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Undeleted > pharmacology of depression > Flashcards

pharmacology of depression Flashcards

1
Q

biogenic amine hypothesis of depression

A

depression is caused by deficiency of monoamines, particularly NE and 5HT

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2
Q

monoamine

A

neurotransmitter containing one amino group, e.g., serotonin, dopamine, epinephrine, norepinephrine

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3
Q

receptor sensitivity hypothesis of depression

A

supersensitivity and upregulation - the post-synaptic neuron tries to compensate for a lack of stimulation due to deficiency of NE & 5HT

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4
Q

lag period

A

time between starting medication and obtaining full symptom relief; believed to occur as a result of down regulation

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5
Q

down regulation

A

reducing stimulation at the post-receptor (post-synaptic) site

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6
Q

bruxism

A

teeth grinding

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7
Q

sympathomimetics

A

compounds mimicking effect of sympathetic nervous system neurotransmitters: catecholamines, epinephrine, norepinephrine, dopamine

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8
Q

monoamine oxidase (MAO)

A

inactivates norepinephrine, dopamine, epinephrine, and serotonin

  • inhibit MAO, increase amount of circulating neurotransmitters
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9
Q

antidepressant rule of thumb

A

NEVER MIX ANTIDEPRESSANTS

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10
Q

antidepressant guidelines

A

start low, go slow
remember lag period
most side effects occur in first 1-2 weeks
suicide risk increases with energy level

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11
Q

antidepressant discontinuation rule of thumb

A

TAPER TAPER TAPER

the shorter the half life, the more likely to have withdrawal

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12
Q

SSRI side effect profile compared to others

A

much lower!

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13
Q

serotonin level in depression is…

A

low 5HT

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14
Q

fluoxetine (prozac)

A

SSRI - first one to be made!

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15
Q

SSRI: moa

A

inhibition of 5HT reuptake

  • result: increased availability, intensified transmission at post-synaptic site
  • adaptive changes occur in response to prolonged uptake blockade
  • smaller doses typically for older adults
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16
Q

SSRI: pharmacokinetics

A
  • highly pound to plasma proteins
  • extensive hepatic metabolism, resulting active metabolites
  • prolonged half life
  • degree of inhibition (platelet aggregation)
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17
Q

SSRI: steady state plasma levels in how long + why?

A

~ 4 weeks, due to prolonged half life

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18
Q

SSRI: degree of inhibition significance (pharmacokinetics)

A

5HT needed to stimulate platelet aggregation!

higher inhibition of 5HT receptors = less 5HT to stimulate aggregation = higher risk of bleeding, hemorrhage (especially taken with NSAID)

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19
Q

SSRI: side effects

A 
nervousness, insomnia, anxiety
headache
nausea
weight loss at first → weight gain
sexual dysfunction common (70%) 
bruxism 
skin rashes *
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20
Q

SSRI: adverse effects

A

risk for hemorrhage
risk for hyponatremia
serotonin syndrome

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21
Q

serotonin syndrome

A

may begin within minutes to hours (up to 72) after initiation of ANY medication that increases serotonin levels

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22
Q

SSRI: why risk for hemorrhage? (ae)

A

serotonin needed for platelet aggregation

  • SSRI blocks reuptake, so aggregation CAN’T occur
  • SSRI decreases coagulation!!!
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23
Q

SSRI: why risk for hyponatremia? (ae)

A

5HT thought to be involved in production of ADH
- water leaves, salt leaves

  • within first few weeks, more common in older adults
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24
Q

too much serotonin is…

A

overly excitatory

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25
Q

zofran, reglan + SSRI = ?

A

serotonin syndrome. zofran and reglan already increase serotonin alone.

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26
Q

serotonin syndrome treatment

A

stop med, stop med combo, treat s/s

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27
Q

mild serotonin syndrome

A

mental status: restless
autonomic activity: diaphoresis, increased HR
neuromuscular: myoclonus (spasm)

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28
Q

moderate serotonin syndrome (full blown!)

