Major Depression Flashcards
What is the difference between a dualist and monist (materialist) view?
dualist - brain and mind are discrete entities
monist - brain an dmind are the same entitiy (preferred today)
True or false: people with MDD experience depression on a continuum ranging from elated to sadness to depression.
false - the experience is that depression is an entirely different beast
What is Beck’s triad of cognitive changes for MDD?
hopelessness, helplessness, and worthlessness
What are the two primary psychiatric depressive disorder?
major depressive disorder
dysthymic disorder
what are the three types of secondary depressive disorders?
- due to general med condition
- substance-induced
- seasonally-mediated
The secondary depressive disorders that are due to a general med condition (NOT neurological) will present with what type of symptoms?
more of the neurovegetative symptoms: fatigue, lethargy, lack of motivation, sometimes sadness
What are some examples of gen medical conditions that can cause a secondary depression?
Nutritional deficiencies (B12, folate, vit D) Anemia Hypothyroidism Adrenal insufficiency brain injury
What are two neurological conditions that can be associated with a secondary depression? With what symptoms?
parkinson’s disease and stroke
they get a full depressive syndrome
What are some drugs that can induce a secondary depression?
alcohol and cannabis (through CNS depressant effects)
cocaine, amphetamine, MDMA (through NT depletion)
Describe how the season can mediate a depressive disorder?
- shortened photo-period
- less light reaches retina
- disrupts circadian rhythm
- neurovegetative changes
- depressive mental state
What gene is especially shown to be a genetic vulnerability for MDD?
serotonin transporter linked promoter region polymorphism
Does the long or short polymorphism of the 5HTTLPR give the vulnerability? Why?
the short promoter - there’s less space for the transcrption machinery to bind, so they get less expression of the serotonin transporter gene
For a diagnosis of MDD, you need at least 2 weeks of either….
low mood or anhedonia (plus other symptoms
What is the lifetime prevalence of MDD?
16.5% (more so in women)
What is the average age of onset for MDD?
32
How do you treat a secondary depression if it’s from a general med condition vs a neurological condition?
general med = just fix the medical problem and the dep will go away
neurological = treat like a MDD
How do you treat a seoncdary depressive disorder that is substance-induced?
abstinence from substance and maybe an antidepressant
How do you treat seasonally mediated secondary depressive disorder?
phototherapy: 10,000 lux for 30 minutes daily
What are the three general arms of treatment for MDD?
lifestyle changes
psychotherapies
somatic treatments
What surprising finding on brain imaging occured after an exercise program in MDD?
it actually reversed hippocampal atrophy (plus releases endorphins)
What are three general types of psychotherapies you can use for MDD? Which is most effective?
cognitive behavioral therapy (most effective)
psychodynaomic psychotherapy
interpersonal therapy
What are the three general types of somatic treatments for MDD?
psychosurgery
neuromodulation
medications
What psychosurgery is still done occasionally for MDD?
anterior cingulotomy (cuts the communication between the dorsolateral prefrontal cortex and the basal ganglia/limbic structures. we don’t know why it works
What are the 3 types of neuromodulation treatments for MDD?
- electroconvulsive therapy
- transcranial magentic stimulation of the dorsolateral PFC
- Deep brain stimulation
Where is the stimulator implanted for deep brain stimulation of MDD?
subcallosal cingulate gyrus
In general, what do MDD medication treatments do?
- manipulate neurotransmission
- increase transcription of BDNF
- enhance neurogenesis
- decrease depressive symptoms (this is why there’s a delay - it takes time to influence gene transcription)
What are the relevant neurotransmitters for medication in MDD?
- 5HT
- NE
- DA
- Glu
What are the 4 adjunctive medications you can give in MDD?
atypical antipsychotics
lithium
thyroid hormone
psychostimulants
What is the archetyapal SSRI?
prozac (fluoxetine)
What is the efficacy of the SSRIs in MDD?
50% of people get 50% better; 1/3 achieve symptom remission
What are the common side effects of SSRIs?
GI (esp diarrhea)
sexual
What are the dangerous side effects of the SSRIs?
platelet dysfunction (bleeding), drug interactions (through cyp2d6), seizure, serotonin syndrome, suicide
What is the archetypal serotonin-norepinephrine reuptake inhibitor?
effexor (venlafaxine)
What are the common side effects of effexor?
GI, sexual, hypertension, tachycardia, discontinuation syndrome
why does effexor have a risk of discontinuation syndrome and prozac doesn’t?
prozac has a much longer half life, so it takes much longer to leave your system, whereas effexor is gone within a day
What is the achetypal dopamine-norepinephrine reuptake inhibitor?
wellbutrin (buproprion)
WHen is wellbutrin most effective?
most useful as an adjunctive therapy with an SSRI or SNRI for residual symptoms (especially when there’s sexual side effects)
What are the common side effects of wellbutrin?
headache, HTN, irritability, increased anxiety
Is wellbutrin better or worse than the SSRIs or SNRIs as reduction of seizure threshold?
worse
What is the archetypal multi-modal antidepressant?
remeron (mirtazapine)
What is the mechanism of remeron?
it increases synaptic NE and 5HT, while blocking post-synaptic 5HT receptor
When is remeron most effective?
it’s very effective, especially in combo with an SNRI like effexor
What are the common side effects of remeron?
sedation and weight gain
What is the dangerous side effect of remeron?
agranulosytosis
In what group of people do we particularly like to use remeron?
the elderly
What is the archetypal TCA?
imipramine
What is the mechanism for the TCAs like imipramine?
increase synaptic serotonin and norepinephrine
Are the TCAs more or less effective than the SSRIs and SNRIs?
more effective
What are the side effects of the TCAs?
dry mouth, sedation, constipation
What are the dangerous side effects fo the TCAs (and why we don’t use them as much)?
drug interactions (cyp2d6), seizure, arrhythmia, lethal overdose
What are the special uses for the TCAs
fibromyalgia
neuropathy
insomnia
What is the archetypal MAOI?
Nardil (phenelzine)
What was the mechanism for the MAOIs?
increase synaptic serotonin, NE,a nd DA
Are the MAOIs more or less effective than the TCAs?
more effective
What were the common side effects of the MAOs?
sedation and weight gain
What are the dangerous side effects of MAOIs?
med interactions, food interactions (tyramine), hypertensive crisis, serotonin syndrome
What is the archetypal atypical antispychotic used as adjunctive therapy for MDD?
abilify (aripiprazole)
What is the mechanism for abilify?
blocks post-synaptic serotonin receptor
also acts as a post-synaptic dopamine receptor partial agonist
What other conditions is abilify used for? (not as adjunctive)
schizophrenia and bipolar
What are the side effects (common and dangerous) of ability?
common - sedation, weight gain, parkinsonian side effects
dangerou - tardive dysinesia
What do we think lithium does NT-wise? By acting through second messenger system
enhance serotonergic NT transmission
What are the side effects of lithium?
lots of them - sedation, weight gain, tremor, toxicity
What is the archetypal agent for thyroid hormone adjunctive therapy?
cytomel (triiodothyronine)
What is the common side effect and dangerous side effect of cytomel?
common - activation in general
dangerous - hyperthyroidism (duh)
In what group of MDD patients would you consider adding a psychostimulant as an adjunct?
those with lethargy, trouble concentrating and poor motivation
What is an example of an NMDA receptor antagonist that is showing recent promise in treatment of MDD?
ketamine
