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Psychopharmacology > Depression > Flashcards

Depression Flashcards

1
Q

Neurochemical implicated in depression

A

Monoamines (serotonin, 5-HT; dopamine; norepinephrine), BDNF (brain-derived neurotrophic factor, CRF (corticotropin releasing factor [or hormone]), Cortisol

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2
Q

What does deficient monoamine signal?

A

Decreases in BDNF: decreases synaptogenesis, neuroplasticity, cell survival, neurogenesis, and increases apoptosis (planned cell death)

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3
Q

Low “level” of the 5-HT system is associated with?

A

Increased “negative affect”: dysphoria, rumination, guilt/distrust, worthlessness, loneliness, fear/anxiety, irritability, hostility, suicidality, particularly affects the prefrontal cortex, amygdada, and hypothalamus

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4
Q

Low “level” of the DA system is associated with:

A

Decreased “positive affect”: dysphoria, anhedonia, loss of motivation & enthusiasm, apathy, anergia or psychomotor retardation, impaired attention and cognition, decreased self-confidence, particularly affects prefrontal cortex, nucleus accumbens, basal ganglia, hypothalamus

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5
Q

Low “level” of the NE system is associated with:

A

Increased “negative affect” and decreased “positive affect”

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6
Q

NT interactions

A

neurotransmitter interactions: they affect each other and thus, the release of their own NTs and other monoamines

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7
Q

Action of anti-depressants

A

Affect the metabolic/gene transcription: decrease various receptors & chemicals associated with stress, depression, anxiety, and increase chemicals associated with healthy neurons, resiliency, less depression & anxiety.

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8
Q

Action of anti-depressants

A

Decrease excessive CRF (corticotropin releasing factor) and cortisol, caused by stress.

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9
Q

What are the impact of too much CRF and cortisol?

A

Cause atrophy in the hippocampus, amygdala, prefrontal cortex, thereby impairing memory, cognitive/executive function, efficient emotional processing (anti-depressants decrease such atrophy associated with deficits)

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10
Q

BDNF (brain-derived neurotrophic factor) and CREB (cAMP response element-binding protein) in hippocampus

A

Increased by anti-depressants in the brain

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11
Q

BDNF

A

cell repair, synaptogenesis, long-term memory, blocks toxic levels of cortisol

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12
Q

Which of the 6 SSRIs is most “guilty” of causing withdrawal symptoms?

A

Paxil

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13
Q

What is the difference between relapse and recurrence?

A

Relapse occurs after continuation of the anti-depressant during the 4-9 month period since beginning the drug (continuation phase). The recurrence period occurs during the maintenance phase after 1+ year of taking the drug.

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14
Q

During what timeframe is the acute phase of beginning an anti-psychotic drug?

A

6-12 weeks.

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15
Q

After 4 different anti-depressants, how many people still have not remitted (have residual symptoms)?

A

33%

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16
Q

What are the least common residual symptoms in non-remitters?

A

Depressed mood, suicidal ideation, & psychomotor retardation

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17
Q

What are the most common residual symptoms in non-remitters?

A

Insomnia, fatigue/pain, concentration, & loss of interest

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18
Q

What populations don’t do as well with anti-depressants (don’t benefit as much, and risk is higher)?

A

adolescents and elderly

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19
Q

What population has not been well studied in terms of the risks and benefits of giving them anti-depressants?

A

children (12 years and under)

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20
Q

How long should anti-depressants be continued after the response or remission, to prevent relapse?

A

4-9 months: If 1st episode, you can probably d/c at the end of the continuation phase (appox. 1 year); If 2nd episode (assess if there are risk factors), and d/c gradually at end of continuation phase if no risk factors, or maintain for life to prevent recurrence in risk factors are present. After 3rd episode, maintain for life. Risk factors: bipolar, family history of mental illness, suicidal or para-suicidal behaviors, substance use

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21
Q

How long should anti-depressants be continued after the response or remission, to prevent relapse?

A

4-9 months: If 1st episode, you can probably d/c at the end of the continuation phase (appox. 1 year); If 2nd episode (assess if there are risk factors), and d/c gradually at end of continuation phase if no risk factors, or maintain for life to prevent recurrence in risk factors are present. Risk factors: bipolar, family history of mental illness, suicidal or para-suicidal behaviors, substance use

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22
Q

How long does it take for neurotransmitters to increase in the brain after an anti-depressant is started?

A

A few days.

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23
Q

How long does it take for receptor sensitivity to decrease in the brain after an antidepressant is started?

A

Same amount of time it takes to experience a clinical effect

24
Q

How do SSRIs work?

