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pharm Flashcards

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1
Q

serotonin - disorders

A
  • decreased in depression, anxiety, insomnia, violent behavior, impulse control, suicide
  • increased in serotonin syndrome and tumors
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2
Q

NE - disorders

A
  • decreased in depression and ADHD

- increased in anxiety

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3
Q

dopamine - disorders

A
  • decreased in depression, parkinsons, ADHD, restless leg syndrome
  • increased in mania, psychosis
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4
Q

why does the clinical effect of SSRIs take so long?

A

takes a long time to regulate B1 and serotonin receptors

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5
Q

SSRI - uses

A

depression (sans fluvoxetine), anxiety disorders, eating disorders, PTSD, premature ejaculation, body dysmorphic disorder, OCD, trichotillomania

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6
Q

SSRI - off label uses

A

cluster B personality disorders, SAD, behavioral problems in dementia or mental retardation

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7
Q

SSRI not to be used in pregancy

A

Paxil (paroxetine)

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8
Q

SSRI most likely to induce mania

A

fluoxetine (Prozac)

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9
Q

Fluoxetine half life

A

long, 2-4 days, wait five weeks before starting MAOI

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10
Q

Fluoxetine SEs

A
  • may increase anxiety and insomnia initially

- CYP2D6 inhibition (inducer)

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11
Q

major SE of citalopram

A
  • long QTc interval, torsade with doses over 40mg/day
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12
Q

differences between citalopram and escitalopram

A

escitalopram is the S isomer, better for GAD, less likely to cause long QT.

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13
Q

fluvoxamine use…

A

OCD only

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14
Q

fluvoxamine SEs

A

GI distress, headaches, sedation, weakness

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15
Q

which SSRI has shortest half life?

A

fluvoxamine

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16
Q

SSRI half lives, short, medium, long

A

short: paroxetine, fluvoxamine, missed doses lead to withdrawal symptoms
medium: sertraline, citalopram, escitalopram
long: fluoxetine, good for people who may miss doses

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17
Q

what does SSRI discontinuation syndrome look like?

A
  • flu like symptoms, agitation, nausea, dysphoria
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18
Q

which SSRI causes the most weight gain?

A

paroxetine

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19
Q

common SSRI SEs

A

sexual, rash, apathy, insomnia, sedation, night sweats, nightmares, tremor, dry mouth, bruising

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20
Q

SSRI electrolyte effect

A

hyponatremia 2/2 to SIADH effect

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21
Q

what does serotonin syndrome look like?

A

common: abd pain, diarrhea, tremor, sweating, restlessness, fever, hyperreflexia, tachycardia, HTN
less common: disorientation, muscle rigidity, myoclonus
least common: death (10%)

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22
Q

SSRI to MAOI switch

A

wait 2 weeks except for fluoxetine which is 5 weeks.

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23
Q

order of 2D6 inhibition in SSRIs

A

fluvoxamine > paroxetine > fluoxetine > sertraline > citalopram > escitalopram

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24
Q

similarities and differences between SNRIs and TCAs

A
  • both work on serotonin and NE

- SNRIs cause fewer antihistamine, anti adrenergic, and anticholinergic SEs

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25
Q

what are the two SNRIs?

A

venlafaxine and duloxetine

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26
Q

what neurotransmitters does bupropion work on?

A

NE and dopamine (NDRI)

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27
Q

where does mirtazapine work?

A

antagonist at a2, serotonin, and H1.

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28
Q

other use for SNRIs besides depression

A

chronic neuropathic pain, diabetic neuropathy (venlafaxine)

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29
Q

other use for bupropion besides depression

A

tobacco addiction

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30
Q

other use for mirtazapine and trazodone besides depression

A

insomnia

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31
Q

venlafaxine ups and downs

A
  • good for geriatrics because fast renal clearance
  • fewer SEs than TCAs
  • short half life so can cause withdrawal symptoms
  • can cause significant nausea
  • 10-15mmHG increase in BP
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32
Q

duloxetine vs venlafaxine?

