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KG - pharmacology 3 > KG - Pharm 3, Exam 1, Antidepressants > Flashcards

KG - Pharm 3, Exam 1, Antidepressants Flashcards

1
Q

what is the amine neurotransmitter DOPAMINE responsible for?

A
  • REWARD, MOTIVATION, EUPHORIA, MOVEMENT

- target of cocaine & amphetamines

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2
Q

what is the amine neurotransmitter NE responsible for?

A
  • REWARD, AROUSAL, ALERTNESS, DECISIONS

- FLIGHT OR FRIGHT

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3
Q

what is the amine neurotransmitter SEROTONIN responsible for?

A
  • MOOD, EMOTION, MEMORY, SLEEP, COGNITION

- target of MDMA, LSD

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4
Q

what is the monoamine hypothesis?

A
  • depression caused by under activity of amines in the brain (DA, NE, serotonin)
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5
Q

moa: uptake inhibitors, short term & long term

A
  • serotonin levels increase but so does feedback inhibition (balances synaptic amine levels)
  • LONG TERM = antidepressants DOWN REGULATE auto-receptors, increases firing rate of serotonin neuron
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6
Q

TCAs: moa

A
  • INHIBIT RE-UPTAKE OF NE & 5-HT

- BLOCK ALPHA-ADRENERGIC, HISTAMINE, MUSCARINIC RECEPTORS

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7
Q

TCAs: use

A
  • depression - limited use bc toxic & potential to overdose
  • CHRONIC PAIN (TMJ)
  • fibromyalgia
  • enuresis
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8
Q

why are TCAs used for chronic pain?

A
  • bc a SMALL DOSE can be used
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9
Q

Amitriptyline & Imipramine: info

A
  • TERTIARY AMINES
  • PRIMARILY INHIBIT 5-HT RE-UPTAKE
  • produce more seizures than secondary amines
  • more sedating than secondary amines
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10
Q

Nortriptyline & Desipramine

A
  • SECONDARY AMINES

- PRIMARILY INHIBIT NE RE-UPTAKE

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11
Q

How do you choose a TCA?

A
  • based on adverse effects
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12
Q

How do you discontinue antidepressant use?

A
  • taper off gradually
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13
Q

TCAs: pharmacokinetics

A
  • oral
  • long half lives
  • once daily dosing
  • METABOLIZED BY CYP2D6 (DRUG INTERACTIONS COMMON!)
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14
Q

TCAs: side effects (histamine, cholinergic, alpha adrenergic)

A
  • BLOCK ALPHA ADRENERGIC, HISTAMINE, CHOLINERGIC RECEPTORS (leads to pharmacologic effects)
  • -> HISTAMINE = drowsiness, fatigue, sedation
  • -> CHOLINERGIC = blurred vision, tachycardia, constipation, urinary retention, dry mouth, palpitations, memory impairment, probs w/ cognition
  • -> ALPHA = cardiac depression, TORSADE DE POINTES, postural hypotension, dizziness, reflex tachycardia
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15
Q

TCAs: side effects, cont

A
  • weight gain
  • TORSADE DE POINTES (arrhythmias)
  • SIADH
  • SEXUAL DYSFUNCTION
  • decr seizure threshold
  • tolerance to sedation & anticholinergic effects
  • ANALGESIA
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16
Q

antidote for torsades de pointes?

A
  • Mg or isoproterenol
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17
Q

TCAs + MAOIs = ______

A
  • SEROTONIN SYNDROME = severe CNS toxicity w/ hyperpyrexia, convulsions, coma (stop TCAs 2-4 wks before starting MAOIs)
  • TCAs compete for metabolism w/ SSRIs
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18
Q

TCAs: drug interactions

A

+ MAOIs = serotonin syndrome
+ sympathomimetics (ie: amphetamine) = HTN
+ alcohol/CNS depressants = extra sedative effects
+ anticholinergics = potentiated effects

–> compete w/ SSRIs

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19
Q

SSRIs: moa

A
  • selectively inhibit 5-HT reuptake
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20
Q

SSRIs: uses

A
  • depression
  • panic disorder
  • OCD, social anxiety = PAROXETINE
  • bulimia
  • alcoholism
  • children & teens
21
Q

DOC depression?

A

SSRIs

22
Q

SSRIs: pharmacokinetics

A
  • well absorbed by gut
  • metabolized by CYP450s
  • inhibit CYP2D6 (fluoxetine, paroxetine)
  • lots of drug interactions
23
Q

Fluoxetine (Prozac): info

A
  • Norfluoxetine = active metabolite (half life 7-9 days)
  • half life 2-3 days
  • MORE DRUG INTERACTIONS THAN OTHER SSRIs
  • impairs blood glucose in diabetics
24
Q

Sertraline (Zoloft): info

A
  • extensive first pass metabolism
  • half life 26 hrs
  • LEAST LIKELY SSRI TO INTERACT W/ OTHER DRUGS
  • preferred in elderly
25
Q

Citalopram: info

A

DOC for depression

26
Q

SSRIs: side effects

A
  • MILD side effects (less than TCAs)
  • GI
  • weight loss/gain
  • SIADH
  • CNS STIMULATION w/ fluoxetine/sertraline, sedation w/ other drugs
  • SEXUAL DYSFUNCTION/DISINTEREST
  • no cardiac probs
  • photosensitivity
27
Q

