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PSYCHIATRY > PPT - DEPRESSION + ANXIETY > Flashcards

PPT - DEPRESSION + ANXIETY Flashcards

1
Q

What are examples of SSRIs?

A

Citalopram
Escitalopram
Fluoxetine
Sertraline
Paroxetine
Dapxetine
Dapoxetine
Fluvoxamine
Vortioxetine

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2
Q

What are the indications for SSRIs?

A

Depression
GAD
OCD
Panic disrder
Severe phobic disorders
Bulimia
PTSD

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3
Q

What are contraindications for all SSRIs?

A

Poorly controlled epilepsy
Manic phase of bipolar disorder

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4
Q

What are additional contraindications for citalopram and escitalopram?

A

Known QR interval prolongation
Concurrent use of drugs known to prolong QT interval

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5
Q

Whats an additional contraindication of sertraline?

A

Severe hepatic impairment

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6
Q

Whats the moa of SSRIs?

A

They block the serotonin transporter which prevents serotonins re uptake from the simpatico space, therefore increasing its availability

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7
Q

What are examples of monoamine uptake inhibitorS?

A

TCAs
SSRIs
SNRIs

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8
Q

Outline the chronic adaptive changes seen with SSRIs?

A

On acute administration, one would expect inhibition of serotonin reuptake to increase the level of 5-HT at the synapse. However, the increase has been observed to be less than expected.
This is because increased activation of 5-HT1A receptors on the soma and dendrites of raphe neurons inhibits these neurons and thus reduces 5-HT release, thus cancelling out to some extent the effect of inhibiting reuptake into the terminals.
On prolonged drug treatment, the elevated level of 5-HT in the somatodendritic region desensitises the 5-HT1A receptors, reducing their inhibitory effect on 5-HT release from the nerve terminals. The need to desensitise somatodendritic 5-HT1A receptors could thus explain in part the slow onset of antidepressant action of 5-HT uptake inhibitors.

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9
Q

Why are SSRIs first-line for depression treatment?

A

Less likely than other antidepressants to cause anticholinergic SE and less dangerous in overdose
Do not cause ‘cheese reactions’ like MAOIs
Less sedative
Less cardiotoxic than TCAs

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10
Q

Whats the half life of SSRIs?

A

Most have half lives of 18-24 hours
Fluoxetine is longer acting with a half life of 24-96 hours

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11
Q

Which SSRIs should not be given concurrently with TCAs and why?

A

Fluoxetine, fluvoxamine and paroxetine
They may increase TCA plasma levels and cause toxicity

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12
Q

What is 5HT1A?

A

A subtype of serotonin receptor located in presynaptic and postsynaptic regions
Upon activation they inhibit firing of 5HT neurons

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13
Q

What are some cardiac adverse effects of SSRIs?

A
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14
Q

Whats the most widely used SSRI for CVD patients?

A

Sertraline - free of Cardiotoxicity

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15
Q

What are possible adverse effects of SSRIs?

A

Most common - GI disturbance at start of treatment , anxiety and agitation early on, loss of appetite and weight loss, insomnia, sweating, sexual dysfunction

Cardiac - palpitations, QT prolongation, rarely tachycardia
GI - reduced appetite, d+v+n, dry mouth, abdominal pain, constipation, altered taste, weight changes
CNS - headache, dizziness, drowsiness, tinnitus, paraesthesia, tremor, sleep disorders, visual impairment, convulsions and movement disorders
Psychiatric - insomnia, agitation, confusion, reduced concentration, anxiety, memory loss, depersonalisation
Skin - rash, hyperhidrosis, Alopecia, pruritus, photosensitivity reaction
Other - haemorrhage, menstrual cycle irregularities, sexual dysfunction, myalgia, urinary disorders, hyponatraemia, SIADH
Serotonin syndrome

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16
Q

What are the signs of serotonin syndrome?

A

Confusion, delirium, shivering, tachycardia, anxiety, agitation, sweating, major changes in blood pressure, diarrhoea, and muscle twitching

Severe - seizures, arrhythmias and unconcious

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17
Q

When may serotonin syndrome occur?

A

when combinations of serotonergic antidepressants are prescribed; most severe cases of serotonin syndrome involve an MAOI (including moclobemide) and an SSRI.
Remember st Johns wort can raise levels of serotonin when combined with SSRI
Ecstacy and amphetamines also increase the risk

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18
Q

What are signs of hyponatraemia?

