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IPAP 21-2 Soph Semester > Depression/ Mania Drugs For Block III > Flashcards

Depression/ Mania Drugs For Block III Flashcards

1
Q

Definition of a:
Receptor-
Neurotransmitter-
Nueromodulator-

A

Receptor: a cellular macromolecule or a macromolecule complex with which a medication interacts to elicit a cellular response

Neurotransmitter: Substance that enables neurons to communicate with each other

Neuromodulator: Any substance that has an effect on neurotransmission

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2
Q

What is the current understanding of neurotransmittion

A

Current understanding that the brain has a combination of voltage and chemical transmission

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3
Q

What is the pathway of a neurotransmitter from Synthesis to reuptake

A

Synth- realease- Effect/activation of receptor- degradation- reuptake

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4
Q

Neurotransmitters action is terminated by what two methods

A

Degradation via enzymes

Reuptake into the presynaptic neuron

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5
Q

What is the major NT in the PNS and SNS and what degrades it

A

Acetylcholine:
Major NT in Parasympathetic & Sympathetic systems (activates Nicotinic & Muscarinic receptors and degraded by Acetylcholinesterase)

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6
Q

What are the three Amino Acid NTs and what degrades them

A

GABA, Glutamate/aspartate, Glycine/taurine

Degraded by Transaminase

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7
Q

What is the effect of GABA stimulation

A

Inhibitory/ Sedative

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8
Q

What is the effect of Gluatmamte/ aspartate NTs

A

Excitatory, Stimulating

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9
Q

What are the 4 types of amines NTs and what degrades them

A

Dopamine, NE, Seretonin, Histamine

Degraded by Monoamine Oxidase

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10
Q

What are the two Neuropeptide NTs and what degrades them

A

Opiods and Techykins

Degraded by peptidases

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11
Q

What does amantadine do

A

Increase the release of Dopamine

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12
Q

What does long term antagonism or reduction of NT release cause

A

Up-regulation of receptors

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13
Q

What does sustained release or slow elimination of NTs cause

A

Down regulation of receptor

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14
Q

Dx Criteria for MDD

A

Depression + 5 S/s of SIGECAPS

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15
Q

What is SIGECAPS

A

Sleep, Interest, Guilt, Energy, Concentration, Appetite, Psychomotor, Suidice

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16
Q

What are the gender differences as it relates to depression

A

Females have less serotonin, earlier onset, longer episodes, greater recurrence and more seasonal

More likely to attempt suicide (but less likely to complete the suicide), 2-4 x increase during menopause

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17
Q

What are the three main classifications of depression

A

Reactive/ Secondary

Unipolar

Bipolar affective

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18
Q

What is the option for refractory depression, depression in therapy, or psychotic depresssion

A

Electro therapy

T.I.D.

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19
Q

What do all medications classified as Antidepressants do

A

increase the synaptic concentration of norepinephrine, dopamine, and/or serotonin

Three ways to increase these neurotransmitters:

  • Inhibit the reuptake of neurotransmitters
  • Block the metabolic degradation
  • Increase the release of the neurotransmitters
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20
Q

Serotonin is released from what kind of neuron

A

Raphe neurons

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21
Q

TCAs, SSRIs, and SNRIs, have what MOA

A

block the reuptake of 5-HT and increase synaptic concentrations

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22
Q

How are BZDs used with antidepressants

A

Not classified as an anti-depressant

Used short-term in acute anxiety management while SSRIs are initiated

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23
Q

What is the difference between tertiary and secondary amines (TCAs)

A

Tertiary amines:
More potent at blocking reuptake of serotonin > norepinephrine
Include: amitriptyline, clomipramine, doxepin, imipramine

Secondary amines:
More potent in blocking reuptake of norepinephrine > serotonin
Include: nortriptyline, desipramine, and protriptyline

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24
Q

TCAs have effect on what Receptors

A

Presynaptic SERT and NET

Postsynaptic A1 blocker

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25
Q

What is the MOA of TCAs

A

Block the reuptake of norepinephrine and serotonin (precursors to SNRI) into the presynaptic neuron which increases the concentrations of monoamines in the synaptic cleft (debated theory)

Also block alpha adrenergic, histamine and muscarinic receptors (anticholinergic side effects)

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26
Q

What is the ADE of TCAs

A

Anticholinergic S/e

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27
Q

Are TCAs first line Tx

A

seldom used as 1st line depression treatment; due to adverse effects and new agents available

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28
Q

What can TCAs be used for

A

Depression
Anxiety Disorders
(NOT 1st LINE!)

