Lecture 4-5: Antidepressants - Pete

Front 1

What is the categorical approach?


What sort of approach is it?

Back 1

Distinctions among members of different categories are qualitative (taxonomy)

“all or none”

Front 2

What does the dimensional approach focus on?

Back 2

1. It focuses on the level of the characteristics

2. place a specific characteristic along an ordered
sequence

Front 3

The dimensional approach places specific characteristic along an __________ _________.

Back 3

The dimensional approach places specific characteristic along an ordered sequence.

Front 4

What two symptoms are required for a Dx of depression?

Back 4

1. Depressed mood
2. Apathy / loss of interest

Front 5

Indications for antidepressants (7)

Back 5

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

Front 6

Efficacy of different antidepressants compared to each?

Back 6

All equally efficacious

Front 7

On antidepresstants there is a ___-____% improvement compared to 30-40% on placebo) and have similar drop-out rates.

Back 7

50-60% improvement compared to 30-40% on placebo) and have similar drop-out rates.

Front 8

Drug choice should be tailored to the individual patient, based on what factors?

Back 8

1. patient choice
2. side effect profile
3. previous response
4. co-morbidity,
5. suicide risk
6. cost

Front 9

Patients on antidepressants seem to have better outcomes if they are given......

Back 9

Given good, clear information about anti-depressants.

Front 10

What are the important determinants of antidepressant efficacy? (6)

Back 10

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

Front 11

How many days of a TCA meds can be a lethal overdose

Back 11

10-15 days of a TCA can be a lethal overdose.

Front 12

There are at least ______ separate pharmacological actions of antidepressants and more than two dozen
antidepressants.

Back 12

There are at least EIGHT separate pharmacological actions of antidepressants and more than two dozen antidepressants.

Front 13

Most antidepressants block ____________ reuptake.

Back 13

Most antidepressants block MONOAMINE reuptake.

Front 14

Some antidepressants block A2 receptors and can therefore increase the release of ____ by blocking this pre-synaptic auto receptor.

Back 14

Some antidepressants block A2 receptors and can therefore increase the release of NA (noradrenaline) by blocking this pre-synaptic auto receptor.

Front 15

Some antidepressants block what enzyme?

Back 15

Some block the enzyme monoamine oxidase.

Front 16

The monamine hypothesis of depression argues that antidepressants increase what?

Back 16

Monamine.

Increase in neurotransmitters cause return to normal state.

Front 17

The neurotransmitter receptor hypothesis of antidepressant action argues that the the antidepressant blocks what?

Back 17

Blocks the reputake pump causing more NT to be in the synapse.

Front 18

The neurotransmitter receptor hypothesis of antidepressant action argues that an increase in neurotransmitters causes receptors to ___________ - _____________.

Back 18

The neurotransmitter receptor hypothesis of antidepressant action argues that an increase in neurotransmitters causes receptors to down-regulate.

Front 19

What % of all patients with depression show full remission with optimised treatment, including trials on numerous medications with and without concurrent
psychotherapy?

Back 19

Fewer than 50% of all patients with
depression show full remission with optimised
treatment, including trials on numerous
medications with and without concurrent
psychotherapy.

Front 20

Do antidepressants elevate mood in
healthy humans?

Back 20

No.

Front 21

___% of patients will have treatment failure
with their first tried antidepressant.

Back 21

40% of patients will have treatment failure
with their first tried antidepressant

Front 22

Imipramine Doxepin Desipramine
Amoxepine Trimipramine Maprotiline
Clomipramine Amitriptyline Nortriptyline
Protriptyline

What class of drugs?

Back 22

Tricyclics and Tetracyclics (TCA).

Front 23

Tranylcypramine Phenelzine
Moclobemide

What class of drugs?

Back 23

Monoamine Oxidase Inhibitors (MAOIs).

Front 24

Fluoxetine
Fluvoxamine Sertraline Paroxetine
Citalopram

What class of drugs?

Back 24

SSRIs

Front 25

Venlafaxine Duloxetine

What class of drugs?