A

Dizziness, drowsiness, confusion, nausea, muscle cramps, or seizures, reduced appetite

Severe - disorientation, agitation, psychosis and fits, coma

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19
Q

What are side effects specific to citalopram or escitalopram?

A

Torsades de pointes

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20
Q

What are some possible drug interactions associated with SSRIs?

A

Antiepileptics
Antidiabetic drugs
Aspirin, NSAIDs, anticoagulants, antiplatelets
Carbamazepine
Cocaine
Grapefruit juice
HIV protease inhibitors
Lithium
MAOIs
SNRIs
Tamoxifen
Other sedative drugs
Opioids, St. John’s wort, Triptans
Drugs which can cause QT interval prolongation
Drugs which are associated with hyponatraemia

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21
Q

What should be prescribed if a patient is taking SSRIs and NSAIDs and why?

A

A proton pump inhibitor due to the increased risk of GI bleeding

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22
Q

What are the most favoured SSRIs?

A

Sertraline and escitalopram

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23
Q

What have NICE suggested doing when choosing SSRI for people who also have a chronic physical health problem?

A

Using citalopram or sertraline as they have a lower propensity for interaction

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24
Q

How should we treat depression when a pt is on warfarin, heparin or aspirin?

A

Use mirtazapine and avoid SSRI
SSRIs inhibit its metabolism so increase the risk of bleeding

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25
Q

How should pts be monitoring following the initiation of SSRIs?

A

patients should normally be reviewed by a doctor after 2 weeks.
For patients under the age of 30 years or at increased risk of suicide they should be reviewed after 1 week.
Try for at least 4-6 weeks before considering trying another antidepressant
If a patient makes a good response to antidepressant therapy they should continue on treatment for at least 6 months after remission as this reduces the risk of relapse.

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26
Q

Which antidepressant is the drug of choice for children?

A

Fluoxetine

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27
Q

Why should citalopram and escitalopram not be used in those with congenital long QT syndrome; known pre-existing QT interval prolongation; or in combination with other medicines that prolong the QT interval?

A

They are associated with dose-dependent QT interval prolongation

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28
Q

What should a pt be warned about when starting an SSRI or changing a dose?

A

It may take a few weeks to start seeing any efferent
Young people under 25 are particularly at risk of sundial thoughts after starting antidepressants
May cause agitation and anxiety in the first few weeks

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29
Q

How should SSRIs be stopped?

A

The dose should gradually be reduced over a 4 week period.
Not for fluoxetine due to its long half life

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30
Q

What are some SSRI discontinuation symptoms?

A

Flu-like symptoms
Insomnia
Nausea and other GI upset
Imbalance
Sensory disturbances e.g. electric shock
Hyperarousal

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31
Q

What are the risks of using SSRIs during pregnancy?

A

During the first trimesters there is a small increased risk of congenital heart defects
Using in the third trimester can result in persistent pulmonary hypertension of the newborn
Paroxetine has an increased risk of congenital malformations, particularly during the first trimester

All small risks and generally considered an option during pregnancy

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32
Q

What is serotonin syndrome?

A

A potentially life-threatening disorder characterised by altered mental status, autonomic hyperactivity and neuromuscular abnormalities

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33
Q

What causes serotonin syndrome?

A

increased serotonergic activity in the central nervous system (CNS) that can be induced by a range of medications that increase serotonergic transmission by altering the neurotransmitter serotonin.
Use of amphetamines, MDMA, cocaine, SSRI, SNRI, MDMA, TCA, MAOI, Buspiron, Triptans and lithium

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34
Q

What causes the most serious form of serotonin syndrome?

A

SS secondary to the use of monoamine oxidase inhibitors is usually more severe and can be fatal.

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35
Q

What are the signs of serotonin syndrome?

A

The typical neuromuscular findings in SS are usually more pronounced in the lower limbs.

Dilated pupils
Flushed skin, diaphoresis
Tachycardia, hypertension
Hyperthermia (>38.0º)
Hyperreflexia
Clonus: repeated, rhythmic contractions
Myoclonus: sudden jerky or spastic contraction
Rigidity
Bilateral upgoing plantars (Babinski sign)

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36
Q

What is the hunter criteria?

