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CNS lectures (Bal) > Module 1.1.2 (Management and Treatment of Depression) > Flashcards

Module 1.1.2 (Management and Treatment of Depression) Flashcards

1
Q

What are the THREE treatment options for depression?

A
  • Psychotherapy
  • Pharmacotherapy
  • Electroconvulsive therapy (ECT)
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2
Q

What is best treatment for the following types of depression: (Use previous slide as a reference)

A) Mild depression

B) Moderate depression

C) Moderate/severe depression

A

A)

  • Psychotherapy > effectiveness than antidepressants

B)

  • Psychotherapy = effectiveness with antidepressants

C)

  • Antidepressants > effectiveness than psychotherapy
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3
Q

What does the psychological treatment of depression consist of?

A
  • Structured problem-solving strategies
  • Stress management strategies
  • CBT
  • Interpersonal psychotherapy (IPT)
  • Short-term dynamic therapy
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4
Q

When is an antidepressant indicated?

A

Antidepressants are indicated in moderate to severe depression

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5
Q

What is the choice of antidepressant based on?

A
  • Prior response
  • Adverse effects profile
  • Family history of response to treatments
  • Potential for drug interactions
  • Safety in overdose & suicidality risk of patient
  • Patient comorbidities
  • Simplicity in dosing
  • Patient preference
  • Cost
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6
Q

For antidepressants;

A) What is first line

B) What is second line

C) Augmentation

D) Other options

A

A)

  • SSRI
  • SNRI
  • Mirtazapine

B)

  • Agomelatine
  • Moclobemide
  • Reboxtine
  • TCAs
  • Mianserin
  • Irreversible nonselective MAOIs

C)

  • Liothyronine (T3)
  • Lithium
  • Anti-pscychotics
  • Pyschostimulants
  • Tryptophan

D)

  • ECT
  • Omega-3-fatty acids
  • Hypericum (St Johns Wort)
  • Exercise
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7
Q

Which SSRI/SNRI will have withdrawal effects? Why? What are these withdrawal effects?

A

Fluvoxamine, paroxetine, and venlafaxine as these have short half lives.

Withdrawal effects for SSRIs and SNRIs: Dizziness, nausea, paraesthesia, anxiety, agitation, tremor, sweating, confusion, electric shock-like sensations

will get withdrawl effects when a dose is missed

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8
Q

What is the SSRI with the longest half life?

A

Fluoxetine

Half life = 24-144 (drug) + 200-330 (active metabolite) hours

  • Low likelihood of withdrawal symptoms
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9
Q

When do SSRI doses need adjustment?

A

Doses usually need adjustment in hepatic impairment

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10
Q

When are SSRI doses usually adminstered?

A

SSRIs are usually taken in the morning to minimize insomnia but can be taken at night if somnolence (sleeping too long or strong desire of sleep) occurs

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11
Q

What differentiates escitalopram from other SSRIs?

A

Escitalopram - causes less sedation, sexual dysfunction and no agitation or weight gain due to high receptor selectivity

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12
Q

Explain the following drug interactions and precuations for SSRI

A) Suicide Risk

B) Serotonin syndrome

C) Platelet aggregation

D) Hyponatraemia risk

E) QT interval prolongation/arrhythmia risk

A

A)

  • Increases risk of suicide when starting

B)

  • Toxicity when SSRIs administered with other seretonergic drugs & opioids

C)

  • Caution with other drugs that effect clotting → bleeding risk (esp GI)
  • E.g. Warfarin + SSRIs may increase anticoagulant effect and risk of bleeding; monitor INR and ↓ warfarin dose as needed.

D)

  • Increase risk with other drugs causing this effect.

E)

  • ↑ risk with other drugs causing this effect.
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13
Q

Which SNRI have risk of withdrawal smyptoms especially when stopped suddenly?

A

All of them?

Desvenlafaxine 11; Duloxetine 8-17; Venlafaxine (apparent half life) 15 ± 6

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14
Q

What type of impairment affects SNRI (metabolism)?