Back 25

Dual Serotonin and Norepinephrine Reuptake Inhibitor (SNRI)

Front 26

Nefazodone* Trazodone

What class of drugs?

Back 26

Serotonin-2 Antagonist and Reuptake Inhibitors (SARIs)

Front 27

Bupropion

What class of drugs?

Back 27

Noradrenaline and Dopamine Reuptake Inhibitor (NDRI)

Front 28

Mirtazapine

What class of drugs?

Back 28

Noradrenergic and Specific Serotonergic Antagonists
(NaSSAs)

Front 29

Reboxetine

What class of drugs?

Back 29

Noradrenaline Specific Reuptake Inhibitor (NRI)

Front 30

Tianeptine

What class of drugs?

Back 30

Serotonin Reuptake Enhancer

Front 31

There are 3 “generations” of drugs to treat
depression and related affective disorders
(anti-depressants). What are they?

Back 31

1. 1st generation: monoamine oxidase inhibitors
(MAOI’s) and tricyclic anti-depressants
2. 2nd generation: selective serotonin reuptake
inhibitors (SSRI’s)
3. 3rd generation: tricyclic anti-depressants with a twist

Front 32

Monoamine Oxidase Inhibitors: ________ the
action of monoamine oxidase which breaks
down what three neurotransmitter?

Where does this breakdown occur?

Back 32

Monoamine Oxidase Inhibitors: INHIBIT the
action of monoamine oxidase which breaks
down dopamine, norepinephrine and serotonin

INSIDE THE TERMINAL.

Front 33

Monoamine Oxidase Inhibitors result in more _____________ to be __-________and
___________.

Back 33

Monoamine Oxidase Inhibitors result in more neurotransmitter to be re-packaged and
released

Front 34

Side effects of MOI include blockage of MAO on what organ?

Back 34

the liver

Front 35

MOI can result in a build-up a ______ (a toxin found in many fermented foods and drinks)

Back 35

build-up a TYRAMINE a toxin found in many fermented foods and drinks)

Front 36

____blood pressure can result fro MOI resulting in an increased risk of what?

Back 36

1. High blood pressure
2. Increased risk of stroke (need very careful diet

Front 37

The four main TCAs are? (tricyclic antidepressants)

Back 37

1. Amitriptyline (Tryptanol)
2. Dothiepin (Prothiaden; Dothep)
3. Imipramine (Tofranil)
4. Clomipramine (Anafranil)

Front 38

TCAs blockof which two neurotransmitters?

norepinephrine and serotonin and thus
elevate neurotransmitter levels in the
synapse

Back 38

1. norepinephrine
2. serotonin and thus:

Elevate neurotransmitter levels in the synapse.

Front 39

TCAs have at least how many other mechanisms of action?

Back 39

THREE. (muscarinic, histamine, adrenergic)

Front 40

In TCAs:

A Block muscarinic cholinergic receptors will result in (5)

Back 40

1. Dry mouth
2. Blurred vision
3. Urinary retention
4. Constipation
5. memory problems

Front 41

In TCAs:

Block H1 histamine receptors will cause?

Back 41

1. Sedation
2. Weight gain

Front 42

In TCAs:
Block 1 adrenergic receptors will cause (2)

Back 42

1. postural hypotension
2. dizziness

Front 43

TCAs can increase the frequency of....

Back 43

Increased frequency of epileptic seizures.

Front 44

Most tricyclics are ________.

Back 44

SEDATIVE.

Protriptyline is not, imipramine is less sedative than most,

amitriptyline and dothiepin are significantly
sedative

Front 45

TCA, the elderly, and cardiotoxicity: Discsuss.

Back 45

Irregularity of heart rate may be a factor in sudden death in elderly patients with heart disease

Front 46

What are the four main SSRIs?

Back 46

1. Fluoxetine (Prozac)
2. Sertraline (Zoloft)
3. Paroxetine (Aropax)
4. Fluvoxamine (Luvox)

Front 47

SSRIs: block the re-uptake of _______ ______.

