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Bloc J - Neuro > Oct15 A3-Antidepressants > Flashcards

Oct15 A3-Antidepressants Flashcards

1
Q

categories of antidepressants

A
  • SSRIs and SNRIs
  • TCAs
  • atypical antidepressants
  • MAOIs
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2
Q

categories of mood stabilizers

A
  • lithium
  • anticonvulsants
  • atypical antipsychotics
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3
Q

charact of adt tx

A
  • only makes you feel less bad, not great
  • takes few weeks before improvement (6 to 12 weeks before full benefit)
  • third people good resp, third = slight improvement, third = no improvement
  • most SEs are in beginning and improve later
  • need daily tx for ­­>6 mo after remission to prevent relapse
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4
Q

what’s the monoamine theory of mood and anxiety disorders

A
  • most adts in market modulate monoamine neurotransmission
  • monoamine = NE, 5HT and dopamine
  • this DOESN’T mean that depression and anxiety are caused by low monoamine lvl
  • 5HT linked to obsessions and OCDs + anxiety and impulsivity
  • NE = fatigue and concentration issues
  • dopamine = reward chemical (drugs, sex, gambling)
  • it is WRONG to say that depression is caused by low dopa and 5HT
  • we DON’T KNOW if adts modify dz or modulate sx
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5
Q

serotonin system

A
  • cell bodies in rostral and caudal Raphe nuclei
  • project neurons to prefrontal cortex, limbic system, spinal cord, etc.
  • 5HT is made of tryptophan which comes from diet
  • ejected in synaptic vesicles
  • act on post syn 5HT Rs. (14 types of them, only some are active in the brain)
  • 5HT1A is the most associated with antidepressant effect
  • 5HT pumped back in pre syn cell after synapse
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6
Q

SSRIs work how

A

increase amount of serotonin in the synapse by blocking SERT (serotonin transporter for reuptake)

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7
Q

SSRIs main benefit in depression

A

main effect is on increased negative affect (feeling bad)

  • dysphoria (state of unease, general dissatisfaction with life)
  • guilty ruminations
  • anxiety
  • irritability
  • suicidal ideation
  • obsessions
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8
Q

diseases where SSRIs are indicated

A
  • major depressive disorder
  • anxiety disorders
  • PTSD
  • OCD
  • premenstrual dysphoric disorder
  • bulimia nervosa
  • bipolar depression (antipsychotic + SSRI)
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9
Q

off label uses of SSRIs

A
  • premature ejaculation
  • anxiety assoc with certain personality disorders (ie. obsessive compulsive personality, avoiding personality, etc.)
  • somatic symptom disorder
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10
Q

SSRI mnemonic (EFSPC)

A

effective for sadness panic compulsions

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11
Q

common SEs of SSRIs

A
  • GI upset
  • headache
  • sexual dysfunction = decreasd interest, orgasm. is the MAIN problem.
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12
Q

uncommon but serious SEs of SSRIs

A
  • switch into mania (if use on bipolar pt)
  • increased bleeding risk like NSAIDs
  • apathy and emotional numbling
  • hyponatremia
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13
Q

duration of SEs with SSRIs

A

1-2 weeks

-apathy and sexual dysfunction are short term

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14
Q

SNRIs are what

A

SEROTONIN norepinephrine reuptake inhibitors

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15
Q

SNRIs general action

A

dual action by blocking both NE and 5HT reuptake

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16
Q

noradrenergic system (norepinephrine)

A
  • nuclei (so cell bodies) in the locus coeruleus in the brainstem
  • projects to brain, limbic system, spinal cord
  • NE comes from tyrosine changing to dopamine
  • NE pumped out in syn vesicles
  • then reuptake
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17
Q

main effect of blocking NE and dopamine reuptake transporters (NOREPINEPHRINE TRANSPORTER = NET) (SNRIs block 5HT and NE reuptake transporters)

A

help for reduced positive affect

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18
Q

other use of SNRIs

A

use for chronic pain conditions because they reduce pain via descending NE and 5HT pathways

