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Neuropsychiatry and Psychopharmacology > L 6+7 - Antidepressants > Flashcards

L 6+7 - Antidepressants Flashcards

1
Q

What are antidepressants used for?

A
  • treat major depression
  • depressive phase in Bipolar
  • depressive episode in schizophrenia
  • preventing relapse
  • adjunct treatment to anxiety disorders, OCD.
  • adjunctive treatment for eating disorders

sometimes… for night sedation.

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2
Q

efficacy of antidepressants?

A

all pretty similar… 50-60% improvement

placebo is 30-40%

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3
Q

What affacts efficacy of antidepressant?

A

 Prior treatment history in
patient/family members
 Patient preferences
 Expertise of prescribing provider
 Side effect profile(sedating or activating)
 Safety in overdose (10-15 days of a TCA can be a lethal overdose)
 Drug-drug interactions

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4
Q

What are some therapeutic targets/mechanisms of actions in antidepressants

A
  • blocking monoamine reuptake
  • block a2 receptor and therefore increase release of NA by blocking presynaptic autoreceptor
  • block enzyme monoamine oxidase (MAO inibitor)

some have multiple actions.

(serotonin is a monoamine)

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5
Q

Do antidepressants help healthy humans?

A

no it does not elevate mood in healthy people

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6
Q

What are the different classes of antidepressants available?

A
  • Tricyclic
  • MAO inhibitors
  • SSRIs
  • SNRIs (dual serotonin and NA)
  • serotonin modulators and stimulators
  • serotonin-2 antagonist and reuptake inhibitors (SARIs)
  • NRI (specific NA reuptake inhibitors)
  • NDRA (NA + DA reuptake inihib)
  • NaSSAs (NA and 5-HT antag)
  • Serotonin reuptake enhancer
  • atypical antipsychotics
  • other .. like ketamine..
  • atypibuspirone, lithium, thyroxine
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7
Q

three generation of antidepressants that we use?

A
  • 1st gen - MAOIs and tricyclics
  • 2nd gen - SSRIs
  • 3rd gen - Tricyclic with a twist
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8
Q

What are 1st gen antidepressants?

A

MAO inhibitors!

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9
Q

Mao inhibitors?

A
  • inhibitor the action of monoamine oxidase, which breaks down dopamine, NA and serotonin.

= mORE NT!

side effect = blocks MAO in the liver, builds up tyramine, high BP and increased risk of stroke.

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10
Q

TCAs? How do they work?

A

Tricyclic antidepressants - blocks the reuptake of NA and serotonin, therefore increase NT in synapse.

  • at least 3 other modes of action - blocking other receptors gives rise to side effects
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11
Q

what are the side effects associated with TCA’s, that are related to certain receptor blockades?

A

 Block muscarinic cholinergic receptors - producing dry mouth, blurred vision, urinary retention, constipation and memory problems

 Block H1 histamine receptors - causing sedation and weight gain

 Block α1 adrenergic receptors - causing postural hypotension and dizziness

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12
Q

What are some generalised side effects of TCAs?

A
  • increased freq of epileptic seizures.
  • sedation
  • cardiotoxicity.
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13
Q

2nd gen antidepressants?

A

SSRIs!

they block the reuptake of serotonin only.

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14
Q

What is the mech of action for SSRIs?

A

specifically blocks the reuptake of serotonin, without affecting other NTs.

 Side effects: nausea, sexual dysfunction (serotonin receptors also in gut, hypothalamus and sex organs)
 Little cardiovascular concern

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15
Q

Side effect of SSRI?

A

Common:
 Stimulant effects such as ‘nervousness’, insomnia
 Other CNS effects: dizziness, headache, tremor
 GI effects: nausea, vomiting, diarrhoea, abdominal discomfort
 Weight loss/gain

Uncommon:
 Sedation; dry mouth; sweating; sexual dysfunction including decreased libido, anorgasmia, delayed ejaculation

Rare:
 Mania; convulsions; movement disorders: tremor, akathisia, dystonia or dyskinesia
 ECG, BP or heart rate changes (arrhythmias)

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16
Q

SSRIs vs Tricyclics?

