Anxiety Meds Names & Facts Flashcards
Psychological Etiology: Unconscious
Unconscious perception of danger: realistic: environmental, Moral: Superego, Id Anxiety: Id
Unconscious triggers: Signal anxiety leading to defenses, when defenses fail, experience more anxiety symptoms
Psychological Etiology: Cognitive Model
Anxiety is triggered when there is an over-evaluation of danger
Anxiety is triggered when there is an underestimation of ability to cope
Perceptions of reality are distorted leading to misunderstandings of “false alarms”
Biological Theories of Anxiety
NOT inconsistent with psychological theories and in fact may go hand in hand
When danger is perceived, a complex network is triggered to prepare the body for “fight or flight.” This network involves nerve pathways, brain structures, and glands
Fight or Flight- mobilizes the body and mind to prepare for potential danger, nonessential physiological processes “shut down,” energy is poured into necessary functions that are responsible for fast action, body shifts into a position of hypervigiance and hyperarousal
Specific pathways (see slides 15 & 16- I don’t think we need to know this much detail)- know amygdala, hypothalamus, and limbic system are involved and NE availability is increased
Chloride Ion Channels also involved (GABA responsible for opening or closing ion channel)
Types of pharmacologic interventions for anxiety
- Anxiolytics (Benzodiazepines, BuSpar)
- Antidepressants (Effexor) (not ideal because cause sedation, but not habit forming, but it is a narrow window between sedation and calming effects so really have to play with dosage)
- Beta Blockers (not as effective as other treatments)
- Antihistamines
- Clonidine
- Tiagabine
Pharmacologic effect
Competes for GABA receptors, which increases the affinity of GABA molecules for their specific receptors
Increases the frequency of anion channel opening
May decrease norepinephrine and serotonin turnover
Absorprtion
Oral- completely absorbed reaching peak plasma levels in 30 minutes to 4 hours
IV_ immediate effect
IM- erratic absorption from muscular injection
Benzodiazepines
Lipophilic- affinity to lipids (love fats)
85-90% bound to plasma proteins
Active metabolites lead to slow elimination, prolonged clinical action, and potential for toxicity
Plasma levels that are twice the recommended amount lead to sedation
lorazepam (Ativan), alprazolam (Xanax), and oxazepam 9Serax) are the safest benzos because they have essentially no active metabolites
Benzos- mechanism
Bind to chloride ion channels further opening the channel and enhancing the flow of negative ions into the cell, producing a widespread calming affect (calming overall brain excitation from the limbic alert)
Benzos- side effects
- Sedation
- Decreased mental acuity
- Decreased coordination
- Combined with drugs increases side effects
- Tolerance, dependence
- Psychological dependence
- Toxicity: particular caution when used with alcohol. 2x the prescribed dose along with alcohol has led to death
- Expected to produce sedation but can cause paradoxical agitation
- Withdrawal- dependence can develop with prolonged use, symptoms subside within 1-4 weeks
Benzos- Other Toxicity warnings
- Pregnancy- safety not established, but drugs do cross the placenta and accumulate in the fetal blood
- Elderly- cautious use due to age related changes in metabolism and increased body fat
- Drug-Drug interactions- MAOI’s potentiate (increase the power) the effects of benzos
Benzos- What patients should know
- Benzodiazepines should not be used in response to minor stresses of everyday life
- Over the counter drugs may potentiate the actions of benzodiazepines
- Driving should be avoided until tolerance develops.
- Alcohol and other CNS depressants potentiate the effects of benzodiazepines
- Hypersensitivity to one benzodiazepine may mean hypersensitivity to another
- Benzodiazepine use should not be discontinued abruptly
Benzos- Cautions for Clinicians
Disinhibition is know to occur with diazepam and possibly other benzos. Sign include: escalating agitation, violence, psychotic terror, explosive behavior, amnesia
Drug is inappropriate for long term use
If client is on high doses of Benzos for >3 months, slow tapered discontinuation is rec.
Alternative treatments include: BuSpar, Effexor, Antidepressants with sedating effects
diazepam
(Valium)-Benzo
“Mothers little helper”
Absorption- IV or oral, peak plasma concentration in 1- 1.5 hours, steady state in 5 days- 2weeks, delayed and decreased when taken with food
Distribution- 98% bound, lipid soluble, found in breast milk
Metabolized in the liver, several active metabolites
Excreted in urine- half life of 24-48 hours
Mechanism- facilities synaptic actions of GABA, inhibits the CNS,diazepam does not act directly on the same site as GABA but on closely linked sites called benzodiazepam receptors
Effects: anxiolytic, sedative, muscle relaxant, anticonvulsant, amnestic
*Onset of action within 30 min and can last 12-24 hours, most effective from 15 min to 1hr after dose
SE: drowsiness, fatigue, muscle weakness, ataxia, seizures with abrupt withdrawal, drug dependence and withdrawal, rebound anxiety
alprazolam
Xanax
Benzo
Oral admin- onset 30 min, peak 1-2 hours, duration 4-6 hours
Half life 12-15 hours
80% protein bound
Metabolized in liver
lorazepam
Ativan
Benzo
Oral or injectable
GABA agonist-pormoting its inhibitory effects
Oral use- anxiety, injection use- first line treatment for status epilepticus, pre anesthesia
Readily absorbed, plasma levels are dose dependent
85% bound
Metabolized in liver
Short half-life
No active metabolites
Do NOT use with other CNS depressants (Alcohol + ativan= respiratory collapse)
clonazepam
Klonopin
benzo
Oral admin- rapidly and completely absorbed. 90% bioavailability
Maximum plasma concentrations reached 1 to 4 hours after admin
85% bound
Half life 30-40 hours
metabolized into pharmacologically inactive metabolites
flumazenil
Romazicon
Benzo
Binds with high affinity to benzo receptors on the GABA complex, but after binding it has no intrinsic activity (thus- competitive with active benzos to the receptor)
It reverses the anti anxiety and sedative effects of any benzo administered prior to flumazenil
Metabolized rapidly in liver and has short half life (about 1 hour)- so reinjection usually required
Acts as an antidote when Benzo OD is suspected
buspirone
BuSpar
NOT a Benzo or barbiturate (in azapirone chemical class)
Oral admin
1-3 weeks to reach therapeutic level
Rapidly absorbed in GI tract
Limited bioavailability given extensive first-pass metabolism (this can be increased with food)
88% bound
*Short half-life (2 to 3 hours)
High affinity for serotonin receptors, but NO significant affinity for benzo receptors (does not affect GABA binding)
Primarily treats GAD
NOT habit forming (as opposed to Benzos)
If previously treated with Benzo- not as effective
Different physiological effect than Benzos
