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152 Cards in this Set
- Front
- Back
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What are the levels of Evidence and describe
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1. At least 2 RCTs and/or meta-analysis
2. 1 RCT and or metanalysis with wide confidence intervals 3. Non-RCT 4. Expert opinion/consensus |
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Lines of treatment?
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1st line: Level 1/2 + clinical support
2nd line: Level 3 evidence + clinical support 3rd line: Level 4 evidence + clinical support |
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Key criteria for MDD?
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Low Mood
or Anhedonia Almost everyday, most days in last 2 weeks + 4 other symptoms for a total of at least 5 sx from MSIGECAPS |
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Difference in Criteria for children?
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can be irritable mood,
regarding weight can be failure to make expected weight gains |
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Key Criteria for Dysthymic Ds?
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Low mood most of the day for more days than not for 2 years
+ 2 other symptoms |
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Give specifiers of MDD/Dysthymic Ds
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Current or Most Recent Episode
mild, mod, severe +/-psychotic sx Melancholic features, Atypical features, Psychotic features Seasonal pattern Catatonic features, Chronic pattern, Postpartum pattern |
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Describe melancholic depression features
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non-reactive mood
anhedonia weight loss guilt psychomotor retardation.agitation Low AM mood early morning awakening excessive/inappropriate guilt |
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Atypical features?
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reactive mood
over-sleeping over-eating leaden paralysis interpersonal rejection sensitivity |
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Catotonic features?
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catalepsy (waxy)
catatonic excitement negativism/mutism mannerisms/stereotypes echolalia/echopraxia |
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chronic depression?
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two years or more with full criteria for MDE
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postpartum depression timing?
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MDE within 4 weeks postpartum
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Dysthymia specifiers?
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early onset before age 21
can have atypical features |
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Prevalance in Canada for Current MDD, 12 month, lifetime?
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1.3 current/1month
4.0 in 12 months 10.8 lifetime likely underestimates because of recall underestimation |
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Incidence formula for MDD
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population:
those who do not have disorder yet and new cases emerging over time |
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What does disease burden depend on along with prevalence?
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time with disorder
severity of disability from ds risk of premature mortality |
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Burden of disease factors?
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prevalence +
course + impairment + premature mortality |
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How did we get estimates of prevalance of MDD in canada nationally?
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1994 National Population Health Survey
used brief version of major depression module from Composite International Diagnostic Interview (CIDI) |
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1st national estimate of prevalence based on full CIDI?
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Canadian Community Health Survey, Mental Health and Wellbeing CCHS 1.2 conducted by stats canada in 2002
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According to CCHS 1.2, the lifetime prevalence of MDD in Canada is ? annual? 1 month prevalence?
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10.8%
4% 1.3% |
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Higher rates of MDD in Canada or US?
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higher in US == 16.2 lifetime, and 6.6 annual
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MDD prevalence greater in men or women, younger or older?
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women, younger
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Prevalence of Dysthymic Disorder?
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3.7% lifetime prevalence
based on Edmonton Study with DSM-III criteria |
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Initial MDE duration
2 weeks ? one month or less? 5 years or longer? |
16%
30% 13.7% |
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NPHS mean duration of MDE?
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17 weeks (4 months)
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Prevalence =
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Incidence X Duration
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Netheralands Mental Health Survey:
% of episodes recovered within 3 months? ?% chronic course persisting longer than 24 months |
50%
20% |
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CCHS 1.2
SIngle episode 2 episodes 3 or more episodes |
56%
28.6% 15.4% |
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What increases risk of suicide attempt along with depression?
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anxiety
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What aprox % do patients with MDD, Double Depression, Dysthymic disorder report severe impairment in quality of life?
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more than half
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Depression link to cardiovasc health?
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Depression recognized as independent risk factor for cv disease and predictor of mortality
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in canada, MDD most linked to what GMC's?
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neurological ds & pain/inflammation ds
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Specific GMC with highest Odds ratio?
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Emphysema/COPD 2.7
Migraine 2.6 MS 2.3 Back problems 2.3 Cancer 2.3 |
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What percent of patients at gp office recognized as depressed, present with somatic sx?
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50% missed
2/3's present with somatic sx only |
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Tx phases of depression?
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acute and
maintenance |
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Acute phase goals?
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eliminate sx
restore fxn |
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Maintenance tx goals?
