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anti-depressants and mood stabilizers Flashcards

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1
Q

what is the biogenic amine hypothesis for depression?

A

a functional deficit of monoamines (mostly NE & 5-HT) is thought to be involved in the pathophys. of depression

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2
Q

which population of pts needs to be warned about which BBW of antidepressants, especially during the initial weeks of treatment?

A

children and adolescents with thoughts of suicide

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3
Q

antidepressant drugs that are substrates for ___________ (MDR1; P-gp) which exists at the BBB limits the ability of drugs to accumulate in the brain

A

ABCB1

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4
Q

name the 4 antidepressants that are substrates for MDR1

A 
citalopram
venlafaxine
paroxetine
amitriptyline
"can't volley proper antidepressants"
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5
Q

name the two antidepressants that are not substrates for MDR1

A

mirtazapine

fluoxetine

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6
Q

what are some of the indications for TCA therapy?

A

major depression, pain/anxiety disorders (OCD, phobias, panic), ADHD, nocturnal enuresis (imipramine), depression assoc. w/ schizophrenia

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7
Q

what is the MOA of TCAs?

A

inhibits the reuptake of 5-HT & NE into presynaptic terminals–> potentiate and prolong the actions of these neurotransmitters–> receptors and transporter regulation w/ repeated treatment
-also block mACh, 5-HT, & histamine receptors

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8
Q

orthostatic hypotension is an AE of TCAs due to antagonism of what receptor?

A

antagonism of alpha-ARs

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9
Q

blurred vision, worsening of narrow-angle glaucoma, dry mouth, constipation, urinary retention, tachycardia are all AEs of TCAs due to antagonism of what receptor?

A

antagonism of mAChR

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10
Q

what are some metabolic/endocrine related AEs of TCAs?

A

weight gain

sexual disturbances

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11
Q

what happens in TCA overdose?

A

has low therapeutic index
CV effects including: arrhythmias, direct myocardial depression, worsening of CHF
-also: acidosis, delirium seizures

“3 C’s: convulsions, coma, cardiotoxicity”

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12
Q

describe some of the PKs of TCAs?

A

high first pass metabolism
high lipid solubility (allows distribution to brain & fat)
highly protein bound (high Vd), which limits excretion (leading to long half-life)

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13
Q

tertiary amines (TCAs) are metabolized to active secondary amines by what?

A

demethylation (imipramine, amitriptyline–> nortriptyline)

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14
Q

the tricylclic ring is subject to oxidation by what cyp enzyme and also can be conjugated?

A

subject to CYP2D6 oxidation & conjugation

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15
Q

name the atypical antidepressant drug: moderate inhibition of serotonin reuptake but primarily acts s a 5-HT2a antagonist & 5-HT1a partial agonist (SARI) useful in the treatment of depression characterized by anxiety and sleep disturbances

A

trazodone

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16
Q

trazodone inhibits which CYP enzyme?

A

CYP3A4

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17
Q

name the drug: analog of mianserin

A

mirtazepine

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18
Q

name the drug: enhances release of serotonin & NE by antagonizing presynaptic alpha-2ARs. Antagonizes 5-HT2 receptors.

A

mirtazepine

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19
Q

what are the AEs of mirtazepine?

A

potent antihistaminic–> sedating
increased weight gain
(tetracyclic antidepressant)

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20
Q

name the drug: weak blocker of DAT, SERT, & NET. active metabolite is a NE reuptake blocker

A

buproprion (also used in smoking cessation)

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21
Q

what are the AEs of buproprion?

A

agitation, anxiety, restlessness

risk of seizure, (no sexual AEs)

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22
Q

name the antidepressant drug: inhibits serotonin & NE reuptake (SNRI). Lacks antihistaminergic, anticholinergic, and antiadrenergic properties–> does not have TCA-like side effects

A

venlafaxine

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23
Q

what are the AEs of venlafaxine?

A

produces a small, sustained HTN, sweating dizzyness, nausea, anxiety

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24
Q

what is the most potent SNRI available?

A

duloxetine (100x more potent than venlafaxine)

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25
Q

describe the bioavailability and protein binding of duloxetine

A

50% bioavailability

highly bound to plasma proteins (95%)

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26
Q

duloxetine is metabolized by what two CYP enzyme?

A

CYP2D6 & CYP1A2

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27
Q

name the drug: recently approved serotonin modulator and stimulator. potent blocker of SERT & high efficacy partial agonist at 5-HT1a receptors. Partial agonist (5-HT-1b) and antagonist at 5-HT1d 3a, & 7 receptors?