Numerous off labeled uses such as:
Treatment for pain syndromes: useful in chronic pain
Migraine prophylaxis

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29
Q

What is the Onset of TCAs

A

2-4 weeks

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30
Q

What are the cautions and warnings for TCAs

A

Most commonly used drug in an overdose
(Avoid in suicidal pts)

Can produce serious, life-threatening cardiac arrhythmias, delirium, coma, seizures, and psychosis
(T.C.A These Cause Arrhythmia’s)

Should not be used in patients with suicidal ideations

Should avoided in patients with cardiovascular conditions, closed angle glaucoma, urinary retention, or severe prostate hypertrophy (Anticholinergic Effects)

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31
Q

What are Anticholinergic Fx

A

Anticholinergic Effects: dry mouth, urinary retention, constipation, blurred vision

Dry mouth is a suggested link to weight gain due to the tendency for patients to drink excessive caloric beverages

The anticholinergic effects will make BPH worse

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32
Q

Are TCAs sedating?

A

Yes they block Histamine

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33
Q

Which TCAs cause the most sedation, Anticholinergic efffects, and Alpha blockade

A

Amitryptyline, Doxepin, Clomipramine

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34
Q

What is Doxepin indicated for

A

Depression and insomnia

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35
Q

What is clomipramine approved for

A

OCD

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36
Q

What TCA can be used for childhood bed wetting in chlidren older than 6

A

Imipramine

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37
Q

Which two TCAs specifically mention weight gain

A

Notriptyline (2kgs) and Amitriptlyine (1.5kgs)

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38
Q

What receptors do SSRIs effect

A

Presynaptic SERT

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39
Q

What is the MOA of SSRI

A

Inhibit serotonin reuptake, without affecting reuptake of norepinephrine or dopamine into the presynaptic neuron

SSRI’s do not significantly effect histamine, muscarinic or other receptors

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40
Q

What is the onset of SSRI

A

3-8 weeks

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41
Q

1st line for depression

A

SSRI

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42
Q

1st line for OCD

A

SSRI

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43
Q

1st line for Panic DO

A

SSRI

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44
Q

1st line for social phobia

A

SSRI

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45
Q

1st line for PTSD

A

SSRI

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46
Q

1st line for Premenstral Dysphoric DO

A

SSRI

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47
Q

1st line for GAD

A

SSRI

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48
Q

What is the advantage of SSRI over TCAs in Tx depression

A

Not as lethal in cases of overdose

Low cost and better pt outcomes

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49
Q

Which SSRI has the longest 1/2 life

A

Fluoxetine

1-3 days for parent drug and active metabolites are 4-16 days

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50
Q

What is the 1/2 life of most SSRI

A

About 1 day, except fluoxetine

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51
Q

Which SSRI has the shortest 1/2 life

A

Fluvoxamine is the shortest with half-life at 15 hours

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52
Q

All SSRI interact with CYP 450 except for

A

Citalopram and escitalopram

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53
Q

What are the SSRI that are most activating

A

Fluoxetine and Sertaline

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54
Q

Which SSRI are most sedating

A

Paroxetine and Fluvoxamine

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55
Q

Which SSRI has the worst wt gain

A

Paroxetine

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56
Q

What are the ADE for SSRI

A

Gastrointestinal: nausea, diarrhea, constipation

CNS: agitation, anxiety, tremor, or panic may be seen in during the early phase of therapy

Sexual Dysfuntion

Serotonin Syndrome

EPS

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57
Q

What are the interventions that can be used to combat the sexual dysfunction of SSRIs