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return to baseline in
fxn quality of life prevent recurrence of sx |
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Duration of acute phase? Activities?
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8-12 weeks
1. Alliance 2. Educate 3. Treat - Rx or CBT 4. Monitor progress |
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Maintence Phase tx duration? activities?
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6 mo to 2 years
1. Educate 2. Rehab 3. Tx comorbidities 4. Monitor for recurrence |
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Chronic Disease Management of MDD?
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Improve detection
Deliver EBM Educate Measure process, outcomes |
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difference between response and remission?
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response = 50% reduction in sx
remission = no sx, normal range score |
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1st line psychotherapies for MDD?
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CBT, IPT both level 1 evidence
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2nd line psychotx for MDD?
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level 1: Bibliotherapy
level 2: behavioural activation CB Analysis System of Psychotherapy Computer assisted CBT Telephone delivered CBT |
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3rd line psychotx for MDD?
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ACT
MI Psychodynamic therapy Emotion-focused therapy |
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How effective is CBT in acute MDD?
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mild to mod depression = to antidepressant = effect size 0.38
for acute phase vs placebo, wait list = 0.82 2 studies no difference between Rx and CBT for severe MDD (without psychotic features) |
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STARD CBT finding?
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2nd level option for pt who failed citalopram, did just as well as switch to another antidepressant with fewer side fx but remission took 3 weeks longer than with medication
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Maintenance phase and CBT outcome?
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if stop rx/cbt; pt who had cbt has lower rates of relapse
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is combined ipt with rx better?
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no evidence
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Psychotx lines in maintenance phase of MDD?
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1st: CBT
2nd: Behavioural activation IPT, MBCT, CBASP 3rd line: nil Insuffient evidence: ACT, MI, Psychodynamic tx, Emotion-focused Tx, Bibliotherapy, Computer-assisted, Telephone Delivered |
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What is Cognitive Behavioural Analysis Stem of Psychotherapy?
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Tx for chronic depression
cog, behav and interpersonal strategies Maladaptive cognitions and behaviours influence and perpetuate negative outcomes therapeutic relationship medium for negative interpersonal behaviours to be changed |
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What is ACT?
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Acceptance and Committment Therapy
Increase acceptance of full range of subjective experiences, including distressing thoughts, beliefs, sensations, and feelings, and subsequently cultivate a mindful outlook |
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mindful outlook?
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awareness of mental events as products of the mind, rather than literal truths
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What is behavioural activation ? theory?
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depression = consequence of few + environment
tx= increase rewarding experiences and emphasize, don't need to be in mood to do things to do things i..e, just do it |
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What is Emotion focused therapy?
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up to 20 sessions
help express emotions change self by focusing on unclear feelings dialogue with one critical internal voice and empty chair dialogue with sig other regarding unresolved issues |
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Most commonly used bibliotherapy?
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Feeling Good (Burns 1980)
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Combined therapy vs psychotherapy alone?
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Combined slightly better
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Combined therapy vs rx alone? line?
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better at relapse prevention
2nd line because of practicality, cost, and availability |
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Discontinuing successful pharmacotherapy and crossing over to psychotherapy has
been shown to be ? to continuing pharmacotherapy. |
not be to superior to continuing therapy
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Mininum duration of rx for MDD?
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6 to 12 months
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What % of patients stop Rx withint 30 days? 90 days?
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30% by 30days
40% by 90 days |
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Reseasons for stopping?
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lack of response,
stimgma side fx |
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Antidepressant selection factors?
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pt preference
sx of pt comorbidity tolerability proflie previous response potential drug drug interactions cost |
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What are classes of 1st line antidepressants?
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SSRI's, SNRI, mirtaz, RIMAO
NDRI (bupropion) also agomelatine, (mt1/2 agonist; 5ht2 antagonist) |
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What are 2nd line rx?
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TCAs, Seroquel, Selegiline Irreversible MAO-B, Trazodone (SRI, 5ht2 antagonist)
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3rd line antidepressants?
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phenelzine
tranylcypromine irreversible MAOI |
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Serious but rare with SSRI's
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Serotonin Syndrome
Gi bleeding with NSAIDS fractures in elderly agranulocytosis/hyponatremia venlafaxine: cardiotoxic in overdose bupropion: increased sz risk over 300mg |
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least tolerable ssri? most ?
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least=fluvoxamine
most= sertaline, escitalopram |
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GI side effects worse in what types of agenets?