A

vortioxetine

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28
Q

name the 5 SSRIs

A

Fluoxetine + Fluvoxamine
Paroxetine
Sertraline
Citalopram

“Flashbacks paralyze senior citizens”

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29
Q

what is the first line therapy in pts diagnosed with major depression?

A

SSRIs (also used to treat panic, OCD, social-anxiety disorder, ADHD, and some eating disorders)

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30
Q

describe the general behavior/clinical effects of SSRIs-acute

A

CNS stim.
anxiety
agitation

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31
Q

describe the general behavior/clinical effects of SSRIs-chronic

A

2-6 wks

improvement of most or all clinical symptoms, CNS activation remains

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32
Q

what are the AEs of SSRIs?

A 
Nausea
decreased libido
sexual dysfunction
low incidence CV & anticholinergic
note: higher therapeutic index
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33
Q

what is the active metabolite of fluoxetine?

A

norfluoxetine-has half life of 7-9 days

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34
Q

most of the SSRIs are metabolized by what CYP enzymes?

A

CYP2D6 (strong inhib.)
CYP2C19 (strong inhib.)
CYP3A4

35
Q

what drug class is contraindicated with SSRIs?

A

MAOIs (taking them together can cause serotonin syndrome)

36
Q

serotonin syndrome is due largely to overstimulation of what receptors in the central grey (midbrain) and medulla?

A

5-HT1A

37
Q

what is the clinical presentation of serotonin syndrome?

A 
hyperpyrexia
hyperreflexia
tremor
shivering
myoclonus
agitation
seizures
confusion
delirium
CV collapse
coma
38
Q

other than MAOis what other drugs can trigger serotonin syndrome?

A

can also be triggered by increased 5-HT release (amphetamines, MDMA) or via 5-HT agonists (LSD, buspirone, L-Tryptophan)

39
Q

name the 4 MAOIs

A

tranylcypromine (not on drug list)
phenelzine
isocarboxazid (not on drug list)
Selegiline (MAO-B inhibitor)

“MAO Takes Pride in Shanghai”

40
Q

what are the indications for MAOis?

A

typically used in pts who are unresponsive to treatment with other antidepressants and for whom ECT is not suitable.
-also used for panic disorder, agoraphobia

41
Q

MOA of the monoamine oxidase inhibitors?

A

blocks oxidative metabolism of monoamines by IRREVERSIBLE inhibition of MAO-A & MAO-B in nerve terminals (MAO-A metabolizes primarily NE, 5-HT, tyramine; MAO-B mostly DA selective)

42
Q

describe the general behavior/clinical effects of MAOIs-acute

A

CNS stim.
agitation
possibly euphoria

43
Q

describe the general behavior/clinical effects of MAOIs-chronic

A

2-6 wks: improvement of most or all symptoms, CNS activation remains

44
Q

what are the AEs of MAOIs?

A 
sleep disturbances (increased arousal)
orthostatic hypotension
weight gain
some sexual dysfunction
hypertensive crisis ( with ingestion of tyramine)
45
Q

MAOIs are inactivated by what process?

A

acetylation (phamacogenomic differences)

46
Q

what are some of the drug interactions for MAOis?

A

foods containing high amounts of tyramine (cheese)

47
Q

what can happen when taking MAOIs & sympathomimetic drugs?

A

acute hypertensive reaction

48
Q

what can happen taking MAOis with meperidine, or dextromethorpham?

A 
hyperpyrexia
delirium
convulsions
coma
death
49
Q

name the 3 drugs used as mood-stabilizers

A

lithium
valproate
carbamazepine

“moody lions value carbs”

50
Q

what are the indications for the mood stabilizers?

A

maintenance of manic depression (bipolar affective disorder)

51
Q

MOA of lithium?

A

most favored hypothesis is Li inhibition of inositol phosphate signaling. also inhibits neurotransmitter-stim. adenylyl cyclase activity. Effective in ~60% of pts

52
Q

what are the adverse effects for lithium?

A

very narrow therapeutic window

  • neurologic/psychiatric: tremor, ataxia, hyperactivity, aphasia, sedation fatigue
  • Glandular: edema, mild hypothyroidism
  • renal: polydipsia, polyuria (nephrogenic diabetes insipidus)
  • cardiac: bradycardia-tachycardia (sick sinus)
    other: acne, folliculitis and exacerbates psoriasis
53
Q

which drug can cause polyuria (nephrogenic diabetes insipidus?