A

Wait-and-see method

Lowering the dose of the SSRI

Switching to bupropion or adding ED medication (i.e. sildenafil)

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58
Q

What are the severe ADE of SSRIs

A

Serotonin Syndrome

Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)
Especially with elderly

EPS side effects:
Include akathisia, dystonias, and parkinsonian symptoms
Reported with all SSRI’s, but paroxetine has the most reported

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59
Q

What is a severe ADE of SSRIs in elderly pts

A

SIADH

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60
Q

What is EPS

A

Include akathisia, dystonias, and parkinsonian symptoms

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61
Q

Which SSRI has the most risk for EPS

A

Paroxetine

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62
Q

How does Seretonin syndrome present

A 
Cognitive effects (thinking) 
Neuromuscular dysfunction (movements) 
Autonomic dysfunction (reflexes, breathing, hr)
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63
Q

What is the Tx for seretonin syndrome

A

Withdraw offending agent(s)!

Supportive care:
Anxiety/seizures -benzodiazepines
Hyperthermia- ice, cooling blankets

Cyproheptadine :
1st generation antihistamine, and 5HT1A and 5HT2 antagonist

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64
Q

What is the warning with Citalopram

A

QT prolongation

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65
Q

Can SSRIs be used with Aspirin or NSAIDS

A

No, DDI, increases bleeding

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66
Q

What enzyme does fluoxetine inhibit

A

2D6

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67
Q

What is the clinical use of sertraline

A

PTSD and MDD

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68
Q

Why is paroxetine not recommended in children

A

Increases SI

69
Q

Can paroxetine be used in pregnancy

A

Cardiac septal defects in 1st trimester exposure (Cat. D/X)

70
Q

What is fluvoxamine clinically approved for

71
Q

What enzyme does fluvoxemine inhibit

72
Q

What is the does restriction with citalopram because of QT elongation

A

No more than 40 mg/day

73
Q

What is the clinical use for the SSRI: vortioxetine

74
Q

Can vortioxetine be dc abruptly

A

May be stopped abruptly, but headaches and muscle tension was evident in clinical trials

Recommend that the dose be decreased to 10mg/day for week before full discontinuation

75
Q

What are the 4 strong CYP2D6 inhibitors

A

bupropion, fluoxetine, paroxetine, or quinidine

76
Q

How should vortioxetine be used with enzyme inhibitors and inducers

A

Strong inhibitor of CYP2D6: reduce Vortioxetine dose by half when given with a strong CYP2D6 inhibitors: bupropion, fluoxetine, paroxetine, or quinidine

Substrate of CYP2D6 and CYP3A4: consider increasing Vortioxetine dose when given with strong CYP inducers: rifampin, carbamazepine, or phenytoin for more than 14 days

77
Q

What receptors do SNRI Fx

A

Presynaptic SERT and NET

78
Q

What is the MOA of SNRIs

A

inhibit the reuptake of 5HT and NE, increasing their levels; little activity for alpha adrenergic, cholinergic, or histamine receptor

79
Q

Which SNRIs have been associated with elevated DBP at high doses

A

Venlafaxine, desvenlafaxine, and duloxetine

80
Q

What is the SE profile for SNRI

A

Similar profile to SSRIs

Common adverse effects:
Nausea
Headache
Somnolence
Dry mouth
Dizziness
Sexual dysfunction
Insomnia
81
Q

Should SNRI and MAOIs be used together

82
Q

What is the MOA of Venlafaxine

A

Mechanism of Action: SNRI with dose-related effect on NE

Doses <150mg/day, primarily a serotonin effect

83
Q

At what dose in venlafaxine primarily a seretonin effect

A

Less than 150 mg/day

84
Q

What is the clinical indication for venlafaxine

A

Severe or treatment-resistant depression

Generalized anxiety disorder (GAD)

PTSD (1st line agent along with SSRIs)

85
Q

What two drugs can be used as 1st line agents for PTSD

A

SSRI and venlafaxine

86
Q

What SNRI can be used when SSRIs fail

A

Venlafaxine

87
Q

How does venlafaxine work at 75 mg/day vs 225 mg/day

A

Works as an SSRI at doses ~75mg/day; SNRI at >225mg/day.