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those involved with serotonin reuptake transporter
agomelatine, bupropion, mirtaz, moclobemide don't so less gi upset |
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What helps decrease SSRI nausea?
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eat with food,
once daily extended releaes versions |
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SSRI's with worse withdrawal?
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Paroxetine
venlafaxine |
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Do SSRI sexual side fx go away on their own?
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no,
reduce dose, switch, add on buprion or mirtaz |
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Rifampin and antidepressants?
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induces several isoenzyme pathways:
2c9, 2c19, 2d6 |
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Agomelatine and
duloxetine are extensively metabolized through the ? pathway and should not be co-administered with drugs that potently inhibit CYP ? (e.g., ???) and hence increase the antidepressant levels. |
1A2
cimetidine, ciprofloxacin and other fluoroquinolone antimicrobials, ticlopidine |
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which antidepressants act as inhibtiors?
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fluoxetine and paroxetine inhibits 2d6 which increase TCAs and beta blockers levels,
codeine less effective because 2d6 converts it to morphine |
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other 2d6 inhibitors?
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bupropion, duloxetine at higher doses
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fluvoxamine intx?
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inhibits 1a2, 2c19, 3a4 so can increase levels of warfarin & statins
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what is P-glycoprotein?
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P-glycoprotein is an important component of the blood
brain barrier and the intestinal barrier, and is responsible for the efflux of several antidepressants, anticancer and cardiac medications |
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? and ? are
potent inhibitors of p-glycoprotein and may increase the levels of substrates including ? |
Paroxetine and sertraline are
potent inhibitors of p-glycoprotein and may increase the levels of substrates including digoxin, cyclosporine, calcium channel blockers and some anticancer agents. |
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What type of drug really avoid with MAO even if reversible?
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other antidepressants
sympathomimetics meperidine |
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linezolid what is it?
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(antibiotic for staph) is a
and is a reversible, nonselective MAO inhibitors |
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Type of depression and rx:
MDD with psychotic features? |
combine with antipsychotic
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seasonal MDD?
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bupropion
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There is some evidence that ? age may respond
preferentially to serotonergic rather than noradrenergic antidepressants, while ?age populations show no differential response (Mulder et al., 2003). |
There is some evidence that younger adults may respond
preferentially to serotonergic rather than noradrenergic antidepressants, while older populations show no differential response (Mulder et al., 2003). |
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only ? has been studied in RCTs involving patients with higher depression severity at baseline; it
was found to be superior to ? and ? (Montgomery et al., 2007). |
only escitalopram has been studied in RCTs
involving patients with higher depression severity at baseline; it was found to be superior to fluoxetine and paroxetine (Montgomery et al., 2007) |
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variations in the gene that encodes for the ? receptor was most predictive of response to citalopramin
the STAR*D database, the largest pharmacogenetic study so far reported (McMahon et al., 2006). |
5HT2A
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Tx of depression with psychotic features?
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treat with antidepressant + antipsychotic
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If pt showing little improvement after 2 weeks, what to do?
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<20% improvement after 2 weeks = dose increase
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What if patient showing more than minimal improvement after 4-6 weeks?
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continue on antidepressant for 2-4 weeks because:
The STAR*D effectiveness trial showed that, of patients who ultimately showed clinical response when treated with open-label citalopram for 12 weeks, 56% first achieved response after 8 or more weeks, while 40% of patients who ultimately remitted first achieved remission after 8 or more weeks (Trivedi et al., 2006b) |
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How long do you wait for people to respond?
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If <20% improvement but improvement then increase dose
If >20% improvement wait for up to 2 months because up to half of patients on citalopram first achieved resonse after 8 or more weeks |
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What do you do when patient does not respond?
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After trying optimization then
1. Reaval Dx 2. Consider Tx issues (adherence, side fx, SI) with validated scales i.e. PHQ-9, QIDS-SR |
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Define Treatment Resistant Depression?
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lack of improvement or <20% reduction in depression sore after 2 or more antidepressant trials
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Options for TRD?
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add Ptx
ECT/TMS Try Alternate Rx strategy like: switch, add-on (combine or augment) |
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How effective is switching?
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It works
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What is better switching to different class of drug or switching in same class of drug?
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STAR-D says no difference; i.e.,
setraline vs bupropionSR/venlafaxine SR had same response remission rates |
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Difference in tx approach for no improvement and partial (>20%) improvement?