A

5HT1a receptor on dendrites or soma (somadendritic autoreceptor) inhibits (reduces) firing and, hence, 5-HT (serotonin) release. They block the reuptake pumps. Also, downregulation of the auto receptors (inhibitors of firing) causes the neuron to release more 5HT at the axon.

25
Q

How do SSRIs work?

A

5HT1a receptor on dendrites or soma (somadendritic autoreceptor) inhibits firing and, hence, 5-HT release.

26
Q

SSRI side effects

A

Acute actions at undesirable postsynaptic receptors

27
Q

SSRI side effects

A

Acute actions at undesirable postsynaptic receptors

28
Q

When do side effects of SSRIs appear?

A

In first 1-2 weeks when postsynaptic receptors (especially 5HTt2) are activated by the increase in 5HT caused by antagonism of transporter. Often they dissipate in several weeks when postsynaptic receptors have down regulated or desensitized.

29
Q

What is the relationship between 5HT1a and 5HT2a?

A

They have opposite effects. 5HT1a=increases DA & NE improving “positive affect” and decreases Glu release decreasing anxiety; 5HT2a=decreases DA & NE decreasing “positive affect”, and increases Glu release increasing anxiety.

30
Q

What is the relationship between 5HT1a and 5HT2a?

A

They have opposite effects.

31
Q

What does acute/excessive activation of other 5-HT receptors cause?

A

Side effects: 5-HT2a/2c in amygdala, prefrontal cortex may cause mental agitation, anxiety, panic; 5HT2a in basal ganglia decreases DA release, thereby causing akathisia, psychomotor retardation, mild parkinsonism, dystonia; 5HT2c in mesolimbic pathway decreases DA release thereby causing apathy anhedonia and decreased libido; 5HT2c/2a in VTA and locus coeruleus decreases DA and NE release, respectively, in prefrontal cortex, thereby causing deficits in attention, cognition. ETC. ETC. ETC. see notes there are too many (slides 49-51). MAIN IDEA: side effects have to do with different receptors, which are located in different areas.

32
Q

What does acute/excessive activation of other 5-HT receptors cause?

A

Side effects: 5-HT2a/2c in amygdala, prefrontal cortex may cause mental agitation, anxiety, panic; 5HT2a in basal ganglia decreases DA release, thereby causing akathisia, psychomotor retardation, mild parkinsonism, dystonia; 5HT2c in mesolimbic pathway decreases DA release thereby causing apathy anhedonia and decreased libido; 5HT2c/2a in VTA and locus coeruleus decreases DA and NE release, respectively, in prefrontal cortex, thereby causing deficits in attention, cognition.

33
Q

SSRIs that increase synaptic concentration of monoamines

A

SSRI + 5-HT1a partial agonist (SPARI) = vilazodone (Viibryd) One method of action of SSRIs which blockade transporters (reuptake pumps); 5-HT1a partial agonism; a2 antagonism; 5-HT2a/2c antagonism/reuptake inhibition; inhibition of monoamine oxidase (MAO)

34
Q

SSRI + 5-HT1a partial agonist (achieved with vilazodone) reduces side effects, can also be achieved through:

A

SSRI plus aripiprazole (Abilify) or quetiapine (Seroquel) - both atypical antipsychotics (FDA approved to augment MDD tx with an SSRI); OR SSRI plus buspirone (BuSpar) - a 5-HT1a partial agonist –> good anti-anxiety effects in addition to anti-depressant.

35
Q

vortioxetine (Brintellix)

A

A complicated multimodal drug that just came out, (not an SSRI), but a partial agonist at multiple receptors, and an antagonist at other receptors, which all lead to precognitive, enhanced antidepressant effect? (not enough time for head on head comparisons yet) and less sexual, nausea SEs

36
Q

What does antagonizing NE reuptake do? (resulting in “low” NE)

A

increase positive affect, decrease negative affect, inhibit pain

37
Q

SNRIs = increase synaptic concentration of monoamines via blockade of transporters (reuptake pumps)

A

serotonin norepinephrine reuptake inhibitors: more active than SSRIs because of NE component. May be more likely to induce mania in bipolar patients. If NE is increased, activation is not usually excessive due to blunting by 5-HT (serotonin). Tend to off-set each other.

38
Q

SNRIs

A

serotonin norepinephrine reuptake inhibitors: more active than SSRIs because of NE component. May be more likely to induce mania in bipolar patients. If NE is increased, activation is not usually excessive due to blunting by 5-HT (serotonin).

39
Q

SNRIs and dopamine

A

NE reuptake inhibition (NRI) also increases DA in prefrontal cortex. They indirectly increase dopamine in the prefrontal cortex. Relevant to ADHD.