A

SS can be diagnosed in a patient taking a serotonergic agent (e.g. SSRI) and presents with one of the following features:
- Spontaneous clonus
- Inducible/ocular clonus and agitation or diaphoresis
- Tremor and hyperreflexia
- Hyperthermia, hypertonia, and ocular/inducible clonus

Serotonin toxicity diagnosis

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37
Q

How do we manage serotonin syndrome?tre

A

Stop serotonergic agent
supportive including IV fluids
benzodiazepines to control agitation
more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazines

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38
Q

What are some complications of serotonin syndrome?

A

Cardiac arrest
Cardiac arrhythmias
Acute kidney injury
Rhabdomyolysis
Disseminated intravascular coagulation
Seizures
Respiratory failure
Venous thromboembolism

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39
Q

How might antiepileptics interact with SSRIs?

A

SSRIs can reduce the seizure threshold

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40
Q

How might antidiabetic drugs interact with SSRIs?

A

SSRIs can affect diabetic control so monitor blood glucose when starting or stopping SSRI

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41
Q

How might carbazmazepine interact with SSRIs?

A

May reduce levels of sertraline

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42
Q

How might cocaine interact with SSRIs?

A

May increase risk of bleeding with citalopram

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43
Q

How might grapefruit juice interact with SSRIs?

A

May modestly increase sertraline levels

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44
Q

How might HIV protease inhibitors interact with SSRIs?

A

They may reduce the efficacy of SSRIS

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45
Q

How might lithium interact with SSRIs?

A

May cause serotonin syndrome or NMS
Lithium can cause QT prolongation so concomitant use may increase this risk

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46
Q

How might MAOIs interact with SSRIs?

A

Serotonin syndrome of NMS

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47
Q

How might SNRIs interact with SSRIs?

A

Risk of serotonin syndrome or NMS
Venlafaxine may also increase risk of QT interval prolongation

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48
Q

How might tamoxifen interact with SSRIs?

A

Avoid concurrent use with fluoxetine or paroxetine as these may reduce plasma concentration of tamoxifen = reduced efficacy

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49
Q

How might sedative drugs interact with SSRIs?

A

SSRIs are sedating so co-administration may have a synergistic effect

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50
Q

why can SSRIs cause hyponatraemia?

A

As they can cause SIADH which leads to hyponatraemia
Particularly in elderly pt

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51
Q

What are examples of SNRIs?

A

Duloxetine
Venlafaxine
Desvenlafaxine

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52
Q

Which SNRI is available in a slow release formulation and why is this useful?

A

Venlafaxine
As it can reduce the incidence of nausea

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53
Q

What are the indications of venlafaxine?

A

Depressive disorder
GAD
Social anxiety disorder
Panic disorder
Menopausal symptoms in women with breast cancer - particularly hot flushes

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54
Q

What are the indications of duloxetine?

A

Depressive disorder
GAD
Diabetic neuropathy
Mod-sev stress urinary incontinence

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55
Q

What is desvenalafaxine?

A

The major active metabolite of venlafaxine

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56
Q

What are the common SE of SNRIs?

A

Headache
Insomnia
Sexual dysfunction
Dry mouth
Dizziness
Sweating
Decreased appetite
(Largely due to enhanced activation of adrenoreceptors)

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57
Q

What are common symptoms of SNRI overdose?

A

CNS depression
Serotonin toxicity
Seizure
Cardiac conduction abnormalities

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58
Q

What are the contraindications of duloxetine?

A

Those with hepatic impairment as it can cause hepatic toxicity

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59
Q

Whats the moa of bupropion?

A

Inhibits noradrenaline and dopamine uptake
Does not induce euphoria like cocaine and doesnt have an abuse potential

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60
Q

What are the indications of bupropion?

A

To aid smoking cessation in combination with motivational support in nicotine-dependent patients

Unlicensed uses - anti-depressant-induced sexual dysfunction, ADHD, depression associated with bipolar disorder, and obesity

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61
Q

Whats the warning that comes with bupropion?

A

Risk of serotonin syndrome with use with other serotonergic drugs

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62
Q

What are the indications of atomoxetine?

A

ADHD

sometimes used off-label to treat adult patients with treatment-resistant depression.

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63
Q

Whats the moa of atomoxetine?

A

Highly selective inhibitors of noradrenaline uptake

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64
Q

What are examples of tricyclic antidepressants?

