Sedative and Hypnotics Flashcards by Iseoluwa Ojo

SEDATIVES – reduce ______ and exert a ______ effect

HYPNOTICS - produces ______ and facilitates the onset and maintenance of _________________

anxiety; calming

drowsiness ;a state of sleep.

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SEDATIVE/HYPNOTICS ANXIOLYTICS

Major therapeutic use is to relief _______(_______) or induce _______(_______)

anxiety (anxiolytics)

sleep (hypnotics).

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Hypnotic effects can be achieved with most anxiolytic drugs

T/F

just by increasing the dose.

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The distinction between a “pathological” and “normal” state of anxiety is easy to draw

T/F

hard

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anxiolytics are among the most prescribed substances worldwide.

T/F

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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

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Pathological Anxiety

Generalized anxiety disorder (GAD): People suffering from GAD have general symptoms of ————, autonomic ______, etc. for at least ________

motor tension; hyperactivity

one month.

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Pathological Anxiety

Phobic anxiety:
Simple phobias. Agoraphobia, fear of ______, etc. Social phobias.

animals

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Pathological Anxiety

Panic disorders: Characterized by (acute or chronic ?) attacks of ___ as compared to the (acute or chronic?) presentation of GAD.

Acute ; fear

Chronic

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Pathological Anxiety

Obsessive-compulsive behaviors: These patients show _________(obsessions) and ___________ (compulsions).

repetitive ideas

behaviors

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Causes of Anxiety

______
_____-induced
Drug ______

Medical
Drug-induced
Drug withdrawal

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Causes of Anxiety
1). Medical:
Respiratory Endocrine Cardiovascular Metabolic Neurologic.

T/F

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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.

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Causes of Anxiety

Drug Withdrawal:
•____,________,_________, other ______,______

BDZs, narcotics, BARBs

sedatives, alcohol.

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Strategy for treatment of anxiety

_______ anxiety without causing ________.

Reduce

sedation

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Anxiolytics

Barbiturates e.g. ________,______,______,_____,_______

Benzodiazepines e.g._______ (Valium), _____ (Versed),_______ (Klonopin) ; ________ (Ormodon), ________ (Rohypnol)

Glutethimide : ____________

Methohexitone, Phenobarbital, Pentabarbital, Thiopentone,Thiamylal

Diazepam; Midazolam; Clonazepam

Nitrazepam; Flunitrazepam

Piperidinediones

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Anxiolytics

Meprobamate : __________ _______

Alcohols : ______,_________,_________

Buspirone : _________

Zolpidem : _____________

Zaleplon : __________

Propanediol carbamates

Ethanol, Chloral hydrate, Paraldehyde

Azaspirodecanedione; Imidazopyridine

Pyrazolopyrimidine

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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

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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

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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

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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

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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

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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

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Benzodiazepines

Treatment : anxiety

It has (more or less?) side effects, dependence

It is (more or less?) effective

Less

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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 1. Depression of CNS: At _____ doses, the barbiturates produce _____ (——- effect, reducing ______). 2. Respiratory depression: Barbiturates suppress the ______ and _______ response to CO2, and overdosage is followed by ———- and _________ 3. 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

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

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

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

Administration of barbiturate is contraindicated in: A. Kernicterus B. Anxiety C. Epilepsy D. Acute Intermittant porphyria

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

Benzodiazepine antagonist is: A. Naloxone B. Zolpidem C. Nalorphine D. Flumazenil

Beta carboline at benzodiazepine receptor act as: A. Agonist B. Inverse agonist C. Antagonist D. Partial agonist

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

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

Which one of the following effects is NOT seen with barbiturates? A. Analgesic B. Anticonvulsant C. Induction and maintenance of anaesthesia D. Sedation

Sleep promoting effect of ramelteon is mediated by receptor: A. GABAA receptor B. Opiate receptors C. GABAB receptor D. Melatonin receptors MT1 and MT2