  • related to central sensitization theory for pain
  • this theory is that in chronic pain, brain gets worse at filtering out painful stimuli
  • brain receives painful signals
  • signal go back down spine to inhibit pain (inhibitory signals)
  • these signals stop working in chronic pain (the inhibitory ones)
  • we get them working again by increasing NE and 5HT pathways (blocking their NET and SERT) with SNRIs
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19
Q

SEs of SNRIs that are related to blocking NET specifically (increasing NE)

A
  • NE beta R: tremor, htn, tachycardia

- NE alpha R: dry mouth, constipation, urinary retention, sweating

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20
Q

SEs of SNRIs related to NET blocking are similar to what med + how to diff

A

like anticholinergics. diff is

  • anticholinergics = dry skin
  • noradrenergic = sweating
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21
Q

TCAs charact

A

tricyclic antidepressants

  • block SERT and NET
  • more SEs bc also block H1 (histamine), alpha 1 (adrenergic) and mAch (muscarinic Ach) Rs.
  • weakly block Na+ channels so can cause seizures and cardiac arrhythmias in overdose. MAIN WORRY IS PT CAN DECIDE TO COMMIT SUICIDE BY OVERDOSING ON IT (which is not possible with SSRIs)
  • block 5HT2 Rs so additional benefit in chronic pain, fibromyalgia, migraine
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22
Q

TCAs use today

A

chronic pain conditions mostly

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23
Q

SEs of TCAs

A
  • alpha1 and beta adrenerg = dizziness and drowsiness
  • antihistamine effect = weight gain and drowsiness
  • antichol effect = constipation, dry mouth, blurred vision
24
Q

atypical antidepressants MOA

A
  • bupriopion weakly blocks dopa and NE reuptake = more transmission
  • another one called mirtazapine, diff MOA (dnm)
  • quetiapine (diff MOA, dnm)
  • vortioexetine (diff MOA, dnm)
25
Q

SEs of atypical atds

A
  • bupriopion = rarely helpful in anxiety disorders, decreases seizure threshold
  • mirtazapine = weight gain and sedation
  • quetiapine = weight gain and sedation
  • vortioxetine = GI SEs
26
Q

main reason to use atypical atds

A

reduced risk of sexual SEs (common benefit to all atypical atds) + one marketed for smoking cessation (one benefit of bupriopion)

27
Q

monoamine oxidase inhibitors (MAOIs) use today

A

rarely used

  • rarely by experts for very tx resistant depression
  • rarely for some anxiety disorders
28
Q

MAOIs 2 types

A

irreversible and reversible (less effective, less risk of 5HT syndrome and no risk of tyramine htn crisis)

29
Q

(imp) main SE of MAOIs

A

2 life threatening drug interaction reactions

  • serotonin syndrome
  • hypertensive crisis
30
Q

(imp) cause of 5HT syndrome

A

when combined with SSRIs and other serotonergic meds or certain drugs of abuse (like MDMA and certain opiates), MAOIs can give the syndrome

31
Q

(imp) cause of hypertensive crisis with MAOI

A

when combined with sympathomimetics and tyramine containing foods (aged cheese, dried meats, soy sauce, draft beer)

32
Q

(imp) tyramine hypertensive crisis def

A

severe, life threatening hypertension

33
Q

(imp) tyramine hypertensive crisis pathophgy

A
  • MOA needed for NE degradation
  • NE in cells of liver and gut not degradated
  • tyramine enters cells of liver and gut and kicks out NE which increases BP
  • high tyramine in diet contributes to that
34
Q

(imp) serotonin syndrome pathophgy

A
  • SERT and MAO are both blocked
  • 5HT accum in synapses and over stim post syn Rs
  • 6-8 hrs after starting or increasing drug
  • tachycardia, agitation, autonomic instability, clonus and tremor, etc.
35
Q

atds and suicidality

A
  • atds decrease the risk of completed suicide
  • atds increase the risk of suicidal behavior but NOT of complete suicide in people <25
  • tx of depression in adolescents DECREASES the risk of suicide
36
Q

why atds increase the risk of suicidal behavior but NOT of complete suicide in people <25

