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20 Cards in this Set

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  • Back
what components of sleep control are found in the hypothal? SCN? Brainstem? Thalamus?
sleep/wake switch. Circadian clock. ARAS and REM, SWS switch. Cortical acticvation, sleep spindles and EEG synchronization
describe chemicals and anatomical locations of wake promotiion.
monoamines (NE,DA, ser, and his) from the brainstem and posterior thal go to the cortex and motor neurons. Ach from the midbrain/pons/posterior thal send info to the thalamus which regulates cortical awakeness. Ach in the basal forebrain goes to the cortex. Tha lateral hypothal sends axons to all these wake promoting areas and the cortex and releases the excitatory peptide NT hypocretin
NREM sleep is regulated by what part of the brain and what NT?
the anterior hypothal via GABA to the wake centers
describe REM regulation via chemicals and anatomy.
Rem on cholinergic neurons in the midbrain are inhbited by aminergic neurons when awake, but when asleep they are disinhibited and then stimulate the thalamus to stimulate the cortex and also have a descending tract that stimulates the glycine tract to inhibit LMN's and NE from the locus cereleus
what are two key features of REM sleep that differentiate it from wakefulness?
absence of activity in the wakefulness-promoting aminergic, ascending pathways and loss of muscle tone during REM sleep.
how do many wake promoting agents such as amphetamines work?
they prevent DA reuptake (and to some extent the other monoamines)
how does modafinil work?
blocks reuptake of NE and DA, thus promoting wake AND inhibiting sleep by more NE blocking the GABA channels
what is the risk of addiction when treating narcoleptics with stimulants?
no significant risk
what insomnias can be treated with hyponotics? Should not be?
acute stress, environmental disturbances, medication changes, and jet leg. Drug/alc abuse, sleep induced respiratory impairment, and clinical med use.
in general how do hypnotics work?
increase GABA signalling in the VLPO descending pathways that innervate wake promoting regions
what are the effects of hypnotics?
shorten sleep latency, increase total sleep time, reduce the frequency of nocturnal awakening
what receptors do benzodiazepines bind to? Nonbenzo hypnotics? Effects of each?
benzos bind to 3 sites (BZD1, 2, and 3) to potentiate GABA. Nonbenzos bind only to BZD 1 (limits therapy but also limits side effects).
what are the "new" hypnotics?
eszopiclone, ramelteon (melatonin), and sodium oxybate
this drug has a very long half life and rapid absorption.
this drug has a short half life and rapid absorption, binds in brain to BZD1 mainly, and might have little potential for abuse, but large doses produce nausea and vomitting.
zolpidem (ambien)
this drug has a fast absorption, peak, and very small half life. Some amnesia, does not help sleep maintenance or increase TST.
what are the side effects of hypnotics?
impaired memory and cognition, ataxia, tolerance, potential for rebound insomnia, withdrawal symptoms with abrupt cessation, daytime carryover
what are the clinical implications for short half life hypnotics? Long half life?
tolerance, rebound insomnia, anterograde amnesia. Day time sedation and hangover
you should use caution when prescribing to what patient populations?
elderly, heavy snorers, renal, hepatic, or pulmonary disease, use other meds, suicidal, hazardous occupations
what are the absolute contraindications for hypnotic use?
sleep apnea, excessive alcohol, need for alert function during normal sleep periods