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no improvement ... usually switch
some ... usually add-on |
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What is effective as an add-on?
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Lithium ... level 1 evidence
Antipsychotics ... level 1 e.g. olanz/fluox; apriprazole level 1 risperidone has +/no major diff evidence |
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Lithium Dosing as add on?
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achieve thereapeutic level:
0.5 to 1 meq/l dose: 650mg X1 week, 900mg X1 week then match to level |
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T3 dosing recommendation level? dosing?
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Level 2
25mcg daily and after 1 week 50mcg if no response after 2weeks try something else |
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Which Rx's had blazeh results for add-on strategy? i.e. Level 3
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Buspirone - StarD
Methylphenidate: Cochrane Modafinil - ? 2 rct's negative |
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Combination of antidepressant evidence?
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Level 2 for bupropion and
mirtazapine |
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What's better switching or adding on?
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Hard to say ... clnical decision weighing past hx, degree of response, side effects of antidepressant, potential side fx of new medication
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How long keep pt on antidepressant once better?
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Not much evidence but PREVENT study with Venlafaxine showed Venlafaxine better than placebo for 2 years at preventing recurrence
Usuall recommendation: 1 episode: no less than 6 months 2 episodes: 2 years >2: 5 years or lifetime |
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Who should be kept on rx longer?
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people with risk factors should be >2 years
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Who might be people with risk factors?
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early onset
depression, psychosocial adversity, and chronic medical illnesses comorbidity |
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Antidepressant often used in pregancy and after?
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sertraline
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Which SSRI may have higher risk of problem?
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Paroxetine, cardiac malformation
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In nursing mothers, first-line antidepressants include because these medications in
therapeutic doses are associated with low to undetectable serum concentrations in breast-fed babies. |
citalopram, sertraline, nortriptyline, and paroxetine
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Youth and TCA's?
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Not recommended , not effective as per meta-analysis
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SSRI's usually recommended in youth? and NNT?
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fluoxetine
citalopram NNT=10 |
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SI increase in youth NNHarm?
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143
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Which rx to avoid in MDD of youth?
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venlafaxine, greater side fx + > SI
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ECT evidence for acute efficacy, relapse prevention, safety?
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level 1
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List Indication for ECT as 1st line Tx?
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Level 1 evidence:
Acute SI MDE w/psychotic features TRD Level 3 evidence: Catatonia Prior response Medication intolerance Deteriorating physical status Pregnancy Patient Choice |
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rTMS relies on electromagnetic induction
to generate a superficial current in |
the dorsolateral prefrontal
cortex (DLPFC) which may be of high intensity or low intensity. |
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The VNS device received approval for
adjunctive long-term use for chronic or recurrent MDD and mech? |
relays a mild electrical pulsed stimulus to the left vagus nerve
which activates limbic structures |
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Describe ECT
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ECT involves the induction of a convulsion (seizure) by the
application of electrical current to the brain. The stimulus parameters are: current (usually 500 to 800 mA); frequency (20 to 120 Hz); pulsewidth (0.25 to 2 ms) and duration (0.5 to 8 or more seconds). The charge of electricity delivered ismeasured in millicoulombs (below 600 mC for machines sold in Canada andUSA but somewhat higher for othermarkets) and the energy is measured in joules. Theminimumcharge to induce a seizure is known as the seizure threshold. The electrodes can be placed bilaterally (either bitemporal or bifrontal) or unilaterally (typically, on the right side — RUL). Markedly suprathreshold ECT is the goal for unilateral placement and entails applying a stimulus dose up to 6 times above seizure threshold. In contrast, moderately suprathreshold ECT is the goal for bilateral placement, which implies 1.5 to 2.5 times threshold. Barely suprathreshold brief-pulse unilateral ECT is remarkably ineffective (Sackeim et al.,1987). Response rates of 80% or higher have been reported with ECT although there are very few comparisons between ECT and first-line antidepressants. |
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Difference between bilateral and unilateral?
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Bitemporal
placement is generally regarded as faster in improving depressive symptoms and more effective than unilateral, at a lower dose of electrical stimulus. However, bitemporal placement is associated with more cognitive side effects (Stoppe et al., 2006). There is evidence that the right unilateral stimulus at suprathreshold dose is as effective as bilateral stimulation and is associated with fewer side effects (Sackeim et al., 1993, 2000). There is also evidence that the less frequently evaluated, bifrontal placement of electrodes is as effective as bitemporal or right unilateral, and is also associatedwith fewer cognitive side effects (Bailine et al., 2000; Eschweiler et al., 2007). |
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Recommended frequency and duration of ECT?
