Depression Flashcards

1
Q

By 2020, the WHO believes depression will rank at this number on leading causes of disability worldwide.

A

2 (behind ischemic heart disease)

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2
Q

How many suicides occur per year in the US?

A

35-40K

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3
Q

What are some morbidities related to depression? (read)

A

Suicide attempts, accidents, other illnesses, lost jobs, failures to achieve, substance abuse

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4
Q

What are some of the societal costs of depression? (read)

A

Dysfunctional families, absenteeism, decreased productivity, job related injuries, adverse effect on quality control in the workplace and school settings

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5
Q

What is the per year cost of depression in the US?

A

$120 billion per year (similar to the cost of CAD or cancer)

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6
Q

What is the lifetime prevalence of depression?

A

12-18%

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7
Q

What is the 1-year prevalence of depression?

A

6-7%

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8
Q

What is the peak age of depression onset?

A

20s (but getting lower)

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9
Q

Sex differences in depression?

A

F:M 2:1

Changes to 1:1 post-menopausaly

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10
Q

How many times greater is your risk of depression if you have a positive family history?

A

2-3x

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11
Q

Generally, what is the root cause of depression in females?

Males?

A

Women: perceived deficiencies in caring relationships and interpersonal loss.

Men: perceived failing to achieve expected goals that lowers their self esteem

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12
Q

Are males or females more likely to express depressive sx somatically?

A

Females

However, if you include sx that many men experience such as anger/aggression, substance abuse, and risk taking, then incidences of depression are =

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13
Q

Name some life events that increase the risk of depression.

A
  • Divorced, separated, unmarried - some risk
  • Early parental losses, postpartum - higher risk
  • Negative life events - highest risk
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14
Q

What months duration is it most common for depressive episodes to last?

A

8-18 months

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15
Q

Recall: what are the recurrence rates for depression after 1 episode? 2? 3?

A

1: 50%
2: 75%
3+: 95%

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16
Q

When are physician depression rates highest?

A

Internship

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17
Q

What are some reasons/theories for the high incidence of depression?

A
  • Greater recognition and awareness
  • Increased genetic predisposition 2/2 greater gene
    pooling
  • Greater expression of certain genes leading to subsequent defective neuronal connections which are more vulnerable to environmental modifiers (chronic stress)
  • Dietary changes: omega‐6‐fatty acids»omega‐3‐fatty acids (corn, soy&raquo_space; fish)
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18
Q

Recall the Kindling theory of depression.

A

With each episode of depression more prone to have further depression with weaker stimuli or stressors

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19
Q

What is the difference between remission and recovery?

A
  • Remission is loss of clinically diagnosable depressive sx for < 1 year in a row
  • Recovery is the same for > 1 year in a row
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20
Q

A slip into depression during “remission” is called ___________, while a slip during “recovery” is called ___________.

A
  • Relapse

- Recurrence

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21
Q

What must happen during depressive tx for there to be considered a “response”?

A

Any decrease in sx

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22
Q

What are the names of the 3 tx phases? (less important)

A
  1. Acute
  2. Continuation
  3. Maintenance (>1 year?)
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23
Q

During depression, recovery begins for 40% of people within _________ (time) of the onset of symptoms.

80% of individuals with their FIRST episode will recovery by ____________ (time) if they receive adequate care.

A

3 months

1 year

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24
Q

What are some features associated with lower recovery from depression?

A
  • Psychotic features
  • Prominent anxiety
  • Personality disorders
  • Symptom severity
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25
Q

What % of ppl w/depression will get help from any professional?

A

50%

35% will see an M.D.; only 15% ever see a Psychiatrist

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26
Q

What are some reasons physicians might fail to treat or refer for depression? (read)

A

Time pressures, close ended interviews, inadequate disease knowledge, discomfort discussing depression

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27
Q

What are some medical system barriers to appropriate depression dx and tx? (read)

A
  • Infrequent visits
  • Total physician reliance
  • Lack of close follow up
  • Lack of time to educate and advocate
  • Lack of monitoring of adherence and outcomes
  • Lack of time to support behavioral changes (exercise, problem solving, etc)
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28
Q

What are the different categories of depressive sx?

A

• Vegetative Symptoms (Classic DSM 5)
• Cognitive Symptoms
• Impulse Control Problems: agitated, irritable (especially in men)
• Behavioral: family and friends
• Physical (Somatic): many people, especially
the elderly

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29
Q

Differentiate psychologizers, initial somaticizers, facultative somaticizers, and persistent somaticizers.

A
  • Psychologizers: all psychologic sx
  • Initial somaticizers: think they only have somatic sx but then realize they may be due to psychologic factors.
  • Facultative somaticizers: realize their somatic sx are due to psychologic causes after some swaying.
  • Persistent somaticizer: they continue to believe their sx are due to physiological problems only

(all relatively equally common)

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30
Q

What is a good question to ask initial somaticizers?

