Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
31 Cards in this Set
- Front
- Back
5HT partial agonist
|
BuSpar (buspirone)
|
|
a2 agonist
|
Catapres (clonidine)
|
|
Beta Blockers
|
Inderal (propanolol)
Tenormin atenolol |
|
Benzodiazepines (anxiety)
|
Valium (diazepam)
Librium (chlordiazepoxide) Serax (oxazepam) Ativan (lorazepam) Xanax (alprazolam) Klonopin (clonazepam) |
|
non-benzodiazepines (sleep)
|
Ambien (zolpidem)
Sonata (zaleplon) Lunesta (eszopiclone) |
|
Natural Sleep products
|
Melatonin
Valerian |
|
Antidepressants used for insomnia
|
Elavil (amitriptylline*)
Desyrel (trazodone*) Serzone* (nefazodone) |
|
Benzodiazepines (sleep)
|
Dalmane (flurazepam)
Restoril (temazepam) Halcion (triazolam) Doral (quazepam) |
|
Antihistamines
|
Diphenhydramine
Doxylamine Hydroxyzine |
|
Melatonin agonist
|
Rozerem (varenicline tartrate)
|
|
Ways panic disorders can be induced.
|
sodium lactate infusion or CO2—mechanism may be stimulation of NE mechanisms in locus coeruleus; associated with increased blood flow in right parahippocampus.
|
|
Brain changes as the result of repeated panic attacks.
|
Temporal lobe abnormalities in white matter, plus ventricular enlargement correlate with number of attacks and age on onset.
|
|
Effect of benzodiazepines on panic attacks.
|
increase inhibitory effects of GABA (which lets Cl- in)
|
|
Effect of Buspar (buspirone)on panic attacks.
|
affects 5HTIA receptors, which have abnormal density in anxiety disorders.
|
|
Factors involved in PTSD
|
genetic, familial, situational
|
|
Probable biological origin of PTSD
|
involves startle response circuits that include NMDA-mediated mechanisms in amygdala and brain-stem pathways, and failure of extinction mechanisms, as well as behavioral sensitization mechanisms (enhanced response magnitudes which probably involve increases in dopamine)
|
|
Likely cause for flashbacks and amnesia from PTSD
|
cell loss in right hippocampus: damage likely by stress-induced glucocorticoids?
|
|
Brain areas with increased metabolism associated with OCD
|
left orbitaofrontal gyrus, cingulate and bilateral caudate
|
|
What other two disorders share the same brain excitation as OCD?
|
Tourette's, and also sometimes in ADHD
|
|
What brain areas show a blood flow increase when OCD symptoms are provoked?
|
right caudate, left anterior cingulate gyrus, and bilateral orbitofrontal
|
|
What neurotransmitter effect does BuSpar have on anxiety?
|
5HT1A partial agonist
|
|
What neurotransmitter effect do alpha-2s have on anxiety?
|
agonists on presynaptic autoreceptors or beta 1 blockers on post-synaptic receptors can inhibit noradrenergic overactivity in locus coeruleus
|
|
What neurotransmitter effect do benzodiazepines have on anxiety?
|
interact with GABA receptors, primarily GABA-A type
|
|
What is the first rule in treating insomnia?
|
First determine the cause, then treat underlying disorder if there is one
|
|
What characterizes the ideal sleep-aid?
|
rapid-onset, short half-life
|
|
What neurotransmitters are implicated in OCD?
|
5HT and DA
|
|
What is the average time for an SSRI to be effective against OCD?
|
4-8 weeks
|
|
What is the preferred course of therapy for OCD?
|
Initially treat with drugs if necessary, but best and longest-lasting treatment is CBT.
|
|
What are treatments options for Panic Disorder and Panic attacks
|
a. SSRI's, but at a lower dose than for depression
b. Other antidepressants c. Benzodiazepines—but these are problematic for long-term use d. CBT is as effective and longer-lasting than any drug treatment |
|
What are treatment options for phobias?
|
1. Specific phobias—treat with desensitization
2. Social phobias—treat with beta blockers for NE overactivity, or SSRI's; as usual, psychotherapy is best approach, especially along with drugs |
|
What is the best psychotropic treatment for PTSD?
|
SSRIs.
|