Sedative and Hypnotics Flashcards
SEDATIVES – reduce ______ and exert a ______ effect
HYPNOTICS - produces ______ and facilitates the onset and maintenance of _________________
anxiety; calming
drowsiness ;a state of sleep.
SEDATIVE/HYPNOTICS ANXIOLYTICS
Major therapeutic use is to relief _______(_______) or induce _______(_______)
anxiety (anxiolytics)
sleep (hypnotics).
Hypnotic effects can be achieved with most anxiolytic drugs
T/F
T
just by increasing the dose.
The distinction between a “pathological” and “normal” state of anxiety is easy to draw
T/F
F
hard
anxiolytics are among the most prescribed substances worldwide.
T/F
T
Manifestations of anxiety:
Verbal complaints. The patient says he/she is __________________
Somatic and autonomic effects: . The patient is _______ and _______, has ______cardia, _____eased sweating, weeping and often gastrointestinal disorders.
Social effects. Interference with _________________ activities.
anxious, nervous, edgy.
restless and agitated; tachycardia, incr
Normal productive
Pathological Anxiety
Generalized anxiety disorder (GAD): People suffering from GAD have general symptoms of ————, autonomic ______, etc. for at least ________
motor tension; hyperactivity
one month.
Pathological Anxiety
Phobic anxiety:
Simple phobias. Agoraphobia, fear of ______, etc. Social phobias.
.
animals
Pathological Anxiety
Panic disorders: Characterized by (acute or chronic ?) attacks of ___ as compared to the (acute or chronic?) presentation of GAD.
Acute ; fear
Chronic
Pathological Anxiety
Obsessive-compulsive behaviors: These patients show _________(obsessions) and ___________ (compulsions).
repetitive ideas
behaviors
Causes of Anxiety
______
_____-induced
Drug ______
Medical
Drug-induced
Drug withdrawal
Causes of Anxiety
1). Medical:
Respiratory Endocrine Cardiovascular Metabolic Neurologic.
T/F
T
Causes of Anxiety
2). Drug-Induced:
– Stimulants
_____,_______,_______,_______.
– Sympathomimetics
_______,________,______,________.
– Anticholinergics\Antihistaminergics
________,________,__________,_________
– Dopaminergics
________,________,________,__________
Miscellaneous:
• Baclofen, cycloserine, hallucinogens, indomethacin.
Amphetamines, cocaine, TCAs, caffeine
Ephedrine, epinephrine, pseudoephedrine phenylpropanolamine
Trihexyphenidyl, benztropine, meperidine diphenhydramine, oxybutinin.
Amantadine, bromocriptine, L-Dopa, carbid/levodopa.
Causes of Anxiety
Drug Withdrawal:
•____,________,_________, other ______,______
BDZs, narcotics, BARBs
sedatives, alcohol.
Strategy for treatment of anxiety
_______ anxiety without causing ________.
Reduce
sedation
Anxiolytics
Barbiturates e.g. ________,______,______,_____,_______
Benzodiazepines e.g._______ (Valium), _____ (Versed),_______ (Klonopin) ; ________ (Ormodon), ________ (Rohypnol)
Glutethimide : ____________
Methohexitone, Phenobarbital, Pentabarbital, Thiopentone,Thiamylal
Diazepam; Midazolam; Clonazepam
Nitrazepam; Flunitrazepam
Piperidinediones
Anxiolytics
Meprobamate : __________ _______
Alcohols : ______,_________,_________
Buspirone : _________
Zolpidem : _____________
Zaleplon : __________
Propanediol carbamates
Ethanol, Chloral hydrate, Paraldehyde
Azaspirodecanedione; Imidazopyridine
Pyrazolopyrimidine
BARBITURATES
Derivatives of ___________
–Hypnotic/anxiolytic effect discovered in the early 20th century (Veronal®, 1903)
– Until the 60s, it was the largest group of _________
– (low or high?) risk of dependence ((mild or severe?) withdrawal symptoms)
barbituric acid
hypnotics; high ; severe
BARBITURATES
– (mild or Strong?) depressant activity on the CNS => ________
– At higher doses it causes respiratory and cardiovascular ________ => very little use today as _______ (only for _______ and ________)
Strong ; anesthesia
hypnotics
epilepsy and anesthesia
Structure-Activity Relationship of Barbiturates
The ________ and ______ forms of barbituric acid with the sites of substitution in the hypnotically active barbiturates