SSRIs: drug interactions

A
  • inhibition CYP3A4, CYP2D6 (fluoxetine)
  • -> TCAs - inhibition metabolism increases toxicity
  • -> Warfarin - increased risk bleeding
  • -> phenytoin, carbamazepine - incr levels and toxicity
  • MAOIs = SEROTONIN SYNDROME
  • St. John’s Wort, Amphetamines = SEROTONIN SYNDROME
  • beta blockers = heart block, hypotension
  • opioids = inhibits conversion to active compound
28
Q

SNRIs: moa

A
  • inhibit NE & 5-HT re-uptake
29
Q

SNRI drugs?

A
  • Venlafaxine (chance cardiac toxicity, incr BP)

- Duloxetine (chance hepatotoxicity)

30
Q

MAOIs: moa

A
  • IRREVERSIBLY INHIBIT MAOs & MAOs METABOLIZE NE, DA, & 5-HT
  • MAO-A metabolizes NE & 5-HT in BOTH CNS and GI tract
  • MAO-B selectively metabolizes DA in CNS
31
Q

Phenelzine: info

A
  • INHIBITS MAO-A & MAO-B
  • INCREASES NE & 5-HT
  • use for depression that hasn’t responded to other drugs
  • DRUG OF LAST CHOICE - SERIOUS SIDE EFFECTS
32
Q

selegiline: info

A
  • SELECTIVELY INHIBITS MAO-B
  • INCREASES DOPAMINE
  • fewer side effects
  • used in Parkinson’s
33
Q

MAOIs: pharmacokinetics

A
  • long half life

- effects persist after stopping drug

34
Q

MAOIs: adverse effects (TYRAMINE)

A
  • TYRAMINE metabolized by MAO in GI TRACT
  • MAOIs inhibit tyramine metabolism
  • increased peripheral noradrenergic effects
  • AVOID FOODS w/ TYRAMINE (RED WINE, BEER, AGED CHEESE, ETC…)

HYPERTENSIVE CRISIS!

35
Q

MAOIs: adverse effects, cont

A
  • tremors, sedation, excitation, insomnia
  • ORTHOSTATIC HYPOTENSION
  • WEIGHT GAIN
  • ANTICHOLINERGIC EFFECTS (blurred vision, dry mouth)
36
Q

MAOIs: drug interactions

A
  • w/ TCAs/SSRIs/St. John’s Wort - SEROTONIN SYNDROME
  • OTC COLD MEDS can lead to severe HTN
  • OPIOIDS & DEXTROMETHORPHAN - can lead to hyperpyrexia, serotonin syndrome
37
Q

Bupropion: moa

A
  • PREFERENTIALLY INHIBITS DOPAMINE RE-UPTAKE
38
Q

Bupropion: use

A
  • COMBINED w/ SSRIs (sometimes)

- ADHD, alcoholism (decreases craving), smoking

39
Q

Bupropion: pharmacokinetics

A
  • extensive first pass metabolism
  • metabolized by CYP2B6
  • inducer CYP2D6
40
Q

Bupropion: side effects

A
  • SEIZURES (MOST SERIOUS)
  • CNS EFFECTS (anxiety, insomnia, restlessness, tremor, psychosis)
  • tachycardia
  • sexual dysfunction (rare)
41
Q

Mirtazapine: moa

A
  • NORADRENERGIC & SPECIFIC SEROTONERGIC ANTIDEPRESSANT
  • BLOCKS PRESYNAPTIC ALPHA 2 RECEPTORS (normally would inhibit release of NE & 5-HT)
  • INCREASES RELEASE NE, 5-HT
  • BLOCKS 5-HT2a, 5-HT3 RECEPTORS
  • blockade of these receptors eliminates side effects of SSRIs
42
Q

Mirtazapine: info

A
  • HISTAMINE ANTAGONIST (produces sedation)

- relieves side effects serotonin

43
Q

Atomoxetine: moa

A
  • SELECTIVE INHIBITOR OF NE RE-UPTAKE

- active metabolite that is DA/D2 antagonist

44
Q

Atomoxetine: info

A
  • TREATMENT ADHD

- last drug of choice depression

45
Q

Atomoxetine: side effects

A
  • liver damage possible, but rare

- side effects like TCAs

46
Q

Trazodone: moa

A
  • 5-HT2a RECEPTOR ANTAGONIST
47
Q

Trazodone: info

A
  • sedating, not good antidepressant
  • antianxiety, antipsychotic
  • OFF LABEL USE = HYPNOTIC/SLEEP AID
  • pain management
48
Q

Trazodone: side effects

A
  • SEDATION
  • dizziness, hypotension, nausea
  • PRIAPISM (rare) - limits use in males
49
Q

St. John’s Wort: info

A
  • may be effective for MILD depression
  • DO NOT COMBINE WITH OTHER ANTIDEPRESSANTS! - SEROTONIN SYNDROME
  • can prolong effects general anesthetics

KG - pharmacology 3 (11 decks)

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