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Pharmacology - Exam 2 > Psychopharmacology: Treatment of Affective Disorders > Flashcards

Psychopharmacology: Treatment of Affective Disorders Flashcards

1
Q

What are the barbiturates we need to know?

A

Phenobarbital

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2
Q

What are the benzodiazapenes we need to know?

A
  • diazepam
  • triazolam
  • alprazolam
  • clonazepam
  • midazolam
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3
Q

What are the benzodiazipine Receptor Agonists that We Need to Know?

A
  • zolpidem
  • eszopiclone
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4
Q

What benzodiazipine receptor antagonist do we need to know?

A

flumazenil

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5
Q

What is a melatonin congener?

A

ramelton

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6
Q

What is a 5-HT1a (minor) receptor agonist?

A

Non-sedative anxiolytic - buspirone

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7
Q

What drug classes act at the GABA receptor?

A

Barbituates

Benzodiazepenes

Benzodiazipine receptor agonists

Benzodiazipine receptor antagonist

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8
Q

Define sedative

A

drug causing a calming effect; tranquilizer

(Ideally, minimal effect on motor fxn or mental status)

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9
Q

Define hypnotic

A

sleep-inducing or promoting drug

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10
Q

What are the anxiolytics?

A

For reduction of anxiety

Note: not all are sedatives

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11
Q

What does the dose-responsive curve for older sedatives (e.g., barbiturates) look like?

A

Linear - anxiolytic and sedative at low doses, at high doses coma and death

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12
Q

What does the dose-response curve for benzodiazepines look like?

A

Linear, but levels off at high doses

anti-anxiety and sedation at low doses

at high doses, harder to cause coma and death (SAFER than older sedatives)

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13
Q

What is the drug of choice for panic disorders?

A

1st line - antidepressants (SSRIs)

2nd line - alprazolam (benzo)

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14
Q

What are the side effects of alprazolam in treatment of anxiety?

A

rebound anxiety when discontinued

risk of dependence

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15
Q

What are the SSRIs?

A

fluoxetine

escitalopram

sertraline

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16
Q

What is an SNRI?

A

duloxetine

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17
Q

What are two TCAs?

A

amitriptyline

desipramine

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18
Q

What is an MAOI anti-depressant?

A

tranylcypromine

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19
Q

What are two “other” antidepressants?

A

bupropion

mirtazapine

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20
Q

What is true about the onset of therapeutic effects for all antidepressants?

A

therapeutic effects are delayed onset - about 2-6 weeks

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21
Q

Serotonin is converted from what and to what?

A

from L-tryptophan

to melatonin (in the pineal gland)

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22
Q

serotonin interferes with the signaling of what other biomolecules?

A

platelets

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23
Q

fluoxetine

A

SSRI

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24
Q

sertraline

A

SSRI

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25
Q

escitalopram

A

SSRI

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26
Q

What is the mechism of action of SSRIs?

A

selectively block the serotonin uptake transporter (SERT), inhibiting the reuptake of 5-HT

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27
Q

what drugs are generally first line for treatment of depression?

A

SSRIs - better tolerated than older drugs

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28
Q

What drug-drug interactions do SSRI’s mainly have?

A

CYP-2D6

(big ones -warfarin, tamoxifen is metabolite of CYP)

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29
Q

what are the t1/2 of most SSRIs?

A

long - about 24 hours

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30
Q

What are the common side effects of SSRIs?

A
  • CNS stimulation (insomnia, agitation)
  • GI problems (nausea, bleeding, diarrhea)
  • sexual dysfunction
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31
Q

Why should you never combine SSRIs with MAO inhibitors?

A

serotonin syndrome

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32
Q

escitalopram has what important side effect?

A

may prolong the QT interval

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33
Q

Other than depression, what are other common indications for SSRIs?

A
  • anxiety disorders
  • eating disorders
  • Premenstrual dysphoric disorder (PMDD)
  • ADD/ADHD
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34
Q

Duloxetine

A

SNRI

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35
Q

What is the key difference in mechanism of action for SNRI’s vs. SSRIs?