A

What is causing your somatic symptoms?

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31
Q

What is a good question to ask facultative somaticizers?

A

Could nerves or worries be contributing to your symptoms?

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32
Q

What are some reasons ppl relapse at 1 year?

A
  1. Noncompliance (similar rates to any dz–50% by 6 months)
  2. New significant life stressor
  3. Loss of medication efficacy
  4. Absence of psychotherapy
  • Feeling better – 55%
  • Adverse Reaction – 23%
  • Fear of Drug Dependence – 10%
  • Lack of Efficacy – 10%
  • Feeling uncomfortable taking meds – 10%
  • 76% of pts told their MD about noncompliance –correlated with strength of Dr.‐pt relationship
  • 59% of MD’s had ego‐defensive reaction (blaming authoritarian: 10% avoided issue; 31% searched for reason
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33
Q

What % of pts withhold the truth from their psychiatrist?

A

70%

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34
Q

What are some reasons a pt might withhold the truth from their physician?

A
  • I found it difficult to talk to my Dr.
  • I thought my Dr. would not take it seriously if I told him
  • I found it embarrassing to tell the truth
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35
Q

In depression, is recovery the rule, the exception, or in-b/w?

A

The rule

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36
Q

Is depression a medical illness, a character defect, or both?

A

Medical illness

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37
Q

What is the goal of depression tx?

A

Complete symptom remission!

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38
Q

Describe the indicated tx’s for mild, mod, and severe depression.

A
  • Mild/moderate depression responds equally well
    to medicine or therapy
  • Severe depression – both medication and therapy are essential, either alone is less valuable. More intensive levels of care might also be indicated, i.e. hospitalization.
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39
Q

What are the differences in severity amongst mild, mod, and severe depression?

A
  • Mild(296.21) meets minimum criteria for MDD and although symptom intensity is distressing, they are manageable; only minor impairment in social or occupational functioning
  • Moderate(296.22) – in‐between minimum and severe
  • Severe(296.23) –most if not all of the MDD criteria, intensity is seriously distressing and unmanageable, social and occupational functioning are very impaired
40
Q

What was the first broad-use effective tx for depression?

A

TCAs (1950s), although ECT present since 1930s

41
Q

TCAs are effective what % of the time in treating depression?

A

60-70%

42
Q

Name some TCAs

A
Imipramine
Amitriptyline
Desipramine
Nortriptyline
Clomipramine
Doxepin
43
Q

TCAs: MoA?

A

Block reuptake of 5-HT and NE at reuptake pump.

44
Q

TCAs: adverse effects?

A
  • H1 blockade: Excessive sedation, fatigue, weight gain
  • M1 blockade: Confusion and memory dysfunction, excessive sedation, fatigue
  • a1 noradrenergic blockade: Orthostatic hypotension, excessive sedation
  • Fast Na+ channel blockade: Cardiotoxicity, cardiac conduction defects, arrhythmia
  • Seizures

3 C’s (tri-Cyclics): cardiac, coma, convulsions

45
Q

You can OD on TCAs in as little as this many day’s worth of medication:

A

10 days

46
Q

Name some MAO-I’s.

A

Phenelzine
Tranylcypromine
Isocarboxazid
Selegiline

47
Q

MAO-I’s: MoA?
Phenelzine, tranylcypromine, isocarboxazid
- vs. -
Selegiline

A

Inhibit MAO-A irreversibly, decreasing intracellular breakdown of DA, NE, 5-HT, and tyramine.

Selegiline: Irreversibly inhibits MAO-B, increasing DA and tyramine at low doses (inhibits MAO-A at high doses)

48
Q

MAO-I’s: adverse effects?

A
GI: nausea, constipation
Orthostasis/dizziness
Sexual dysfunction
Sleep disturbances: insomnia and day/night shifting 
Sedation
Weight gain
- Hypertensive crisis
- Risk of serotonin syndrome (myoclonus, seizures, CV collapse, disorientation, hyperthermia, psychosis, coma...)
49
Q

What tyramine-containing foods should be avoided with MAO-Is to avoid a hypertensive crisis?

A
  • Fermented goods, aged cheeses, cured meets, liqueurs.

- Also w/drugs that increase adrenergic stimulation, NE reuptake blockers

50
Q

Which MAO-i is available transdermally?

A

Selegiline

51
Q

Indications for SSRIs?

bulimia or anorexia?

A
  • Depression
  • GAD
  • Panic d/o
  • PTSD
  • OCD
  • Impulse control d/o’s
  • Bulimia (not anorexia)
  • Social anxiety d/o
  • Cardiac d/o ppx
52
Q

SSRIs: adverse effects?

