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
Q

mirtazapine

A

noradrenergic and specific serotonergic antidepressants (NaSSAs)

26
Q

rTMS

A

repeated transcrainial magnetic stimulation; brief magnetic stimulation, localized to a brain area

27
Q

HPA axis pathway

A
  • 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
Q

plasma levels of cortisol in depressed patients

A

increased cortisol levels, indicative of hyperactive HPA axis

29
Q

relationship between cortisol levels and BDNF

A

increased cortisol levels, decreased BDNF

30
Q

Decreased levels of BDNF linked to:

A

atrophy of neurons and decreased neuronal survival

31
Q

Role of BDNF

A

important for the birth and growth of neurons

32
Q

Where does adult neurogenesis occur?

A

hippocampus

33
Q

certain antidepressants can increase ____

A

neurogenesis in the hippocampus

34
Q

What receptors could another class of next generation antidepressants target?

A

NMDA glutamate receptors

35
Q

GLYX13

A

glycine site partial agonist on NMDA receptors; phase 3 clinical trials in 2016

36
Q

Phase I drug trials

A

small group to evaluate saftey, dosage, & side effects

37
Q

Phase II drug trials

A

larger group to access efficacy and safety

38
Q

Phase III drug trials

A

large group to confirm efficacy, monitor side effects, and compare to other treatments

39
Q

Phase IV drug trials

A

drug marketed, but efficacy and side effects are sill monitored