Antidepressants Flashcards

1
Q

When is ECT used?

A

suicidal depression

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2
Q

ECT

A
  • patient anestethized and given a muscle relaxant
  • electric current passed through head for .5s - 4s
  • induces a grand mal seizure
  • low level of current used, short duration
  • memory loss can occur
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3
Q

depressive disorder

A
  • prolonged disturbance of mood
  • sad, empty, or irritable modd accompanied by: somatic and cognitive changes that affect individuals capacity to function
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4
Q

MDD symptoms

A
at least two weeks of depressed mood or anhedonia and:
-weight change
-sleep problems
-psychomotor agitation
-fatigue
-feelings of worthlessness/guilt
-difficulty concentrating
-thoughts of death/suicide
episodes can last months to years
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5
Q

monoamine oxidase inhibitors

A

block monoamine oxidase in nerve terminals and glia, as well as liver and kidney

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6
Q

catechol-o-methyltransferase is invovled in:

A

monoamine degredation

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7
Q

How many forms of mao are there? Which degrades monoamines?

A
  • two forms (a and b)

- a degrades monoamines

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8
Q

limitations/side effects of maois

A
  • lots of side effects due to the widespread location of maos
  • interact with foods rich in tryptamine (life-threatening)
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9
Q

monoamine theory of depression and its problems

A
  • hypoactivity of mono amino neurons causes depression

- problem: why is there a theraputic lag in the imporvement of symptoms?

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10
Q

maois given chronically and numbers of mao receptors:

A

neurons down-regulate the numbers of mao receptors on post synaptic neuron

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11
Q

revised monoamine theory of depression

A
  • the hypoactivity of monoamine neurons increases postsynaptic receptor sensitivity, causing depression
  • antidepressants decrease postsynaptic receptor sensitivity
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12
Q

tricyclic antidepressants

A
  • closely related in structure to phenothiazines (antipsychotics)
  • inhibit NE/5-HT uptake
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13
Q

second generation antidepressants

A
  • fewer side effects
  • 5-HT reuptake inhibitors
  • NE reuptake inhibitors
  • DA reuptake inhibitors
  • 5-HT/NE reuptake inhibitors
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14
Q

Paxil, Prozac, Zoloft

A

SSRIs

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15
Q

Reboxetine

A

NRIs

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16
Q

Wellbutrin

A

DA reuptake inhibitor

17
Q

Effexor

A

SNRI (5-HT/NE reuptake inhibitors)

18
Q

autoreceptors function to

A

shut off neurotransmitter release from neurons

19
Q

do autoreceptors have high or low affinity for neurotransmitters? why?

A

high affinity; there is low neurotransmitter concentration of the edge of the synapse

20
Q

chronic reuptake inhibition and autoreceptors

A

chronic reuptake inhibition results in autoreceptor downregulation (consistent with theraputic lag)

21
Q

further refinement of monoamine theory of depression

A
  • hyopactivity of monoamine neurons increases autoreceptor sensitivity
  • antidepressants decrease autoreceptor sensitivity
22
Q

What do all antidepressants act on?

A

5-HT2 autoreceptors; reduce 5-HT2a binding

23
Q

What does ECT do to 5-HT2a binding?

A

increases 5-HT2a binding

24
Q

newest antidepressants:

A

noradrenergic and specific serotonergic antidepressants (NaSSAs)

25
mirtazapine
noradrenergic and specific serotonergic antidepressants (NaSSAs)
26
rTMS
repeated transcrainial magnetic stimulation; brief magnetic stimulation, localized to a brain area
27
HPA axis pathway
- in response to stress the hypothalamus secretes corticotropin releasing hormone - then the anterior pituitary relases adrenocorticotropin hormone - the adrenal gland relased glucocorticoids - glucocorticoids have a negative feedback to the hypothalamus and hippocampus
28
plasma levels of cortisol in depressed patients
increased cortisol levels, indicative of hyperactive HPA axis
29
relationship between cortisol levels and BDNF
increased cortisol levels, decreased BDNF
30
Decreased levels of BDNF linked to:
atrophy of neurons and decreased neuronal survival
31
Role of BDNF
important for the birth and growth of neurons
32
Where does adult neurogenesis occur?
hippocampus
33
certain antidepressants can increase ____
neurogenesis in the hippocampus
34
What receptors could another class of next generation antidepressants target?
NMDA glutamate receptors
35
GLYX13
glycine site partial agonist on NMDA receptors; phase 3 clinical trials in 2016
36
Phase I drug trials
small group to evaluate saftey, dosage, & side effects
37
Phase II drug trials
larger group to access efficacy and safety
38
Phase III drug trials
large group to confirm efficacy, monitor side effects, and compare to other treatments
39
Phase IV drug trials
drug marketed, but efficacy and side effects are sill monitored