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167 Cards in this Set
- Front
- Back
What is the categorical approach? |
Distinctions among members of different categories are qualitative (taxonomy)
“all or none” |
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What does the dimensional approach focus on?
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1. It focuses on the level of the characteristics
2. place a specific characteristic along an ordered sequence |
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The dimensional approach places specific characteristic along an __________ _________.
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The dimensional approach places specific characteristic along an ordered sequence.
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What two symptoms are required for a Dx of depression?
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1. Depressed mood
2. Apathy / loss of interest |
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Indications for antidepressants (7)
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1. Treatment of depressive illness - major depressive episode (single/recurrent)
2. Depressive phases of bipolar affective disorder 3. Depressive episodes occurring in schizophrenia 4. Preventing recurrence of depressive episodes 5. Adjunctive treatment of anxiety disorders, includes obsessive-compulsive disorder 6. Adjunctive treatment of eating disorders 7. Occasionally, night sedation |
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Efficacy of different antidepressants compared to each?
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All equally efficacious
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On antidepresstants there is a ___-____% improvement compared to 30-40% on placebo) and have similar drop-out rates.
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50-60% improvement compared to 30-40% on placebo) and have similar drop-out rates.
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Drug choice should be tailored to the individual patient, based on what factors?
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1. patient choice
2. side effect profile 3. previous response 4. co-morbidity, 5. suicide risk 6. cost |
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Patients on antidepressants seem to have better outcomes if they are given......
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Given good, clear information about anti-depressants.
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What are the important determinants of antidepressant efficacy? (6)
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1. Prior treatment history in patient/family members
2. Patient preferences 3. Expertise of prescribing provider 4. Side effect profile (sedating or activating) 5. Safety in overdose (10-15 days of a TCA can be a lethal overdose) 6. Drug-drug interactions |
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How many days of a TCA meds can be a lethal overdose
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10-15 days of a TCA can be a lethal overdose.
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There are at least ______ separate pharmacological actions of antidepressants and more than two dozen
antidepressants. |
There are at least EIGHT separate pharmacological actions of antidepressants and more than two dozen antidepressants.
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Most antidepressants block ____________ reuptake.
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Most antidepressants block MONOAMINE reuptake.
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Some antidepressants block A2 receptors and can therefore increase the release of ____ by blocking this pre-synaptic auto receptor.
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Some antidepressants block A2 receptors and can therefore increase the release of NA (noradrenaline) by blocking this pre-synaptic auto receptor.
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Some antidepressants block what enzyme?
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Some block the enzyme monoamine oxidase.
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The monamine hypothesis of depression argues that antidepressants increase what?
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Monamine. |
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The neurotransmitter receptor hypothesis of antidepressant action argues that the the antidepressant blocks what?
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Blocks the reputake pump causing more NT to be in the synapse. |
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The neurotransmitter receptor hypothesis of antidepressant action argues that an increase in neurotransmitters causes receptors to ___________ - _____________. |
The neurotransmitter receptor hypothesis of antidepressant action argues that an increase in neurotransmitters causes receptors to down-regulate. |
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What % of all patients with depression show full remission with optimised treatment, including trials on numerous medications with and without concurrent
psychotherapy? |
Fewer than 50% of all patients with
depression show full remission with optimised treatment, including trials on numerous medications with and without concurrent psychotherapy. |
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Do antidepressants elevate mood in
healthy humans? |
No.
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___% of patients will have treatment failure
with their first tried antidepressant. |
40% of patients will have treatment failure
with their first tried antidepressant |
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Imipramine Doxepin Desipramine
Amoxepine Trimipramine Maprotiline Clomipramine Amitriptyline Nortriptyline Protriptyline What class of drugs? |
Tricyclics and Tetracyclics (TCA).
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Tranylcypramine Phenelzine
Moclobemide What class of drugs? |
Monoamine Oxidase Inhibitors (MAOIs).