A

mental status: agitation, LOC
autonomic activity: hypertension, shivering –> hyperthermia
neuromuscular: rigidity

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29
Q

severe serotonin syndrome

A

mental status: coma
autonomic activity: shock
neuromuscular: tonic-clonic seizures

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30
Q

SSRI interaction: TCA

A

potentiates

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31
Q

SSRI interaction: lithium

A

potentiates

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32
Q

SSRI interaction: MAOI

A

serotonin syndrome

NO NO NO NO NO NEVER MIX

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33
Q

SSRI: withdrawal + fix

A

abrupt, persists 1-2 weeks
severity depends on: duration, dosage, half life
s/s: GI, neuro, somatic, psychological
“fix” = take med again

34
Q

tricyclic antidepressants (TCA): moa

A
  • inhibits reuptake of NE and 5HT
    • moa varies by med (primarily NE, 5HT less)

intermediary neurochemical events and/or changes occur over time

35
Q

TCA compared to SSRI

A

more effective, but worse side effect profile

36
Q

TCA: why “dirty drug” and results

A

because varying affinity for MANY receptor sites

  • block muscarinic receptors (anticholinergic side effects)
  • block histamine receptors (sedation, weight gain)
  • love adrenergic receptors (dizzy, hypotension, increased fall risk)

MANY SE DUE TO PERIPHERAL EFFECTS ON OTHER NT SYSTEMS

37
Q

TCA: minimize AE by avoiding… (2)

A 
anticholinergic drugs
cns depressants (alcohol, opioids, barbituates)
38
Q

TCA: AE

A 
hypotension
horrible anticholinergic SLUD
sedation
diaphoresis
cardiotoxicity
seizures
hypomania
yawngasm
muscarinic: flushing, pupil dilation, hyperthermia
39
Q

TCA: most dangerous adverse effect & why

A

cardiotoxicity: decrease vagal influence, act directly on heart to slow conduction

40
Q

hypomania + TCA, MAOI: why?

A

sudden increase in monoamines!

41
Q

TCA interactions (4)

A

cns depressants
anticholinergics
sympathomimetics
MAOI

42
Q

TCA + MAOI = ?

A

NEVER EVER EVER EVER DO THIS

hypertensive crisis can result!!!!

43
Q

TCA toxicity: cardiotoxicity

A

direct/indirect causes

44
Q

TCA toxicity: anticholinergics

A

only takes 8x daily dose to be LETHAL

–> atropine psychosis

45
Q

atropine psychosis: cause + s/s

A

sign of TCA toxicity!
early s/s: agitation, confusion
late s/s: seizures, coma

aka anticholinergic delirium

46
Q

TCA: what to monitor (2)

A 
baseline EKG regardless of age
plasma levels (only in case of overdose)
47
Q

MAOI rule of thumb

A

NEVER MIX MAOI WITH OTHER ANTIDEPRESSANTS

48
Q

MAOI compared with SSRI

A

more effective, but more significant side effect profile

49
Q

MAO action

A

degrades monoamines after reuptake
important role in metabolism of many drugs

  • MAOI inhibits both MAO-A and MAO-B
50
Q

MAO-A

A

inactivates dopamine

51
Q

MAO-B

A

inactivates 5HT, NE

52
Q

MAOI wash out period

A

10 - 14 days before new MAO is synthesized after discontinuing MAOI

53
Q

MAOI appropriate for (disease + patient types)

A

depression, bulimia, ocd, panic disorders, more

give to patients highly likely to conform to restrictions (med, diet)

54
Q

MAO: decrease in liver = ?

A

decreased metabolism of many drugs

MAO plays important role in metabolism of many drugs

55
Q

MAOI: moa

A
  • prevents inactivation of NE and 5HT by mao
    = increased transmitters released into synaptic cleft
  • irreversible inhibition for 10-14 days
    = effects continue up to 2 weeks after medication stopped
56
Q

phenelzine sulfate (nardil)

A

MAOI in USA

57
Q

tranylcypromine sulfate (parnate)

A

MAOI in USA

58
Q

selegiline transdermal system (emsam)

A

MAOI in USA

less likely to react with food, but still needs regulation

59
Q

isocarboxazid (marplan)

A

MAOI in USA

60
Q

MAOI: drug interactions

A
  • anesthesia
  • narcotics
  • antidepressants
  • sympathomimetics
  • cocaine
  • antihypertensives
61
Q

MAOI: food interactions

A

TYRAMINE!!!!

dairy
protein-rich (esp processed; salami, sausage, tofu, pickled fish)
fruits, veg (fig, banana, avocado)
desserts, sweets (chocolate!)
alcohol (red wine, beer)
some fats (salad dressing)
yeast products
soy sauce, meat tenderizers
ginseng (MANIC REACTION)
caffeinated bevs
62
Q

tyramine

A

MAJOR INTERACTION WITH MAOI

moa: pressor, increases BP if not inactivated by MAO
- MAOI increases availability leading to
- - hypertension, hypertensive crisis

63
Q

tyramine + MAOI = ?