- Which is more prone to causing anxiety during 1st week of use?

A

A/w too much 5-HT agonism:
GI: low appetite, N/D, constipation, dry mouth
Anxiety during 1st week use (esp. paroxetine)
CNS: insomnia, sedation, HA, dizziness
Sex dysfunction: loss of libido, impotence, anorgasmia
Emotional numbing
Akithisia/involuntary movements

53
Q

Which SSRI and which SNRI are most a/w discontinuation syndrome?

A

SSRI: paroxetine
SNRI: venlafaxine

54
Q

Do SSRIs pose a greater risk of miscarriage?

A

Probably not

55
Q

Which SSRI is most a/w congenital craniofacial abnormalities when taken during pragnancy?

A

Paroxetine

56
Q

Women exposed to SSRIs 1st trimester slightly higher risk of this mental d/o in their child.

A

Autism

  • Can also see R amygala decrease in volume (2/2 cortisol exposure)
57
Q

Does SSRI get into the breast milk?

A

Yes, but minimal and not harmful

58
Q

How does the suicide risk change in adolescence who are on SSRIs?

A

Risk from 2% jumps to 4% in studies but no actual
completed suicides > 4000 patients

(Results: black box warning, 25% less antidepressants since 2004 in children – recent uptick in completed suicides in adolescents)

59
Q

How do adverse effects of SNRIs contrast to SSRIs?

A
  • Same side effect profile as SSRIs but milder.
  • Dose-dependent increase in BP (venlafaxine)
  • Diaphoresis (via NE-reuptake inhibition)
  • Discontinuation syndrome (esp. venlafaxine, desvenlafaxine–taper when discontinuing)
60
Q

Mirtazepine: MoA?

A
  • Blockade of both NE and 5-HT2/3 nerve terminals’ presynaptic alpha2 receptors (increases 5-HT, NE activity)
61
Q

Mirtazepine: adverse effects?

A

5-HT1A agonist: antidepressant/anti-anxiety effects
5-HT2A antagonism: sleep restoration, no sexual dysfunction (which is caused by agonism there)
5-HT2C antagonism: weight gain
5-HT3 antagonism: GI side effects (combats those of SSRIs/SNRIs)
Sedating at low doses (helps w/insomnia), may be stimulating at high doses.

62
Q

Buproprion: MoA?

A

NE and DA reuptake inhibitor. Resembles amphetamine.

63
Q

Buproprion: indications?

A

Depression; tobacco dependence.

May be most effective antidepressant in BD

64
Q

Buproprion: adverse effects?

A
  • Dry mouth
  • Nausea
  • Insomnia
  • Decreases seizure threshold (esp. at high doses)

No weight gain (perhaps minor weight loss), no sexual side effects, no sedation, no orthostatic hypotension.

65
Q

Buproprion: contraindications?

A
  • Those w/eating disorders (due to weight loss SE and increased seizure risk)
  • Epilepsy
  • Don’t use w/panic disorder
66
Q

Nefazodone: MoA?

Adverse effects?

A

5-HT2A antagonist and 5-HT reuptake inhibitor

Nausea
Dry mouth
Increased appetite
No sexual dysfunction

67
Q

Vilazodone (Viibryd®): MoA?

Adverse effects?

A

5-HT reuptake inhibitor and partial 5-HT1A agonist.

GI: N/V/D
Insomnia
No weight gain
No sexual dysfunction

68
Q

Vortioxetine (Brintellix®): MoA?

Adverse effects?

A

5-HT reuptake inhibitor and partial 5-HT1A agonist (similar to vilazodone, but lower affinities at NE and DA uptake sites). Also 5-HT1B agonist, as well as 5-HT3/7 (targets of atypical antipsychotics).

GI: N > V/D/constipation
Some sexual dysfunction at higher doses
No weight gain

69
Q

What is the response rate of sx in SSRIs compared to PBO?

A

65‐75%

- placebo as high as 45%

70
Q

If patient stays in treatment for depression, there is a >__% chance of symptom REDUCTION.

A

> 98%

71
Q

What does remission mean, generally?

A

• Presence of mental health: optimism, vigor, self‐confidence
• Return to one’s usual self
• General sense of well being
• Very low number or severity of symptoms if using a rating scale
(Chance of relapse much higher without remission)

72
Q

What are some initial therapeutic questions you can ask with depression?

A
  • Ask patients their theories as to why they are depressed
  • Ask patients what they think it will take for them to
    improve
  • Work off of those ideas for best compliance and
    recovery
73
Q

What are some indications for psychotherapy alone with depression tx?

A
  • Patient preference
  • Mild‐to‐moderate functional impairment
  • Acute onset related to adverse event(s)
  • First depressive episode
  • Availability of competent therapists
74
Q

Describe the approach of Cognitive Therapy.

