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Pharm II > Depression meds > Flashcards

Depression meds Flashcards

1
Q

major depression is characterized by?

A

feelings of intense sadness, despair, mental slowing, loss of concentration, pessimistic worrying, agitation, self-deprecation

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2
Q

criteria for persistent depression?

A

meet 3 of the criteria =
for 2 years (1 year of youth)
milder, higher functioning

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3
Q

criteria for major depression?

A

meet 5 of the criteria
for 2 wks
lower functioning

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4
Q

criteria for depression?

A

sleep problems, disinterest, low self-esteem, energy problems, poor concentration, appetite change, agitated or slow
suicidal ideal

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5
Q

physical ssxs of depression?

A

insomnia, hypersomnia, anorexia, wt loss, some will overeat as a coping mechanism
decreased energy
decreased libido

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6
Q

pneumonic for depression?

A 
S: sleep pattern changes
I: interests change, activities change
G: guilty feelings or increased worry
E: energy changes
C: concentration changes
A: appetite changes
P: psychomotor disturbances
S: suicidal ideation
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7
Q

what do most antidepressants act on?

A

act on metabolism of monoamine neurotransmitters and receptor sites (NE and serotonin)

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8
Q

monoamines include?

A

dopamine, NE, serotonin

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9
Q

amphetamines also act as?

A

monoamines

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10
Q

theory of depression?

A

deficiency of monoamines such as NE or serotonin in parts of the brain
can be dt genetics, environment, biochemical factors, dopaminergic activity, endocrine factors

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11
Q

aside from affecting monoamine levels, how else do antidepressants work?

A

possibly also down-regulate the # of receptor sites in response to an increased neurotransmitter availability

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12
Q

indications of antidepressants?

A 
moderate to severe depressive illness
severe anxiety and panic attacks
OCD
chronic pain
eating d/os
post-traumatic stress d/o
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13
Q

when antidepressants and EtOH are consumed, what is a possible outcome?

A

seizures as it lowers the threshold for seizure

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14
Q

6 major categories of antidepressants?

A 
monoamine oxidase inhibitors
tricyclic antidepressants
tetracyclic antidepressants
serotonin re-uptake inhibitors
serotonin and NE re-uptake inhibitors
NE and dopamine re-uptake inhibitors
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15
Q

3 additional classes of antidepressants?

A

selective serotonin re-uptake enhancers
NE re-uptake inhibitors
novel antidepressants

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16
Q

4 MAOIs?

A

tranylcypromine/parmate
phenelzine/nardil
isocarcarboxazie/marplan
selegiline/eldepryl

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17
Q

why are MAOIs less commonly used?

A

severe SEs include: weakness, dizziness, H/As, tremors, potential for marked HTN
can potentiate the effects of sympathomimetics such as NE

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18
Q

what amino acid is normally broken down by monoamine oxidase? where is this a.a. found? what does this mean in regards to monoamine oxidase inhibitors and this a.a.?

A

tyramine
found in cheese, soy, raisins, meats and red wine
since MAO is essential for adequate breakdown of tyramine, anyone suing MAOIs should avoid foods w/high levels of tyramine

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19
Q

what happens if a pt on an MAOI ingests too much tyramine?

A

can cause potentially toxic levels of catecholamines resulting in severe H/As, nausea and HTN

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20
Q

MOA of increased tyramine in the bloodstream while on MAOIs?

A

tyramine displaces NE from neuronal storage vesicles which causes vasoconstriction and increased HR and BP
also acts directly as a neurotransmitter, acts on TA1 receptor

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21
Q

indications for tricyclic antidepressants?

A 
OCD
enuresis
panic attacks
chronic pain
migraines
depression
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22
Q

what do tricyclic antidepressants cause in regards to neurotransmitters?

A

inhibit reuptake of serotonin and NE which increases amount left in neurotransmitter in synaptic cleft

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23
Q

how long can it take for tricyclic antidepressants to work?

A

can take up to 4 wks to work and need to take as PRESCRIBED not as needed
usu taken at bedtime; only take once a day

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24
Q

SEs of tricyclic antidepressants?

A

dry mouth, constipation, urinary hesitancy, orthostatic hypotension, sedation

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25
Q

why is dry mouth a SE of tricyclic antidepressants?

A

b/c affects the muscarinic cholinergic receptors

26
Q

primary cause of orthostatic hypotension with tricyclic antidepressant use?

A

blockade of alpha-adrenergic receptors

27
Q

heart rate variability tricyclic antidepressants can cause?