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Some studies
(Shapira et al., 2000), but not all (The UK ECT Review Group, 2003), support a faster onset of action when patients receive the treatment 3 times per week. On the other hand, patients receiving a twice weekly regimen have decreased frequency and intensity of cognitive side effects compared to those on a three times weekly schedule |
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ECT response rates?
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80-90% as first line
50-60% for TRD |
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ECT and relapse prevention
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the Consortium for Research in ECT (CORE) (Kellner et al.,
2006) and Columbia University Consortium (CUC) (Sackeim et al., 2001a,b,c) support the combination of nortriptyline plus lithium for relapse prevention in patients who responded to ECT. The CORE study reported that both continuation pharmacotherapy and maintenance ECT were equally effective for relapse prevention during the first 6months after responding to ECT (Kellner et al., 2006). Maintenance ECT ranging from one per week to one per month is associated with low rates of cognitive side effects (Vothnecht et al., 2003). However, there is insufficient evidence to recommend one frequency over another for maintenance ECT. Maintenance treatments should be reviewed every 6 months. |
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ECT mortality per treatment?
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ECT is a safe procedure with a very low mortality rate (0.2
per 100,000 treatments), approximating the risk of general anaesthesia (Kramer, 1999). Patients who have myocardial ischemia, cardiac arrhythmias, or abdominal aortic aneurysms carry higher morbidity and mortality risks. |
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The most frequently reported short-term side effects of ECT are:
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nausea,
headache, muscle pain, oral lacerations, dental injuries, and persistent myalgia |
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Cognitive side fx of ECT?
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have to weighed against cog side fx of MDD:
particularly acute confusional states, anterograde and retrograde amnesia, word finding difficulties, and deficits in autobiographical memory. There is evidence to show impairment in verbal learning after three treatments (Porter et al., 2008), although this did not correlate with long-term memory function. |
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How reduce Cog side fx?
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Reducing the frequency of treatments (from 3 to 2 per
week), the use of brief pulse rather than sine wave ECT machines, right unilateral or bifrontal positioning of the electrodes (instead of bitemporal) and lower dose stimuli should reduce the frequency and intensity of cognitive side effects (Sackeim et al., 2007). |
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Does ECT has brain damage?
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Claims that ECT may result in structural brain damage are
unsubstantiated (Devanand et al.,1994; Zachrisson et al., 2000). In fact, consistent with evidence about various antidepressant treatments, ECT stimulates neurotrophic growth factors including brain derived neurotrophic factor (BDNF), causing migration and growth of new neurons in the hippocampus (Marano et al., 2007), and this may contribute to the antidepressant effect. |
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Should ECT be given with Antidepressant?
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evidence of nortriptyline with ECT increasing remission rates vs ECT+placebo;
Lithium doses usually omitted pre-ect because of concern of confusion and delirium Benzo and anticonvulsants best avoided |
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Types of rTMS?
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1. Low frequency (at or below 5hz) which reduces exitability
2. High frequency (over 5hz) increase excitability |
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rTMS target areas?
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The intensity of the stimulus is based on the individual
motor threshold (the minimal intensity required to produce muscle twitches), and usually is between 90% and 120% of this threshold. Target areas to be stimulated are left or right DLPFC. There is most evidence to support high-frequency rTMS applied to the left DLPFC, |
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How many sessions should be done in TMS?
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20 better than 10
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use of rTMS for maintenance, relapse prevention?
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not much evidence
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rTMS side fx?
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In general, rTMS is a safe and well-tolerated treatment.
Common short-term side effects include headaches and scalp pain usually responding well to symptomatic treatments. Because of concerns about hearing loss (due to the clicking noise of the apparatus), both patients and staff should use ear plugs with 30 dB protection during the treatment process. rTMS does not involve general anaesthesia or seizure induction and is not associated with adverse cognitive effects. There is no evidence of cognitive impairment with rTMS rare seizure |
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rTMS contraindications?