A

– Wide applicability
– Here and Now
– Very little exploration of the person
– Correction of abnormal thought connections due to one’s experience
– Catastrophic thinking, black and white thinking, overvaluation, etc.
– Homework, repetition

75
Q

Describe the approach of Interpersonal Therapy.

A

– Narrower applicability
– Here and Now
– Use the Relationship, with you as a vehicle
– Grief, role transition, role dispute, interpersonal deficits the main areas of focus
– Patterns of past poor interactions
– Redefine one’s relationship with others

76
Q

Describe the approach of Behavioral Therapy.

A

– Learning models, healthy eating
– Relaxation models, exercise
– Specific techniques and general techniques
– Very effective for anxiety disorders and many types of “stress”
– Common for all of us to use some of this ‐ very few
masters

77
Q

Describe the approach of Solution-Based Therapy.

A

– Positive psychology
– Determine what should change for the patient to feel better
– Look at what strategies and skills the pt already has from the past that might prove helpful again
– Based on the pt’s strengths, come up with new or better ways to manage
– Try to change external situations to the betterment of the pt’s condition

78
Q

What are some complementary techniques/strategies to include w/therapy (not meds).

A
  • omega 3 fatty acids
  • Exercise
  • Mindfulness based therapies
79
Q

Describe the approach of Mindfulness-Based Therapy.

A

– Present centered thought awareness: each thought, feeling, sensation acknowledged and accepted
– Self regulation; adopting curiosity
– Optimizes PFC regulation of the amygdala and balances right and left activity of the prefrontal areas (left-reward; right‐avoidance)

80
Q

Describe the approach of Insight-Oriented Treatment.

A

– Very powerful but long process of therapy and training
– Based on Freud and childhood developmental traumas
– Very hard to determine outcome
– Personality change part of the therapy
– Expensive and not for everyone
– Predominant Rx from 1920’s ‐ 1970’s

81
Q

Which therapeutic technique is most often used?

A

Supportive (Ego Binding)

- E.g., what are the pluses and minuses of doing this vs that

82
Q

What are some specifiers to MDD and other depressive dx’s?

A
  • With anxious distress (note overlap w/ GAD)
  • With mixed features (some hypomanic symptoms)
  • With psychotic features
  • With melancholic features
  • With catatonia
  • With peripartum onset
  • With seasonal mood pattern
  • With atypical features
83
Q

What is “melancholic depression”?

A

A. During worst of the depression either loss of all
pleasure or lack of reactivity to usually pleasant things
B. 3 or more of the following:
– Distinct quality of depressed mood
– Worse in the AM
– Early awakening (2 hrs before normal)
– Psychomotor agitation/retardation
– Weight loss (vs. weight gain in “atypical depression”)
– Guilt

(Classic depressive syndrome, thought to be
predominantly biological based due to the severity and
symptom presentation)

84
Q

In which demo can depression be more likely to p/w:

somatic, irritable sx

A

Elderly

85
Q

In which demo can depression be more likely to p/w: behavioral changes, changes in friends, grades, use of drugs

A

Adolescents

86
Q

In which cx can depression be more likely to p/w stoicism?

A

Azns

87
Q

In which cx can depression be more likely to p/w exagerated sx?

A

Hispanics

88
Q

In which cx can depression be more likely to p/w minimized sx?

A

African-Americans

89
Q

In what % of cases of depression can another co-morbidity be found?

A

60%

  • 25% of the time there are 3 or more Psychiatric disorders identified
  • More comorbidites = worse prognosis
90
Q

What are some d/o’s that are commonly comorbid w/MDD?

A
– Substance Abuse
– Anxiety Disorders (Panic, GAD, Social Anxiety)
– Somatoform Disorders
– OCD
– Eating Disorders
– Personality Disorders
– Trauma
91
Q

In Recurrent Major Depression, the need for

_______________ therapy has been well documented.

A

maintenance

92
Q

What is the DOC for pediatric depression?

A

Fluoxetine (Prozac)

93
Q

*What is the triad of sx seen in serotonin syndrome?

A
  • AMS
  • Autonomic dysregulation
  • Neurmuscular hyperactivity (e.g. myoclonus)
94
Q
  • Most SSRIs should be d/c’d __ weeks prior to beginning an MAO-i to avoid serotonin syndrome.
  • What SSRI requires longer?
A

2 weeks

Fluoxetine (Prozac)
- 5 weeks (longer T1/2)

95
Q

What are the features of “atypical depression”?

A
  • Mood reactivity (i.e., mood brightens in response to actual or potential positive events)
  • 2+ of the following:
  • Weight gain
  • ^ sleeping (as opposed to the insomnia in melancholic depression)
  • Leaden paralysis
  • Interpersonal rejection sensitivity –> social or occupational impairment