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Brain And Behavior Exam 4 > Lec 74 Antidepressants > Flashcards

Lec 74 Antidepressants Flashcards

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1
Q

What are the classes of antidepressants?

A
  • MAO inhibitors
  • tricyclic antidepressants
  • selective serotonin reuptake inhibitors
  • antidepressants with multiple receptor targets
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2
Q

What is therapeutic use of MAO inhibitors?

A

atypical depression
anxiety
hypochondriasis

treatment resistant depression/panic disorder/social anxiety disorder

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3
Q

What is mech of action of MAO inhibitors?

A
  • irreversibly inhibit degradation of MAOs in presynaptic terminals
  • causes increase 5HT, NE, DA in presynaptic terminals and synaptic cleft
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4
Q

What are substrates of MAO-A vs MAO-B?

A

MAO-A: 5HT, NE, DA

MAO-B: phenylethylamine, DA [NOT 5HT, NE]

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5
Q

What is first aid mnemonic for MAO inhibitors?

A

MAO takes pride in shanghai

  • MAO
  • Tranylcypromine
  • Phenelzine
  • Isocarboxazid
  • Selegiline
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6
Q

What are the side effects of MAO inhibitors?

A

serotonin syndrome if combined w/ other 5HT drugs

hypertension if combined with tyramine diet or drugs that are adrenergic agonists

orthostatic hypotension, weight gain, insomnia, sexual dysfunction, rare hepatotoxicity [for phenelzine + iso]

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7
Q

What are symptoms of serotonin syndrome?

A

symptoms: ab pain, diarrhea, sweating, tremor, hyperthermia, tachycardia, hypertension, myoclonus, irritability, delirium, death

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8
Q

What causes serotonin syndrome?

A

selected drugs in combo with MAOI

  • other antidepressants
  • cyclobenzapine
  • carbamazepine
  • dextromethorphan
  • opiaties: meperidine, fentanyl, methadone
  • tramadol
  • st johns wort
  • SSRI
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9
Q

What is a hypertensive crisis? symptoms?

A

defined by diastolic BP > 120

symptoms: headache, palpitations, stiff/sore neck, N/V, sweating, dilated pupils, photophobia

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10
Q

What triggers hypertensive crisis? what drugs to avoid?

A

triggered by noradrenergic drug + MAO inhibitor

avoid

  • decongestants
  • stimulants [amphetamines]
  • appetite suppressants
  • antidepressants with NRI [TCAs, SNRIs, buproprion]
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11
Q

What is a tyramine-induced hypertensive crisis?

A
  • ingestion of tyramine-rich foods in presence of MAO-I can trigger hypertensive crisis
  • tyramine is a catecholamine releasing agent
  • intestinal wall MAO-A breaks down tyramine before absorption
  • if tyramine gets access to NE sympathetic neurons –> will release NE; but don’t have to worry about it because MAO-A breaks down tyramine before it gets a chance

if you inhibit MAO-A –> can’t handle dietary tyramine, release NE and no MAO-A to destroy it –> increased BP

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12
Q

What foods should you avoid on MAO-I?

A

avoid: soy, beer, red wine, aged cheese, dried sausage, fava beans, liver, smoked fish, sauerkraut

continue diet for 2 wks after stopping MAO-I to allow re-synthesis of MAO-A

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13
Q

What is EMSAM?

A

selegiline transdermal path for treatment of depression

  • at low levels selegiline inhibits MAO-B but at antidepressent level inhibits A and B
  • goal to bypass GI tract and liver to minimize chance of hypertensive crisis if tyramine is ingested

dietary restriction at > 6mg/24 hr

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14
Q

What kind of drug is phenelzine?

A

MAO inhibitor

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15
Q

What kind of drug is tranylcypromine?

A

MAO inhibitor

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16
Q

What kind of drug is selegiline?

A

MAO inhibitor –> selective for MAO-B at low doses; but acts on both at anti-depressant levels

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17
Q

What is therapeutic use for tricyclic antidepressants?

A
  • major depression
  • OCD [clomipramine]
  • fibromyalgia
depression + treatment resistant depression
childhood enuresis [imipramine]
generalized anxiety disorder
insomnia
obsessive compulsive disorder
migraine
cataplexy syndrome [imipramine]
fibromyalgia
prurits/dermatologic
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18
Q

What is mech of action tricyclic antidepressants?

A
  • block presynaptic reuptake of NE and 5HT
  • secondary = NE only; tertiary = NE + 5HT
  • causes NT accumulation in synaptic cleft
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19
Q

What are side effects of TCAs?

A

sedation, weight gain [H1 block]

a1 blockade –> orthostatic hypotension, dizziness

atropine [anti-ACh] side effects: urinary retention, dry mouth, tachycardia

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20
Q

What are side effects unique to despiramine?

A
  • less sedating [H] but higher seizure incidence

- least alpha 1 blockade

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21
Q

Do tertiary or secondary amines have more anticholinergic effects?

A

tertiary > secondary

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22
Q

what are the Tri-C’s of tricyclic antidepressants?

A

TriC = convulsion, coma, cardiotoxicity [arrhythmias]

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23
Q

Why should you use nortriptyline in elderly?

A

its a secondary amine = less anti-ACh effects

causes confusion and hallucination in elderly

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24
Q

How do you treat tricyclic antidepressant cardio toxicity?

A

NaHCO3

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25
Q

Which TCAs have least anticholinergic effects?

A

secondary amines [desipramine, nortriptyline]

26
Q

Which TCAs have most antihistamigeric effect?