88
Q

What is Desvenlafaxine

A

Active metabolite of venlafaxine

89
Q

What is the clinical use for desvenlafaxine

A

2nd line agent for MDD

90
Q

What is the MAO of Duloxetine

A

SNRI with dose dependent NE reuptake inhibition

91
Q

What is the clinical use of Duloxetine

A

Severe or treatment-resistant depression

Generalized anxiety disorder

Diabetic peripheral neuropathy!

Fibromyalgia!

Chronic musculoskeletal pain caused by chronic lower back pain or osteoarthritis pain!

92
Q

Which SNRI really works on chronic and muscular pain

A

Duloxetine

93
Q

What pts should Duloxetine be avoided in

A

Should NOT be used in patients with hepatic insufficiency, end-stage renal disease requiring dialysis, or severe renal impairment

94
Q

What vital sign should be monitored with Duloxetine

95
Q

What is the MOA of levomilnacipran

A

Stronger inhibitor of norepinephrine reuptake than duloxetine (Cymbalta) or venlafaxine (Effexor)

96
Q

What is the clinical use of levomilnacipran

A

Only for depression

97
Q

What are the ADE of SNRI: levomilnacipran

A

May cause hyponatremia and increase bleeding risk

Blood pressure elevation and orthostatic hypotension can occur

98
Q

What is the difference with milnaciprin and levomilnacipran

A

More active isomer of the SNRI milnacipran (Savella)

Milnacipran (Savella) approved for fibromyalgia, not depression

99
Q

When do NDRIs have an effect

A

On the presynaptic NE reuptake receptor

100
Q

What is the MOA of Bupropion

A

dopamine and norepinephrine reuptake (at high doses) inhibitor with minimal activity on serotonin

101
Q

What are the clinical uses of Bupropion

A

MDD

Smoking cessation

Unlabeled: ADHD adjunct

102
Q

What are the ADE of bupropion

A

Headache, insomnia, irritability, nausea, vomiting, decreased appetite

Weight loss ~4kg

Increased risk of seizures
To reduce seizures: avoid use in susceptible patients;
History of seizure disorders, eating disorders

Associated with less sexual dysfunction than other anti-depressants

103
Q

Bupropion has what contraindication

A

: patients at risk for seizures

including patients with seizure disorders, history of anorexia or bulimia, or using or withdrawing from medications such as alcohol or benzodiazepines

104
Q

What is the prominent DDI of bupropion

A

MAO inhibitors

Allow 14 days elapse

105
Q

What are the common affects of SRAs

A

Antagonists of 5HT2 family of receptors

Antagonists of α1 receptors

Antagonists of Histamine1 (H1) receptors – causes drowsiness

106
Q

What is the MOA of trazadone

A

modestly inhibit serotonin reuptake (less than SSRIs), antagonist for postsynaptic 5HT2A, H1, and α1 receptors

107
Q

What is the clinical use for Trazodone

A

Depression in combination with SSRi/ SNRI in patients with sleep DO

108
Q

ADE of Trazadone

A

Drowsiness and Ortho Hypotension (A1 blockade)

109
Q

What is the MOA of mirtazapine

A

SRA Inhibits 5HT2A, 5HT3, H1, α1 and α2 receptors, does not have reuptake inhibition effect.

110
Q

What is the clinical use for mirtazapine

A

MDD, better than TCAs, used with SSRI and SNRI for MDD with sleep DO

111
Q

What are the ADE of mirtazapine

A

Sedative, low dose sleepiness, high dose insomnia

Reported to have less sexual side effects than the SSRIs
Increased appetite, significant weight gain and hyperlipidemia
Constipation
Dry mouth
Asthenia

112
Q

How is mirtazapine cleared

A

Renally!! Lower dose if CrCl <30ml/min

113
Q

What is the MOA of Nefazadone

A

Inhibits 5HT2 family of receptors, α1 receptors, and reuptake of serotonin + norepinephrine