A

Imipramine
Desipramine
Amitriptyline
Nortriptyline
Clomipramine

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65
Q

Whats the moa of TCAs?

A

block the uptake of amines by nerve terminals, by competition for the binding site of the amine transporter
Most TCAs inhibit noradrenaline and 5-HT uptake but have much less effect on dopamine uptake.

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66
Q

Why do TCAs have so many unwanted effected?

A

As in addition to their effects on amine uptake, most affect other receptors including muscarinic ACh receptors, histamine and serotonin receptors

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67
Q

What side effects do TCAs cause?

A

Cardiac - tachycardia, palpitations, arrhythmias, AV block, bundle branch block, QT prolongation, hypertension, MI, sudden cardiac death
Vision - accommodation disorder, Mydriasis and blurred vision
GI - dry mouth, reduced apparition, altered taste, constipation, N+d+v, abdo pain, paralytic ileus and weight changes
CNS - tremor, dizziness, reduced concentration, confusion, headache, drowsiness, speech disorders, movement disorders, peripheral neuropathy, seizure, sleep disorders, tinnitus
Psychiatric - aggression, confusion, anxiety, agitation, delirium, hallucinations, suicidal behaviours
Skin - skin reactions, Alopecia, facial oedema, photosensitivity reactions
Others - bone marrow depression, gynaecomastia, hyperhidrosis, hyponatraemia, NMS, sexual dysfunction, thrombocytopenia and urinary disorders

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68
Q

What are the most common TCA side effects?

A

Anti muscarinic effects - dry mouth, blurred vision, constipation, urinary retention
Alpha-adrenergic receptor blockade - postural hypotension
Histaminergic receptor blockage - weight gain and sedation
Cardiotoxic effects - QTc prolongation, ST elevation, heart block and arrhythmias

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69
Q

What effects would TCAs have in non-depressed humans?

A

Sedation
Confusion
Motor incoordination
(Effects also occur in depressed pt in the first few days of treatment but wear off in first 1-2 weeks)

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70
Q

What are the contraindications of TCAs?

A

Recent MI, arrhythmias, severe liver disease and mania
With acute porphyrias (lofepramine).

Others:
With heart block.
With severe renal impairment (lofepramine).
Taking a monoamine oxidase inhibitor (MAOI).

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71
Q

Why do you have to be wary when taking TCAs with antipsychotic drugs or steroids?

A

As TCAs rely on hepatic metabolism by CYP450
But these can be inhibited by competing drugs e.g. antipsychotics and steroids
= reduced metabolism = increased toxicity

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72
Q

What are the effects of TCAs with alcohol/anaesthetic agents?

A

TCAs can potentiates their effects and deaths have occurred as a result of this
I.e. severe resp depression after drinking on TCAs

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73
Q

What are the dangers with TCAs?

A

Dangerous in overdose.
Narrow therapeutic index
Commonly used in suicide attempts
Can cause convulsions, coma, respiratory depression
Cardiac dysrhythmias and sudden death may occur from VF

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74
Q

Why may side effects develop slowly with TCAs?

A

As half lives are generally long, ranging from 10-20hours and can be even longer in elderly pt
Gradual accumulation is possible leading to slowly developing Sid effects

75
Q

How should any antidepressant drug be monitored?

A

Patients should be reviewed every 1–2 weeks at the start of antidepressant treatment. Treatment should be continued for at least 4 weeks (6 weeks in the elderly) before considering whether to switch antidepressant due to lack of efficacy. In cases of partial response, continue for a further 2–4 weeks (elderly patients may take longer to respond).

Following remission, antidepressant treatment should be continued at the same dose for at least 6 months (about 12 months in the elderly), or for at least 12 months in patients receiving treatment for generalised anxiety disorder (as the likelihood of relapse is high). Patients with a history of recurrent depression should receive maintenance treatment for at least 2 years.

76
Q

Which antidepressants are most likely to cause hyponatraemia?

A

All types have an association. More common in elderly and possible due to SIADH
Repotted most frequently with SSRIs

77
Q

What are second line options for managing depression?

A

A different SSRI or mirtazapine
SNRI
?augmenting agent
(TCAs for more severe forms and MAOIs only prescribed by specialists)
ECT in severe refractory depression

78
Q

Whats drugs should be used for GAD?

A

SSRI
SNRI

79
Q

Whats drugs should be used for panic disorder?