keto and enol tautomeric
Structure-Activity Relationship of Barbiturates
Substitution at carbon 5 = *_____ activity is introduced
_______ chain >- greater hypnotic activity
______ group (like ________) -> Greater anticonvulsant activity
Presence of ______philic groups decreases lipophilicity so decreases activity
Hypnotic; Branched
Phenol; phenobarbital
hydro
Benzodiazepines
_____,_______,_______,_____, and _________ properties.
Treatment : _______
At low doses are useful _______ and high doses produce a ________ effect
sedative, hypnotic, anti-anxiety, anticonvulsant, and muscle relaxant
anxiety; sedatives; hypnotic
Benzodiazepines
Absorption and distribution: ___philic, are (slowly or rapidly?) and (completely or incompletely?) absorbed after _____ administration and distribute throughout the body.
Excreted in the urine as ________ or ______ metabolites.
lipo; rapidly ; completely
oral
glucuronides; oxidized
Benzodiazepines
Treatment : anxiety
It has (more or less?) side effects, dependence
It is (more or less?) effective
Less
More
What are the different types of benzodiazepines?
Several types with differences in potency, speed at which they are metabolized, and “half-life” and therapeutic use.
Vary mostly in their ________
duration of action
Benzodiazepines
A substituent in the position _____, such as a _______, or ________ group, is required for sedative-hypnotic activity
7
halogen or a nitro
benzodiazepines
List 4
Clonazepam
Diazepam
Lorazepam
Flunitrazepam
Anxiolytics
_______ (BZDs).
___________ (BARBs).
_________ receptor agonists.
_____,______, and ______ receptor
antagonists.
If ANS symptoms are prominent:
_______________ antagonists.
_________ agonists (clonidine).
Benzodiazepines (BZDs).
Barbiturates (BARBs).
5-HT1A receptor agonists.
5-HT2A, 5-HT2C & 5-HT3 receptor
antagonists.
ß-Adrenoreceptor
Alpha2-AR
Anxiolytics
Other Drugs with anxiolytic activity.
–_____(_______). Used for Obsessive compulsive Disorder.
–________. Used in panic attacks.
– Anti_____ agents. Present in over the counter medications.
– Anti________ (Ziprasidone).
TCAs (Fluvoxamine)
MAOIs; histaminic
psychotics
Anxiolytics
Other Drugs with anxiolytic activity.
Novel drugs. (Most of these are still on clinical trials).
-_____ (e.g. CCK4).
–______/_______ (e.g. HA966).
CCKB
EAA’s/NMDA
Anxiolytics
Other Drugs with anxiolytic activity.
– TCAs (Fluvoxamine). Used for ________________
– MAOIs. Used in _______
Obsessive compulsive Disorder.
panic attacks.
Sedative/Hypnotics
A hypnotic should produce, as much as possible, a state of _____ that resembles _______
sleep
normal sleep.
Sedative/Hypnosis
By definition all sedative/hypnotics will induce sleep at _____ doses.
Normal sleep consists of distinct stages, based on three physiologic measures: ____________gram, ______gram, ____________gram.
high
electroencephalo; electromyo
electronystagmo
Sedative/Hypnosis
Two distinct phases are distinguished which occur cyclically over —— min:
1)___________(NREM). _____% of total sleep. Has _____ stages. Most sleep leads to stage ____.
2)__________ (REM). Recalled _____.
90
Non-rapid eye movement
70-75; 4; 2
Rapid eye movement; dreams
Properties of Sedative/Hypnotics in Sleep
1) The _______ of sleep onset is ____eased (time to ______).
2) The duration of stage ___ ——— sleep is increased.
3) The duration of _____ sleep is decreased.
4) The duration of ___-wave sleep is decreased.
Tolerance occurs after ______
latency; Decr; fall asleep
2 NREM; REM
slow; 1-2 weeks
slow-wave sleep , when ____________ and —————- occur
somnambulism and nightmares
Other Properties of Sedative/Hypnotics
Some sedative/hypnotics will depress the CNS to stage ______ of anesthesia.
Due to their (slow or fast?) onset of action and (short or long?) duration, barbiturates such as _______ and ________ are used as _____ in general anesthesia.
III ; fast ; short
thiopental and methohexital
adjuncts
Sedative/Hypnotics
All of the anxiolytics/sedative/hypnotics should be used only for __________
*****
All the drugs used alter the normal _____ and should be administered only for _______________, never for _________.