Back 47

SSRIs: block the re-uptake of serotonin only

Front 48

Elevate serotonin levels in the synapse without directly influencing other _____________.

Back 48

Elevate serotonin levels in the synapse without directly influencing other neurotransmitters

Front 49

Side effects of SSRIs (2) and why? (3 areas)

Back 49

1. nausea
2. sexual dysfunciton

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

Front 50

Cardiovascular concern and SSRI's

Back 50

Little cardiovascular concern.

Front 51

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?

Back 51

common

Front 52

SSRI and SEs

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

common, uncommon or rare?

Back 52

uncommon

Front 53

SSRI and SEs

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

common, uncommon or rare?

Back 53

Rare

Front 54

SSRIs versus tricyclics: (2 points)

Back 54

1. more selective action on serotonin uptake - less
anticholinergic side effects

2. Free from membrane stabilising effects on the heart -
less cardiotoxic side effects

Front 55

are SSRIs more effective than TCA? (2)

Back 55

No more effective. They're the same.

No more rapid in onset of action (NB fluoxetine steady
state reached in 2-6 weeks)

Front 56

SSRI vs TCA

Different side effect profile of SSRI may have advantages including

Back 56

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

Front 57

SSRI can be helpful where depression complicated by _________ or _________ ________ but more gastro-intestinal side effects

Back 57

SSRI can be helpful where depression complicated by obesity or heart disease but more gastro-intestinal side effects.

Front 58

Which class of antidepressants may be helpful in patients unable to tolerate TCAs?

Back 58

SSRIs.

Front 59

Suicide risk important - if high risk - probably safer to prescribe an ____

Back 59

SSRI

Front 60

TCA vs SSRI in terms of cost?

Back 60

SSRIs more expensive

Front 61

If TCAs have worked before – _________.

Back 61

continue

Front 62

Anti-depressants: 3rd generation

Act as SSRIs but also antagonists at _______ and _________ receptors so restrict serotonin’s action to _________ receptors.
receptors

Back 62

Act as SSRIs but also antagonists at 5-HT2 and 5-HT3 receptors so restrict serotonin’s action to 5-HT1 receptors

Front 63

5-HT3 receptor stimulation will cause what symptom?

Back 63

nausea

Front 64

5-HT2 receptor stimulation will cause what symptom?

Back 64

sexual dysfunciton

Front 65

Anti-depressants: 3rd generation
Venlafaxine (Efexor): 1

Different mechanism of action from tricyclics and SSRIs; i.e. it has _____

Back 65

Different mechanism of action from tricyclics and SSRIs; i.e. it has BOTH

Front 66

Anti-depressants: 3rd generation
Venlafaxine (Efexor): 1

Selective inhibition of reuptake of which two neurotransmitters? (and, to lesser extent,
dopamine)

Back 66

Selective inhibition of reuptake of serotonin and
noradrenaline (NA) (and, to lesser extent,
dopamine).

Front 67

Shares similar advantages with the what class of antidepressant over tricyclics?

Back 67

Shares similar advantages with the SSRIs over
tricyclics.

Front 68

Potential advantages of Venlafaxine (Efexor) over SSRIs? (2)

Back 68

1. Increase in efficacy at higher doses
- consistent with the addition of 2nd action
(on NA), at 225 mg/day

2. magnitude of the antidepressant effect is
50% higher than that seen with SSRIs

RCTs in hospitalised patients with melancholia: 225
mg/day venlafaxine superior to placebo and fluoxetine

Front 69

Other Potential advantages of Venlafaxin over SSRIs (3)

Back 69

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

Front 70

Disadvantages of Effexor (Venlafaxine) relative to the SSRIs? (3)

Back 70

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

Front 71

Three most common side effects of Effexor?

Back 71

1. nausea
2. dizziness
3. sedation

Front 72

Effexor:
At higher doses (i.e., above 225mg), dose-dependent increases in:

Back 72

1. blood pressure (rarely observed below 225 mg/day)
2. sweating
3. tremors

Front 73

Bupropion is marketed as Zyban and Wellbutrin for what two conditions?