A

SSRIs
SNRI

80
Q

Whats drugs should be used for OCD and PTSD and phobic states?

A

SSRIs

81
Q

What is clomipramine most selective for?

A

Serotonergic transmission

82
Q

What is imipramine most selective for?

A

Nor adrenergic transmission

83
Q

Who might we give TCAs with sedative properties to?

A

Those who are agitated and anxious
Not withdrawn and apathetic pt

84
Q

What are the TCAs with sedative properties?

A

Amitriptyline
Clomipramine

85
Q

What are the TCAs with less sedative properties?

A

Imipramine
Lofepramine
Nortriptyline

86
Q

What are the pros and cons of lofepramine (TCA)?

A

Lower incidence of SE and less dangerous in overdose
Infrequently associated with hepatic toxicity

87
Q

What are the pros and cons of imipramine (TCA)?

A

Well established but more marked antimuscarinic SE than other TCAs

88
Q

What are the pros and cons of amitryptiline (TCA)?

A

Effective but particularly dangerous in overdose and so are not recommended for treatment of depression

89
Q

When and how often are TCAs taken?

A

Once a day usually at night
(Long half life)

90
Q

Whats the STOPP criteria?

A

Screening Tool of Older Person’s potentially Inappropriate prescriptions

evidence-based criteria used to review medication regimens in elderly people.

91
Q

Whats the STOPP criteria for TCAs?

A

if prescribed in those with dementia, narrow angle glaucoma, cardiac conduction abnormalities, prostatism, or history of urinary retention - risk of worsening these conditions

if initiated as first-line antidepressant treatment - higher risk of adverse drug reactions than with SSRIs or SNRIs

92
Q

What are some possible drug interactions associated with TCAs?

A

Clonidine
Lithium
MAOIs
Other sedative drugs
Phenothiazines
SSRIs and SNRIs
Tramadol
Warfarin
Drugs which prolong QT interval

93
Q

How might TCAs interact with clonidine?

A

Antihypertensive effects of clonidine may be reduced by TCAs
Monitor bp and adjust dose of hypertensive if required

94
Q

How might TCAs interact with lithium?

A

Concurrent use with TCA may cause neurotoxicity, serotonin syndrome or NMS
Also both drugs have been associated with QTc prolongation or torsades de pointes

95
Q

How might TCAs interact with MAOI?

A

Risk of serotonin syndrome

96
Q

How might TCAs interact with phenothiazine?

A

Concentrations of both drugs may be increased
Increasing risk of tardive dyskinesia and antimuscarinic adverse effects
Risk of QT interval prolongation
If have to be take together, consider ECG monitoring

97
Q

How might TCAs interact with SSRI/SNRIs?

A

TCA concentrations my be increased leading to adverse effects
SSRI and SNRI associated with QT interval prolongation so maybe increased risk of arrhythmias

98
Q

How might TCAs interact with Tramadol?

A

Increases risk of SS

99
Q

How might TCAs interact with warfarin?

A

TCAs may affect prothrombin time

100
Q

What drugs may increase levels of TCAs?

A

Antifungal
Bupropion
Cimetidine
Diltiazem
Verapamil
HIV protease inhibitors

101
Q

What drugs may reduce levels of TCAs?

A

Carbamazepine
Phenobarbital
Rifampicin

102
Q

What are TCAs widely used for?

A

Treatment of neuropathic pain as smaller doses are typically required compared with treatment for depression

103
Q

Which TCAs are particularly dangerous in overdose?

A

Amitriptyline and dosulepin

104
Q

What are the features of TCA overdose?

A

Early features relate to anticholinergic properties - dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision

Arrhythmias, seizures, metabolic acidosis, coma

105
Q

What can ECG tell us about TCA overdose?

A

ECG changes include:
sinus tachycardia
widening of QRS
prolongation of QT interval

Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

106
Q

How do we manage TCA overdose?

A

IV bicarbonate (if QRS interval >100msec or a ventricular arrhythmia)
Other drugs for arrhythmias
?IV lipid emulsion to bind free drug and reduce toxicity

107
Q

What are examples of MAOIs?

A

Phenelzine
Tranylcypromine
Isocarboxazid
Moclobemide

108
Q

Why are MAOIs used much less frequently than other antidepressants?

A

Dangers of dietary and drug interactions

109
Q

What are the 2 types of MAOIs?

