tremor, polydipsia and polyuria, weight gain

Long-term effects:
– Hypothyroidism – usually reversible
– Renal impairment – usually irreversible (and occurs most at above therapeutic doses)
– Therefore annual U&Es and TFTs

115
Q

lithium toxicity summary

A
116
Q

which anticonvulsants are used as mood stabilisers

A

– Sodium Valproate – avoid in women of child bearing age due to teratogenicity. Check LFTs before and soon after starting
– Carbamazepine – less often used
– Lamotrigine – potential for Stevens Johnson Syndrome –only for bipolar depression

117
Q

lamotrigine indication

A

Used to treat bipolar depression. It is less teratogenic than the other mood stabilizers and therefore usually the drug of choice in women of child bearing age. Lamotrigine does not treat or prevent manic episodes.

118
Q

MOA of lamotrigine

A

Lamotrigine is thought to work by inhibition of sodium and calcium channels in presynaptic neurons and subsequent stabilization of the neuronal membrane.

119
Q

side effects of lamotrigine

A

GI disturbances, rash (in around 5% of patients), headache and tremor.

BEWARE OF STEVEN JOHNSON SYNDROME

120
Q

Second Generation Antipsychotics (SGAs) in bipolar mood disorder

A
  • Quetiapine now first line treatment for bipolar – probably more to do with potential for lithium toxicity rather than better efficacy
  • All SGAs have effectiveness - so do FGA’s
  • Doses and monitoring the same as for psychosis
121
Q

soidum valproate as a mood stabiliser

A

Comparable efficacy to lithium as a mood stabilizer. If lithium (and an atypical antipsychotic) is ineffective or unsuitable in acute mania. Used in combination with lithium for rapid cycling bipolar affective disorder.

122
Q

side effect of sodium valproate

A

GI disturbances, Very fat (􏰁 weight), Aggression, LFTs 􏰁, Platelets low (thrombocytopenia), Reversible hair loss (in 10%), Oedema (peripheral), Ataxia, Tremor/Tiredness/Teratogenic, Emesis.

123
Q

side effect for sodium valproate

A

Avoid in pregnancy (can cause neural tube defects in the fetus and result in spina bifida), hepatic dysfunction and porphyria

124
Q

Second Generation Antipsychotics (SGAs) in bipolar mood disorder

A
  • Quetiapine now first line treatment for bipolar – probably more to do with potential for lithium toxicity rather than better efficacy
  • All SGAs have effectiveness - so do FGA’s
  • Doses and monitoring the same as for psychosis
125
Q

drugs used to treat ADD and ADHD

A
  • Methylphenidate
  • Dextroamphetamine
  • Atomoxetine
126
Q

Methylphenidate

A
  • most commonly prescribed
  • often given with a combination of immediate and sustained release (in the same tablet)
127
Q

dextrophetamine

A
  • Stimulants have potential for misuse and dependency
  • Monitor weight, height (in children) and pulse
128
Q

atomoxetine

A

– Noradrenaline re-uptake inhibitor
– Used according to patient preference, unable to tolerate stimulants, or (sometimes) in instances of previous drug dependence

129
Q

Drugs used for cognitive symptoms of dementia

A
  • Do not prolong life or slow down neurodegenerative changes
  • Improve cognitive and emotional/behavioural symptoms

Types
- Acetylcholinesterase inhibitors – often called cholinesterase inhibitors
- Memantine

130
Q

Cholinesterase inhibitors

A
131
Q

memantine

A
132
Q

formulation of antidepressants

A

tablets, some in liquid form, no injectables

133
Q

formulation of antipsychotics

A

– Tablets and liquid or dispersible melt in the mouth tablets
– Some short acting injections – haloperidol IM for rapid tranquilisation
– Some long acting injections – Depots given once a week to once a month

134
Q

formualtion of benzos

A

– Tablets and liquid
– Short acting injections – IM lorazepam for rapid tranquilisation

135
Q

formulation of lithium

A

tablet only

136
Q

formulation of sodium valproate

A

tabelt and liquid

137
Q

formualtion formof hypnotics

A

tabelts and liquid

138
Q

formualtion of hypnotics

A

tabelts and liquid

139
Q

formulation of promethazine

A

sedating antihistamine – tablets and IM short acting for rapid tranquilisation

140
Q

formation of procyclidine

A

tablets and short acting IM injections

Psychiatry (Y4) (15 decks)

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