A
  • bc these people have some type of bipolar disorder
  • you’re activating them into an agitated state
  • a mood stabilizer is better for these pts
37
Q

(imp) what meds can give a true serotonin syndrome

A

MOAIs ONLY
-SSRIs and SNRIs can both give serotonin effects (bad headaches, feeling unwell), especially if combine them but not 5HT syndrome

38
Q

considerations in initial tx of depression

A
  • first line meds are SSRIs, SNRIs, bupriopion, vortioxetine and mirtazapine
  • the 3 atypical atds for less risk of sexual SEs
39
Q

lithium used for what

A

tx of mania and prevention of mood episodes in bipolar disorder
(also in combination with atds for tx resistant depression)
(may reduce suicidal thinking and aggression)

40
Q

lithium MOA

A
  • is a salt, given as lithium carbonate
  • interacts with 2nd messenger systems inside the cell
  • promotes neuronal survival and synaptongenesis, neural plasticity, neural protection
  • no metab by liver. excreted unchanged by the kidney
41
Q

SEs of lithium

A
  • short term: GI, tremor, polyuria, polydipsia

- long term (after years): 10-20% nephrogenic diabetes insipidus, 20% CKD (chronic renal insufficiency), hypoT

42
Q

(imp) bad SEs of lithium

A

teratogenic, risks for pregnancy

  • cardiac malformations
  • assoc with Epstein abnormality (a specific cardiac abnormality)
  • also not compatible with lactation
43
Q

lithium toxicity

A
  • narrow therapeutic index
  • toxicity possible in dehydration and diarrheal illnesses
  • sx of lithium toxicity = GI sx, ataxia, confusion, seizures, renal failure, arrhythmias
  • no tx = long term neuro problems
44
Q

tx of lithium toxicity

A

IV fluids, hemodialysis maybe

45
Q

mnemonic for lithium SEs

A
  • L = leukocytosis
  • I = insipidus (diabetes)
  • T = tremors
  • H = hypothyroid
  • I = increased urine (polyuria)
  • M = mom’s beware (teratogenicity)
46
Q

anticonvulsant used for tx of mania and prevention of mood episodes

A

valproate (epival, depakote)

-anticonvulsant and antimigraine effec ttoo

47
Q

MOA of valproic acid

A
  • block Na and Ca channels
  • increases GABA
  • inhibits histone deacetylace
  • modulates 2nd messengers
48
Q

SEs of valproate

A
  • GI
  • weight gain
  • sedation
  • polycystic ovary
49
Q

contraindication of valproate use

A

pregnancy

  • neural tube defects
  • dev delay
  • CAN lactate while taking it however
50
Q

anticonvulsant used to prevent depressive episodes in bipolar disorder

A

lamotrigine (lamictal)

  • well tolerated
  • MOA = block Na channels leading to decreased glutamate release
51
Q

SEs of lamotrigine

A
  • drowsiness
  • rashes
  • rare Steven-Johnson syndrome (severe life threatening rash)
52
Q

antipsychotics in bipolar disorders

A
  • can be used to tx mania no matter if pt has psychosis or not
  • used when pts are agitated (works faster than lithium and valproate)
  • long acting injectable format available
  • some antidepressant effects also
53
Q

antipsychotics MOA

A

decrease dopamine activity (increased dopamine is probably the cause of manic episodes in bipolar disorders)

54
Q

considerations in tx of bipolar disorder

A
  • lithium (classic manic depressive illness, not in pt with kidney prob)
  • valproate (irritability and mixed states, migraine, epilepsy. but teratogenic)
  • lamotrigine (prevents depression, helps epilepsy)
  • 2nd generation antipsychotics (tx and prevent mania. watch out for sedation)
55
Q

main categories of antidepressants

A
  • SSRIs
  • SNRIs
  • TCAs
  • MAOIs
  • novel antidepressants
56
Q

what all currently prescribed atds do

A

modulate monoamine ntrs (dopa, 5HT, NE) synaptic transmission

57
Q

meds used to tx bipolar disorders

A
  • lithium
  • valproate
  • lamotrigine
  • 2nd generation antipsychotics

Bloc J - Neuro (60 decks)

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