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39 Cards in this Set

  • Front
  • Back
Name the classifications of drugs that are commonly used as sedatives.
Anti-depressants, barbituates, benzodiazepines, typical antipsychotics, atypical antipsychotics; non-benzodiazepine sedatives (newest)
what is the main control center of the circadian rhythms of sleep and temperature?
the SUPRACHIASMATIC NUCLEUS (SCN) - part of the hypothalamus (located above the optic chiasm) - controls synchronized sleep according to patterns of light and dark
what endocrine gland does the suprachiasmatic nucleus regulate and what does it secrete?
SCN regulates the pineal gland (posterior to thalamus): PG secretes melatonin (hormones increases sleepiness)
what receptors does melatonin act on?
MT1, MT2, and MT3 receptors
What are the stages of normal sleep?
stage 1 (drowsiness), Stage 2 (light sleep), Stage 3&4 (deep, "slow-wake" sleep), REM (rapid eye movement "dream sleep", almost awake, occurs mostly in morning)
explain the order of the sleep patern stages.
go 1-2-3-4-3-2-REM-2-3-4-3-2-REM (each cycle lasts ~90minutes)
explain when stages 3 and 4 occur and what about the stages length?
stage 3 and 4 occur early in the night and the length will decrease as the night progresses
what part of the CNS is responsible for arousal?
reticular formation in midbrain (extends from the medulla to the forebrain)
name the area and neurons that are important for promoting sleep.
ventrolateral preoptic area (VLPA) contains ventrolateral preoptic nucleus that inhibits other neurons that are responsible for wakefulness. it sends inhibitory GABA projections to places that keep you awake: locus coeruleus (NE), raphe (5-HT), and the tuberomammillary nucleus (histamine)
if you were to lesion the VLPA (ventrolateral preoptic area) what would happen?
lesions produce total insomnia, leading to death
what waves will predict the onset of REM? where is this activity first detected?
PGO (pontogeniculooccipital) waves- high amplitude electrical potentials; pons --> lateral geniculate of hypothalamuc --> occipital cortex
what neurotransmitter and what part of the pons is responsible for modulating REM?
ACh neurons in the peribrachial pons modulate REM sleep; increase ACh, increase REM; these peribrachial neurons fire at a high rate during REM
explain the production of rapid eye movement.
pontine ACh neurons project to the thalamus (control cortical arousal), to the forebrain (arousal and desynchrony), and to the TECTUM (RAPID EYE MOVEMENT)
name the area that is anterior and dorsal to the hypothalamus that contains cells that extend throughout the thalamus and cerebral cortex; it release inhibitory GABA (essential for sleep) as well ACh for arousal.
basal forebrain
name and describe two sleep disorders.
INSOMNIA: difficulty getting to or remaining asleep and NARCOLEPSY: falling asleep at odd times; narcopleptics have a reduced CSF levels or altered activity of the neuropeptide OREXIN(neuropeptide transmitter responsible for the ability to stay awake)
What is orexin and what does it stimulate?
orexin is a peptide neurotransmitter released in a pathway from the hypothalamus that is highly responsible for the ability to stay awake; it stimulates ACh-releasing cells in the forebrain and brainstem
what does adenosine do in regard to sleep and arousal?
accumulation of adenosine in the brain will inhibit the basal forebrain cells responsible for arousal and CAUSE SLEEP. (caffeine blocks adenosine receptors)
in order to go to sleep, you must have decreased arousal. how does this occur?
to go to sleep: 1. the brain and body decrease its temperature, 2. decrease stimulation by finding a quiet environment, 3. the brain accumulates adenosine - inhibits the basal forebrain cells from releasing ACh
Describe the different types of insomnia.
TRANSIENT: <3days and caused by brief environmental or situational stress; SHORT-TERM: 3days - 3weeks caused by stressors such as illness, grief, or job problems; LONG-TERM INSOMNIA: lasting for more than 3 weeks (causes: major pychiatric illnesses and drugs, medical condition, or conditioned or learned behavior, sleep apnea)
If a depressed patient is on an SSRI and she can't sleep, what maybe should you try?
switch her to trazodone; anti-depressent that is good at inhibiting serotonin reuptake (structure similar to a BZD)
when should you not use a sedative-hypnotic?
sleep apnea
Name some sedative-hypnotics that don't really help the quality of sleep.
Barbituates decrease REM; Benzodiazepines reduce slow-wake non-REM sleep and produce cognitive changes (next day confusion, falling, rebound next-day anxiety, worsen sleep apnea)
when a person is on a long-term treatment with a Benzodiazepine, what do you have to be careful of when taking them off?
taper it down, may cause seizures, rebound insomia, and altered sleep patterns
in deciding what sedative is best, which 3 are preferred over barbituates?
benzodiazepines, and non-BZD: zolpidem and zaleplon
what sedative-hypnotics are preferred in elderly?
What drugs should be avoided in treating insomnia?
avoid barbs, glutethimide and meprobamate (all have high abuse potential and easy to overdose)
name 2 short active barbituate sedative hypnotics.
pentobarbital sodium and secobarbitoal sodium (good for s/term tx of insomnia or preoperatively)
what is the MOA of most sedative hypnotics?
most sedative hypnotics bind to the GABA receptor and cause Cl- channels to open, thus hyperpolarizing and inhibiting the effect of neuronal excitability
what is the MOA of barbituates?
multiple MOA: 1. increase GABA effect (increase Cl channel opening duration), 2. directly activate GABAa channels at high concentrations; 3. block glutamate NT effects; 4. Block Na channels; barbs DO NOT relieve pain and may lead to tolerance and dependence and death by overdoes: NOT GENERALLY USED TODAY FOR SLEEP-AIDs
in order for a benzodiazepine to bind to the GABA receptor, what must be present?
BZDs need GABA to be present on the GABA receptor in order to work; it will cause an even greater influx of Cl and hyperpolarize with greater affinity
name some non-benzo sedatives; how long are they recommended for use?
zolpidem and zaleplon (recommended for 7-10 days only); and chloral hydrate (older, cheap, converted to trichlorothanol, slow clearance)
name barbituates toxicities/side-effects that may occur.
alcohol and barbs - respiratory and CV depression; ADDITIVE: CNS depression; anterograde amnesia with Benzos (date rape);;;;Barbs use cyt P450 enzymes
Name a drug that has been approved for narcolepsy, excessive somnolence and obstructive sleep apnea. explain its MOA.
modafinil; MOA: activates orexin producing neurons (alpha agonist, facilitates Glu, reduces GABA)
what is the drug ramelteon (Rozerem)'s MOA and what are its indications?
used to tx adults with difficulty of sleep onset; not a controlled substance; MOA: melatonin receptor (MT1, MT2) agonist (not to be used in renal impairment)
name the BNZ antagonist that can halt the effects of benzodiazepines.
name a common side-effect of high dose Benzodiazepines.
anterograde amnesia
Name drugs that are used to treat insomnia.
BNZs(daytime sedation, REM reduced; rebound with bizzare dreams); NON-BZDs(less daytime sedation and no effects on REM): ZOLPIDEM (can eat, cook, and drive while asleep) and ZALEPLON
what alpha receptors will BZDs use? which ones are good for sedation, anxiety, and which will produce anterograde amnesia?
BZDs are sensitive to alpha 1,2,3,5; 1 is good for sedation; 2&3 are good for anti-anxiety; 1&5 will produce amnesia
what are common long-term effects of BZD abuse?
lethargy, irritability, nausea, loss of sexual interest, increased appetite, and increased weight