A

Non-selective and selective

110
Q

Whats the MOA of MOAIs?

A

Monoamine oxidase enzymes are responsible for breaking down neurotransmitters such as dopamine, norepinephrine, and serotonin in the brain.
MAOIs inhibit this enzyme so these neurotransmitter levels remain high - particularly serotonin and to a lesser extent NA
Non selective MAOIs inhibit both MAO-A and B
Selective MAOIs only inhibit MAO-B which only increases dopamine levels

111
Q

What is selegiline?

A

A selective MAOI for MAO-B which increased dopamine levels and can be used to treat Parkinson disease sympotms

112
Q

Which group of patients respond best to MAOIs?

A

Phobic pt
Depressed pt with atypical, hypochondriacal or hysterical features

113
Q

When can you start other antidepressants after stopping MAOIs?

A

At least 2 weeks
Or 3 weeks if starting Clomipramine or imipramine

114
Q

When can you start an MAOI after stopping another class of antidepressants?

A

1-2 weeks after TCAs
1 week after SSRIs (at least 5 weeks if fluoxetine)

115
Q

What are the unwanted effects of MAOIs?

A

Hypotension
Tremors, excitement, insomnia and convulsions due to excessive central stimulation
Increase appetite and weight gain
Atropine like side efefcts (dry mouth, blurred vision, urinary retention)

116
Q

What is the cheese reaction?

A

A direct consequence of MAOIs and occurs when tyramine is ingested
Tyramine is normally metabolised by MAO in the gut wall and liver so little dietary tyramine reaches the systemic circulation
MAOI allow for tyramine to be absorbed and enhances the sympathomimetic effect
The result is acute hypertension

Because MAOIs bind irreversibly to MAO-A , amine may accumulate to dangerously high levels, precipitating a life-threatening hypertensive crisis

117
Q

What are the symptoms of the ‘cheese reaction’?

A

Severe throwing headache and occasionally can cause intracranial haemorrhage

118
Q

What are the main causes of the cheese effect?

A

Ripe cheeses
Concentrated yeast products like marmite
Amphetamines
TCAs

119
Q

Why does moclebemide not cause the ‘cheese reaction’?

A

As its a MAO-A inhibitor so tyramine can still be metabolised by MAO-B

120
Q

What are the major drugs used to treat bipolar disorder?

A

Lithium (mood stabilise of choice)
Antiepielptics e.g. valproate, carbamazepine and lamotrogine
Some antipsychotic drugs e.g. olanzapine, risperidone, quetiapine or aripiprazole

121
Q

How do you manage mania or hypomania?

A

Consider stopping antidepressants
Antipsychotic therapy

122
Q

How do you manage depression in bipolar disorder?

A

Talking therapies or fluoxetine

123
Q

Why do we give mood stabilisers in bipolar disorder?

A

They prevent the swings of mood and thus can reduce both the depressive and manic phases of the illness
Given over long periods

124
Q

Why is lithium such a dangerous drug?

A

It has a very narrow therapeutic range and a long plasma half-life being excreted primarily by the kidneys
Therapeutic levels are 0.5-1 mmol/L. Toxic levels are >1.5mmol/L and dangerously toxic levels are >2mmol/L

125
Q

What are the 2 theories of MOA of lithium?

A

Interferes with inositol triphophate formation
Interferes with cAMP formation

126
Q

Why should you avoid a low-sodium diet when taking lithium?

A

As lithium is a mono alert cation similar to sodium which can mimic its role
Sodium depletion reduces the rate of excretion by increasing the reabsorption of lithium by the proximal tubule = increases likelihood of toxicity

127
Q

What can predispose you to lithium toxicity?

A

Low sodium diet
Diuretics
Renal disease NSAIDS, ARBs, ACEi
Dehydration
Haloperidol
Carbamazepine
Dapagliflozin

128
Q

What are ther adverse effects of lithium treatment?

A

Nausea, vomiting, direhoea
Fine tremor
Precipitates or worsens skin problems
Renal effects - polyuria and polydipsia
Thyroid enlargement / ?hypothyroidism
Weight gain
hair loss
Leukocytosis
Hyperparathyroidism and resultant hypercalcaemia

129
Q

Why may lithium treatment cause polyuria?

A

As lithium can cause nephrogenic diabetes insipidus

130
Q

At what concentration does lithium toxicity occur?

