Depression meds Flashcards
major depression is characterized by?
feelings of intense sadness, despair, mental slowing, loss of concentration, pessimistic worrying, agitation, self-deprecation
criteria for persistent depression?
meet 3 of the criteria =
for 2 years (1 year of youth)
milder, higher functioning
criteria for major depression?
meet 5 of the criteria
for 2 wks
lower functioning
criteria for depression?
sleep problems, disinterest, low self-esteem, energy problems, poor concentration, appetite change, agitated or slow
suicidal ideal
physical ssxs of depression?
insomnia, hypersomnia, anorexia, wt loss, some will overeat as a coping mechanism
decreased energy
decreased libido
pneumonic for depression?
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
what do most antidepressants act on?
act on metabolism of monoamine neurotransmitters and receptor sites (NE and serotonin)
monoamines include?
dopamine, NE, serotonin
amphetamines also act as?
monoamines
theory of depression?
deficiency of monoamines such as NE or serotonin in parts of the brain
can be dt genetics, environment, biochemical factors, dopaminergic activity, endocrine factors
aside from affecting monoamine levels, how else do antidepressants work?
possibly also down-regulate the # of receptor sites in response to an increased neurotransmitter availability
indications of antidepressants?
moderate to severe depressive illness severe anxiety and panic attacks OCD chronic pain eating d/os post-traumatic stress d/o
when antidepressants and EtOH are consumed, what is a possible outcome?
seizures as it lowers the threshold for seizure
6 major categories of antidepressants?
monoamine oxidase inhibitors tricyclic antidepressants tetracyclic antidepressants serotonin re-uptake inhibitors serotonin and NE re-uptake inhibitors NE and dopamine re-uptake inhibitors
3 additional classes of antidepressants?
selective serotonin re-uptake enhancers
NE re-uptake inhibitors
novel antidepressants
4 MAOIs?
tranylcypromine/parmate
phenelzine/nardil
isocarcarboxazie/marplan
selegiline/eldepryl
why are MAOIs less commonly used?
severe SEs include: weakness, dizziness, H/As, tremors, potential for marked HTN
can potentiate the effects of sympathomimetics such as NE
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.?
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
what happens if a pt on an MAOI ingests too much tyramine?
can cause potentially toxic levels of catecholamines resulting in severe H/As, nausea and HTN
MOA of increased tyramine in the bloodstream while on MAOIs?
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
indications for tricyclic antidepressants?
OCD enuresis panic attacks chronic pain migraines depression
what do tricyclic antidepressants cause in regards to neurotransmitters?
inhibit reuptake of serotonin and NE which increases amount left in neurotransmitter in synaptic cleft
how long can it take for tricyclic antidepressants to work?
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
SEs of tricyclic antidepressants?
dry mouth, constipation, urinary hesitancy, orthostatic hypotension, sedation
why is dry mouth a SE of tricyclic antidepressants?
b/c affects the muscarinic cholinergic receptors
primary cause of orthostatic hypotension with tricyclic antidepressant use?
blockade of alpha-adrenergic receptors
heart rate variability tricyclic antidepressants can cause?
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
compare/contrast toxicity of SSRIs to tricyclic antidepressants
tricyclic antidepressants can be fatal in doses as little as 10x the daily dose
toxicity to tricyclic antidepressants is dt what?
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
class of amitriptyline/elavil? indications? MOA? how to give? how does it primarily act?
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
SEs of amitriptyline/elavil? what can abrupt discont of the drug cause?
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)
mirtazapine enhances what activity?
noradrenergic and serotonin activity
acts as a central presynaptic alpha 2 adrenergic inhibitor receptors
mirtazapine is a potent/moderate antagonist of what neurotransmitter, hormone and what receptors?
potent antagonist of 5-HT2 and 5-HT3 receptors
potent antagonist of histamine receptors
moderate antagonist of peripheral alpha 1 adrenergic receptors
class of trazodone/desyrel? other effects? off-label uses?
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
class of trazodone/desyrel? indications? MOA?
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
adverse effects of trazodone? relative safety?
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
b/c of trazodones lack of anticholinergic SEs, when is it esp useful to use?
when antimuscarinic effects are particularly problematic: prostatic hypertrophy, closed-angle glaucoma, severe constipation
the possible resulting hypotension in pts of trazodone is from what?
1-adrenergic receptor blockade
what is the most commonly prescribed category of antidepressant drugs?
SSRIs
main MOA is blockade of serotonin reuptake at the presynaptic terminal which results in subsequent increased level of serotonin available for further neurotransmission
SSRIs are documented to help what %age of pts w/depression?
50-70%
SEs of SSRIs? what age group is particularly at risk for a fatal SE?
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
where does serotonin come from?
brainstem - raphe nuclei
all SSRIs potently decrease the action of the presynaptic serotonin reuptake pump by what %age? importance?
60-80%
this increases the length of time that serotonin is available in the synapse and increases postsynaptic serotonin receptor occupancy
how long can it take to see therapeutic effects of SSRIs?
can take 3-8 wks
effect of SSRIs on other neurotransmitters?
initial increase in synaptic serotonin eventually leads to increased production of neuroprotective proteins such as brain-derived neurotrophic factor and Bc1-2
what is mood anesthesia?
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
class of fluoxetine/prozac? indications? MOA?
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
how to give fluoxetine/prozac? SEs?
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)
what class of meds can affect the efficacy of SSRIs?
painkillers of the NSAID class (aspirin, ibuprofen, naproxen)
5 serotonin and NE reuptake inhibitors?
duloxetin/cymbalta desvenlafaxine/pristiq milnacipran/dalcipran nafazodone/serzone venlafaxine/effexor
duloxetine/cymbalta is C/I in what pts? approved use?
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
most common SEs of duloxetine/cymbalta? what age group is at increased risk for a fatal SE?
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
class of bupropion/wellbutrin? indications? aids in what?
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)
MOA of buproprion/wellbutrin? SEs? potential increase in what behavior with all antidepressants?
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
if being used as a smoking cessation age, when does the pt need to start taking zyban?
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
MOA of chantix? SEs of chantix? neuropsychiatric sxs?
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
diet related possible cause of depression?
folate deficiency
levomefolic acid= active form
purpose of methyltetrahydrofolate in neurotransmitter production?
acts as a co-enzyme modulator in the synthesis of dopamine, serotonin, NE
what is a supplement useful for augmenting antidepressants in pts w/inadequate responses to SSRIs?
SAMe - share w/MTHF the ability to regulate methylation
significance of folate deficiency and depression?
folate deficiency can increase the risk of depression and reduce the action of antidepressants
“medical food” brand name of levomefolic acid?
deplin - indicated for the management of suboptimal folate levels in depressed pts
what is methylated folic acid used for?
DNA replication, cysteine cycle and regulation of homocysteine among multiple other factors
important coenzyme utilized in the production of catecholamine neurotransmitters