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Fluoxetine
Fluvoxamine Sertraline Paroxetine Citalopram What class of drugs? |
SSRIs
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Venlafaxine Duloxetine
What class of drugs? |
Dual Serotonin and Norepinephrine Reuptake Inhibitor (SNRI)
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Nefazodone* Trazodone
What class of drugs? |
Serotonin-2 Antagonist and Reuptake Inhibitors (SARIs)
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Bupropion
What class of drugs? |
Noradrenaline and Dopamine Reuptake Inhibitor (NDRI)
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Mirtazapine
What class of drugs? |
Noradrenergic and Specific Serotonergic Antagonists
(NaSSAs) |
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Reboxetine
What class of drugs? |
Noradrenaline Specific Reuptake Inhibitor (NRI)
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Tianeptine
What class of drugs? |
Serotonin Reuptake Enhancer
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There are 3 “generations” of drugs to treat
depression and related affective disorders (anti-depressants). What are they? |
1. 1st generation: monoamine oxidase inhibitors |
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Monoamine Oxidase Inhibitors: ________ the |
Monoamine Oxidase Inhibitors: INHIBIT the
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Monoamine Oxidase Inhibitors result in more _____________ to be __-________and
___________. |
Monoamine Oxidase Inhibitors result in more neurotransmitter to be re-packaged and
released |
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Side effects of MOI include blockage of MAO on what organ?
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the liver
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MOI can result in a build-up a ______ (a toxin found in many fermented foods and drinks)
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build-up a TYRAMINE a toxin found in many fermented foods and drinks)
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____blood pressure can result fro MOI resulting in an increased risk of what?
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1. High blood pressure
2. Increased risk of stroke (need very careful diet |
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The four main TCAs are? (tricyclic antidepressants)
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1. Amitriptyline (Tryptanol)
2. Dothiepin (Prothiaden; Dothep) 3. Imipramine (Tofranil) 4. Clomipramine (Anafranil) |
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TCAs blockof which two neurotransmitters?
norepinephrine and serotonin and thus elevate neurotransmitter levels in the synapse |
1. norepinephrine
2. serotonin and thus: Elevate neurotransmitter levels in the synapse. |
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TCAs have at least how many other mechanisms of action?
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THREE. (muscarinic, histamine, adrenergic)
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In TCAs:
A Block muscarinic cholinergic receptors will result in (5) |
1. Dry mouth
2. Blurred vision 3. Urinary retention 4. Constipation 5. memory problems |
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In TCAs:
Block H1 histamine receptors will cause? |
1. Sedation
2. Weight gain |
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In TCAs:
Block 1 adrenergic receptors will cause (2) |
1. postural hypotension
2. dizziness |
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TCAs can increase the frequency of....
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Increased frequency of epileptic seizures.
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Most tricyclics are ________.
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SEDATIVE.
Protriptyline is not, imipramine is less sedative than most, amitriptyline and dothiepin are significantly |
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TCA, the elderly, and cardiotoxicity: Discsuss.
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Irregularity of heart rate may be a factor in sudden death in elderly patients with heart disease
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What are the four main SSRIs?
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1. Fluoxetine (Prozac)
2. Sertraline (Zoloft) 3. Paroxetine (Aropax) 4. Fluvoxamine (Luvox) |
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SSRIs: block the re-uptake of _______ ______.
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SSRIs: block the re-uptake of serotonin only
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Elevate serotonin levels in the synapse without directly influencing other _____________.
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Elevate serotonin levels in the synapse without directly influencing other neurotransmitters
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Side effects of SSRIs (2) and why? (3 areas)
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1. nausea
2. sexual dysfunciton Side effects: nausea, sexual dysfunction (serotonin receptors also in gut, hypothalamus and sex organs) |
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Cardiovascular concern and SSRI's
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Little cardiovascular concern.
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SSRI and SEs
Stimulant effects such as ‘nervousness’, insomnia Other CNS effects: dizziness, headache, tremor GI effects: nausea, vomiting, diarrhoea, abdominal discomfort Weight loss/gain common, uncommon or rare? |
common
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SSRI and SEs
Sedation; dry mouth; sweating; sexual dysfunction including decreased libido, anorgasmia, delayed ejaculation common, uncommon or rare? |
uncommon
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SSRI and SEs
Mania; convulsions; movement disorders: tremor, akathisia, dystonia or dyskinesia ECG, BP or heart rate changes (arrhythmias) common, uncommon or rare? |
Rare
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SSRIs versus tricyclics: (2 points)
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1. more selective action on serotonin uptake - less
anticholinergic side effects 2. Free from membrane stabilising effects on the heart - less cardiotoxic side effects |
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are SSRIs more effective than TCA? (2)
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No more effective. They're the same.
