Pharmacology of anxiolytic drugs Flashcards
What are the type of anxiety disorders
generalized anxiety disorder, Obsessive compulsive disorder,
What is the development of anxiety
Pre-existing sensitivity (gene plus environment) -> learning of fear (index traumatic event) -> consolidation of fear (hours to days following event) -> expression of anxiety (memories, flashbacks, nightmares, avoidance, startle)
What is the organ in the brain that drives a short term fear response and fear learning
Amygdala (site of BZD action)
T/F: Smell and touch bypass the thalamus go straight to amygdala inducing a much stronger stress response then sound and visual stimuli
True
What part of the brain causes the symptoms of fear and anxiety, symptoms
Locus ceruleus/ rapid hearbeat, increased blood pressure, sweating, pupil dilation
What is the organ in the brain that drives a long term fear response
Bed nucleus of the stria terminalis (site of BZD)
T/F: Memory consolidation happens in the hippocampus
True
What is fear extinction, what are the relevant structures involved
Decrease in fear responses during repeated presentations of the conditioned stimuli without the unconditioned stimulus reinforcement/ amygdala, hippocampus and cortex
T/F: A sedative calms a patient while a hypnotic drug produces drowsiness
True
What is the real approval time frame for BZDs
2-4 weeks
T/F: All BZDs have the same efficacy but there is a difference pharmcokinetics that influence the drug chosen
True
T/F: BZDs can cause tolerance to sedation effects BUT NOT Anxiety effects
True
What occurs when a GABA receptor is activated
Diffusion of chloride ions across the cell membrane
Where does GABA bind, where does BZDs bind
between alpha-beta subunit, bind at the alpha-gamma interface
T/F: BZDs are GABA agonists
False: BZDs are allosteric modulators that increased the affinity of GABA to the receptor
What is a competitive BZD antagonist
Flumazenil
T/F: BZDs are both allosteric modulators BUT BARBITURATES can activate Cl channel opening in the ABSENSE of GABA
TRUE
T/F: Barbiturates increase the open time of GABA channels
True
How come BZDs are not anesthetics
Patients can still feel pain
Why do BZDs have abuse potential
DOPAMINE is dumped by ventral tegmental area into the Nucleus accumbens, Dopamine causes medium spiny neurons to inhibit GABA from inhibiting dopamine release to cause the cycle to continue
What effects of BZDs causes tolerance
Sedation/hypnotic (greater with short half life BZDs) and Anticonvulsant/muscle relaxant
What effects of BZDs do not cause tolerance
Anxiolytic, dependence potential (greater potential for dependance in short half life BZDs), amnesia
T/F: Chronic use of BZDs is associated with dementia even after discontinuation
True
What are the short acting BZDs
Midazolam and Triazolam
What are the intermediate acting BZDs
Alprazolam, Clonazepam, Estazolam, Lorazepam, Oxazepam, Temezepam
What are the long acting BZDs
Chlordiazepoxide, Clorazepate, Diazepam, Flurazepam, Quazepam
Which BZDs can be given IM
Chlordiazepoxide (L), Diazepam (L), Lorazepam (I), Midazolam (S)
What BZDs can be given IV
Chlordiazepoxide (L), Diazepam (L), Lorazepam (I), Midazolam (S)
What is the only BZD that can be given rectally
Diazepam
What are withdrawl effects of BZDs
anxiety, increased sensitivity to light and sound, muscle cramps, myclonic jerks, sleep disturbances, Seizures and delirium (high dose)
T/F: Drug accumulation is most likely to happen in BZDs that are long acting
True
What is the anti-anxiety MOA of busprione, anti depressant property
Full agonist at the pre-synaptic 5-HT1 receptors inhibiting 5-HT synthesis and firing, partial agonist at post synaptic 5-HT1A
What are the benefits of buspirone over BZDs
Nonwithdrawl syndrome, no tolerance to anxiolytics effects
T/F: Just like BZDs there is no evidence of tolerance to anxiolytic effects when using buspirione
True
Which hypertensive drug decreases norephinephrine therefore decreasing the anxiety response
Clonidine
