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14 Cards in this Set
- Front
- Back
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Describe the history of sedatives |
- phenobarbital was introduced, one of the first barbiturates - chlordiazepoxide was marketed as first sedative anxiolytic benzo - Benzos had one major advantage over barbiturates: they were rarely ever fatal - it was thought that barbiturates acted through nonselective neuronal depression - |
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How do Benzos work? (pharmacodynamics) |
- they are PURE GABA AGONISTS because they facilitate binding of GABA by binding to a site adjacent to the GABA receptor, producing a three-dimensionalconformational change in the receptor structure that, in turn, increasesthe affinity of GABA for the receptor - this in turn facilitates influx of CL ions, causing hyperpolarization of the post synaptic neuron - they exert anxiolytic properties by acting on the limbic centers like amygdala OFC insula |
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Can you blackout with sedatives? What happens? |
Yep! Just like alcohol, if you reach a high dose, it can produce anterograde amnesia - this stage is distinct from effects that produce lack of consciousness. The person can be fully awake and yet have amnesia (organic dementia) - in a blackout on sedatives, mental content, intellectual function, insight+judgement, sensorium, affect are affected
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Describe barbituates (5) Why are they no longer used as much? (4) |
- short half life & lipid soluble - low selectivity- cant achieve anxiolysis without sedation - REM is suppressed - they are cognitive inhibitors since they depress memory functioning - barbituates stimulate the synthesis of liver enzymes that metabolize barbiturates as well as other drugs, an effectthat produces significant tolerance to the drugs. (withdrawal may result in hallucinations, restlessness, and convulsions) - their use has declined rapidly bc of the lethal overdose, narrow therapeutic to toxic range, high tolerance potential, interact with many other drugs |
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What are nonbarbituate sedative-hypnotic drugs? |
- they are pharmacologically interchangeable with barbituates and offer NO advantages - they are obsolete in medicine but are sometimes abused - Meprobamate, Carsiprodol, Methaqualone - GHB (sched 1), useful in treating narcolepsy |
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Describe the pharmacokinetcs of Benzos |
- well aborbed when takend orally - peak plasma concentration at 1hour - sme are metabolized into pharm inactive substances and excreted, others into active products which have a second metabolism. Others still are metabolized into long-lasting active metabolites (such as nordiazepam which has a half life or 60 hrs) - elderly have reduced ability tometabolize long-acting benzodiazepines and their active metabolites. Must be careful to avoid cognitive side effects (dementia!) |
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The behavioral rewarding effects, drug abuse potential, and psychologicaldependency of benzos likely come from... |
actions on GABA receptors thatmodulate the discharge of neurons located in the ventral tegmentumand the nucleus accumbens. |
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What is the most common therapies Benzos are used for? |
- short term treatment of anxiety that is extremely debilitating - panic attacks and phobias (although not as effective as SSRIs - used as hypnotics for treatment of insomnia - can also be used for producing long-lasting amnesia if needed (injection) This is actually the only area where benzos cannot be replaced by other drugs |
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What are the side effects of Benzos? |
- impairment of motor ability - when used for insomnia, REM rebound, insomnia and anxiety - cognitive deficits - learning, academic performance, psychomotor - taken in first trimester can cause fetal abnormalities and fetus dependence |
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Flumazenil |
- benzo that binds with highaffinity to benzodiazepine receptors on the GABAA complex, but afterbinding, it exhibits no intrinsic activity. As a consequence, it competitivelyblocks the access of pharmacologically active benzodiazepines tothe receptor, effectively reversing the antianxiety and sedative effects ofany benzodiazepines administered before flumazenil. - shorter hald life than most benzos |
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What are BZRAs? |
- benzo receptor agonists wich bind to the benzo receptor and can exert agonistic action to increase GABA activity - benzos are obviously in this category, but so are some nonbenzo drugs - Zolpidem binds to BAGA1A and is more sedative than anxiolytic - Zaleplon also binds to GABA1A but is even shorter acting that zolpidem - Eszopiclone is the active isomer of zopiclone that has a half life of 5-7 hours may have next day sedation though - partial agonists of BZRsare being identified to try to get rid of the side effects of "full" agonists |
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General Anesthetics |
- used to produce amnesia and loss of consciousness- either inhaled or injected into vein - dose-dependant depression of CNS |
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Ramelteon ; Serotonin receptor agonists as anxyolitics (2) |
- melatonin receptor agonist - insomnia, but not effective except for jet-lag - nonaddicting, no rebound insomnia ; - Serotonin 5HT 1A receptors are in high density in areas involved in fear + anxiety - Buspirone is a weak agonist at these receptors and is unique in that it relieves anxiety without sedation/hyponotic, does not exhibit cross-tolerance, has a gradual onset (better for long term not immediate relief), antidepressant effect, little abuse potential |
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Antiepileptic drugs (2) + 3 examples |
- sedative hypnotics have been used to help treat epilepsy, as well as chronic pain, PTSD, withdrawal etc - antiepileptic drugs may increase risk of suicidal thoughts - phenobarbital was common but not not used - valproic acid is helpful in treating petit mal seizures, but is short acting - Carbamazepine- less intense sedation,but alters white blood cell count, and increases the productionof drug-metabolizing enzymes in the liver |