No more rapid in onset of action (NB fluoxetine steady state reached in 2-6 weeks) |
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SSRI vs TCA
Different side effect profile of SSRI may have advantages including |
1. less sedation
2. anticholinergic effects 3. cardiotoxicity 4. weight gain helpful where depression complicated by obesity or heart disease but more gastro-intestinal side effects |
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SSRI can be helpful where depression complicated by _________ or _________ ________ but more gastro-intestinal side effects
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SSRI can be helpful where depression complicated by obesity or heart disease but more gastro-intestinal side effects.
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Which class of antidepressants may be helpful in patients unable to tolerate TCAs?
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SSRIs.
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Suicide risk important - if high risk - probably safer to prescribe an ____
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SSRI
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TCA vs SSRI in terms of cost?
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SSRIs more expensive
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If TCAs have worked before – _________.
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continue
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Anti-depressants: 3rd generation
Act as SSRIs but also antagonists at _______ and _________ receptors so restrict serotonin’s action to _________ receptors. receptors |
Act as SSRIs but also antagonists at 5-HT2 and 5-HT3 receptors so restrict serotonin’s action to 5-HT1 receptors |
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5-HT3 receptor stimulation will cause what symptom?
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nausea
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5-HT2 receptor stimulation will cause what symptom?
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sexual dysfunciton
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Anti-depressants: 3rd generation |
Different mechanism of action from tricyclics and SSRIs; i.e. it has BOTH |
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Anti-depressants: 3rd generation |
Selective inhibition of reuptake of serotonin and |
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Shares similar advantages with the what class of antidepressant over tricyclics? |
Shares similar advantages with the SSRIs over
tricyclics. |
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Potential advantages of Venlafaxine (Efexor) over SSRIs? (2)
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1. Increase in efficacy at higher doses |
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Other Potential advantages of Venlafaxin over SSRIs (3)
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1. Clinically meaningful more rapid onset of action (within 1 week)
2. Safety in over dosage is high 3. Probably less interactions with other drugs |
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Disadvantages of Effexor (Venlafaxine) relative to the SSRIs? (3)
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1. 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
2. Original need for twice a day dosing schedule now overcome with extended release formulation 3. Dose needs to be titrated |
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Three most common side effects of Effexor?
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1. nausea
2. dizziness 3. sedation |
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Effexor:
At higher doses (i.e., above 225mg), dose-dependent increases in: |
1. blood pressure (rarely observed below 225 mg/day)
2. sweating 3. tremors |
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Bupropion is marketed as Zyban and Wellbutrin for what two conditions?
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Zyban for smoking cessation
Wellbutrin for treating depression |
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What is the only non-nicotine medication approved for smoking cessation?
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Bupropion (Zyban)
Only non-nicotine medication approved for smoking cessation (abstinence rates double placebo; efficacious as maintenance medication for 6 months post cessation) |
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What is the mechanism of Zyban / Bupropion?
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Blocks neural re-uptake of dopamine and/or
noradrenaline. Weak if any effect in the re-uptake of serotonin |
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Which antidepressant is associated with decreased levels of sexual side-effects in depression?
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Bupropion
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Physical Sx of depression : appetite and sleep: respond best to what?
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antidepressant medication
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Cognitive and behavioural Sx of depression respond best to?
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Psychological strategies (i.e. increasing activity,
structured problem solving, CBT, assertiveness and communication training) |
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In terms of recovery from depression, what tends to improve first, second, and last?
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1st Appetite and sleep tend to improve first
2nd behaviour second 3rd thoughts and feelings improve last |
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Effects of treatment of antidepressants.
We expect full antidepressant treatment effects and side effect subsiding by what week? |
4
SE and treatment effect crossover is at two weeks. |
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Cognitive therapy and antidepressant medications have __________ _______ _______ ___________.
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Cognitive therapy and antidepressant medications have COMPARABLE SHORT TERM EFFECTS.
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Drug effect accounts for ___% of measured improvement in depression.
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20 - 25%. Same as placebo!
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Placebo effects are a ________ ________ of the
measured improvement in treatment for depression. |
Placebo effects are a major portion of the
measured improvement. Studies reporting large effect sizes for medication also had large effect sizes for placebos. |
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In the treatment of depression, the amount of improvement is a function of ___________ __________.
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Amount of improvement was a function of BASELINE SEVERITY: ....