************ USE FOR \_\_\_\_\_\_\_-TERM TREATMENT ONLY!!
symptomatic relief.
sleep cycle
days or weeks; months
SHORT
Barbiturates
Long acting
___________
Short acting
___________ , ___________
Ultra-short acting
___________
___________
Phenobarbitone
Butobarbitone ,Pentobarbitone
Thiopentone
Methohexitone
Benzodiazepines
Hypnotic
List 6
Antianxiety
List 5
Anticonvulsant
List 4
Diazepam Flurazepam Nitrazepam Alprazolam Temazepam Triazolam
Diazepam Chlordiazepoxide
Oxazepam Lorazepam Alprazolam
Diazepam Lorazepam
Clonazepam Clobazam
Non Benzodiazepine hypnotics
List 3
Miscellaneous
List 2
ZOLPIDEM
ZALEPLON
ZOPICLONE (ESZOPICLONE)
MELATONIN RAMELTEON
GABA-A Receptor
Major player in ______ Synapses.
It is a ____ Channel.
Binding of GABA causes the channel to ____ and ____ to flow ____ the cell with the resultant membrane _____________.
Inhibitory
Cl- ; open
Cl- ; into
hyperpolarization
GABA Receptor
Increase in Cl− permeability can depolarize the target cell under some conditions of ________________. This in turn potentially can _____________ or to activate _______ via voltage-gated channels and has been proposed as a physiologically relevant event, especially in embryonic neurons.
high intracellular Cl−
excite the cell to fire
Ca2+ entry
GABA Receptor
GABAB receptors were identified by their __________ to the GABAA antagonist _______.
insensitivity; bicuculline
GABA Receptor
The GABA analog (−) ________ was found to be a potent and selective GABA___ agonist.
baclofen
B
GABA Receptor
Baclofen (__________________________________ acid)
β-(4-chloro-phenyl)-γ-aminobutyric
GABAB receptors are coupled (directly or indirectly?) to ___ channels.
When activated, these receptors can ____ease _____conductance and ____ cAMP production via intracellular mechanisms mediated by G proteins.
Indirectly; K+
decr; Ca2+; inhibit
GABAB receptors can mediate ___________________________________ inhibition.
both postsynaptic and presynaptic
GabaB
Presynaptic inhibition may occur as a result of GABABreceptors on nerve terminals causing a ____ease in the influx of _____, thereby reducing the release of neurotransmitters.
it is known that these _________ increase the frequency of channel opening in response to GABA,
decr; Ca2+
benzodiazepines
benzodiazepine site is coupled allosterically to the ______ and ______ sites.
Benzodiazepine receptors are _______geneous with respect to affinity for certain ligands.
A wide variety of nonbenzodiazepines, such as the _____,________, and ______, also bind to the benzodiazepine site.
barbiturate and picrotoxin
hetero
β- carbolines, cyclopyrrolones and imidazopyridines
Barbiturates
• enhance the binding of GABA to ______ receptors
•Prolonging ________
•Only _____ (not ____ ) subunits are required for barbiturate action
•(wide or narrow?) therapeutic index
•in _____ doses, barbiturates increase reactions to painful stimuli.
GABAA; duration
α and β ; Υ
Narrow; small
Hence, they cannot be relied on to produce sedation or sleep in the presence of even moderate pain.
Barbiturates can be relied on to produce sedation or sleep in the presence of moderate pain.
T/F
F
they cannot be relied on to produce sedation or sleep in the presence of even moderate pain.
Bezodiazepines
• enhance the binding of GABA to ______ receptors
•Increasing the ________
•Unlike barbiturates, benzodiazepines do ___________
GABAA
frequency
not activate GABA
BARBITURATES or BENZODIAZEPINES
Has a Respiratory depression steeper dose-response relationship than
BARBITURATES or BENZODIAZEPINES
BARBITURATES
BENZODIAZEPINES
BARBITURATES
ACTIONS
- Depression of CNS: At _____ doses, the barbiturates produce _____ (——- effect, reducing ______).