A

> 1.5mmol/L

131
Q

What are the features of lithium toxicity?

A

Coarse tremor or extremities and lower jaw
Diarrhoea, vomiting
Muscle weakness
Dizziness
Ataxia
Blurred vision
Hyperreflexia
Acute confusion
Polyuria
Seizure
Coma, convulsions and death is plasma concentration reaches 3-5mmol/L

132
Q

Why should you always prescribe lithium by brand name?

A

As preparations vary widely in bioavailability

133
Q

Who should you not prescribe lithium to?

A

Cardiac disease associated with rhythm disorders.
Clinically significant renal impairment.
Untreated or untreatable hypothyroidism.
Brugada syndrome or family history of Brugada syndrome.
Low sodium levels, including people that are dehydrated and those on low-sodium diets.
Addison’s disease.

134
Q

How should you monitor someone taking lithium?

A

Lithium levels are normally measured one week after starting treatment, one week after every dose change, and weekly until the levels are stable.
Once levels are stable, levels are usually measured every 3 months.

Measure weight or Body Mass Index (BMI), urea and electrolytes estimated glomerular filtration rate (eGFR), calcium and thyroid function tests every 6 months (more often if there is evidence of impaired renal function).

If there is a risk factor for, or existing, cardiovascular disease, an ECG is normally performed before treatment begins.

135
Q

How soon after taking lithium, should you check the sample when considering monitoring?

A

12 hours post dose

136
Q

What advise should you give to someone taking lithium?

A

Carry a lithium card
Regular blood tests are important and results should be recorded in their lithium record booklet
What adverse effects to expect
How to recognise symptoms of lithium toxicity
Not to take NSAIDs
That episodes of d+v (or any form of dehydration) will lead to sodium depletion and increase plasma lithium levels. Maintain fluid intake particularly when unwell or after sweating
If a dose is mossed to take it as soon as possible but never double the daily dose
Not to stop taking lithium abruptly

137
Q

Which recreational drugs can increase the risk of serotonin syndrome?

A

Ecstacy and amphetamines

138
Q

If a person cannot tolerate SSRIs or SNRIs for anxiety management, what drug should you give?

A

Pregabalin

139
Q

What is pregabalin used to treat?

A

Epilepsy
Anxiety
Neuropathic pain

140
Q

Whats the moa of pregabalin for helping manage GAD?

A

Pregabalin is a structural analogue of GABA
It’s thought to exert its anxiolytic effects by binding to voltage gated calcium channels in ‘over excited’ presynaptic neurones, reducing release of excitatory neurotransmitters

141
Q

When should you offer benzodiazepines for GAD?

A

Only in crises as a short-term measure
E,g, in a particularly severe period of anxiety

142
Q

Why can’t benzos be used long term for anxiety?

A

Because they become addictive and pt build dependance and tolerance

143
Q

How soon do benzos work to treat anxiety?

A

30-90 minutes

144
Q

How long can you be prescribed benzos for when managing anxiety?

A

No longer than 2-4 weeks at a time

145
Q

Which benzodiazepine is usually given for severe anxiety?

A

Diazepam

146
Q

Whats the first line drug treatment for panic disorder?

A

SSRI
If not suitable then imipramine or clomipramine (not licensed but shown to be effective)

147
Q

What medicines can be used to treat PTSD?

A

Paroxetine and sertraline

148
Q

What medications can be used for OCD?

A

SSRIs

149
Q

What medications can be used to manage phobic disorders?

A

Clomipramine

150
Q

What medications can be used to manage social anxiety disorder?

A

SSRIs
Monclobemide

151
Q

When are beta blockers indicated for anxiety?

A

To manage the physical signs of anxiety e.g. heart palpitations

152
Q

Which beta blocker is typically used for anxiety?

A

Propanolol

153
Q

Whats the moa of benzodiazepines?

A

They bind to GABA A receptors at a location separated to where GABA itself binds and exerts an influence over GABA binding. This results in increased action at the GABA receptor. It opens ion channels to allow the passage of Cl- into then ruin. This pushes the membrane potential further from 0, hyperpolarising it, which makes it less likely the neuron will fire an action potential

154
Q

What are the effects of benzodiazepines?

A

They have sedation, hypnotic, anxiolytic, anticonvulsant and muscle relaxant effects

155
Q

How should you withdraw a benzodiazepines?