A
  • Dosage adjustments required in renal impairment (CrCl < 30ml/min)
  • Hepatic impairment - variable recommendations depending on the agent (duloxetine contraindicated)
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15
Q

Interactions of the following SNRIs (CYP)

A) Desvenlafaxine

B) Duloxetine

C) Venlafaxine

A

A)

  • metabolized by conjugation and to a lesser extent CYP3A4

B)

  • metabolized by CYP2D6 and CYP1A2

C)

  • metabolized by CYP2D6 and CYP3A4
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16
Q

Explain the side effects for SNRI to do with:

A) Serotonin reuptake inhibition

B) Noradrenaline reuptake inhibition

A

A)

  • Nausea, insomnia, tremor, sexual dysfunction

B)

  • Hypertension, sweating, dry mouth
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17
Q

What are the adverse effects of SNRIs? how do they differ from SSRIs?

A

Similar adverse effects and precautions to SSRIs due to serotonergic actions

  • Suicide risk, serotonin syndrome, hyponatraemia, risk of bleeding, narrow angle glaucoma

> narrow angle glaucoma is a NA side effect

Cardiac effects

  • Use cautiously in patients with cardiac disease
  • Increases in BP reported with desvenlafaxine, duloxetine (infrequent) & venlafaxine
  • Control hypertension before starting desvenlafaxine or venlafaxine

Lipid effecs

  • Elevations have occurred with desvenlafaxine – use with caution

Liver enzymes

  • ↑ serum transaminases with duloxetine
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18
Q

What is the MOA of Mirtazapine? What happens to sedation at higher doses?

A

Acts by postsynaptic blockade of serotonin 5HT2 and 5HT3 receptors, a2 adrenoreceptors and also a potent H1 antagonist which accounts for sedative effects

  • Sedation is decreased at higher doses (>15 mg)
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19
Q

For mirtazapaine;

A) What is the half life?

B) Excretion

C) Precautions

D) When is the dose taken

E) interactions/metabolism

A

A)

  • 20-40, longer half lives of up to 65 hours have occasionally been recorded, shorter half lives seen in young men (withdraw slowly)

B)

  • Clearance can be ↓ in both hepatic and renal insufficiency - ↓ dose

C)

  • Epilepsy: can ↓ seizure threshold
  • Diabetes: may disrupt glycaemic control – monitor closely – adjust doses if necessary

D)

  • Dose taken at night

E)

  • CYP2D6 and 3A4 substrate
  • Serotonin toxicity
  • Additive sedative effects
  • Warfarin: monitor INR
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20
Q

For Agomelatine;

A) What is the MOA?

B) What are the side effects?

C) When is the dose taken?

D) Which patients not to use it in?

E) What are THREE practice points

A

A)

  • Agonist of melatonin receptors (MT1 and MT2) and antagonist of (5HT2C) receptors
  • Improves sleep quality

B)

  • Less GI side effects (vomiting, constipation), sexual function (↓ libido) and no cardiovascular side effects compared with other antidepressants

C)

  • At night

D)

  • dont use in patients >75 yo

E)

  • Initial suicide risk
  • Lack of abuse potential or withdrawal effects
  • Can be started when beginning to taper an SSRI or SNRI
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21
Q

When is agomelatine contraindicated?

A
  • Contraindicated in hepatic impairment or if aminotransferase concentration is > 3 X ULN.
  • Caution if aminotransferases are already elevated or other risk factors for hepatic damage
  • Additive hepatotoxic effects with other drugs
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22
Q

Interactions/metabolism of agomelatine?

A

CYP1A2 (90%) and CYP2C9/CYP2C19 (10%) toxicity

  • CYP1A2 inhbitor will increase agomelatine concentration
  • CYP1A2 will decrease efficacy
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23
Q

What is the MOA of moclobemide? How do they compare to 1st line antidepressants?

A
  • Competitive and reversible inhibition of MAO with relative selectivity for type A (MAO-A).
  • Synaptic concentrations of serotonin, noradrenaline and dopamine are increased.

> free of cardiovascular and sexual side effects compared to 1st line antidepressants

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24
Q

For Moclobemide;

A) When is the dose given?