A
  • SSRIs are more selective with serotonon… less anticholinergic effects
  • SRRIS free from membrane stabilising effects on the heart, therefore does not affect cardiac risk

but

not more effective
action is not faster.

but less side effects :)
less sedation, anticholinergic effects, cardiotoxicity and weight gain.

BUT more gastro effects

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17
Q

What to prescribe if suicide risk is high

A

better to prescribe SSRI than TCA. easier tolerated.

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18
Q

3rd gen antidepressant

A

“tricyclics with a twist”
- they do a rang eof things… SSRI+ almost..

  • acts as an SSRI but also antagonises 5-ht2 and 5-ht3 receptors…therefore restricting action to only 5-ht1 receptor
  • efexor (venlafaxine; SNRI), mitazapine
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19
Q

Venlafaxine?

A

aka Efexor

  • does bOTH what SSRI and TCAs do

**Selectively inhibits reuptake of serotonin and NA (and, to lesser extent, dopamine)

**Shares similar advantages with the SSRIs over tricyclics

potential advantages over SSRIs.

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20
Q

Advantages of venlafaxine over ssri?

A
  • increase in efficacy at higher doses, due to addition of second action on NA.
  • effect is 50% higher than SSRIs.
  • more rapid onset of action (1 week)
  • safe at high dosage
  • less interactions with other drugs.
21
Q

Disadvantages of venlafaxine, when compared to SSRI?

A

 potential for blood pressure elevation at higher doses - requires BP to be monitored closely during first 2 months of being stabilised on any dose above 225 mg/day

 Original need for twice a day dosing schedule now overcome with extended release formulation

 dose needs to be titrated

22
Q

Side effects of venlafaxine/efexor?

A

Most common side effects:  nausea
 dizziness  sedation

At higher doses, dose-dependent increases in:
 blood pressure (rarely observed below 225 mg/day)  sweating
 tremors

23
Q

Bupropion

A
  • aka zyban also used for smoking cessation
  • bLOCKS REUPTAKE of DOPAMINE and/or NA.
  • very weak effect on serotonin, if at all.
  • decreased level of side effects in depression
  • not much of an effect on anxiety
24
Q

Which classes of antidepressant have sedative effect?

A

tricyclic and SSRIs.. some

25
Q

Classes of symptom in depression?

A
  • physical - appetite, sleep

- cognitive and behavioural

26
Q

What kind of symptoms is best alleviated by antideprssants?

A

physical ones - sleep disturbance, appetite.

27
Q

What helps most with . cognitive and behavioural problems ?

A

CBT… psych strategies

28
Q

What is the usual course of recovery in depression

A

appetite and sleep improve first

then behaviour second

thoughts and feelings last.

29
Q

What is the difference in presentation for someone with DA dysfunction and someone with 5-HT dysfunction?

A

DA dysfunction = REDUCED POSITIVE AFFECT
- loss of happiness, anhedonia, fatigue, decreased alertness, decreased self confidence

5-HT dysfunction = INCREASED NEGATIVE AFFECT
-depressed mood, guilt, disgust, anxiety, hospility, irritability, loneliness

NA dysfunction is in between both of these… can swing eac way but not as severe.

30
Q

What NT systems would you modify for fatigue and concentration problems?

A

NA and DA.

so use...
NDRI,
NRI
SNRI
MAOI 
stimulants
31
Q

what NT systems would you modify for sleep problemms

A

5-HT and GABA and histamine systems

hyponotics
sedating antidepressants - mirtazapine

32
Q

Usually, with antidepressants, what is the course of recovery …

A

therapeutic effects are slow.. then quickly go up to plateu.

side effects more quickly commence… then decrease over time…

33
Q

What are the first line monotherapies for depression then?

A 
SSRI
NDRI
SNRI
SDA
BP
BP - lamotrigine (antipsychotic/anticonvulsant)
34
Q

What age range do antidepressants work best for

A

26-64 - adults

35
Q

Placebo role in antidepressants?