Back 73

Zyban for smoking cessation

Wellbutrin for treating depression

Front 74

What is the only non-nicotine medication approved for smoking cessation?

Back 74

Bupropion (Zyban)

Only non-nicotine medication approved for smoking cessation (abstinence rates double placebo; efficacious as maintenance medication for 6 months post cessation)

Front 75

What is the mechanism of Zyban / Bupropion?

Back 75

Blocks neural re-uptake of dopamine and/or
noradrenaline.

Weak if any effect in the re-uptake of
serotonin

Front 76

Which antidepressant is associated with decreased levels of sexual side-effects in depression?

Back 76

Bupropion

Front 77

Physical Sx of depression : appetite and sleep: respond best to what?

Back 77

antidepressant medication

Front 78

Cognitive and behavioural Sx of depression respond best to?

Back 78

Psychological strategies (i.e. increasing activity,
structured problem solving, CBT, assertiveness and communication training)

Front 79

In terms of recovery from depression, what tends to improve first, second, and last?

Back 79

1st Appetite and sleep tend to improve first

2nd behaviour second

3rd thoughts and feelings improve last

Front 80

Effects of treatment of antidepressants.

We expect full antidepressant treatment effects and side effect subsiding by what week?

Back 80

4

SE and treatment effect crossover is at two weeks.

Front 81

Cognitive therapy and antidepressant medications have __________ _______ _______ ___________.

Back 81

Cognitive therapy and antidepressant medications have COMPARABLE SHORT TERM EFFECTS.

Front 82

Drug effect accounts for ___% of measured improvement in depression.

Back 82

20 - 25%. Same as placebo!

Front 83

Placebo effects are a ________ ________ of the
measured improvement in treatment for depression.

Back 83

Placebo effects are a major portion of the
measured improvement.

Studies reporting large effect sizes for medication also had large effect sizes for placebos.

Front 84

In the treatment of depression, the amount of improvement is a function of ___________ __________.

Back 84

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.

Front 85

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)

Back 85

“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)

Front 86

“… 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)

Back 86

“… 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)

Front 87

Criticisms of the antidepressant Rx meta-anaylsis by prof Gordon Parker? (3).

Back 87

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.

Front 88

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.

Back 88

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.

Front 89

Supporting antidepressant Management. 4 key points?

Back 89

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’

Front 90

In terms of treatment for depression, it is helpfully to help patients and providers identify: (3)

Back 90

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

Front 91

The key treatment of Tx with antidepressants include: (3)

Back 91

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

Front 92

When should you change antidepressant medication if there is an inadequate response?

Back 92

Usually after 8-10 weeks

Front 93

Max dose of
Fluoxetine Paroxetine Citalopram Duloxetine

Back 93

60 mg

Front 94

Max dose of Escitalopram?

Back 94

30mg

Front 95

Max dose of Sertraline?

Back 95

200mg

Front 96

Max dose of Venlafaxine?

Back 96

300mg

Front 97

Max dose of Buproprion SR?

Back 97

450mg

Front 98

Max dose of Nortriptyline?

Back 98

Nortriptyline 125 mg (check serum level)

Front 99

Max dose of Desipramine?

Back 99

200 mg (check serum level)

Front 100

In the Tx of depression and to prevent relapse, it is important to emphasise?

Back 100

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

Front 101

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

Back 101

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

Front 102

SE in antidepressant.

Four strategies for short term? (4)

More longer term options? (2)

Back 102

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

Front 103

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

Back 103

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

Front 104

How long should you treat all adults for after the initial response?

Back 104

4 to 9 months.

Front 105

How long should you treat all adults at high risk for relapse?

Back 105

Treat those at high risk for relapse for 2 years or longer.

Some may need lifetime treatment.

Front 106

What dose should be given of antidepressants to prevent relapse?

Back 106

Maintenance treatment should be at FULL dose.

Make a relapse prevention plan.

Front 107

What should you do to avoid a discontinuation syndrome when ceasing antidepressant use?