A

Dose should be withdrawn in steps of about 1/8th the daily dose every fortnight

156
Q

What happens if pt withdraw too quickly from benzos?

A

They may experience benzodiazepine withdrawal syndrome
This may occur up to 3 weeks after stopping a long-acting drug

157
Q

What are features of benzodiazepine withdrawal syndrome?

A

Insomnia
Irritability
Anxiety
Tremor
Loss of appetite
Tinnitus
Perspiration
Perceptual disturbances
Seizures

158
Q

Why is midazolam given when undergoing a GI endoscopy?

A

It achieves moderate levels of sedation and causes anterograde amnesia

159
Q

How does the BNF group benzodiazepines?

A

Hypnotics and anxiolytics

160
Q

What are hypnotics used to treat?

A

Insomnia short term

161
Q

What are Z-drugs?

A

non-benzodiazepine hypnotics, developed with the intention of overcoming some of the adverse effects of benzodiazepines but there is no firm evidence that there is a difference

162
Q

What are the two Z-drugs available in the UK?

A

Zolpidem and zopiclone

163
Q

What are the indications of Z-drugs in the UK?

A

Short term management of insomnia

164
Q

What are examples of short acting benzodiazepines?

A

Lorazepam
Oxazepam
Alprazolam

165
Q

What are examples of long acting benzodiazepines?

A

Chlordiazepoxide
Clonazepam
Diazepam

166
Q

What are the indications of benzodiazepines?

A

Anxiety disorders - short term relied of anxiety that is severe
Insomnia - only when severe or disabling

?Alcohol withdrawal
?Akathisia
?Acute mania or psychosis

167
Q

Why should benzos and Z-drugs be avoided in the elderly?

A

Because they are at greater risk of becoming ataxic and confused, leading to falls and injuries

168
Q

What are the side effects of benzodiazepines?

A

Drowsiness
ataxia
Loss of memory
Reduced motor coordination
Increased anxiety
Behavioural changes
Delirium
Depress respiration in those with chronic resp disease
Risk of dependance

169
Q

Why might benzodiazepines cause resp depression in those with chronic resp conditions?

A

Because of their muscle relaxant effects
Contraindicated in those with myasthenia gravis, sleep apnoea, bronchitis and COPD

170
Q

What are the indications of buspirone?

A

Anxiety short term

171
Q

Whats the moa of buspirone?

A

5-HT1A receptor agonist (these are autoreceptors) = inhibits 5HT release

172
Q

Why does buspirone take up to 2 weeks to exert its effects?

A

Because it induces desensitisation of somatodendritic autoreceptors overtime

173
Q

How soon after starting benzos do effects start?

A

Within an hour!

174
Q

What type of drug is reboxetine?

A

A selective inhibitor of noradrenaline re-uptake

175
Q

What are the indications of reboxetine?

A

Major depression

176
Q

What type of drug is mirtazapine?

A

A noradrenergic and specific serotonergic anridepressant

177
Q

Whats the moa of mirtazepine?

A

It blocks presynaptic alpha 2 receptors = increased release of noradrenaline and serotonin from presynaptic neurones

178
Q

What are the indications of mirtazapine?

A

Severe depression

179
Q

What are contraindications for MAOIs?

A

Phaeochromocytoma
CVD
Hepatic impairment
Mania

180
Q

Why should you be cautious of prescribing lithium alongside antipsychotics?

A

Antipsychotics may synergistically increase lithium-induced neurotoxicity

181
Q

What is lithium induced neurotoxicity?

A

When chronic lithium therapy predisposes to gradual accumulation of lithium in the brain = demyelination = persistent neurologic deficits

182
Q

What are contraindications for lithium therapy?

A

Pregnancy
Breast feeding
Renal insufficiency
Thyroid disease
Cardiac conditions
Neurological conditions e,g, parkinsons or Huntingtons

183
Q

What should you do if you miss more than 48 hours worth of clozapine doses?

A

If doses are missed for more than 2 consecutive days (48 hours), you will need to restart their clozapine slowly (like when they first started on it). This restart of treatment needs to be under the direction of a Psychiatrist. This is because when you start Clozapine after a break of >48 hours, it can make side effects worse, such as blood pressure changes, drowsiness and dizziness.

PSYCHIATRY (20 decks)

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