- Respiratory depression: Barbiturates suppress the ______ and _______ response to CO2, and overdosage is followed by ———- and _________
- Enzyme induction: Barbiturates (induce or inhibit?) P450 microsomal enzymes in the liver.
low; sedation; calming ;excitement
hypoxic and chemoreceptor; respiratory depression and death.
induce
BARBITURATES
ACTIONS
1. Depression of CNS: At low doses, the barbiturates produce sedation (calming effect, reducing excitement).
2. Respiratory depression: Barbiturates suppress the hypoxic and chemoreceptor response to CO2, and overdosage is followed by respiratory depression and death.
3. Enzyme induction: Barbiturates induce P450 microsomal enzymes in the liver.
BARBITURATES PHARMACOKINETICS
All barbiturates redistribute in the body.
Barbiturates are metabolized in the ____, and inactive metabolites are excreted in the ________.
liver
urine
BARBITURATES PHARMACOKINETICS
Toxicity: Extensions of CNS depressant effects
dependence liability (> or <?) benzodiazepines.
>
BARBITURATES PHARMACOKINETICS
Interactions: Additive CNS depression with ________ and many other drugs (induction or inhibition?) of hepatic drug-metabolizing enzymes.
ethanol
induction
Barbiturates readily cross the placenta and can depress the fetus.
T/F
T
THERAPEUTIC USES
ANESTHESIA (THIOPENTAL, METHOHEXITAL)
Selection of a barbiturate is strongly influenced by the desired _________________________
The ultra______-acting barbiturates, such as thiopental, are used _______________ to induce anesthesia.
duration of action.
short; intravenously
THERAPEUTIC USES
ANESTHESIA (THIOPENTAL, METHOHEXITAL)
ANXIETY
Barbiturates have been used as (mild or severe ?) sedatives to relieve anxiety, nervous tension, and insomnia.
When used as hypnotics, they suppress ________ more than other stages. However, most have been replaced by the _______________.
mild; REM sleep
benzodiazepines
THERAPEUTIC USES
ANTICONVULSANT: (PHENOBARBITAL, MEPHOBARBITAL)
Phenobarbital is used in (short or long?) -term management of _______ seizures, status ___________, and eclampsia.
Long
tonic-clonic ; epilepticus
THERAPEUTIC USES
ANTICONVULSANT: (PHENOBARBITAL, MEPHOBARBITAL)
However, phenobarbital can depress ____________ in children, and the drug should be used ______.
cognitive performance; cautiously
THERAPEUTIC USES
ANTICONVULSANT: (PHENOBARBITAL, MEPHOBARBITAL)
Phenobarbital has specific _________ activity that is distinguished from the ___________ CNS depression.
anticonvulsant
nonspecific
___________ has been regarded as the drug of choice for treatment of young children with recurrent febrile seizures.
Phenobarbital
Adverse effects of Barbiturates
CNS: Barbiturates cause drowsiness, impaired _________
Drug hangover: Hypnotic doses of barbiturates produce a feeling of
_________ well after the patient wakes.
Barbiturates (induce or inhibit?) the P450 system.
concentration ; tiredness
Induce
Adverse effects of Barbiturates
Drug hangover:
By inducing ___________________, barbiturates increase porphyrin synthesis, and are contraindicated in patients with ____________________
aminolevulinic acid (ALA) synthetase
acute intermittent porphyria.
ADVERSE EFFECTS of Barbiturates
Physical dependence: Abrupt withdrawal from barbiturates may cause ______, anxiety, weakness, ________, nausea and vomiting, seizures, delirium, and _____________
Poisoning: Barbiturate poisoning has been a leading cause of death resulting from drug overdoses for many decades.
It may be due to ____________
tremors; restlessness; cardiac arrest.
automatism
Barbiturates: adverse effects
Severe depression of _______ is coupled with _______________ depression, and results in a _____-like condition with shallow, infrequent breathing.
respiration
central cardiovascular
shock
THE TREATMENT OF ACUTE BARBITURATE INTOXICATION
Treatment includes _______ and ________________________ if the drug has been recently taken.
artificial respiration ; purging the stomach of its contents
Mention 2 specific barbiturate antagonist
No specific barbiturate antagonist is available.
THE TREATMENT OF ACUTE BARBITURATE INTOXICATION
General supportive measures.
___________ or ___________ is necessary only rarely.
Use of CNS ______________ is contraindicated because they increase the mortality rate.
Hemodialysis or hemoperfusion
stimulants
THE TREATMENT OF ACUTE BARBITURATE INTOXICATION
If renal and cardiac functions are satisfactory, and the patient is hydrated, __________ and ___________ of the urine will hasten the excretion of phenobarbital.