B) How hepatic impairment affect dosing

C) Interactions/metabolism

D) Practice points/precautions

A

A)

  • Dose given in the morning/midday to decrease risk of insomnia

B)

  • dose by half to 1/3 in severe hepatic impairment

C)

  • CYP2C19 and CYP2D6 – some are poor metabolisers
  • Drug combinations – contraindications SSRIs, SNRIs or TCAs, buproprion, dextromethorphan, linezolid, pethidine, selegilene, tramadol, triptans

D)

  • Initial suicide risk
  • Additive toxicity – serotonin syndrome
  • Avoid use in acute confusional states (rare AE = agitiation, nightmare, hallucination)
  • Best taken with or soon after food
  • Potential hypertensive reactions in patients with hyperthyroidism –> more common in non-selecitive MAOIs
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25
Q

For Reboxetine;

A) What is the action

B) What are the adverse effects

C) What is the practice points/precautions

D) When is decrease in dose required

E) CI?

F) What enzyme should it be avoided use with>

A

A)

  • Highly selective and potent inhibitor of noradrenaline uptake.
  • Only weak effects on serotonin reuptake and does not affect the uptake of dopamine

B)

  • Tachycardia, dry mouth, constipation, insomnia, impotence
  • Urinary retention, dysuria common –> not useful for older patients

C)

  • Initial suicide risk
  • Risk of angle closure glaucoma
  • Epilepsy & administered with drugs that ↓ seizure threshold
  • Exacerbation of urinary retention or bladder obstruction
  • Cardiovascular - ↑ risk of orthostatic hypotension, tachycardia and hypertension

D)

  • Decrease dose in moderate to severe renal and hepatic impariment

E)

  • CI with MAOIS

F)

  • CY3A4: Avoid with inducers or inhibitors of this enzyme
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26
Q

When are TCAs used? What do they have a role in? When are they potentially lethal?

A

Used generally after unsuccessful trials of at least 2 first-line treatments

  • Have a role in severe melancholic depression
  • Potentially lethal in overdose!!! (cardiotoxicity)
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27
Q

What is the MOA of TCA? What are the precautions?

A

Inhibit reuptake of noradrenaline and serotonin into pre-synaptic terminals

Precautions: suicide risk, CV disease, elderly, epilepsy (lowers seizure threshold like all antidepressants), hyperthyroidism

28
Q

Which TCAs have;

A) greater effect on serotonin transport?

B) lower incidence of anticholinergic side effects, orthostatic hypotension and sedation?

A

A)

  • Clomipramine has > effect on serotonin transport

B)

  • Nortriptyline has a lower incidence of anticholinergic side effects, orthostatic hypotension and sedation
29
Q

Which patients are more susceptible to anticholinergic and sedating side effects?

A

ELDERLY patients more susceptible to anticholinergic and sedating side effects

30
Q

What are the interactions of TCAs?

A

CYP450, anticholinergic, serotonergic drugs, drugs that prolong QT interval, other antidepressants

31
Q

How is Mianserin better than other TCAs? What is the MOA?

A

Has fewer CV and anticholinergic effects than TCAs and a wider margin of safety in overdose.

  • MOA: inhibits NA reuptake
32
Q

For Mianserin;

A) When it CI?

B) AE?

C) What is required before treatment?

D) What needs to be checked at baseline?

A

A)

Contraindicated in severe liver disease

B)

Sedation, orthostatic hypotension, (conversely) hypertension, weight gain (infrequently) and rarely neutropenia and deaths from agranulocytosis

C)

FBC require before initation of treatment

  • Watch for signs suggestive of neutropenia (infection, sore throat)

D)

Check hepatic function at baseline

  • Stop treatment if jaundice occurs
33
Q

What are TWO examples of irreversible MAOIs? How many times are they given a day? What time should be they given?

A

Tranylcypromine & Phenelzine

  • Given either daily, bd or three times a day
  • Take last dose of the day before 3 pm, might have trouble sleeping if taken later
34
Q

What are the adverse effects of irreversible MAOIs? What are the interactions and what happens when combined with tytramine rich foods?

A

Adverse effects

  • Orthostatic hypotension, dry mouth, blurring of vision, constipation, sexual dysfunction, weight gain, insomnia and arousal

Interactions

  • Tyramine-containing foods (avoid during and for 2 weeks after stopping treatment), serotonergic drugs, sympathomimetic amines (indirectly acting ones), hypotensive drugs, insulin and oral hypoglycaemics

CAN CAUSE SIGNIFICANT HYPETENSION WHEN COMBINED WITH CERTAIN FOOD (hypertensive crisis –> death)

> tyramine rich foods: pepperoni, salami, cheese, beer + wine, nuts

35
Q

Combinations with the following drugs are contraindicated while taking a MAOI and for 14 days after stopping it (21 days for clomipramine and imipramine) because of the possibility of either severe hypertension (resulting from the accumulation of endogenous catecholamines) or the development of serotonin toxicity during this period

What are some examples of these drugs?

