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40 Cards in this Set

  • Front
  • Back
Panic Disorder:
A panic attack is an acute, discrete period of intense
fear and discomfort associated with a number of somatic and cognitive
symptoms that include: heart palpitations, sweating, trembling, shortness
of breath, sensations of choking, chest pain, nausea, dizziness, tingling,
chills or blushing, hot flashes.
Panic Disorder is diagnosed when
a person has experienced at
least two unexpected panic attacks and develops persistent worry about
subsequent attacks or changes his/her behavior to avoid attacks.
Social Anxiety Disorder (SAD):
characterized by marked and
persistent anxiety in social situations, including performances and public speaking.
Generalized Anxiety Disorder (GAD):
a period of anxiety
and worry of > 6 months duration accompanied by multiple associated
symptoms. Need to rule out other anxiety disorders.
Obsessive-Compulsive Disorder (OCD):
Obsessions are recurrent,
intrusive thoughts, images, ideas or impulses perceived as being
inappropriate, grotesque or forbidden.
Compulsions are repetitive
behaviors or mental acts that are performed to alleviate the anxiety
Post-traumatic stress disorder (PTSD):
Acute Stress Disorder refers to anxiety and behavioral disturbance (eg. nightmares) after an
extreme trauma (near-death experience, rape, witnessing a murder, etc). If symptoms and behaviors persist for >1 month and if features
are associated with functional impairment, it is now considered PTSD
Panic Disorder Theories
suggest that in anxiety disorders, there is an alteration in the
normal “stress response”
The stress response is the coordinated reaction to threatening stimuli and
involves:
• Avoidance Behavior
• Increased vigilance and alertness
• Activation of SNS
• Activation of HPA axis, ultimately releasing cortisol from adrenals
hippocampus and amygdala,
two areas that are part of the limbic system
that help to regulate the body’s normal response to stress, tightly regulate control of the HPA axis.
Theory of Anxiety
Inappropriate activation of the amygdala and subsequent activation of HPA axis has been associated with some anxiety
disorders.
The hippocampus
normally decreases HPA responses by a negative
feedback mechanism as cortisol levels rise. With chronic stress cortisol receptors in
hippocampus may downregulate or die resulting in a decline in the negative feedback pathway resulting in further
dysregulation of the HPA axis by the amygdala
Theory summed up
So, the combination of hyperactivity of the amygdala and under-activity of the hippocampus may underlie some of the etiology of anxiety disorders.
Neurotransmitter involvement
NE, 5-HT and GABA
There is a complex interaction between 5-HT, GABA and NE neurons in anxiety
disorders as SSRIs and SNRIs are effective for chronic treatment of most anxiety
disorders.
NE,
In animal models, stress results in elevation of NE in amygdala and
hypothalamus and an elevation of ACTH release. Stress-induced NE release facilitates a number of anxiety-like behavioral
responses in animal models.
5-HT
Stress results in decreased 5-HT in hypothalamus. 5-HT1A knockout mice are used as a model of anxiety.Full or partial 5-HT1A
agonists have utility in treatment of certain types of anxiety disorders.
GABA
Agents (eg. Benzodiazepines) that potentiate effects of GABA on GABA-A
receptors are very effective in reducing stress responses.
FDA-approved agents for GAD
Alprazolam*
Buspirone
Duloxetine
Escitalopram
Paroxetine
Venlafaxine
FDA-approved agents for SAD
Paroxetine
Fluvoxamine
Sertraline
Venlafaxine
FDA-approved agents for OCD
Clomipramine
Fluoxetine
Fluvoxamine
Paroxetine
Sertraline
FDA-approved agents for PANIC
Alprazolam*
Clonazepam*
Paroxetine
Sertraline
Venlafaxine
FDA-approved agents for PTSD
Paroxetine
Sertraline
Off-label or general use in various anxiety disorders
Beta blockers
Other benzodiazepines (diazepam*, oxazepam)
Buspirone
(Buspar) for GAD
5-HT1A partial agonist
may also act as a partial agonist of D2 receptors.
No sedation
does not possess anticonvulsant or muscle-relaxant properties
Buspirone Pharmacokinetics, Adverse Effects, Interactions:
administered twice daily; onset of anxiolytic effect
may require 2 weeks
Metabolized primarily by
CYP 3A4.