A

at medium to high doses, they block the reuptake of norepinepherine

*important - 5-HT and alpha-2 receptors are on BOTH noradrenergic and serotonergic neurons

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36
Q

duloxetine has a __________ t/12

A

short. shortest of the antidepressants

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37
Q

how are SSRIs and SNRIs excreted?

A

hepatic and renal

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38
Q

what is a unique adverse effect of SNRIs?

A

increase BP at high doses

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39
Q

duloxetine has two unique indications - what are they?

A

fibromyalgia

diabetic neuropathy

No one knows the mechanism here

40
Q

What other drugs have high MAOI inhibitor activity and therefore should not be taken with SSRIs or SNRIs?

A

St. John’s wort

linezolid

41
Q

What is serotonin syndrome?

A

if you OD on SSRIs/SSNRIs, you will get this (can get it other ways):

hyperthermia

muscle rigidity

myoclonus

fluctuating vital signs & mental status

hyperreflexia

42
Q

Why would you give an SNRI vs. an SSRI?

A

Individualized - some patients respond better to one class as opposed to the other

43
Q

amitryptyline

A

TCA (tertiary amine)

44
Q

desipramine

A

TCA (secondary amine)

45
Q

Why are TCA’s not the first line for treament of depression?

A

They have a low TI - dangerous in overdose and they have more drug-drug interactions than SSRI/SNRIs

46
Q

What is the mechanism of action for TCAs?

A

They block the neuronal reuptake pumps for both 5-HT and NE

Secondary preferentially block NET

teritary preferentially block SERT

BUT, tertiary are metabolized to secondary, so they really do BOTH

47
Q

What is it about TCA’s that caues so many side effects?

A

They block the receptors for many NT

muscarinic

alpha-1 adrenergic

histamine

48
Q

What is the t1/2 of most TCAs?

A

Long, as are the metabolites

49
Q

What are the adverse effects of TCAs?

A
  • tachycardia, palpitations
  • conduction block, arrhythmias
  • orthostatic hypotension
  • dry mouth, constipation, urinary retention
  • sedation, confusion, memory impairment
  • increased appetite, weight gain
  • sexual
50
Q

What are other indications for TCAs?

A

enuresis

anxiety disorders

pain (neuropathic and migraine)

51
Q

What are some major concerns with TCAs and overdose?

A

cardiac arrhythmias

low TI, used for suicide

52
Q

Tranylcypromine

A

Monoamine Oxidase Inhibtor (MAOIs)

53
Q

What is the mechanism of action of MAOIs?

A

they irreversibly inhibit monoamine oxidase, an enzyme involved in the break down of 5-HT and NE [and dopamine, but that’s from another lecture]

*two types MAO-A and MAO-B - found in brain and at periphery

most inhibit both types

54
Q

MAOIs have a high incidence of ___________?

A

side effects

55
Q

What is the difficulty of changing drugs with MAOIs?

A

must allow a long time before changing to or from them, or you risk serotonin syndrome

56
Q

MAOIs have what unusual side effect?

A

postural hypotension

57
Q

What foods can you not eat with MAOIs?

A

foods containing tyramine

cheese, wine

*acts as an indirect sympathomimetic

58
Q

What are MAOIs best for treating?

A

atypical depression

SSRIs might work, but NOT TCAs

59
Q

What do atypically depressed people crave?

A

carbohydrates

60
Q

Bupropion

A

dopamine reputake inhibitor

61
Q

Mirtazapine

A

autoreceptor antagonist

62
Q

Buproprion is used for what besides depression?

A

smoking cessation

63
Q

What is unique about mirtazapine?

A

It has strong sedative properties and it is also an appetite stimulant

64
Q

Buproprion’s mechanism of action?