A

Atomoxetine, cocaine, desvenlafaxine, dexamfetamine, dextromethorphan, duloxetine, entacapone, ephedrine, fentanyl, linezolid, methylphenidate, mianserin, oxycodone, pethidine, phentermine, phenylephrine, pseudoephedrine, reboxetine, St John’s wort, SSRIs, TCAs, tramadol and venlafaxine

> use direct acting drugs sympathomimmetic agent like isoprenaline if required

36
Q

For Vortioxetine:

A) MOA?

B) Negative effect

C) What are the adverse reactions

D) What makes it special

E) What enzyme does it have interactions with?

A

A)

  • Inhibits the serotonin transporter, acts as a antagonist and agonist at different 5HT receptor subtypes. Thought to ↑ serotonin in the CNS

B)

  • May contribute to serotonin toxicity

C)

  • Adverse reactions: nausea, vomiting, constipation, dry mouth, itch, dizziness, sexual dysfunction, abnormal dreams, flushing

D)

  • Can be stopped without tapering

E)

  • Drug interactions involve inhibitors and inducers of CYP2D6
37
Q

When does serotonin toxicity occur? Provide THREE different reasons

A
  • Overdose of a single agent
  • Simultaneous use of two serotonergic agents
  • Failing to use appropriate washout period when switching agents
38
Q

For serotonin toxicity:

A) What are mild symptoms

B) What are the moderate symptoms

C) What are the severe symptoms

A

A)

  • Mydriasis, shivering sweating mild tachycardia

B)

  • disorientation, excitement, rigidity, tachycardia, hyperthermia (> 40) tremor, clonus, hyperreflexia

C)

  • Delirium, hypertension, hyperthermia, muscle rigidity, tachy
39
Q

What are the mental status changes that occur with serotonin toxicity?

A
  • Confusion, agitation, hypomania, hyperactivity, restlessness

Can be a medical emergency and deaths have occurred

Fatalities have mostly occurred through the use of two drugs with different mechanisms for increasing serotonergic activity (e.g SSRIs and MAOIs)

40
Q

What are te TWO treatment options for serotonin toxicity?

A
  1. Cyproheptadine: 12mg single dose or 4 to 8mg tds
  2. Chlorpromazine: 12.5 to 50mg slow IV infusion over 30 to 50min
41
Q

What are the drugs that have been associated with serotonin toxicity?

A

See attached image

42
Q

For antidepressants;

A) When is the highest rate of improvement?

B) When is the lowest rate of improvement?

A

A)

  • Highest rate of improvement during weeks 1-2

B)

  • Lowest rate of improvement during weeks 4-6
43
Q

How to commence antidepressants?

A

Generally commence antidepressants with a low dose and gradually increase over 2 to 4 weeks

44
Q

When is the full effect of antidepressants seen?

A

Full effects may take 4 to 8 weeks but improvement seen within 1 to 3 weeks

45
Q

How long to continue drug treatment for after a single episode of major depression?

A

Continue drug treatment for 4 to 12 months after a single episode of major depression

  • High risk of relapse
46
Q

How to adjust treatment for depression medication?

A
  • Increase dose if full response not achieved (check adherence before adjusting therapy)

> Up to maximum possible dose

> Depending on side effects

  • If a change is necessary can switch to an antidepressant from the same or a different class
47
Q

What to do for patients who fail to respond to antidepresasnt therapy? What are the key questions in assessing failure to respond to psychotropic drugs?

A
  • Refer to a psychiatrist – check diagnosis
  • May need to sequentially trial a number of drugs to achieve remission
48
Q

What are the FOUR options in treatment of resistant patients (refractory depression)?

A
  1. Switching antidepressants
  2. Augmentation strategies
  3. Antidepressant polypharmacy
  4. Electroconvulsive therapy (ECT)
49
Q

For switching antidepressants;

A) What requires long washout periods?

B) TCAs and most SSRI (except fluoxetine) clear the drugs from the body within how long?

C) For other switches, what needs to be considered?