114
Q

What is the clinical use of Nefazadone

A

Anxious depression, or in SSRI with too much sex dysfuntion

115
Q

What is the black box warning with nefazadone

A

Risk of liver failure

116
Q

What is the MOA of MAO-I

A

blocks the enzyme responsible for the break down of norepinephrine, dopamine and serotonin which increases the stores of these transmitters in the neurons

117
Q

What is the clinical use of MAO-I

A

Atypical depression
(hypersomnia, hyperphagia, and mood reactivity)

Patients refractory to other anti-depressant agents

118
Q

What are MAO-I food interactions

119
Q

What are the ADE of MAO-I

A

Hypertensive Crises: increased levels of catecholamines, which can be the result of ingestion of tyramine containing foods

Serotonin Syndrome: when levels of 5HT become too high usually as the result of multiple serotonergic agents

Orthostatic hypotension

Peripheral edema

Weight gain

Sexual dysfunction

120
Q

Are MAO-I such as phenelzine and Tranylcypromine 1st line agents

A

No, considered last line agents

121
Q

What foods should be avoided with MAOIs

A

avoid use with cheese, wine, beer, sausage, liver and several other items

122
Q

How long should the waiting period be when switching someone to a MAOI

A

Wait 2 weeks after discontinuing antidepressant before initiating the MAOI

Except Fluoxetine waiting period should be 5-6 weeks

123
Q

What is the MOA and Clincal use of selegiline

A

MAOI

Clin use: MDD

(High doses require diet modification, Tyramine)

124
Q

Adequate trial of any drug includes:

A

Adequate trial of any agent includes full therapeutic doses for 2-8 weeks and in some cases for up to 12 weeks

If no response at that point, the drug can be considered a failure

125
Q

What are the strong inhibitors of 2D6

A

Bupropion
Fluoxetine
Paroxetine

126
Q

What is the strongest inhibitor of 3A4

A

Nefazadone

127
Q

What two drugs can be used if the pt has sex dysfunction with SSRI, SNRI

A

Bupropion is not likely to cause sexual dysfunction

Mirtazapine has a lower risk than an SSRI or SNRI to cause sexual dysfunction

128
Q

What drugs can be used if the pt is putting on weight with antidepressants

A

Bupropion and Fluoxetine are less likely to cause weight gain

129
Q

TCA’s, Mirtazapine, paroxetine, and trazodone- ALL CAUSE what>?

A

Somnolence

130
Q

Is bupropion activating or sedating

A

Activating, increases energy

131
Q

What drugs should be used with a pt with antidepressants and needs pain control

A

Duloxetine (Cymbalta) or venlafaxine in depression plus fibromyalgia or neuropathic pain

Amitriptyline and Imipramine have indication for diabetic neuropathy

132
Q

Which two TCAs are indicated for diabetic neuropathy

A

Amitriptyline and Imipramine have indication for diabetic neuropathy

133
Q

What SSRI should be used in pts with CV Dz

134
Q

Which SSRI should not be used in obese pts

A

Paroxetine

135
Q

Which SSRI should be avoided in pts with insomnia

A

Fluoxetine and sertaline

136
Q

Which SSRi should be avoided in pregnancy

A

Paroxetine and fluoxetine

137
Q

Which SSRI should be avoided in the elderly

A

Paroxetine

138
Q

SNRI should not be used in pts with

A

HTN or Agitation/ Insomina

139
Q

Mirtazapine should not be used in pts with

A

Obesity or hyperlipidemia

140
Q

Bupropion should not be used in pts with

A

SZR, HTN, or agitation/ insomina

141
Q

Vortioxetine should not be used in pts with

A

Nausea or Vomitting

142
Q

What is the tapering method for paroxetine

A

Decrease by 10 mg q 1-2 weeks

143
Q

What is the tapering method for Sertaline

A

Decrease by 50 mg q 1-2 weeks

144
Q

What is the tapering method for TCAs

A

10-25% q 1-2 weeks

145
Q

Do you have to taper Fluoxetine or Bupropion

146
Q

What are the two 2* antipsychotics that are approved for depression augmentation

A

Only Aripiprazole (Abilify) and Quietiapine (Seroquel) have FDA approval

147
Q

What is the clinical use of lithium

A

Effective for manic and depressive components

Acts as a mood stabilizer during manic phase

Does not work well in patients who are rapid cyclers (four or more episodes per year)