A

HUGE ROLE…. 20-25% of the effect for antidepressants…

50% natural cause of illness

then 20-25% is down to the actual antiderpssant

36
Q

When a meta analysis was run.. what was found for the effect of SSRIs?

A
  • did not meet 3 point drug-placebo criterion for clinical significance.
  • improvement was a function of baseline severity. those those at the tail ends improved least, those in the middle had the largest gains.

drug type didnt mediate this effect.

37
Q

Why might some studies find a greater effect for antidepressant in extremely severe patients?

A

because the placebo effect is less in those severely depressed

(this is when looking at drug vs placebo effect)

38
Q

efficacy of psychotherapy vs combined with medication?

A

 Mean effect size for the difference between PT and
combined therapy was 0.35
 Differences between PT and combined was smaller in those studies that employed CBT
 At follow up at 3, 6 and 12 mths; no difference between PT and combined

Conclusion: Combined therapy is more effective than PT treatment alone, but it is not clear whether this difference is relevant from a clinical perspective

39
Q

key principles for using antidepressants?

A

 Use antidepressants, not minor tranquilizers /
benzodiazepines
 Use adequate doses for an adequate amount of time
 Start slow and work with side effects but titrate to an effective dose as needed

Change medication if not effective
 Usually after 8-10 weeks

40
Q

how long should you wait until you say a medication is not working (antidepressant)

A

usually 8-10 weeks.

change medication

41
Q

How should we education patients on antidepressants

A

Key messages
 How do these medications work?
 By restoring a chemical imbalance in the brain
 There are several options (over 20 available medications)

Anticipate
 Patient concerns about medications  Side effects (these can be managed)  Problems with adherence

Reinforce
 Need for continuation or maintenance treatment to prevent relapse even after the patient feels better

42
Q

What happens if they dont respond to SSRI

A

about one in four patients who are changed to either another SSRI, Buproprion-SR, or Venlafaxine XR will respond to the new drug

27–32 % of patients will respond to augmentation with Buspirone or Buproprion

43
Q

How to manage side effects?

A

Short term strategies
 Wait and support (e.g., GI side effects)
 Adjust medication timing (e.g., take sedating meds at bedtime)
 Consider temporary dose reduction
 Treat side effects (see intervention manual)

Change to a different antidepressant

Change to or add psychotherapy

44
Q

When to stop antidepressants?

A

 Treat all adults for 4-9 months after initial response.
 Treat those at high risk for relapse for 2 years or longer. Some
may need lifetime treatment.

 Maintenance treatment should be at full dose.
 Make a relapse prevention plan.
 Taper antidepressants slowly to avoid discontinuation syndrome.

45
Q

What are the guidelines for treatment with moderate depression

A

all antidepressants, CBT & IPT equally effective

46
Q

What are the guideless for treatment of severe depression

A

all antidepressants, psychotherapy later.

47
Q

What are the guidelines for severe depression with psychosis

A

ECT alone or TCA plus antipsychotic is superior to TCA alone.

48
Q

What are the long term effecst when you compare antidepressant and Cog therapy

A

prior treatment with CT protected against relapse of depression at least as well as continued provision of ADM and better than ADM treatment that was subsequently discontinued.

more people relapse with discontinue medication, than those who discontinue cognitive therapy…. CT has more enduring effect

While acute changes with the either CT or ADM might be due to a similar mechanism, CT can be assumed to also produce changes that ADM does not.

49
Q

neurological explanation for why cog therapy is more beneficial and enduring than medication?

A

 Acutely depressed individuals are characterised by decreased prefrontal function possibly arising from increased amygdala reactivity
 CT operates by increasing prefrontal function, while ADM operates more directly on the amygdala
 These treatments might thus result in end states that are, in one important respect, similar: normalised amygdala and PFC activity in the short term
 If the amygdala is the “point of entry” for environmental stressors, cessation of ADM could leave the person at risk of having strong maladaptive reactions to new environmental insults
 By contrast, CT works by building the skills that require active operation of PFC, thus making the effects more enduring

Neuropsychiatry and Psychopharmacology (12 decks)

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