A

slow intra-cardiac conduction and cause various arrhythmias including tachycardia, ventricular fibrillation, ventricular premature complexes
ECG changes may occur - benign or otherwise, but do not reduce CO

28
Q

compare/contrast toxicity of SSRIs to tricyclic antidepressants

A

tricyclic antidepressants can be fatal in doses as little as 10x the daily dose

29
Q

toxicity to tricyclic antidepressants is dt what?

A

toxicity usu dt prolongation of QT interval leading to arrhythmias
can cause death dt dysrhythmia or heart block
week’s supply of tricyclic taken at once can be fatal

30
Q

class of amitriptyline/elavil? indications? MOA? how to give? how does it primarily act?

A

class: tricyclic antidepressant
indications: major depression, bipolar d/o, migraines, tension H/A, chronic pain
MOA: CNS modulation of both serotonin and NE, increases levels of each
give via PO or IM, usu take at bedtime to minimize SEs of drowsiness and dizziness
acts primarily as a serotonin-NE reuptake inhibitor w/strong actions on the serotonin transporter and moderate effects on NE transporter

31
Q

SEs of amitriptyline/elavil? what can abrupt discont of the drug cause?

A

SEs: dizziness, drowsiness, anticholinergic effects such as dry mouth, constipation, urinary hesitancy, blurred vision
stopping tx abruptly can cause withdrawal-like sxs - nausea, H/A, dizziness, lethargy, flu-like sxs (discontinuation syndrome)

32
Q

mirtazapine enhances what activity?

A

noradrenergic and serotonin activity

acts as a central presynaptic alpha 2 adrenergic inhibitor receptors

33
Q

mirtazapine is a potent/moderate antagonist of what neurotransmitter, hormone and what receptors?

A

potent antagonist of 5-HT2 and 5-HT3 receptors
potent antagonist of histamine receptors
moderate antagonist of peripheral alpha 1 adrenergic receptors

34
Q

class of trazodone/desyrel? other effects? off-label uses?

A

class: tetracyclic antidepressant of serotonin antagonist and re-uptake inhibitor class
also has anti-anxiety and sleep-inducing effects
off label uses: fibromyalgia, complex regional pain syndrome, control of nightmares, panic d/o, diabetic neuropathy, bulimia nervosa, OCD, EtOH withdrawal, ED

35
Q

class of trazodone/desyrel? indications? MOA?

A

class: tetracyclic
indications: major depressive d/o, anxiety, panic d/o, insomnia
MOA: serotonin re-uptake inhibitor and partial antagonist
decreased serotonin reuptake at presynaptic cleft allows for increased serotonin levels in the synapse and increased serotonin made available at post-synaptic receptor sites

36
Q

adverse effects of trazodone? relative safety?

A

sedation, orthostatic hypotension, fatigue, possible cardiac dysrhythmias, possible mania in pts w/bipolar d/o, increased risk of suicide
appears relatively safer than TCAs, MAOIs and a few of the other 2nd generation antidepressants in overdose situations, esp when only agent taken
fatalities are rare

37
Q

b/c of trazodones lack of anticholinergic SEs, when is it esp useful to use?

A

when antimuscarinic effects are particularly problematic: prostatic hypertrophy, closed-angle glaucoma, severe constipation

38
Q

the possible resulting hypotension in pts of trazodone is from what?

A

1-adrenergic receptor blockade

39
Q

what is the most commonly prescribed category of antidepressant drugs?

A

SSRIs
main MOA is blockade of serotonin reuptake at the presynaptic terminal which results in subsequent increased level of serotonin available for further neurotransmission

40
Q

SSRIs are documented to help what %age of pts w/depression?

A

50-70%

41
Q

SEs of SSRIs? what age group is particularly at risk for a fatal SE?

A

SEs: dizziness, nausea, H/A, fatigue, diarrhea, anxiety, insomnia, impotence
despite wide range of potential SEs, still best benefit to risk ratio of the antidepressant drugs
adolescents at increased risk of suicide while on SSRIs

42
Q

where does serotonin come from?

A

brainstem - raphe nuclei

43
Q

all SSRIs potently decrease the action of the presynaptic serotonin reuptake pump by what %age? importance?

A

60-80%
this increases the length of time that serotonin is available in the synapse and increases postsynaptic serotonin receptor occupancy

44
Q

how long can it take to see therapeutic effects of SSRIs?

A

can take 3-8 wks

45
Q

effect of SSRIs on other neurotransmitters?