A

block both dopamine norepinephrine reuptake

Also: potent antagonist at nicotinic receptor

65
Q

how is buproprion metabolized

A

hepatic

66
Q

What are the notable possible AE of buproprion?

A

anxiety (weird)

seizures (esp. in eating disorders)

but, less sexual side effects

67
Q

How does mirtazapine work?

A

potent alpha 2 antagonist

*also at 5-HT2A/C receptors

68
Q

how is mirtazapine excreted?

A

hepatic CYP metabolism

69
Q

what are the advantages and disadvantages of mirtazapine?

A

advantage: fewer sexual side effcts, sedative effects can be useful, good in resistant patients
disadvantages: increast appetite, weight gain, drug-drug interaction

70
Q

What should you do with a depressed patient who is pregnant?

A

best to give SSRI - fluoxetine or sertraline

lowest risks for these - others have bigger risks to fetus

71
Q

What is the only anti-depressant drug labeled for use in children?

A

fluoxetine

escitalopram

72
Q

What are the 5 Ds of antidepressant therapy for poor responders?

A
  1. dose?
  2. duration? 1-6 weeks
  3. diagnosis?
  4. drugs? (additional to increase response)
  5. Different treatment?
73
Q

what are the drugs used to treat bioplar disorder?

A

lithium

olanzapine

valproate

lamotrigine

74
Q

What would you use olazopine to treat in bipolar disorder?

A

acute manic episode - sedation

this is an atypical antipsychotic

75
Q

What can you use to treat an acute manic episode in bipolar disorder?

A

atypical antipsychotics

benzodiazepines

valproate - anticonvulsants

76
Q

What is the leading mood stabilizer used in the treatment of bipolar disorder?

A

lithium

77
Q

What can we use to treat bipolar disorders at both poles?

A
  • lithium
  • anticonvulsants - valproate, lamotrigene
  • atypical antipsychotics - olanzapine
78
Q

What is the mechanism for action for Lithium?

A

unknown, dampens IP3 messenger system

79
Q

What else is lithium indicated for?

A

depression as an adjunct

schizoaffective disorder (along with antipsychotics)

80
Q

How is lithium excreted?

A

urine

narrow TI - need blood monitoring

81
Q

Don’t use lithium with which drugs?

A

loop diuretics

NSAIDS

ACE inhibitors

82
Q

When is it useful to treat with valproic acid in bipolar disorder?

A

useful for rapid cycling, mixed states

83
Q

what is unique about lamotrogine in the treatment of bipolar disorder?

A

has significant anti-depressant activity (this is not proven for other anticonvulsants)

84
Q

What is a serious side but rare side effect of lamatrogine?

A

Stevens-Johnson’s syndrome

85
Q

What are the side effects of olanzapine?

A

weight gain

hyperlipidemia

hyperglycemia

(basically antipsychotic effects)

86
Q

What is the drug of choice to treat social phobia?

A

clonazepam

87
Q

what is the first line treatment for agoraphobia

A

alprazolam

88
Q

what drugs are used as sedatives?

A

antipsychotics

antidepressants - TCA, mirtazapine

barbiturates

benzodiazepines

89
Q

what is the major inhibitory neurotransmitte in the brain?

A

GABA

90
Q

phenobarbital is what kind of drug?

A

a barbituate

91
Q

what is the mechanism of action for barbituates?

A

binds to site on GABAa - increase Cl- flux

supress glutamate transmission via AMPA

92
Q

what is the t1/2 life of phenobarbital

A

long - over 60 h

93
Q

how is phenobarbital eliminated?

A

hepatic metabolism/renal elimination

94
Q

what are the dangers with barbituates?

A

relatively low TI

additive with EtOH

dependence and addiction

95
Q

phenobarbital is used for what today?

A

seizure disorders

96
Q

What is the mechanism of action for benzodiazepines?

A

Binds to GABAa and facilitates Cl- influx

Needs GABA to act (cannot open channel alone)

97
Q
A

Pharmacology - Exam 2 (14 decks)

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