A

doxepin

27
Q

Which TCAs have least alpha 1 blockade?

A

secondary amines [desipramine, nortriptyline]

28
Q

What happens in TCA overdose?

A

lethal

29
Q

Who should you avoid TCA in?

A

pts with narrow angle glaucoma, recent cardiac events, cardiac conduction delays, prolonged GTc

30
Q

Are tertiary or secondary amines beter in elderly?

A

secondary

31
Q

What is the phrase for anticholinergic toxicity?

A 
red as a beet
dry as a bone
blind as a bat
mad as a hatter
hot as a hare
full as a flask
32
Q

How are TCAs metabolized?

A

by cyp450
tertiary –> secondary
1/2 life 10-70 hrs

33
Q

What drug-drug interactions with TCAs?

A
  • block effect of antihypertensives
  • additive tox with anti-arrhythmics/QTc prolonging agents, anticholinergics, CNS depressants, sympathomimetics
  • drugs that increase TCA level: cimetidine, fluoxetine, ritonavir
  • drugs that decrease TCA: carbamazepine, rifampin, phenytoin, nictonie, barbituates

MAOIs: wait 14 days between MAOI and TCA

34
Q

What is dosing/monitoring of TCA?

A
  • narrow therapeutic index
  • similar dose range and plasma levels for most
  • lower doses for pain
  • unclear value in monitoring drug levels
35
Q

What are uses for SSRIs?

A
  • depression
  • generalized anxiety
  • panic disorder
  • PTSD
  • OCD
  • premenstrual dysphoric disorder
  • social phobias
  • bulimia
36
Q

What is mech of action SSRIs?

A

bind to serotonin transporter and inhibit reuptake of 5HT into presynaptic nerve terminals

37
Q

What is first aid mnemonic for SSRI names?

A

Flashbacks paralyze senior citizens

  • Fluoxetine
  • paroxetine
  • setraline
  • citalopraom
38
Q

Which SSRI has highest potency for DA?

A

setraline

39
Q

Which SSRIs have highest potency for NE?

A

fluvoxamine

paroxetine

40
Q

Which SSRIs are most selective for 5HT reuptake?

A

citalopram

fluoxetine

41
Q

What are common side effects of SSRIs?

A 
GI distress 
sexual dysfunction (anorgasmia and decrease libido)
weight gain
tremor
sweating

serotonin syndrome with any drug that increases 5HT [MAOI, SNRI, TCA] –> hyperthermia, confusion, myoclonus, flushing, diarrhea, seizures

42
Q

What is treatment for serotonin syndrome?

A

cyproheptadine = 5HT2 receptor antagonist

43
Q

What is metabolism of SSRI?

A

significant 1st pass

metabolized in liver by CYP enzymes

44
Q

Which SSRIs have less drug-drug interactions?

A

citalopram and escitalopram

45
Q

Which SSRIs have more drug drug interactions?

A

fluxoamine

46
Q

Which SSRI has longest half life and least withdrawal?

A

fluoxetine

47
Q

What are properties of fluoxetine?

A
  • activating, may cause insomnia
  • long half life
  • least withdrawal symptoms
  • more drug-drug interactions than others
48
Q

What are properties of sertraline?

A
  • activating

- mild DA reuptake inhibitor

49
Q

What are properties of paroxetine?

A
  • short half life
  • withdrawal symptoms
  • control release form available
  • blocks NE reuptake, some anti-ACh activity, more sedation, dry mouth, weight gain
50
Q

What happens in SSRI withdrawal? treat?

A
  • if abrupt discontinuation after >6 wks of treatment
  • dizziness, weakness, nausea, headache, anxiety, insomnia, paresthesias, flu-like symptoms, muscles aches

usually resolves within 3 wks

can treat with fluoxetine

51
Q

What are advantages of SSRIs over older agents?

A

standard dosing = easy to titrate
often get clinical response at starting dose
usually not lethal in overdose
no arrhythmias/disturbance in BP/seizure/coma/resp depression
fewer drug-drug interactions
no special diet

52
Q

What is use of SNRIs?

A
  • depression
    venlafaxine = also generalzie anxiety + panic disorders
    duloxetine = also diabetic peripheral neuropathy

fibromyalgia, painful physical symptoms of depression, stress urinary incontinence, vasomotor symptoms

53
Q

What is mech of SNRIs?

A

at low dose < 150mg/day act as SSRI

at higher doses –> SNRI = inhibit 5HT and NE reuptake

54
Q

What are side effects of SNRIs?

A

increase BP [more in venlafaxine than duloxetine], stimulant effects, sedation, nausea

55
Q

What is unique about bupropion’s side effects?

A

no sexual dysfunction or weight gain

stimulant effects: tachycardia, insomnia; headache, seizure in bulimic pts

56
Q

What are side effects of mirtazapine?

A

Sedation [may be desirable in depressed pts with insomnia]

increased appetite, weight gain [may be desirable in elderly or anorexic]

dry mouth

57
Q

What is use of mirtazapine?

A
  • depression
  • insomnia
  • appetite stimulation
58
Q

Which anti-depressant is known for its priapism effects?

A

trazodone

59
Q

What causes the therapeutic delay in onset of antidepressant action?

A

downregulation of serotonergic receptors

may enhance neruonal regeneration process + restore cortical dendrites

60
Q

Which type of antidepressants best for co-morbid pain disorders?

A

SNRI

Brain And Behavior Exam 4 (24 decks)

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