A

A)

  • Specified long washout periods are mandatory for irreversible MAOIs
  • Non selective irreversible MAOI and serotonin toxicity drug stays in body 2-3 weeks after it has been ceased –> severe HTN and serotonin toxicity

B)

  • around 5 days, they half lifes around 20-30 hours

C)

  • Clinical urgency for change/potential for relapse and exacerbation
  • Potential for withdrawal effects and need for tapering dose of agent being ceased
  • Half life of drug & continued effects → potential for interaction/toxicity during switch if the drug has a long half life
50
Q

What are the methods of switiching antidepressants? Include why the switch is done.

A
  1. Conservative switch
  • Gradual tapering and cease
  • Washout period of 5 half lives
  • New drug commenced at dose as per guidelines

Why: reduce risk of adverse effects like serotonin toxicity, but patient’s risk of relapse is high as there is no antidepressant in the system. Withdrawl effects are worse but safer.

  1. Moderate switch
  • Gradual tapering and cease
  • Washout period of 2 to 4 days
  • New drug commenced at low dose

Why: reduce risk of adverse effects like serotonin toxicity, but patient’s risk of relapse is high as there is no antidepressant in the system. Withdrawl effects are worse but safer.

  1. Direct switch
  • First drug stopped
  • New drug commenced the next day at a therapeutic dose

Why: very severe side effect eg. full body rash, stopped medication suddenly. Some antidepressants cause mania so has to be stopped suddenly. Patient preference is the third reason (e.g. venlafaxine, when tapering doses, withdrawal effects start and last for weeks/months, some patients prefer to ‘suffer for a few days’ and get over it.

  1. Cross taper switch
  • Gradual tapering and cease
  • New drug commenced at low dose at some stage in the reduction
  • Dose increased to therapeutic dose when first drug has been ceased

Why: less withdrawal effect, less risk of relapse as there is medication in the body. Risk is that there is a larger risk of adverse effects as combining 2 antidepressants at the same time –> potential for serotonin syndrome and other side effects.

Hospital –> cross taper

Community –> cross taper if patient is at high risk of relapse or high risk of withdrawal symptoms

51
Q

For changeover:

A) What drugs are category A changeover?

B) What drugs are category B changeover?

C) What drugs are category C changeover?

Expalain the consequences

A

A)

  • Fluoxetine, phenelzine, tranylcypromine, vortioxetine

LONG HALF LIFE

> wait 14 days before starting new drug

B)

  • TCAs, SSRIs (excpet fluxoetine), mianserin, mirtazapine

DRUGS WITH HALF LIFE OF 24-48 hours

> wait for 2-4 days before starting next antidepressant

> withdraw gradually to prevent withdrawal symptoms

> withdrawal symptoms rare for mianserin

C)

  • Agomelatine, moclobemide, reboxetine, SNRIs

DRUG with short half life of <18 hours

> SNRI: withdraw gradually to prevent withdrawal symptoms

> Agomelatine, moclobemide, reboxetine = rare/not reported withdrawal symptoms

> Agomelatine can be started immediately if switching from an SSRI or SNRI –> doesn’t have withdrawal effects even though it has a short half life .. unique drug innit

52
Q

What two antidepressants are most common for withdrawal effects? What is the general rule for discontinuing a drug?

A

Paroxetine and venlafaxine

  • Halve the dose every week until the daily dose is half of the lowest unit available, then stop after 1 week
53
Q

Discontinuation symptoms may arise when the drug is stopped abruptly and are more likely to occur with a ?

A
  • Higher dose
  • Longer treatment duration
  • Shorter half life drugs –> go out of system faster
54
Q

What are some withdrawal effects of antidepressants?

What in particular for phenelzine and tranylcypromine?

A

See attached image

phenelzine: psychosis and seizures
tranylcypromine: may cause delirium

55
Q

What can rapid withdrawal of the more potently anticholinergic tricyclic antidepressants (TCAs) (eg amitriptyline) result in?

A

Cholinergic rebound (agitation, headache, sweating, gastrointestinal symptoms), parkinsonism and problems with balance.

> sailvation, lacrimation, urination, diarrhoea, GI distress, emesis SLUDGE = cholinergic effects

56
Q

What drugs are used for augmentation of antidepressants?