Back 107

Taper antidepressants slowly to avoid discontinuation syndrome.

Front 108

There are over __ FDA approved antidepressants and all are effective in about __% & of patients.

Back 108

There are over 20 FDA approved antidepressants and all are effective in ~ 50 % of patients.

Front 109

it may take ______ ______ until an effective medication is identified for a particular patient.

Back 109

it may take several trials until an effective medication is identified for a particular patient

Patients need support during this time

Front 110

If medications are not effective after 8-10 weeks at a
therapeutic dose (4)

Back 110

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)

Front 111

How long is a full treatment course of antidepressants?

Back 111

12 months

Front 112

RANZCP Guidelines:
Moderate depression: What are all equally effective? (4)

Back 112

all anti-depressants, CBT & IPT equally effective

Front 113

RANZCP Guidelines:
Severe depression: (2)

Back 113

all anti-depressants, psychotherapy later

Front 114

RANZCP Guidelines:
Severe depression with psychosis

Back 114

ECT alone or TCA plus antipsychotic

Front 115

RANZCP Guidelines:
Augmentation:

Severe uncomplicated:

Back 115

TCA, venlafaxine or CBT/IPT

Front 116

RANZCP Guidelines:
Augmentation:

Severe with melancholia? (2)

Back 116

TCA or venlafaxine

Front 117

RANZCP Guidelines:
Augmentation:

Atypical:

Back 117

Phenelzine or CBT/IPT

Front 118

Cognitive therapy and antidepressant medications have comparable________ ________ _________.

Back 118

Cognitive therapy and antidepressant medications have comparable short term effects.

Front 119

What does CT prior to treatment with antidepressants protect against?

Back 119

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.

Front 120

Likelihood of relapse:
___ % of ADM responders relapsed following
medication withdrawal compared with a only
___ % of the patients who had been treated with
cognitive therapies.

Back 120

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.

Front 121

Cognitive therapy has an
________ ____________ that is not found with ADM.

Back 121

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.

Front 122

Antidepressant medications (ADM) seem to be __________ _________ rather than ___________.

Back 122

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.

Front 123

This suggests that the causal mechanisms of depression are unchanged by ADM and so patients are left with an elevated risk for .... ?

Back 123

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

Front 124

Acutely depressed individuals are characterised by decreased ___________ __________ function possibly arising from ________ amygdala
_________.

Back 124

Acutely depressed individuals are characterised by decreased prefrontal function possibly arising from increased amygdala reactivity

Front 125

CT operates by increasing ___________ _________, while ADM operates more directly on the ___________.

Back 125

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.

Front 126

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.

Back 126

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

Front 127

By contrast, CT works by building the skills that require active operation of _____, thus making the effects more enduring.

Back 127

By contrast, CT works by building the skills that require active operation of PFC, thus making the effects more enduring.

Front 128

________ hyperactivity leads to decreased _____ function or efficiency.

Back 128

AMYGDALA hyperactivity leads to decreased PFC function or efficiency.

Front 129

CT increases _____ functioning.

Back 129

CT increases PFC functioning.

Front 130

ADM decreases amygdala ___________ ____________.

Back 130

ADM decreases amygdala hyperactivity directly.

Front 131

Increase PFC function leads to decreased ___________ _________.

Back 131

Increase PFC function leads to decreased amydala reactivity.

Front 132

The effect size of the antidepressants is ___ _______, but is significant

Back 132

The effect size of the antidepressants is not
large, but is significant

Front 133

Who receives the most benefit from ADM?

Back 133

More severe patients achieve the most benefit

Front 134

__________ agents can impact upon the
depressive disorders.

Back 134

Numerous agents can impact upon the
depressive disorders

Front 135

All ADM are mediated through which three neurotransmitters? (3)

Back 135

1. monoamines,
2. NA

3. 5HT

Front 136

Depression Dx:

Depressed mood and apathy/loss of interest + four or more of... (7)

Back 136

1. Weight/appetite changes

2. Sleep disturbance

3. Psychomotor agitaiton/retardation

4. Guilt/worthlessnes

5. Executive Dysfunction

6. Suicidal ideation

7. Fatigue

Front 137

TCA's block the re-uptake of (2) to elevate neurostransmitters in the synapse

Back 137

1. Norepinepherine

2. Serotonin

Front 138

S/E: Postural hypotension and diziness.