A
  • duloxetine doesn’t cause increase in BP, better for those with HTN
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33
Q

mirtazapine and dosage

A
  • 30mg is the cut off between the H1, serotonin effects and the a2 effects
  • sedating under 30, activating NE effects over 30
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34
Q

trazadone - possible SE

A

priapism - painful erection that needs to be treated in ER

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35
Q

secondary vs tertiary TCAs

A

tertiary - imipramine, amitriptyline, doxepin, chlomipramine - more SEs than secondary, get metabolized to secondary
secondary - nortriptyline, desipramine

36
Q

what are three categories of SEs of TCAs? examples

A

anticholinergic

  • dry mouth
  • constipation
  • blurred vision
  • urinary retention
  • arrhythmias

antiadrenergic
- anti a1, orthostatic hypotension

antihistaminergic

  • sedation
  • weight gain
37
Q

serious TCA warnings

A
  • 3 C’s, convulsions, coma, cardiotoxic in overdose (don’t give to suicidal patients)
  • can push undiagnosed BPAD into mania
  • can cause long QT even at therapeutic serum levels, so have to obtain EKGs
38
Q

SE unique to MAOIs

A

acute hypertensive crisis, worsened by sympathomimetic stimulants such as cold remedies, tyramine containing foods

39
Q

how does selegiline differ from other MAOIs?

A
  • it is selective for MAO-B at low doses (parkinson) so diet is not an issue
  • at higher doses it acts as a typical MAOI
  • Emsam - patch for depression
40
Q

where is lithium limited in affective disorders?

A
  • less effective in rapidly cycling bipolar or in mixed states
41
Q

labs for lithium

A

creatinine, TSH, CBC, pregnancy test (ebsteins anomaly)

42
Q

lithium blood level goal

A

.8-1.2

43
Q

lithium major SEs

A
  • mild: polyuria/polydipsia 2/2 to nephrogenic DI
  • severe: coarse tremor, gait instability, vomiting, diarrhea, confusion, cognitive slowing, renal failure, seizures
  • hypothyroid
  • ebstein anomaly
  • risk factors: salt restriction, sweating, NSAIDs other than aspirin, diuretics, ACE/ARBs
44
Q

valproic acid vs lithium uses

A

valproic acid better in rapid cycling states

45
Q

valproic acid, other uses

A

migraines, seizures

46
Q

valproic acid labs

A

LFT, pregnancy, CBC

47
Q

valproic acid monitoring

A

steady state after 4-5 days, recheck labs

goal is 80-120

48
Q

valproic acid SEs

A
  • nausea, weight gain, sedation, unsteadiness, hair loss, tremor
  • liver dysfunction
  • thrombocytopenia
  • hyperammonemia
  • neural tube defects
  • acute pancreatitis (rare)
  • PCOS (rare)
49
Q

carbamazepine labs

A

LFT, CBC, EKG

50
Q

carbmazepine monitoring

A
  • same as valproic acid, steady state in 4-5 days, recheck labs
  • 8-12
51
Q

carbamazepine SEs

A

GI: nausea, constipation, decreased appetite, diarrhea
CNS: sedation, dizziness, unsteadiness, confusion
Derm: SJS
birth: cleft palate, IUGR
cardio: AV conduction delays
heme: agranulocytosis/aplastic anemia
SIADH

52
Q

drugs that increase carbamazepine levels/toxicity

A

acetazolamide, cimetidine, clozapine, VPA, diltiazem, INH, fluvoxamine

53
Q

drugs that decrease carbamazepine efficacy

A

neuroleptics, barbs, phenytoin, TCAs

54
Q

lamotrigine best for…..

A

bipolar depression, bipolar maintenance therapy

55
Q

lamotrigine SEs

A
  • SJS/TEN titrate slowly

- aseptic meningitis

56
Q

what increases/decreases lamotrigine levels?

A
  • valproic acid increases

- carbamazepine decreases

57
Q

four brain pathways:

A

mesocortical - ventral tegmentum to cortex, too little dopamine, negative symptoms
mesolimbic - ventral tegmentum to limbic system, too much dopamine, positive symptoms
nigrostriatal - substantia nigra to basal ganglia, smooth movement regulation, parkinsons
tuberoinfundibular - hypothalamus to anterior pituitary, blocking dopamine causes hyperprolactinemia

58
Q

mechanism of typical vs atypical antipsychotics

A

typical are dopamine antagonists, atypical are dopamine and serotonin antagonists

59
Q

high potency vs low potency typical antipsychotics

A

high potency - bind D2 more tightly, cause more EPS
low potency - bind D2 less tightly but also bind muscarinic receptors leading to cardio toxicity and anti-cholinergic effects