A

hypertensive crisis!!!!

64
Q

MAOI: interaction with anesthesia

A
  • anesthesia
  • narcotics
  • antidepressants
  • sympathomimetics
  • cocaine
  • antihypertensives
65
Q

MAOI: interaction with narcotics

A

especially opioids

66
Q

MAOI: interaction with SSRI

A

serotonin syndrome

DON’T MIX

67
Q

MAOI: interaction with TCA

A

hypertensive crisis

DON’T MIX

68
Q

MAOI: interaction with OTC

A

+ St. John’s Wort = bad
+ cough medicine = bad

CONSULT PHARMACIST FIRST

69
Q

MAOI: interaction with antihypertensives

A

excessive hypotension (MAOI already = hypotension, so potentiated hypotension)

70
Q

MAOI: adverse effects

A
  • hypertensive crisis!!!
71
Q

hypertensive crisis: definition, cause, risk

A

sudden, severe increase in BP

  • massive vasoconstriction of entire body
  • excessive stimulation of the heart
    • due to high tyramine levels
    • result of MAOI interactions (+food/tyramine, +TCA)

risk: intracranial hemorrhage, stroke

72
Q

hypertensive crisis: treatment

A
  • call 911

- take IMMEDIATE measures to decrease BP (nifedipine or other antihypertensive)

73
Q

hypertensive crisis: s/s

A 
major:
throbbing, occipital headache
retroorbital pain
stiff neck
apprehension
flushing of skin
palpitations
chest pain

minor: nausea, chills, fever, pallor, sweating

74
Q

atypical antidepressant list (4)

A

SNRI (serotonin-norepinephrine reuptake inhibitor)
- venlafaxine (effexor)

NDRI (norepinephrine-dopamine reuptake inhibitor)
- bupropion (wellbutrin)

heterocyclic
- trazodone (desyrel)

NaSSA (norepinephrine and serotonergic specific antidepressant) OR TeCA (tetracyclic antidepressant)
- mirtazepine (remeron)

75
Q

venlafaxine (effexor)

A

atypical antidepressant: SNRI (serotonin-norepinephrine reuptake inhibitor)

does not block cholinergic, histamine, alpha1-adrenergic
- very selective, no peripheral side effects

use: bipolar disorder (if more depressive)

side effects (common): headache, anorexia, insomnia

  • increased 5HT = more excitatory!
  • increased NE = excitatory (in this case)

adverse effects (less common): serotonin syndrome, neuroleptic malignant syndrome, hypertension, bleeding, increased serum lipids, activation of mania

76
Q

bupropion (wellbutrin)

A

atypical antidepressant: norepinephrine-dopamine reuptake inhibitor

moa: inhibits nicotinic receptors
- does NOT block 5HT!!

smoking cessation (Zyban)

side effects: weight loss, dizziness, dry mouth (NE effects!)
nausea, headache, insomnia, tremor, agitation (direct stimulation effects!)

increased risk for seizures!

77
Q

the only activating antidepressant is…

A

bupropion (wellbutrin): atypical antidepressant, SNRI

78
Q

Zyban

A

atypical antidepressant: norepinephrine-dopamine reuptake inhibitor – bupropion (wellbutrin)

EXCEPT USED FOR SMOKING CESSATION

79
Q

trazodone (desyrel)

A

atypical antidepressant: heterocyclic

moa: SSRI and 5HT2 antagonist

use: adjunct
- sedation for insomnia, potentiates SSRI
- dose for depression alone too high

side effects: sedation, hypotension, nausea, vomiting, priapism

  • sedative due to histamine activation
  • similar to TCA (increase in 5HT and NE levels = added sedative effects)
  • priapism due to alpha-adrenergic blocking
80
Q

mirtazepine (remeron)

A

atypical antidepressant: NaSSA/TeCa – norepinephrine and serotonergic specific antidepressant; also tetracyclic antidepressant

moa: moa: blocks alpha-2 adrenergic receptors (those inhibit release of NE & 5HT)

elimination half-life: 20 to 40 hours

side effects: somnolence (> 50%), increased appetite, cholesterol, dizziness, weight gain (significant: 50-60lbs/year)

    • give at bedtime
    • increase dose = somnolence decreases

dosing: 15mg QHS, max 30mg

quick dissolve - first antidepressant with this route

  • great for compliance (can’t hide in cheek, spit out)
    • esp. dementia patients with depressive features
81
Q

atropine psychosis aka

A

anticholinergic delirium

82
Q

trazodone + SSRI

A

augment each other, good combo

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