What's being blocked?

Back 138

a1 andrenergic receptors

Front 139

S/E: sedation and weight gain

What's being blocked?

Back 139

H1 Histamine receptors

Front 140

S/E: dry mouth, blurred vision, urinary retention, constipation, and memory problems.

What's being blocked?

Back 140

Muscaric cholinergic receptors

Front 141

If someone has epilepsy, which antidepressant WOULDN'T you prescribe?

Back 141

TCA (as it increases seizure risk!)

Front 142

If someone has heart problems, which AD wouldn't you prescribe? (3)

Back 142

TCA, MOAI, SNRI (all cary cardiovascular heart risksI)

Front 143

If someone is fat, which wouldn't you prescribe? (2)

Back 143

TCA and mirtazepine (both cause weight gain).

Front 144

Which is the only antidepressant that doesn't help with anxiety?

Back 144

Buproprion

Front 145

Which two antidepressants might be helpful to assist with pain?

Back 145

TCA and SNRI

Front 146

If someone has no drive, which two anti-depressants would you avoid?

Back 146

TCA and Mirtazpapine

Front 147

Which anti-depressants might improve sleep? (3)

Back 147

TCA, SNRI and Mirtazepine

Front 148

Which three antidepressants are good if someone is on a shizload of drugs (want to avoid interactions)?

Back 148

1. SSRI

2. Buproprion,

3. Mirtazepine

Front 149

Which antidepressant has a weak (if any) reuptake of serotonin?

Back 149

Buproprion

Front 150

If someone is having problems concentrating, which AD might be helpful and why?

Back 150

1. Buproprion (NDRI)

Front 151

What might we tackle sleep with? (3)

Think: 5HT/GABA/Histamine

Back 151

1. Hypnotics

2. Sedating antidpressants

3. STOP activating antidepressants

Front 152

Antidepressants in children 6 - 12?

Back 152

no

Front 153

When does the decline in AD take place in terms of lifespan?

Back 153

>65

Front 154

Cuijiper found what in their meta-analysis?

Back 154

That the effects of psychotherapy might be overstated

Front 155

What should the plan B look like for SSRI-non responders?

Back 155

1. Change to another SSRI, Bupproprion- or Venlafaxine.

27-32% of patients will respond to augmentation with Buproprion

Front 156

Monoamine Oxidase Inhibitors: inhibit the
action of monoamine oxidase which.... does what? (3)

Back 156

breaks down dopamine, norepinephrine and serotonin inside the terminal

Front 157

Side effects of MAOI include a blockade of what where?

Back 157

MAO in liver

Front 158

What is tyramine commonly found in?

Back 158

many fermented foods and drinks (cheese!!)

Front 159

TCA's block the re-uptake of both (2)

Back 159

norepinephrine and serotonin

Front 160

What is the mechanism of Buproprion?

Back 160

Mechanism: blocks neural re-uptake of dopamine and/or noradrenaline. Weak if any effect in the re-uptake of
serotonin

Front 161

What meds might assist with problems concentrating in depression are attributable to dysfunciton DLFPC? (2)

Back 161

Buproprion

Modafinil

Front 162

Medications for dysfuncitoning amygdala in depression? (2)

Back 162

SSRI

SNRI

CBT and BZD might also assist.

Front 163

With anxiety: Target (2)

Back 163

5ht

GABA

Front 164

Antidepressants are most effective in which age group?

Back 164

Adults 26 - 64.

Front 165

What is the key message to communicate to patients re: AD meds?

Back 165

By restoring a chemical imbalance in the brain

Front 166

Long-term possible S/E of antidepressant meds?

Back 166

Sexual dysfunction

Front 167

treatment of choice after failuer of other anitd

Back 167

effexor