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Social And Behavioral 2 > Major Depression > Flashcards

Major Depression Flashcards

1
Q

What is the difference between a dualist and monist (materialist) view?

A

dualist - brain and mind are discrete entities

monist - brain an dmind are the same entitiy (preferred today)

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2
Q

True or false: people with MDD experience depression on a continuum ranging from elated to sadness to depression.

A

false - the experience is that depression is an entirely different beast

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3
Q

What is Beck’s triad of cognitive changes for MDD?

A

hopelessness, helplessness, and worthlessness

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4
Q

What are the two primary psychiatric depressive disorder?

A

major depressive disorder

dysthymic disorder

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5
Q

what are the three types of secondary depressive disorders?

A
  1. due to general med condition
  2. substance-induced
  3. seasonally-mediated
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6
Q

The secondary depressive disorders that are due to a general med condition (NOT neurological) will present with what type of symptoms?

A

more of the neurovegetative symptoms: fatigue, lethargy, lack of motivation, sometimes sadness

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7
Q

What are some examples of gen medical conditions that can cause a secondary depression?

A 
Nutritional deficiencies (B12, folate, vit D)
Anemia
Hypothyroidism
Adrenal insufficiency
brain injury
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8
Q

What are two neurological conditions that can be associated with a secondary depression? With what symptoms?

A

parkinson’s disease and stroke

they get a full depressive syndrome

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9
Q

What are some drugs that can induce a secondary depression?

A

alcohol and cannabis (through CNS depressant effects)

cocaine, amphetamine, MDMA (through NT depletion)

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10
Q

Describe how the season can mediate a depressive disorder?

A
  1. shortened photo-period
  2. less light reaches retina
  3. disrupts circadian rhythm
  4. neurovegetative changes
  5. depressive mental state
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11
Q

What gene is especially shown to be a genetic vulnerability for MDD?

A

serotonin transporter linked promoter region polymorphism

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12
Q

Does the long or short polymorphism of the 5HTTLPR give the vulnerability? Why?

A

the short promoter - there’s less space for the transcrption machinery to bind, so they get less expression of the serotonin transporter gene

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13
Q

For a diagnosis of MDD, you need at least 2 weeks of either….

A

low mood or anhedonia (plus other symptoms

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14
Q

What is the lifetime prevalence of MDD?

A

16.5% (more so in women)

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15
Q

What is the average age of onset for MDD?

A

32

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16
Q

How do you treat a secondary depression if it’s from a general med condition vs a neurological condition?

A

general med = just fix the medical problem and the dep will go away
neurological = treat like a MDD

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17
Q

How do you treat a seoncdary depressive disorder that is substance-induced?

A

abstinence from substance and maybe an antidepressant

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18
Q

How do you treat seasonally mediated secondary depressive disorder?

A

phototherapy: 10,000 lux for 30 minutes daily

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19
Q

What are the three general arms of treatment for MDD?

A

lifestyle changes
psychotherapies
somatic treatments

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20
Q

What surprising finding on brain imaging occured after an exercise program in MDD?

A

it actually reversed hippocampal atrophy (plus releases endorphins)

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21
Q

What are three general types of psychotherapies you can use for MDD? Which is most effective?

A

cognitive behavioral therapy (most effective)
psychodynaomic psychotherapy
interpersonal therapy

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22
Q

What are the three general types of somatic treatments for MDD?

A

psychosurgery
neuromodulation
medications

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23
Q

What psychosurgery is still done occasionally for MDD?

A

anterior cingulotomy (cuts the communication between the dorsolateral prefrontal cortex and the basal ganglia/limbic structures. we don’t know why it works

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24
Q

What are the 3 types of neuromodulation treatments for MDD?

A
  1. electroconvulsive therapy
  2. transcranial magentic stimulation of the dorsolateral PFC
  3. Deep brain stimulation
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25
Q

Where is the stimulator implanted for deep brain stimulation of MDD?

A

subcallosal cingulate gyrus

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26
Q

In general, what do MDD medication treatments do?

A
  1. manipulate neurotransmission
  2. increase transcription of BDNF
  3. enhance neurogenesis
  4. decrease depressive symptoms (this is why there’s a delay - it takes time to influence gene transcription)
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27
Q

What are the relevant neurotransmitters for medication in MDD?

A
  1. 5HT
  2. NE
  3. DA
  4. Glu
28
Q

What are the 4 adjunctive medications you can give in MDD?