A

Many drugs are used for augmentation of antidepressant treatment but evidence to support their use is limited

  • Lithium augmentation with SSRIs and TCAsn
  • Liothyronine (T3) augmentation
  • Second generation antipsychotic augmentation –> only quetiapine indicated as adjunctive therapy in australia.
57
Q

What is the cobinations that are used for antidepressants? How is it different to augmentation

A
  • Mirtazapine + SSRIs
  • Mirtazapine + Venlafaxine
  • SSRI + TCA

Different to augmentation = Involves using 2 or more antidepressant medications typically from 2 different mechanism classes

> Avoid using > 1 antidepressant drug –> Insufficient evidence to support combination therapy –> Serious adverse effects can occur

58
Q

What is Electro-convulsive therapy (ECT)?

A

Delivery of an electric current to induce a seizure for a therapeutic response (uni or bilateral)

  • Indicated for severe and unresponsive forms of depression
  • Response rate of 50 to 80%
59
Q

How often is ECT given? What is done to prevent high relapse rate? What are the side effects?

A
  • Treatments given 3 times weekly or ↓ if cognitive impairment emerges
  • 6 to 14 treatments (up to 24 treatments)

Relapse rate high

  • Maintain recovery with pharmacotherapy (that has not been previously ineffective), lithium or mood stabiliser or combination

Side effects

  • Memory loss, muscle aches and pains, headaches, transient confusion
60
Q

Pharmacotherapy considerations for ECT:

A) What to do for BZDs?

B) Side effect of Lithium?

C) Using antiepileptic drugs?

D) Can antipsychotics be used/

A

A)

  • Benzodiazepines should ceased because they raise seizure threshold and ↓ efficacy

B)

  • Lithium doesn’t ↓ efficacy but may ↑ postictal confusion

C)

  • Continuation of antiepileptic drugs during ECT may ↓ efficacy, prolong course and ↑ cognitive adverse effects

D)

  • Unless antipsychotics are ineffective or result in problems with ECT (e.g. clozapine and prolonged seizures) they can be continued and may improve results
61
Q

Explain St Johns Wort (hypericum perforatum) as alternative trearment

A
  • Efficacy in acute mild-moderate disease
  • Mechanism unknown – may involve increasing synaptic availability of serotonin and other neurotransmitters n
  • Longer-term efficacy and safety not established
  • Risk of serotonin toxicity
62
Q

Explain Omega-3 Fatty Acids as alternative treatments

A
  • Mood improvement demonstrated in a study with dose of 1g per day
  • Several recent studies indicate not superior to placebo in major depressive disorders
63
Q

How does exercise alleviate symptoms of depression?

A
  • ↑ energy
  • Improve sleep
  • Positive distraction
  • Social support
  • ↑ sense of control and self-esteem
  • May change levels of neurotransmitter

Trials have demonstrated regular exercise to be equally effective as antidepressants in mild to moderate depression

> decrease risk of developing depression

64
Q

Key Messages about depression

A
  • Depression may result in significant disability
  • Depression may be associated with a number of medications and medical conditions, in particular co-morbid psychiatric illnesses
  • Pharmacotherapy is indicated in moderate to severe MDD only
  • SSRIs are first line (in general) – need to consider what is best for the individual
  • Drug choice should be based on patient preference, past history of response, adverse effect profile, potential for toxicity in overdose, potential for drug interactions
  • Consider interactions due to CYP450 enzymes
  • Monitor for serotonin syndrome
  • Avoid withdrawal syndrome
  • Observe washout periods when switching antidepressants to reduce adverse effects
  • There is little evidence to support combinations of antidepressants, although the risk of adverse events is well documented
65
Q

Antidepressants can cause hyponatraemia and this leads to SIADH, what is the solution?

> All antidepressants can cause SIADH and would require close monitoring.

A

Cease antidepressant –> SIADH resolves quickly on cessation of causative drug

Do not taper if acute nature

Assess fluid status (SIADH –> euvolaemic hyponatraemia, but patient may be dehydrated due to vomiting – hypovolaemic).

If euvolaemic and sodium remains low, consider fluid restrictions (500-800mL daily) depending on severity of CNS symptoms.

If hypovolaemic give NaCl 0.9% solution

If CNS symptoms are severe hypertonic saline may be administered (depending on urine osmolality)

CNS lectures (Bal) (29 decks)

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