Lecture 7 Depression Treatment Flashcards

1
Q

Only effective treatment of MD prior to 1950

A

Electroconvulsive Therapy

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2
Q

Procedure of ECT

A
  • apply brief electrical current to brain
  • results in temporary seizures
  • a course of 6-10 treatments administered
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3
Q

Pros and cons of ECT

A

Pros:

  • effective for severe depression (85%+)
  • still used in people not responsive to other treatments
  • few side effects

Cons:

  • relapse common
  • STM loss
  • uncertain why/how ECT works
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4
Q

1st wave of drugs

A

Monoamine Oxidase Inhibitors (MAOIs)

introduced in 1956 (iproniazide)

14-21 days to effect

MAO breaks down serotonin/norepinephrine, MAO inhibitors block MAO A and B

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5
Q

side effect of MAOIs

A

hypertension -> stroke if not on strict diet

Must avoid Tyramine (beer, red wine, cheeses)

Ideally should inhibit MAO-A only

still used: Parnate (tranylcypromine), Nardil (phenelzine)

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6
Q

2nd wave of drugs

A

Tricyclic medications

introduced in 1960s (imipramine) for psychosis

14-21 days to effect

block presynaptic reuptake of serotonin and norepinephrine

still widely used

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7
Q

side effects of tricyclic medications

A

Vegetative symptoms lift first: increased suicide risk between 10th-14th day

negative side effects: dry mouth, blurred vision, tremor, emotional blunting, drowsiness, anxiety, confusion, restlessness, dizziness, muscle twitches, weakness, nausea, vomiting, constipation, memory

cardiotoxicity

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8
Q

3rd wave of drugs

A

selective serotonin reuptake inhibitors (SSRIs)

introduced in 1980s (prozac)

all waves of drugs are equally effective, only difference is side effects

more specifically block reuptake of serotonin, only act on serotonin so less side effects

drugs of choice at present

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9
Q

side effects of SSRIs

A

fewer and less serious

insomnia, agitation, nausea, sexual dysfunction

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10
Q

other 3rd wave drugs

A

serotonin and norepinephrine reuptake inhibitors (SNRIs)

norepinephrine and dopamine reuptake inhibitors (NDRIs)

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11
Q

Cognitive Behavioural Therapy

A

addresses cognitive biases in thinking (NOT positive thinking)

behavioral components: behavioral activation, behavioural experiments

outcomes comparable to drug therapy, lower relapse rates vs drug treatment alone (29 vs 60%)

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12
Q

Interpersonal Psychotherapy (IPT)

A

not dealing with depression, dealing with interpersonal world
target beginning / exacerbation of depression: Interpersonal/role disputes
Role transitions
Interpersonal deficits

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13
Q

Mindfulness-based cognitive therapy (MBCT)

A

specifically developed to reduce relapse (after 1 episode 50%, 3 episodes 90%)

as effective as prophylactic treatment with maintenance antidepressant medication

notice and distance from mild depressive thoughts (easier and easier to trigger depression)

mechanism: reduces rumination (my thoughts are simply symptoms, divert attention to something else), increases self compassion, increases meta-awareness

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14
Q

prevelance of depression in children

A

<1% preschool

2-3% school-age

15-30% adolescence (14-18)

risk rises greatly in late adolescence

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15
Q

gender difference in depression

A

female:male 2:1

dramatic difference emerge during early-to-mid adolescence

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16
Q

cognitive diathesis-stress model

A

Beck: negative schema

Seligman: helplessness, negative attributions

Cognitive style + negative events -> depression

predict depression from 12-14 years

17
Q

critical time for major depression

A

mid adolescence because:

negative cognitive styles consolidated

increased stress during adolescence

18
Q

why increase especially in females

A

possible: reporting difference, self-medication in males, hormonal difference

higher stress exposure:

  • sexual victimisation (16-19 peak age of rape)
  • body image concerns (80% girls)
  • interpersonal negative events
  • vicarious stress in social network

higher negative cognitive style

different coping responses to stress
-rumination vs distraction/problem-solving

19
Q

causes of depression in preadolescents

A

negative cognitive styles in children

negative events -> cognitive style -> depression

role of depressed parent: model depressive behaviour, non-contingent responsiveness (most important risk factor, 4-5 times more risk)

emotional abuse, neglect

20
Q

medication treatment for preadolescence depression

A

TGA: no SSRIs or antidepressants currently approved in Australia for treatment in children/adolescence

fluoxetine and escitalopram approved by FDA in USA

Australia guidelines:

  • fluoxetine only in moderate/severe MDD
  • when psychological therapy not effective
  • must occur in context of ongoing management plan: close monitoring of symptom severity and adverse effects + protocol in place for managing suicidal thinking
21
Q

treatment for preadolescent

A

CBT derived from adult approaches

prevention:
-psychoeducation and CBT
-universal prevention: given to all students
-indicated prevention: aimed at children or adolescents with high scores on symptom scales
-selective prevention: target high risk groups
e.g.children of depressed parents
programme effective on ST, but effect dissipate after 4 months
booster sessions result in higher LT effectiveness