A

atypical antipsychotics
lithium
thyroid hormone
psychostimulants

29
Q

What is the archetyapal SSRI?

A

prozac (fluoxetine)

30
Q

What is the efficacy of the SSRIs in MDD?

A

50% of people get 50% better; 1/3 achieve symptom remission

31
Q

What are the common side effects of SSRIs?

A

GI (esp diarrhea)

sexual

32
Q

What are the dangerous side effects of the SSRIs?

A

platelet dysfunction (bleeding), drug interactions (through cyp2d6), seizure, serotonin syndrome, suicide

33
Q

What is the archetypal serotonin-norepinephrine reuptake inhibitor?

A

effexor (venlafaxine)

34
Q

What are the common side effects of effexor?

A

GI, sexual, hypertension, tachycardia, discontinuation syndrome

35
Q

why does effexor have a risk of discontinuation syndrome and prozac doesn’t?

A

prozac has a much longer half life, so it takes much longer to leave your system, whereas effexor is gone within a day

36
Q

What is the achetypal dopamine-norepinephrine reuptake inhibitor?

A

wellbutrin (buproprion)

37
Q

WHen is wellbutrin most effective?

A

most useful as an adjunctive therapy with an SSRI or SNRI for residual symptoms (especially when there’s sexual side effects)

38
Q

What are the common side effects of wellbutrin?

A

headache, HTN, irritability, increased anxiety

39
Q

Is wellbutrin better or worse than the SSRIs or SNRIs as reduction of seizure threshold?

A

worse

40
Q

What is the archetypal multi-modal antidepressant?

A

remeron (mirtazapine)

41
Q

What is the mechanism of remeron?

A

it increases synaptic NE and 5HT, while blocking post-synaptic 5HT receptor

42
Q

When is remeron most effective?

A

it’s very effective, especially in combo with an SNRI like effexor

43
Q

What are the common side effects of remeron?

A

sedation and weight gain

44
Q

What is the dangerous side effect of remeron?

A

agranulosytosis

45
Q

In what group of people do we particularly like to use remeron?

A

the elderly

46
Q

What is the archetypal TCA?

A

imipramine

47
Q

What is the mechanism for the TCAs like imipramine?

A

increase synaptic serotonin and norepinephrine

48
Q

Are the TCAs more or less effective than the SSRIs and SNRIs?

A

more effective

49
Q

What are the side effects of the TCAs?

A

dry mouth, sedation, constipation

50
Q

What are the dangerous side effects fo the TCAs (and why we don’t use them as much)?

A

drug interactions (cyp2d6), seizure, arrhythmia, lethal overdose

51
Q

What are the special uses for the TCAs

A

fibromyalgia
neuropathy
insomnia

52
Q

What is the archetypal MAOI?

A

Nardil (phenelzine)

53
Q

What was the mechanism for the MAOIs?

A

increase synaptic serotonin, NE,a nd DA

54
Q

Are the MAOIs more or less effective than the TCAs?

A

more effective

55
Q

What were the common side effects of the MAOs?

A

sedation and weight gain

56
Q

What are the dangerous side effects of MAOIs?

A

med interactions, food interactions (tyramine), hypertensive crisis, serotonin syndrome

57
Q

What is the archetypal atypical antispychotic used as adjunctive therapy for MDD?

A

abilify (aripiprazole)

58
Q

What is the mechanism for abilify?

A

blocks post-synaptic serotonin receptor

also acts as a post-synaptic dopamine receptor partial agonist

59
Q

What other conditions is abilify used for? (not as adjunctive)

A

schizophrenia and bipolar

60
Q

What are the side effects (common and dangerous) of ability?

A

common - sedation, weight gain, parkinsonian side effects

dangerou - tardive dysinesia

61
Q

What do we think lithium does NT-wise? By acting through second messenger system

A

enhance serotonergic NT transmission

62
Q

What are the side effects of lithium?

A

lots of them - sedation, weight gain, tremor, toxicity

63
Q

What is the archetypal agent for thyroid hormone adjunctive therapy?

A

cytomel (triiodothyronine)

64
Q

What is the common side effect and dangerous side effect of cytomel?

A

common - activation in general

dangerous - hyperthyroidism (duh)

65
Q

In what group of MDD patients would you consider adding a psychostimulant as an adjunct?

A

those with lethargy, trouble concentrating and poor motivation

66
Q

What is an example of an NMDA receptor antagonist that is showing recent promise in treatment of MDD?

A

ketamine

Social And Behavioral 2 (18 decks)

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