In the event of renal failure - _________
circulatory collapse is a major threat. So __________ must be corrected & blood pressure can be supported with ———.
Acute renal failure consequent to ______ and ________ accounts for perhaps one-sixth of the deaths.
forced diuresis and alkalinization
hemodialysis; hypovolemia; dopamine
shock and hypoxia
Effects of benzodiazepine
On increasing the dose, sedation progresses to ______ and then to ________.
But the drugs do not cause a true general anesthesia because
- ________________________
-___________________ to allow surgery cannot be achieved.
However at “preanesthetic” doses, there is ________.
hypnosis; stupor
awareness usually persists
-immobility sufficient
amnesia
Effects of benzodiazepines on the (EEG) and Sleep Stages
_____eased sleep latency
_____eased number of awakenings
_____eased time spent in stage 0, 1, 3, 4
_____eased time spent in REM sleep (_____eased number of cycles of REM sleep)
____eased total sleep time (largely by increasing the time spent in stage ___)
Decr; Decr
Decr; Decr
incr; Incr
2
Respiration-Hypnotic doses of benzodiazepines are (with or without?) effect on respiration in normal subjects
CVS-In preanesthetic doses, all benzodiazepines ____ease blood pressure and ____ease heart rate
without
decr
incr
PHARMACOKINETICS of benzodiazepines
A (short or long?) elimination half-life is desirable for hypnotics, although this carries the drawback of increased _____________ and ____________ after drug discontinuation.
Most of the BZDs are metabolized in the ____ to produce (active or inactive ?) products (thus long duration of action).
After metabolism these are ______ and are excreted via ________.
Short
abuse liability and severity of withdrawal
liver; active
conjugated; kidney
ADVERSE EFFECTS of BZDs
Light-headedness, Fatigue
____eased reaction time
Motor _______
_______,__________ amnesia
Incr; incoordination
Confusion, Antero-grade
Adverse effect of BZDs
________ appears to be affected less than ___________.
All of these effects can greatly impair _______ and other psychomotor skills, especially if combined with ———-.
Cognition
motor performance
driving; ethanol
FLUMAZENIL: A BENZODIAZEPINE RECEPTOR ANTAGONIST
competitively antagonism
Flumazenil antagonizes both the electrophysiological and behavioral effects of agonist and inverse-agonist ___________ and _________.
Flumazenil is available only for ________ administration.
benzodiazepines and β -carbolines
intravenous
FLUMAZENIL: A BENZODIAZEPINE RECEPTOR ANTAGONIST
On intravenous administration, flumazenil is eliminated almost entirely by hepatic metabolism to (active or inactive?) products with a t1/2 of ~________ ; the duration of clinical effects usually is only _________
Inactive
1 hour
30-60 minutes.
FLUMAZENIL: A BENZODIAZEPINE RECEPTOR ANTAGONIST
PRIMARY INDICATIONS FOR THE USE OF FLUMAZENIL ARE:-
Management of suspected ________________
Reversal of _______ effects produced by benzodiazepines administered
The administration of _________ injections is preferred to ———— injection.
benzodiazepine overdose.
sedative
a series of small
a single bolus
Novel Benzodiazepine Receptor Agonists
Z compounds
________,________,_________,____________
structurally (related or unrelated?) to each other and to benzodiazepines
zolpidem , zaleplon , zopiclone and eszopiclone
Unrelated
Novel Benzodiazepine Receptor Agonists
Z compounds
therapeutic efficacy as hypnotics is due to agonist effects on the ______ site of the _____ receptor
benzodiazepine; GABAA
Novel Benzodiazepine Receptor Agonists
Z compounds
Compared to benzodiazepines, Z compounds are
-(more or less?) effective as anticonvulsants or muscle relaxants
-which may be related to their relative selectivity for ______ receptors containing the ____ subunit.
Less
GABAA
α1
The clinical presentation of overdose with Z compounds is similar to that of benzodiazepine overdose and can be treated with the ____________________
benzodiazepine antagonist flumazenil.
Zaleplon and zolpidem are effective in relieving sleep-onset ______. Both drugs have been approved by the FDA for use for up to __________ at a time.
________ and _______ have sustained hypnotic efficacy without occurrence of rebound insomnia on abrupt discontinuation.
insomnia
7-10 days
Zaleplon and zolpidem
RAMELTEON
Synthetic tricyclic analog of _________.