40
Q

SNRIs and dopamine

A

NE reuptake inhibition (NRI) also increases DA in prefrontal cortex.

41
Q

NDRI (norepinephrine dopamine reuptake inhibitor)

A

Increase dopamine in the mesolimbic pathway. Can be diagnosed alone, or as an augmenting agent (ex: buproprion being added to an SSRI) –> often increases positive affect, decreases negative affect, and reduces sexual SEs.

42
Q

NDRI (norepinephrine dopamine reuptake inhibitor)

A

Increase dopamine in the mesolimbic pathway

43
Q

What is the typical order of antidepressants that will be given/tried?

A

SSRI –> SNRI –> NDRI

44
Q

Alpha-2 Antagonism = Increase synaptic concentration of monoamines via a2 antagonism

A

What occurs when there is an increase in synaptic concentration of monoamines. Increased release and re-uptake of NE and 5-HT neurons. (mirtazapine=NaSS=norepinephrine and specific serotonergic antagonist). Decreases nausea, vomitting, diarrhea, but also blocks H1 receptors which causes daytime sleepiness. Also, might get weight gain from blocking H1 + 5-HT2c together.

45
Q

Blockage of H1 + 5-HT2c =

A

weight gain.

46
Q

Increased synaptic concentration of monoamines via 5-HT2a/2c antagonism/reuptake inhibition

A

Another mechanism of action for antidepressants (SARI - serotonin 2a/2c antagonist/reuptake inhibitor) - ex: trazodone (Desyrel, Oleptro). Used mainly for insomnia at low dose. Very sedating (blocks H1 and a1 receptors), with no “morning hangover” (short T1/2). Also used as an adjunct to other Ads by blocking some side effects associated with stimulation of 5HT2a receptors (anxiety, agitation, insomnia, sexual dysfunction).

47
Q

Increase synaptic concentration of monoamines via inhibition of monoamine oxidase (MAO)

A

Another mechanism of action of antidepressants - 2 forms MAOa and MAOb

48
Q

MAOa

A

metabolizes 5-HT, NE, DA, tyramine (found in gut and brain) - inhibition has antidepressant effect.

49
Q

MAOb

A

metabolizes DA, tyramine (in brain) - inhibition has no antidepressant affect.

50
Q

MAOa + MAOb =

A

Robust antidepressant effect. Irreversible MAOIs - permanently inhibit MAOs; new enzymes must be synthesized (takes 2 weeks). Considered “gold standard” because they’re so powerful, but they’re not given often because they’re irreversible. (experts believe underutilized)

51
Q

Why are MAOIs used so infrequently?

A

many other others, dangerous side effects, and incomplete or incorrect beliefs concerning them

52
Q

Tyramine

A

An amine found in some foods that potently increases the release of NE, increasing blood pressure. Normally MAO is able to metabolize the extra tyramine and NE and result in no increase in blood pressure.

53
Q

Tyramine

A

An amine found in some foods that potently increases the release of NE, increasing blood pressure. Normally MAO is able to metabolize the extra tyramine and NE and result in no increase in blood pressure.

54
Q

Foods high in tyramine

A

dried, aged, smoked, fermented, spoiled, improperly stored meat, poultry, fish, broad bean pods (e.g., fava beans), aged cheese, NOT processed cheese slices, cottage cheese, ricotta cheese, yogurt, cream cheese, most cheese in most commercial chain pizzas. Tap and non-pasteurized beers, but NOT canned or bottled. Many wines have low amounts. Marmite, sauerkraut, soy products, tofu.

55
Q

Foods high in tyramine

A

dried, aged, smoked, fermented, spoiled, improperly stored meat, poultry, fish, broad bean pods (e.g., fava beans), aged cheese, NOT processed cheese slices, cottage cheese, ricotta cheese, yogurt, cream cheese, most cheese in most commercial chain pizzas. Tap and non-pasteurized beers, but NOT canned or bottled. Many wines have low amounts. Marmite, sauerkraut, soy products, tofu.

56
Q

Serotonin syndrome

A

More serious condition that can occur when MAOIs are combined with other drugs, but can occur with only one drug - myoclonus, agitation, diaphoresis (sweating), tremor, hyper-reflexia. Greater risk associated with greater selectivity for 5-HT transporter. D/C immediately, do not titrate off. Do not combine any MAOI with another drugs that increases serotonin.

57
Q

Serotonin syndrome

A

more serious condition that can occur when MAOIs are combined with other drugs - myoclonus, agitation, diaphoresis (sweating), tremor, hyper-reflexia. Greater risk associated with greater selectivity for 5-HT transporter. D/C immediately, do not titrate off.

Psychopharmacology (2 decks)

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