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Absolute contraindications include seizures, the presence
of ferromagnetic material anywhere in the head (excluding the mouth) such as cochlear implants, brain stimulators or electrodes, aneurysm clips, plates, etc. Cardiac pacemakers are also a contraindication. Increased intracranial pressure, severe cardiovascular disease, epilepsy and other serious medical conditions are also contraindications |
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VNS involves implantation of a bipolar electrode around the
?(right or left) vagus nerve. Why that side? |
left,
because less cardiac effects |
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Which patients to consider for VNS?
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Results from an acute phase pilot study of 59 TRD
participants suggest that patients with chronic or recurrent, TRD may show long-term benefit when treated with VNS (Nahas et al., 2005). In practice, it would be reasonable to consider patients who have failed at least 4 prior treatments at adequate dose and duration for the current episode. Failure to respond to ECT is not a prerequisite. |
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VNS side fx?
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Hoarseness 54%–68% [Level 2] Neck pain 13–21% [Level 2]
Cough 6–29% [Level 2] Headache 4–22% [Level 2] Dyspnoea 15–23% [Level 2] Dysphagia 4–21% [Level 2] |
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Deep brain stimulation target?
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To date, the subcallosal cingulate gyrus (SCG)
(approximately Brodmann Area 25) has been evaluated most. The rationale for this site comes from evidence that healthy volunteers experiencing sadness during functional neuroimaging display increased activity in BA 25 and depressed patients responding to antidepressant medications demonstrate a reduction |
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Side fx of DBS?
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pain,
bleeding infection hypomania |
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What is dose of light therapy?
|
Light therapy consists of daily exposure to bright light,
usually administered at home with a fluorescent light box. The standard “dose” of light is 10,000 lux (intensity) for 30 min per day given in the early morning. |
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When does light therapy response usually occur?
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Response usually occurs
within 1–3 weeks |
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Bright light side fx?
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The side effects of bright light therapy include headache, eye
strain, nausea, and agitation, but these are generally mild and rarely lead to treatment discontinuation. Bright light exposure may trigger hypomanic or manic episodes, particularly in susceptible individuals such as those with bipolar disorder. |
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Bright light therapy level of evidence?
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Level 1 evidence, first line treatment for seasonal MDD.
There is also Level 2 evidence for its use as an adjunctive treatment in mild to moderate non-seasonal MDD, and thus, is recommended as a second-line treatment |
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Sleep deprivation line of treatment?
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n summary, there is Level 2 evidence for sleep deprivation as
adjunctive treatment in the acute management of mild to moderate MDD, and some limited support for its use in seasonal, antepartum and postpartum MDD, (Table 2). However, it is recommended as third-line due to the practical difficulties associated with sustaining treatment. |
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Exercise evidence level and for what?
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In summary, there is Level 2 evidence for the benefit of
exercise as adjunct to medications in mild to moderate MDD, but not as monotherapy |
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Yoga line? level of evidence?
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In summary, there is Level 2 evidence to support the use of
yoga, but the quality of trials makes it difficult to interpret these results (Table 2). As with all group treatments, the nonspecific benefits of group dynamics cannot be entirely separated from the benefits of yoga. Thus, yoga may be considered a second-line adjunctive treatment in mild to moderate MDD, if available. |
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Accupuncture and Level of evidence?
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In summary, the current evidence does not support the
use of acupuncture for the management of MDD |
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Omega 3 indication? evidence level? line of therapy?
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up to moderate MDD,
Level 1 2nd line as monotx and add-on |
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SAMe indication, ev, line?
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up to moderate,
level 1 2nd line as monotx |
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DHEA
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up to mod
level 2 3rd line mono |
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Tryptophan
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no enough evidence to say
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Folic acid for indication, evidence, line?
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up to moderate
level 2 3rd line add-on |
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St. John's wort, level of evidence? line?
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level 1 up to mod, 1st line monotx
for mod/severe: level 2, 2nd line addon |
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Crocus Sativus: indication, level of ev? line?
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up to mod, level 2, 3rd line
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St. John's Wort Side fx?
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Adverse effects include photosensitivity and drug interactions
with immunoregulatory compounds, anticoagulants, anti-infective agents and oral contraceptives, attributed in part to its effect on cytochrome P450 enzymes (Golan et al., 2007). Serotonin syndrome, when it is added to antidepressants, and induction of hypomania have also been reported (NaturalMedicines, 2009c). Therefore, combining St. John's wort with other medications, including antidepressants, should be done with caution. |