A

lithium

54
Q

which drug can cause bradycardia-tachycardia (sick-sinus)?

A

lithium

55
Q

which drug can exacerbate psoriasis?

A

lithium

56
Q

what are the drug interactions with lithium?

A

sensitive to diuretics & NSAIDs

57
Q

name the two anticonvulsants that are now frequently used in the management of bipolar disorder

A

valproate & carbamazepine

58
Q

what are the advantages of valproate and carbamazepine over Lithium?

A

increase dose faster, quicker response, better therapeutic index

59
Q

what are the disadvantages valproate and carbamazepine compared to lithium?

A

less experience, efficacy questionable in severe disease

60
Q

which drug is first line for bipolar disorder?

A

lithium (however milder forms of bipolar disorder may be treated with anticonvulsants)

61
Q

what is the drug of choice when absence seizures are also accompanied with tonic-clonic seizures?

A

valproic acid

62
Q

what is the MOA of valproic acid?

A

inhibits voltage-gated Na+ channels by stabilizing the inactivated state of the channel. Block of channel activity is use-dependent.

  • Also blocks Ca2+ channels (T-type) to a lesser extent
  • can also stim. GABA synthesis & inhibit GABA degradation
  • at high doses may increase resting K+ conductances
63
Q

valproate inhibits its own metabolism and the metabolism of other drugs via which CYP enzyme?

A

CYP2C

64
Q

what are the AEs of valproate?

A

nausea, abd. pain, heartburn, sedation may be a problem, hepatotoxicity can be common (recomend liver function test)

65
Q

what is the drug of choice for partial seizures, also may be used for generalized tonic-clonic seizures, also effective for trigeminal neuralgia?

A

carbamazepine

66
Q

MOA for carbamazepine?

A

inhibition of Na channels (prolongs recovery time from inactivation)

67
Q

which drug is metabolized primarily by CYP3A4 to an active metabolite 10,11-epoxide?

A

carbamazepine

68
Q

name the two SNRIs

A

venlafaxine

duloxetine

69
Q

name the TCAs (8)

A 
Amitriptyline
nortriptyline
imipramine
desipramine
protriptyline

(all TCAs end in iptyline or ipramine except doxepin and amoxapine)

70
Q

what are the drug interactions for carbamazepine?

A

carbamazepine is a broad spectrum inducer of CYP2C & 3A families & in addition to induction of UGTs

71
Q

what are the AEs of carbamazepine?

A 
diplopia & ataxia are common
mild GI upset
at high doses drowsiness
rash common idiosyncratic reaction
some occurences of aplastic anemia
72
Q

name the drug that matches the pt with most benefit: elderly pt; a pt with agitated depression or pt w/ GI distress

A

citalopram

73
Q

name the drug that matches the pt with most benefit: noncompliant or forgetful pt; excessive fatigue

A

fluoxetine

74
Q

name the drug that matches the pt with most benefit: less likely to produce initial anxiety &/or insomnia

A

paroxetine

75
Q

name the drug that matches the pt with most benefit: the medical/surgical pt on one or more drugs. initial activation and increased alertness desired

A

sertraline

76
Q

name the drug that matches the pt with most benefit: pts with menopausal symptoms or failing an SSRI trial. At higher doses pts with chronic pain

A

venlafaxine

77
Q

name the drug that matches the pt with most benefit: pt with depression and chronic pain (effects on pain are dose-dependent) pt failing an SSRI trial

A

duloxetine

78
Q

name the drug that matches the pt with most benefit: the medically ill pt with weight loss, insomnia and nausea

A

mirtazapine

79
Q

name the drug that matches the pt with most benefit: the now depressed or potentially bipolar pt. The apathetic, low energy pt. Pts motivated to stop smoking. Helpful for ADHD

A

buproprion

80
Q

which antidepressant is “unlikely” to cause sexual dysfunction?

A

mirtazapine

81
Q

which antidepressant “rarely” causes sexual dysfunction?

A

buproprion

82
Q

name the drug that matches the pt with the least benefit: pts who are agitated, very anxious &/or panicky. Pts at risk for seizures &/or w/ hx of head trauma, substance abuse, eating disorder or electrolyte disturbance

A

buproprion

83
Q

name the drug that matches the pt with the least benefit: pts who are agitated, very anxious &/or panicky. Pts at risk for seizures &/or w/ hx of head trauma, substance abuse, eating disorder or electrolyte disturbance

A

buproprion

PSYCH (8 decks)

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