Drug type did not mediate this effect, although venlafaxine and paroxetine had larger effect sizes relative to placebo than did fluoxetine. |
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Kirsch et al, 2008: Results
“the overall effect of new-generation antidepressant medications is below recommended criteria for clinical significance. We also find that efficacy reaches clinical significance only in trials involving the most extremely depressed patients, and that this pattern is due to a decrease in the response to placebo rather than an increase in the response to medication” (p. 265-266) The differences between drug and placebo were not clinically significant in clinical trials involving either moderately or very severely depressed patients, but did reach the criterion for trials involving patients whose mean initial depression scores were at the upper end of the very severe depression category” (p. 266) |
“the overall effect of new-generation antidepressant medications is below recommended criteria for clinical significance. We also find that efficacy reaches clinical significance only in trials involving the
most extremely depressed patients, and that this pattern is due to a decrease in the response to placebo rather than an increase in the response to medication” (p. 265-266) The differences between drug and placebo were not clinically significant in clinical trials involving either moderately or very severely depressed patients, but did reach the criterion for trials involving patients whose mean initial depression scores were at the upper end of the very severe depression category” (p. 266) |
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“… little evidence to support the prescription of
antidepressant medication to any but the most severely depressed patients, unless alternative treatments have failed to provide benefit.” (p. 266) “the response to placebo in these trials was exceptional and large, duplicating more than 80% of the improvement observed in the drug groups.” (p. 266) “… the increased benefit for extremely depressed patients seems attributable to a decrease in responsiveness to placebo, rather than in an increase in responsiveness to medication.” (p. 266) |
“… little evidence to support the prescription of
antidepressant medication to any but the most severely depressed patients, unless alternative treatments have failed to provide benefit.” (p. 266) “the response to placebo in these trials was exceptional and large, duplicating more than 80% of the improvement observed in the drug groups.” (p. 266) “… the increased benefit for extremely depressed patients seems attributable to a decrease in responsiveness to placebo, rather than in an increase in responsiveness to medication.” (p. 266) |
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Criticisms of the antidepressant Rx meta-anaylsis by prof Gordon Parker? (3).
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1. “... results based on patients who “bear very little
correlation to the people we see in real-life clinical practice” (Australia, Feb 27, ‘08) 2. … i.e. the studied patients were usually hospital outpatients rather than admitted patients, were not suicidal and did not have the co-morbidity of drug and alcohol problems 3. Patients with melancholic depression, are often not included in clinical trials, but 65 to 70% of these patients respond to antidepressants, whereas only 10 to 15%improved taking placebo. |
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Combined (PT and RX) Tx for depression.
Conclusion: Combined therapy is _____ ______ effective than (psychotherapy) PT treatment alone, but it is not clear whether this difference is relevant from a clinical perspective. |
Conclusion: Combined therapy is MORE EFFECTIVE than (psychotherapy) PT treatment alone, but it is not clear whether this difference is relevant from a clinical perspective.
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Supporting antidepressant Management. 4 key points?
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1. Become familiar with commonly used antidepressant medications medication doses
2. Provide basic patient education about antidepressants 3. Support antidepressant medication adherence 4. Know when treatment is ‘not working’ |
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In terms of treatment for depression, it is helpfully to help patients and providers identify: (3)
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1. Potentially inadequate doses
2. Ineffective treatment (e.g., persistent depression after adequate duration of antidepressant trial) 3. Side effects - Facilitate patient-provider communication about antidepressant medications - Consult with team psychiatrist about medication questions |
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The key treatment of Tx with antidepressants include: (3)
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1. Use antidepressants, not minor tranquilizers /
benzodiazepines 2. Use adequate doses for an adequate amount of time 3. Start slow and work with side effects but titrate to an effective dose as needed |
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When should you change antidepressant medication if there is an inadequate response?
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Usually after 8-10 weeks
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Max dose of
Fluoxetine Paroxetine Citalopram Duloxetine |
60 mg
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Max dose of Escitalopram?
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30mg
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Max dose of Sertraline?
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200mg
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Max dose of Venlafaxine?
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300mg
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Max dose of Buproprion SR?
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450mg
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Max dose of Nortriptyline?
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Nortriptyline 125 mg (check serum level)
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Max dose of Desipramine?
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200 mg (check serum level)
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In the Tx of depression and to prevent relapse, it is important to emphasise?
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Need for continuation or maintenance treatment to prevent relapse even after the patient feels better
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Plan B: antidepressant RX for SSRI non responders.
About _____ 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 |
About ONE in four patients who are changed to either another SSRI, Buproprion-SR, or Venlafaxine XR will respond to the new drug
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SE in antidepressant.