A

initial increase in synaptic serotonin eventually leads to increased production of neuroprotective proteins such as brain-derived neurotrophic factor and Bc1-2

46
Q

what is mood anesthesia?

A

closely related to sexual SEs attributed to anti-depressant drugs, esp the SSRIs
includes emotional blunting: apathy, lack of motivation, emotional numbness, feelings of detachment, indifference to surroundings, “not caring about anything anymore”
all SSRIs, SNRIs and serotonergic TCAs can cause this to varying degrees

47
Q

class of fluoxetine/prozac? indications? MOA?

A

class: SSRI
indications: major depressive d/o, OCD, bulimia, panic d/o
MOA: decreased serotonin reuptake at presynaptic cleft allows for increased serotonin levels in the synapse and increased serotonin made available at post-synaptic receptor sites
to be avoided in children and teens

48
Q

how to give fluoxetine/prozac? SEs?

A

give PO, once a day dosing, generally takes weeks to achieve full therapeutic effects
SEs: serotonin syndrome = fever, agitation, diarrhea, elevated BP; sexual dysfxn common (lack of interest, impotence, anorgasmia)

49
Q

what class of meds can affect the efficacy of SSRIs?

A

painkillers of the NSAID class (aspirin, ibuprofen, naproxen)

50
Q

5 serotonin and NE reuptake inhibitors?

A 
duloxetin/cymbalta
desvenlafaxine/pristiq
milnacipran/dalcipran
nafazodone/serzone
venlafaxine/effexor
51
Q

duloxetine/cymbalta is C/I in what pts? approved use?

A

C/I: pts w/heavy EtOH use or chronic liver dz, can increase levels of certain liver enzymes that can lead to acute hepatitis or other dzs in certain at risk pts
approved for major depressive d/o, generalized anxiety d/o chronic MS pain, chronic osteoarthritis pain, chronic low back pain, fibromyalgia

52
Q

most common SEs of duloxetine/cymbalta? what age group is at increased risk for a fatal SE?

A

H/A, somnolence, fatigue, nausea, xerostomia, insomnia, ED
children, adolescents and young adults at increased risk of suicidal thinking and behavior w/taking cymbalta and major depressive d/o or another psychiatric d/o

53
Q

class of bupropion/wellbutrin? indications? aids in what?

A

class: NE and dopamine reuptake inhibitor and nicotine receptor antagonist
indications: major depression, bipolar d/o, attention deficit d/o
adis in smoking cessation (Zyban when used for this purpose)

54
Q

MOA of buproprion/wellbutrin? SEs? potential increase in what behavior with all antidepressants?

A

MOA: blockade of NE and dopamine reuptake increases the available pool of these amines in the synaptic cleft
SEs: H/A, insomnia, dry mouth, tremors, restlessness, agitation, anxiety, sweating, dizziness
all of the antidepressants are being looked at for potential increase in suicidal behavior

55
Q

if being used as a smoking cessation age, when does the pt need to start taking zyban?

A

need to start taking 1 week before target quit date since it takes 5-7 days to reach steady state in blood
recommended duration of tx is 7-12 wks

56
Q

MOA of chantix? SEs of chantix? neuropsychiatric sxs?

A

MOA: partial nicotine agonist indicated for use as an aid to smoking cessation
SEs: neuropsychiatric effects - depression, suicidal thoughts, suicide; nicotine withdrawal sxs and exacerbation of underlying psychiatric illness
DO NOT RECOMMEND USING THIS DRUG b/c of neuropsychiatric effects even in those who have never experienced psychiatric complaints before

57
Q

diet related possible cause of depression?

A

folate deficiency

levomefolic acid= active form

58
Q

purpose of methyltetrahydrofolate in neurotransmitter production?

A

acts as a co-enzyme modulator in the synthesis of dopamine, serotonin, NE

59
Q

what is a supplement useful for augmenting antidepressants in pts w/inadequate responses to SSRIs?

A

SAMe - share w/MTHF the ability to regulate methylation

60
Q

significance of folate deficiency and depression?

A

folate deficiency can increase the risk of depression and reduce the action of antidepressants

61
Q

“medical food” brand name of levomefolic acid?

A

deplin - indicated for the management of suboptimal folate levels in depressed pts

62
Q

what is methylated folic acid used for?

A

DNA replication, cysteine cycle and regulation of homocysteine among multiple other factors
important coenzyme utilized in the production of catecholamine neurotransmitters

Pharm II (18 decks)

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