CNS: dizziness (12%); drowsiness (10%); headache (6%); hostility or agitation
GI: N/V
Nonselective MAO inhibitors
Sedatives
are agents that reduce anxiety and exert a calming effect
Hypnotics
are agents that produce drowsiness and encourage the onset and maintenance of
sleep.
Most common FDA-approved agents for insomnia
Benzodiazepines
Estazolam
Flurazepam
Lorazepam*
Quazepam
Temazepam
Other
Eszopiclone*
Zalepion
Zolpidem*
Diphenhydramine
Doxylamine
Mechanism of Action (Barbiturates, Benzodiazepines, non-benzodiazepines,)
target the
GABA-A receptor.(a ligand-gated Cl- channel.) Upon binding the Cl- channel opens to produce hyperpolarization of the cell.decreasing activity of the neurons on which it resides.
GABA-A receptors
are hetero-pentamers comprised of 3 different subunits (a, b and
g) that form the Cl- channel. subunits have heterogeneity as well in that there
are at least 5 a and at least 3 b subunits that allow for a number of combinations in
channel structure to exist.
Benzodiazepines activate GABA-A receptors comprised of all the a subunits (1-5),
newer hypnotics selectively activate only GABA-A receptors comprised of a1
subunits.
Barbiturates***
Amobarbital
Secobarbital
Butabarbital
Pentobarbital
Phenobarbital
FDA-approved agents for insomnia
***Insomnia is no longer an accepted use of barbiturates; safer benzodiazepines
and the newer hypnotics have mostly replaced this indication.
Barbiturates Mechanism of Action that contribute to barbiturates’ ability
to produce general anesthesia and more CNS depression than benzodiazepines
act
as positive allosteric modulators of the GABA-A receptor.When GABA is present they increase the duration of GABA channel openings. high concentrations may directly open GABA-A
channels.
may also block excitatory amino acid AMPA receptors,
reducing effects of glutamate.
benzodiazepines and newer non-benzodiazepine hypnotics (eg. Zolpidem) MOA
act as allosteric modulators of the GABA-A channel by increasing the frequency of
GABA channel openings, making channels more sensitive to the effects of GABA
Barbiturates Indications
Insomnia (not recomended); preoperative anxiety; sedation induction
(surgical procedures); sedation maintenance (surgery); some for seizure disorders
Barbiturates Pharmacokinetics
Phenobarbital: Very long T1/2 of 50-120, metabolized CYP 2C9, inducer of many enzymes, Short acting with duration of 1-4 hrs.
Amobarbital: IV or IM only; 10-12 hr duration.
Butabarbital: oral, 6-8 hr duration. 45-60 min onset. Complete metabolism in
liver, excreted by kidney as metabolites.
Barbiturates Adverse Effects/Toxicity:
• CNS deoression
• Respiratory depression
• CV depression
• Tolerance
• Cross-tolerance to ethanol
• Physical dependence:
o Withdrawal symptoms:
• All are teratogens, Pregnancy Category D
Barbiturates Pharmacodynamic Interactions:
CNS depressants: antihistamines, alcohol, opiates, tricyclic antidepressants,
phenothiazines, anticonvulsants
Benzodiazepines Pharmacokinetics:
Phase I metabolism that results in active metabolites,
some with very long T1/2. These metabolites may then undergo Phase II conjugation
reactions and then be eliminated by urinary excretion.
Benzodiazepines Adverse Effects/Toxicities:
• CNS effects: euphoria, drowsiness, amnesia, sleep driving, sleep walking, binge
eating while asleep, impaired judgment, diminished motor skills
• CV depression
• Respiratory depression
• Daytime sedation with longer T1/2 agents if used for insomnia.
• Tolerance after use of >1-2 weeks
• Physical dependence (similar to barbiturates)
Benzodiazepines Adverse Effects/Toxicities: cont
• Rebound insomnia may result if used for more than 1-2 weeks
• Shorter T1/2 drugs have more withdrawal symptoms after chronic use
• Toxicities in overdose are less severe than with barbiturates, but still dangerous.
• All agents mentioned are Pregnancy Category D and considered teratogens.
Benzodiazepines Pharmacodynamic Interactions
• CNS depressants
Top 200 Benzodiazepine Agents:
• Diazepam (Valium, generic, Diastat rectal gel)
• Lorazepam (Ativan, generic)
• Alprazolam (Xanax XR, Niravam ODT, generic)
• Clonazepam (Klonopin, generic)