Four strategies for short term? (4) More longer term options? (2) |
1. Wait and support (e.g., GI side effects)
2. Adjust medication timing (e.g., take sedating meds at bedtime) 3. Consider temporary dose reduction 4. Treat side effects (see intervention manual Also: Change to a different antidepressant Change to or add psychotherapy |
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Risk of relapse following the discontinuation of antidepressatns
if 1 prior episode = if 2 prior episodes = if 3 prior episodes = Also increased with dysthymia and residual depressive symptoms |
Risk of relapse
50% if 1 prior episode 75% if 2 prior episodes 90% if 3 prior episodes Also increased with dysthymia and residual depressive symptoms |
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How long should you treat all adults for after the initial response?
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4 to 9 months.
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How long should you treat all adults at high risk for relapse?
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Treat those at high risk for relapse for 2 years or longer.
Some may need lifetime treatment. |
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What dose should be given of antidepressants to prevent relapse?
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Maintenance treatment should be at FULL dose.
Make a relapse prevention plan. |
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What should you do to avoid a discontinuation syndrome when ceasing antidepressant use?
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Taper antidepressants slowly to avoid discontinuation syndrome.
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There are over __ FDA approved antidepressants and all are effective in about __% & of patients.
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There are over 20 FDA approved antidepressants and all are effective in ~ 50 % of patients.
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it may take ______ ______ until an effective medication is identified for a particular patient.
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it may take several trials until an effective medication is identified for a particular patient
Patients need support during this time |
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If medications are not effective after 8-10 weeks at a
therapeutic dose (4) |
1. make sure patient is taking medication as prescribed
2. consult with prescribing provider 3. consult with team psychiatrist 4. a change in treatment plan is likely indicated (e.g., change in medication, augmentation of medication, switch to psychotherapy or other depression treatment) |
|
How long is a full treatment course of antidepressants?
|
12 months
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RANZCP Guidelines:
Moderate depression: What are all equally effective? (4) |
all anti-depressants, CBT & IPT equally effective
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RANZCP Guidelines:
Severe depression: (2) |
all anti-depressants, psychotherapy later
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RANZCP Guidelines:
Severe depression with psychosis |
ECT alone or TCA plus antipsychotic
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RANZCP Guidelines:
Augmentation: Severe uncomplicated: |
TCA, venlafaxine or CBT/IPT |
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RANZCP Guidelines: |
TCA or venlafaxine |
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RANZCP Guidelines:
Augmentation: Atypical: |
Phenelzine or CBT/IPT
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Cognitive therapy and antidepressant medications have comparable________ ________ _________.
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Cognitive therapy and antidepressant medications have comparable short term effects.
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What does CT prior to treatment with antidepressants protect against?
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The data demonstrates that 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.
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Likelihood of relapse:
___ % of ADM responders relapsed following medication withdrawal compared with a only ___ % of the patients who had been treated with cognitive therapies. |
Likelihood of relapse:
76% of ADM responders relapsed following medication withdrawal compared with a only 31% of the patients who had been treated with cognitive therapies. |
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Cognitive therapy has an
________ ____________ that is not found with ADM. |
Cognitive therapy has an enduring effect that is not found with ADM.
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. |
|
Antidepressant medications (ADM) seem to be __________ _________ rather than ___________.
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Antidepressant medications (ADM) seem to be symptom suppressive rather than curative.
ADM is effective in the treatment of an acute depressive episode, and is preventive so long as its use is maintained, no published findings today to suggest that ADM’s reduced future risk of depressive episodes once their use is terminated. |
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This suggests that the causal mechanisms of depression are unchanged by ADM and so patients are left with an elevated risk for .... ?
|
This suggests that the causal mechanisms of depression are unchanged by ADM and so patients are left with an elevated risk for subsequent episodes if they stop taking their medication
|
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Acutely depressed individuals are characterised by decreased ___________ __________ function possibly arising from ________ amygdala
_________. |
Acutely depressed individuals are characterised by decreased prefrontal function possibly arising from increased amygdala reactivity
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CT operates by increasing ___________ _________, while ADM operates more directly on the ___________.
|
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. |
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If the amygdala is the “point of entry” for environmental stressors, cessation of ADM could leave the person at risk of having strong
________ __________ to new environmental insults. |
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
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By contrast, CT works by building the skills that require active operation of _____, thus making the effects more enduring.
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By contrast, CT works by building the skills that require active operation of PFC, thus making the effects more enduring.
|
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________ hyperactivity leads to decreased _____ function or efficiency.
