Anxiety is a state of pervasive apprehension that may be triggered by specific environmental or personal factors. Many patients with anxiety disorders do not respond completely to initial treatment and prescribers often combine an antidepressant with an effective anxiolytic drug that has a different mechanism of action. See what you know by taking this quiz.
Age
Environment
Gender
Genetics
All of the above
GABA inhibition
GABA activation
Glutamate inhibition
Glutamate activation
None of the above
SSRIs
Benzodiazepines
Psychotherapy
TCAs
All of the above are options for slow therapeutic treatment of high anxiety
Hippocampus
Frontal lobe
Amygdala
A & B
B & C
Plays a role in disorders involving very distinct fears
Processing threatening stimuli
Storage of emotional memories
A & C
B & C
Enlarged in size
Secrete more GABA than any other brain section
Reduced in size
Secretes less GABA than any other brain section
Two of the above
Antidepressants (SSRIs)
Buspirone
Benzodiazepines
Cognitive-behavioral therapy
All the treatment options above have the same effect on antianxiety time.
Partial agonist at the 5HT(1A) receptor
Partial antagonist at the 5HT(1A) receptor
Selective agonist at the GABA(A) receptor
Selective antagonist at the GABA(A) receptor
Selective reuptake inhibitor of 5-HT
Preferred as treatment for patients with chronic anxiety who are not responding to acute stresses
S/E profile: nausea, dizziness, headaches, and fatigue
Was discovered because practitioners were concerned about the S/E profile and risk of benzodiazepines
S/E profile: sedation, psychomotor impairment, dependence, withdrawal syndrome, and abuse potential
All of the above are characteristic of buspirone
True
False
True
False
Partial agonist at the 5-HT(1A) receptor
Partial antagonist at the 5-HT(1A) receptor
Agonist at the GABA(A) receptor
Antagonist at the GABA(A) receptor
Selective reuptake inhibitor of 5-HT
Enhance the response to serotonin; opening the 5-HT receptors
Depress the response to serotonin; closing the 5-HT receptors
Depress the response to serotonin; opening the 5-HT receptors
Enhance the response to GABA; opening the GABA(A) receptors
Depress the response to GABA; closing the GABA(A) receptors
Decrease frequency of channel opening
Increase frequency of channel opening
Decrease duration of channel opening
Increase duration of channel opening
Two of the above
Na+
K+
Mg++
Ca++
Cl-
GABA transaminase (GABA-T)
Glutamic acid decarboxylase (GAD)
GABA decarboxylase (GDC)
Succinic semialdehyde dehydrogenase (SSADH)
GABA is synthesized from the precursor succinic semi-aldehyde only, not Glutmate
Activation leads to repolarization
A channel for sodium (Na+) ions
Hexameric structure (6 subunits)
Is the binding site for both GABA and benzodiazepines
None of the above are true statements
Alpha
Beta
Gamma
All of the above
None of the above
Alpha
Beta
Gamma
All of the above
None of the above
Strong anxiolytic effect
All agents are schedule IV (C-IV)
Slow on/off kinetics
Low risk of interaction with other medications
Good safety profiles, compared to older agents such as barbituates
Rate of uptake into the brain
Rate of uptake into adipose tissue
Equilibration between serum and plasma
Equilibration between adipose tissue and serum
Equilibration between brain and plasma
Distribution; slowly
Metabolic processes; slowly
Distribution; rapidly
Metabolic processes; rapidly
Reduction
Glucuronidation
Transamination
Electrophilic substitution
Oxidation
Sooner
Later
At the same time
Time to Cp,ss is variable with the benzodiazepine agent
S/E's are subtractive with the concurrent intake of alcohol
Higher risk of interdose symptoms breakthrough
Require more care in tapering after prolonged use
Short term S/E include: sedation, fatigue, ataxia, slurred speech, impaired cognitive and motor performance
Effects wash out sooner after discontinuation than long half-life BZD's
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