It was approved for the treatment of _______, specifically ________ difficulties.
MELATONIN; insomnia
sleep onset
RAMELTEON
MECHANISM OF ACTION of melatonin
Melatonin levels in the _______ nucleus rise and fall in a circadian fashion
concentrations increasing in the _____ as an individual prepares for sleep, and then reaching a ______ and ultimately ____easing as the night progresses.
suprachiastmatic
evening; plateau
decr
MELATONIN CONGENERS
Mechanism of Action
Two GPCRs for melatonin, MT1 and MT2, are found in the suprachiasmatic nucleus, each playing a different role in sleep.
RAMELTEON binds to both MT1 and MT2 receptors with (low or high?) affinity.
Binding of Melatonin to MT1 receptors promotes _____________
Binding of Melatonin to MT2 receptors _————- of the circadian system.
High; the onset of sleep.
shifts the timing
RAMELTEON is efficacious in combating _____________ insomnia
both transient and chronic
Management of Patients after Long-Term Treatment with Hypnotic Agents
If a benzodiazepine has been used regularly for >2 weeks, it should be ______ rather than ____________.
In some patients on hypnotics with a short t1/2, it is easier to switch first to a hypnotic with a ______ and then to _______.
The onset of withdrawal symptoms from medications with a long t1/2 may be _____.
Consequently, the patient should be warned about the symptoms associated with withdrawal effects.
tapered; discontinued abruptly
long t1/2(taper; delayed
Atypical Anxiolytics
List 3
Buspiron
Ipsapirone Gepirone
Buspirone relieves ______ without causing marked ______, hypnotic, or euphoric effects.
- no _______ or _________ properties.
Buspirone does not interact directly with ________ systems.
anxiety; sedative
anticonvulsant or muscle relaxant
GABAergic
Anxiolytic effects of buspirone is by acting as a _________ at brain ________ receptors.
partial agonist
5-HT1A
Buspirone
the anxiolytic effects of buspirone may take more than ______
unsuitable for management of ______ states
____ rebound anxiety or withdrawal signs on abrupt discontinuance
a week; acute anxiety
no
Buspirone
The drug is effective in blocking the acute withdrawal syndrome resulting from abrupt cessation of use of benzodiazepines or other sedative-hypnotics
F
The drug is not effective in blocking the acute withdrawal syndrome resulting from abrupt cessation of use of benzodiazepines or other sedative-hypnotics
Buspirone has (minimal or maximal?) abuse liability
The drug is used in _______ states but is less effective in _____ disorders
Minimal
generalized anxiety
panic
True statement about zolpidem:
A. Relieve sleep onset insomnia
B. Cause profound rebound insomnia
C. Cause profound REM suppression
D. Has strong anticonvulsant effect
A
Which is NOT true about Flumazenil?
A. Acts on GABAA receptor
B. Specific antagonist of benzodiazepine C. Given intravenously
D. May be used in barbiturate poisoning
D
Administration of barbiturate is contraindicated in:
A. Kernicterus
B. Anxiety
C. Epilepsy
D. Acute Intermittant porphyria
D
Benzodiazepines act by:
A. Activating GABAA receptors directly
B. Modulating the effects of GABA on GABAA receptors
C. Antagonistic effect on GABAA receptors D. GABA mimetic effect
B
Benzodiazepine antagonist is:
A. Naloxone
B. Zolpidem
C. Nalorphine
D. Flumazenil
D
Beta carboline at benzodiazepine receptor act as:
A. Agonist
B. Inverse agonist
C. Antagonist
D. Partial agonist
B
True statement about effect of bezodiazepines on sleep is:
A. Time spent in stage 2 is decreased
B. Time spent in stages 1, 3 and 4 is increased
C. Shortening of REM sleep
D. Increase sleep latency
C
An ideal hypnotic drug should NOT have:
A. rapid onset of action
B. sustained effect throughout the night
C. without any residual effect in the following morning
D. increase in sleep latency
D
Which one of the following effects is NOT seen with barbiturates?
A. Analgesic
B. Anticonvulsant
C. Induction and maintenance of anaesthesia
D. Sedation
A
Sleep promoting effect of ramelteon is mediated by receptor:
A. GABAA receptor
B. Opiate receptors
C. GABAB receptor
D. Melatonin receptors MT1 and MT2
D
