Walden 6630 Psychopharmacology Midterm Study Guide
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Terms in this set (180)
In addition to MDD SNRIs treat Anxiety and neuropathic pain (peripheral neuropathy)
Medication specific indications urinary incontinence and Fibromyalgia
of duloxetine:
Medication specific indications social anxiety, panic disorders, PTSD, OCD, postmenopausal hot flashes
of venlafaxine:
Six common side effects of Insomnia, nausea, sexual dysfunction, hypertension, sweating, headaches
SNRIs include:
Severe side effect of SNRIs in suicidal ideation
children/adolescents under age
25 years old:
Life threatening adverse effect Serotonin Syndrome
of SNRIs, especially when used
in combination with other
serotonergic drugs:
This SNRI is an inhibitor of venlafaxine
Cytochrome P450 enzymes:
This SNRI is hepatotoxic: duloxetine
MAOIs increase the levels of: Serotonin, Norepinephrine, and Dopamine
Norepinephrine regulates: alertness and focus
Dopamine regulates: cognitive function, motivation, and awakeness
In the synaptic cleft, Monoamine Serotonin, Norepinephrine, and Dopamine
Oxidase A breaks down:
In the synaptic cleft, Monoamine Dopamine
Oxidase B breaks down:
Atypical depression (mood responds to positive events and
MAOIs are especially effective
in: symptoms include increased appetite, weight gain,
sleepiness, and fatigue)
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Non-selective MAOIs inhibit MAO-A and MAO-B
enzymes:
Selective MAOIs only inhibit the MAO-B
enzyme:
Three non-selective MAOIs: isocarboxazid, phenelzine, tranylcypromine
Non-selective MAOIs increase Serotonin, Norepinephrine, Dopamine
the levels of these
neurotransmitters:
These three non-selective MAOIs isocarboxazid, phenelzine, tranylcypromine
bind irreversibly to MAO
enzymes to
permanently block their function:
Two selective MAOIs: selegeline, rasagiline
Selective MAOIs increase the Dopamine
level of this neurotransmitter:
These selective MAOIs are more selegeline, rasagiline
commonly prescribed to treat
Parkinson's Disease (a
neurodegenerative disorder that
effects the dopaminergic
neurons in the substantia nigra
region of the brain):
Adverse effects of MAOIs Serotonin syndrome and hypertensive crisis
include:
Before starting another Two weeks (to allow for the body to replace MAO enzymes
antidepressant MAOIs so that serotonin syndrome does not occur)
should be stopped for at
least:
Five main symptoms of hyperthermia, hypertension, tachycardia, arrhythmias, agitation
hypertensive crisis:
Hypertensive crisis commonly tyramine (cheese, wine, beer, cured/smoked meats)
occurs when people taking
MAOIs consume foods or
drinks high in:
Foods and drinks rich in cheese, wine, beer, cured/smoked meats
tyramine:
When uninhibited, these two MAO-A and MAO-B
enzymes are responsible for
breaking down tyramine:
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When tyramine is not broken Norepinephrine
down, it increases the release
of this
neurotransmitter,
which causes
hypertensive crisis:
Due to its action as an adrenergic Phentolamine
antagonist this drug is the
treatment of hypertensive
crisis:
TCAs are subdivided into these Tertiary TCAs and Secondary TCAs
two groups:
Three Tertiary TCAs: amitriptyline, imipramine, clomipramine
Two Secondary TCAs: desipramine, nortriptyline
Tertiary TCAs are non-selective Serotonin and Norephinephrine transporters (increase 5HT and NE)
and act on:
Secondary TCAs are selective Norepinephrine transporters (increase NE)
and act only on:
Therapeutic benefits from TCAs 2-4 weeks
typically take approximately:
In addition to treatment of Phobic disorders, chronic neuropathic pain, migraine prophylaxis
depression, other
indications for TCAs
include:
Medication specific indication OCD
for clomipramine:
Medication specific indication Nocturnal enuresis
for imipramine:
In addition to SERTs and NETs, Histamine (H1) receptors, Muscarinic receptors, and Alpha 1 receptors
TCAs block (causes side
effects):
TCAs inhibitory effects on sedation
Histamine (H1) receptors
results in this side effect:
TCAs inhibitory effects on anticholinergic side effects
Muscarinic
receptors results in this side
effect profile:
These TCAs more commonly amitriptyline, imipramine, clomipramine (Tertiary TCAs)
cause anticholinergic side
effects:
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