60
Q

typical antipsychotics by potency

A

low: thioridazine, chlorpromazine (low EPS, high AC)
medium: perphenazine, loxapine, molindone, thiothixene, trifluoperazine (high EPS, medium AC)
high: haloperidol, fluphenazine, pimozide (high EPS, low AC)

61
Q

EPS includes

A
  • dystonia
  • parkinsonism (akinesia)
  • akathisia
  • tardive dyskinesia
62
Q

EPS - acute dystonia, description and treatment

A
  • sustained contraction of throat, tongue, neck, eyes
  • can be live threatening
  • starts within few minutes to an hour
  • treat with benztropine or benadryl
63
Q

EPS - parkinsonism, description and treatment

A
  • pill rolling, shuffling, masked facies, cog wheeling, muscle stiffness, drooling
  • beyond 1 week after starting med
  • treat with benxtropine or benadryl
64
Q

EPS - akathisia, description and treatment

A
  • restlessness, repeated movement, unable to sleep
  • generally in first weeks of treatment
  • treat with beta-blocker or benzo
65
Q

EPS - TD, description and treatment

A
  • usually irreversible spastic movements of face

- more than 6 months of use

66
Q

NMS - cause, description, treatment

A
  • usually high potency FGAs, but SGAs are possible
  • pipe-like rigidity, fever, tremor, altered consciousness
  • hypotension, tachycardia
  • rhabdomyolysis
  • mortality 10-20%
67
Q

labs in NMS

A

high WBC and CK

68
Q

AC side effects

A
  • dry mouth
  • blurred vision
  • constipation
  • urinary retention
  • sedation
  • tachycardia
  • confusion
  • delirium
  • mydriasis
  • cycloplegia
69
Q

hyperprolactinemia SEs

A
  • amenorrhea, galactorrhea, gynecomastia, sexual dysfunction
70
Q

general SEs of typical antipsychotics

A
  • neutropenia
  • seizures
  • cardiac arrhythmias
  • hyperthermia
  • cataracts
  • priapism
  • metabolic syndrome (mostly SGA)
71
Q

4 important inducers, what is their effect?

A
  • smoking
  • carbamazepine
  • barbs
  • st. john’s wort

decrease blood concentration of other drugs

72
Q

5 important inhibitors, what is their effect?

A
  • fluvoxamine
  • fluoxetine
  • paroxetine
  • duloxetine
  • sertraline

increase blood concentration of other drugs

73
Q

which SSRI has a weekly dosing option?

A

fluoxetine

74
Q

which SSRI causes the most GI SEs?

A

sertraline

75
Q

which SSRI has the most drug interactions?

A

paroxetine

76
Q

which SSRI is most likely to cause withdrawal symptoms?

A

paroxetine

77
Q

which SSRI has the most anti-cholinergic effects?

A

paroxetine

78
Q

symptoms of serotonin syndrome

A
  • flushing
  • fever
  • diaphoresis
  • shivering
  • hypertension
  • hyperreflexia
  • delirium
  • tachycardia
  • “electric jolt” limb movements
79
Q

how does trazodone work?

A

serotonin receptor antagonist

80
Q

what are two tetracyclic antidepressants?

A
  • amoxapine

- maprotiline

81
Q

name 4 MAOIs

A
  • selegiline
  • phenelzine
  • tranylcypromine
  • isocarboxazid
82
Q

3 new expensive atypical antipsychotics

A
  • paliperidone (invega) - metabolite of risperidone
  • asenapine
  • iloperidone
83
Q

thioridazine can cause…

A

retinal pigmentation

84
Q

toxic and lethal blood levels of lithium

A

toxic 1.5

lethal 2.0

85
Q

benzodiazepines by length of acting

A

long acting (>20 hours): diazepam, clonazepam

medium acting (6-20 hours): alprazolam, lorazepam, oxazepam, temazopam

short acting (

86
Q

benzos not metabolized by the liver

A
  • lorazepam
  • oxazepam
  • temazepam
87
Q

how does buspirone work? when used?

A
  • 5HT-1A partial partial agonist
  • in addition to SSRI for anxiety symptoms
  • good for alcoholics in place of benzo

psych rotation (2 decks)

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