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AMYGDALA hyperactivity leads to decreased PFC function or efficiency.
|
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CT increases _____ functioning.
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CT increases PFC functioning.
|
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ADM decreases amygdala ___________ ____________.
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ADM decreases amygdala hyperactivity directly. |
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Increase PFC function leads to decreased ___________ _________. |
Increase PFC function leads to decreased amydala reactivity. |
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The effect size of the antidepressants is ___ _______, but is significant
|
The effect size of the antidepressants is not
large, but is significant |
|
Who receives the most benefit from ADM?
|
More severe patients achieve the most benefit
|
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__________ agents can impact upon the
depressive disorders. |
Numerous agents can impact upon the |
|
All ADM are mediated through which three neurotransmitters? (3)
|
1. monoamines, 3. 5HT |
|
Depression Dx: Depressed mood and apathy/loss of interest + four or more of... (7) |
1. Weight/appetite changes 2. Sleep disturbance 3. Psychomotor agitaiton/retardation 4. Guilt/worthlessnes 5. Executive Dysfunction 6. Suicidal ideation 7. Fatigue |
|
TCA's block the re-uptake of (2) to elevate neurostransmitters in the synapse |
1. Norepinepherine 2. Serotonin |
|
S/E: Postural hypotension and diziness.
What's being blocked? |
a1 andrenergic receptors |
|
S/E: sedation and weight gain
What's being blocked? |
H1 Histamine receptors |
|
S/E: dry mouth, blurred vision, urinary retention, constipation, and memory problems.
What's being blocked? |
Muscaric cholinergic receptors |
|
If someone has epilepsy, which antidepressant WOULDN'T you prescribe? |
TCA (as it increases seizure risk!) |
|
If someone has heart problems, which AD wouldn't you prescribe? (3) |
TCA, MOAI, SNRI (all cary cardiovascular heart risksI) |
|
If someone is fat, which wouldn't you prescribe? (2) |
TCA and mirtazepine (both cause weight gain). |
|
Which is the only antidepressant that doesn't help with anxiety? |
Buproprion |
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Which two antidepressants might be helpful to assist with pain? |
TCA and SNRI |
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If someone has no drive, which two anti-depressants would you avoid? |
TCA and Mirtazpapine |
|
Which anti-depressants might improve sleep? (3) |
TCA, SNRI and Mirtazepine |
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Which three antidepressants are good if someone is on a shizload of drugs (want to avoid interactions)? |
1. SSRI 2. Buproprion, 3. Mirtazepine |
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Which antidepressant has a weak (if any) reuptake of serotonin? |
Buproprion |
|
If someone is having problems concentrating, which AD might be helpful and why? |
1. Buproprion (NDRI) |
|
What might we tackle sleep with? (3)
Think: 5HT/GABA/Histamine |
1. Hypnotics 2. Sedating antidpressants 3. STOP activating antidepressants |
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Antidepressants in children 6 - 12? |
no |
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When does the decline in AD take place in terms of lifespan? |
>65 |
|
Cuijiper found what in their meta-analysis? |
That the effects of psychotherapy might be overstated |
|
What should the plan B look like for SSRI-non responders? |
1. Change to another SSRI, Bupproprion- or Venlafaxine.
27-32% of patients will respond to augmentation with Buproprion |
|
Monoamine Oxidase Inhibitors: inhibit the
|
breaks down dopamine, norepinephrine and serotonin inside the terminal
|
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Side effects of MAOI include a blockade of what where? |
MAO in liver |
|
What is tyramine commonly found in? |
many fermented foods and drinks (cheese!!) |
|
TCA's block the re-uptake of both (2) |
norepinephrine and serotonin |
|
What is the mechanism of Buproprion? |
Mechanism: blocks neural re-uptake of dopamine and/or noradrenaline. Weak if any effect in the re-uptake of |
|
What meds might assist with problems concentrating in depression are attributable to dysfunciton DLFPC? (2) |
Buproprion Modafinil |
|
Medications for dysfuncitoning amygdala in depression? (2) |
SSRI SNRI
CBT and BZD might also assist. |
|
With anxiety: Target (2) |
5ht GABA |
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Antidepressants are most effective in which age group? |
Adults 26 - 64. |
|
What is the key message to communicate to patients re: AD meds? |
By restoring a chemical imbalance in the brain |
|
Long-term possible S/E of antidepressant meds? |
Sexual dysfunction |
|
treatment of choice after failuer of other anitd |
effexor |