148
Q

Does lithium work well in pts with cyclothimic mania

149
Q

What is the Therpuic Index for Lithium

A

Narrow therapeutic index: requires serum blood level monitoring Lithium level (0.8-1.2mEq/L is therapeutic)

150
Q

What are the conditions that effect lithium concentration

A

Conditions that raise lithium levels: dehydration, fever, vomiting, crash diets and sodium restricted diets can all increase lithium levels

151
Q

What is the standard Lithium W/Up

A

CBC

Electrolytes

Renal function

Thyroid function tests

Urinalysis

Electrocardiogram (ECG)

Pregnancy test (childbearing age)

152
Q

What are the ADE of lithium

A 
Lethargy
Coarse tremor
Confusion
Neurologic and Psychiatric: 
Higher plasma levels can cause tremors, convulsions, confusion

Seizures
Coma
Cardiac Effects: dysrhythmias can occur at lithium toxicity, which can result in death

153
Q

What effect does lithium have on the thyroid

A

Decreases thyroid function

154
Q

What renal effects does lithium have

A

Nephrogenic Diabetes Insipidus/Renal Effects:

Blocks the responsiveness of the renal collecting tubule to vasopressin

Polyuria and polydipsia

155
Q

Can lithium be used in pregnancy

A

Avoid in 1st trimester in possible

156
Q

How do NSAIDS and lithium interact

A

NSAIDs will increase Lithium levels due to an enhanced reabsorption of sodium and lithium secondary to inhibition of prostaglandin synthesis

157
Q

What level is severe lithium toxicity

A

Severe toxicity occurs (level>3mEq/L), hemodialysis may be indicated

158
Q

What is the DOC in manic indications

A

Valproic ACid and Divaproex sodium

159
Q

What anticonvulsant is the DOC for rapid cycles

A

Valproic Acid and Divalproex sodium

160
Q

What are the ADE of Valproic Acid and Divalproex sodium

A

neurotoxicity, sedation, hair loss, teratogenic

causes spina bifida

161
Q

What is the clin use for carbamazepine

A

Effective for acute mania and maintenance therapy

Used for long-term management

Can be added to lithium for patients who have not responded to monotherapy

Carbamazepine (Equetro) approved by the FDA for acute manic/mixed episodes

162
Q

What pts should be screened prior to carbamazepine use

A

Screen for HLA-B*1502 (Asian and Asian Indian) population

Increased risk of severe rash (Steven’s Johnson syndrome)

If positive; carbamazepine should not be used

163
Q

What are the ADE of carbamazepine

A

Hyponatremia, including SIADH can occur

Rash/Steven’s Johnson Syndrome

Agranulocytosis

164
Q

What is the clin use of lamotrigine

A

Approved for maintenance therapy

Appears to be effective against the depressed phase of bipolar disorder

165
Q

How should the use of lamotrigine and valproic acid be used together

A

Valproic acid inhibits the metabolism of lamotrigine and increases the risk of severe skin reactions

Double the dose of lamotrigine if given with carbamazepine

166
Q

What is the primary concern of using lamotrigine

A

Rash that may present of SJS

Associated with aseptic meningitis in adult and pediatric patients

167
Q

What is the clincal use of BZD in Bipolar DO

A

ACUTE treatmet,

Useful for insomnia, hyperactivity, and agitation

168
Q

Which two atypical antipsychotics are not approved for use in manic pts

A

Clozapine and Iloperidone

169
Q

Which 2* antipsychotics are approved for bipolar maintenance monotherapy

A

Olanzapine (Zyprexa)

Aripiprazole (Abilify)

IPAP 21-2 Soph Semester (20 decks)

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