Miscellaneous Quiz / Sedative Hyponotic Drugs

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Can you name the Sedative Hyponotic Drugs?

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Amobarbital class
Drug use: Decreases sleep latency -- induction of sleep, BDZ1Subclass specific. Used in those who have difficulty falling asleep or going back to sleep
Secobarbital class
Class effects: Dose dependent decrease in firing rate of critical neurons throughout the brain. GABAergic activation leads to a succession of effects that include sedation, reduced
Drug interactions: rifampin (inducer of CYP3A4) may decrease t1/2, inhibitors of CYP3A4 may increase t1/2
Meprobamate class
Drug use: Anxiety disorders, seizure disorders, ETOH withdrawal
Drug P-kinetics: Intermediate-acting: Peak levels 2-4 hrs, 1/2 life 10-20 hrs. no active metabolites, non-liver metabolism
Drug interactions: inhibitors of CYP 1A2 (ciporfloxacin, fluvoxamine, tacrine, zileuton) & CYP2C9 (fluconazole)
Ethchlorvynol class
Clinical use: BDZ OD
Drug P-kinetics: oral, t1/2 35-50 hrs, redistribution reduces duration
Drug SE: dizziness, n/v, hypotension & facial numbness, Hangover. marked excitement w/ pain. Contraindicated in pts w/ intermittent porphyria
Eszopiclone class
Drug P-kinetics: t1/2 4-10 hrs, oral (disagreeable taste) or rectal damages tissue, IV, 75% metabolized in liver 25% exhaled
Drug P-kinetics: Long-acting: peak levels 2 hrs, 1/2 life 39 hrs, Active metabolites with long 1/2 life
Drug P-kinetics: oral, t1/2 10-70
Drug use: sedation
Aprobarbital class
Class P-kinetics cont. Excretion - mostly glucuronides in the urine. Factors affecting 'biodisposition' - liver function (increased or decreased microsomal enzymes); pharmacokineti
Buspirone class
Drug Use: Seizure disorders, SE, daytime sedation
Clorazepate class
Drug P-kinetics: oral, rectal, t1/2 5-10 hrs, converted to trichloroethane (active metabolite)
Drug MOA: antihistamine
Drug Use: Insomnia & anxiety disorders
Drug SE: Unlike BDZs it has NO hypnotic, anticonvulsant or muscle relaxant effects. Less psychomotor impairment than diazepam. It may cause tachycardia, palpitations, nervousness,
Hydroxyzine class
Drug P-kinetics: oral, IM IV, t1/2 10-40 hrs, Na+ salts only for parenteral admin. Short acting (3-8 hours).
Drug MOA: may act as a partial agonist of the 5-HT 1A (maybe D2) receptor. Metabolite has α-2 activity.
Drug use: 'Chronic insomnia. Note: does not interact with GABA receptors. Reduces sleep latency with little effect on sleep architecture. '
Class P-kinetics cont.: Bound to plasma proteins (lipophilic molecules more):[CSF] = free drug in plasma. Volume of distribution increase in elderly: decreased water volume + incre
Drug Use: Insomnia, preop sedation, emergency mgmt of seizures
Drug use: Decreases sleep latency, increases NREM, decreaseds REM (high doses) -- insomnia (efficacy similar to that of hypnotic benzodiazepines), BDZ1Subclass specific. Used to in
Drug Use: Barbituate for insomnia
Drug SE: acidosis, hepatitis, bleeding gastritis & nephrosis
Quazepam class
Drug P-kinetics: Short-acting: t1/2 2hrs, most rapidly metabolized benzo. For anesthesia, not active metabolites
Diazepam class
Class P-kinetics: All absorbed well orally (except one which is converted to an active metabolite), in the stomach. IM variable bioavailability.Distribution into & out of (redistri
Drug P-kinetics: effects may take weeks to establish, extensive first pass, active metabolites, t1/2 2-4 hrs
Drug P-kinetics: Long-acting: Peak levels 1-2 h, 1/2 life 40-100 hrs. active metabolites w/ 1/2 lives
Pentobarbital class
Drugs MOA: Selectively binds to the BZ1 (omega1)-GABA-A channel separate from GABA binding site & increases frequency of opening of GABA bound GABA-A channels resulting in & increa
Class P-kinetics cont: Most are metabolized to H2O-soluble derivatives in the liver --> excretion in urine. Parent drug T 1/2 does not always effect DOA. Several metabolites are ac
Drug SE: Agitation, confusion, dizziness, and nausea, also induce seizure in BDZ dependent pts, abstinence syndrome in BDZ dependent pts.
Drug Effects: unclear, anxiolytic w/o sedative side effects
Drug Effects: similar to barbituates
Alprazolam class
Drug Use: Insomnia, preop sedation
Drug SE: Dizziness, somnolence, fatigue, endocrine changes (↓testosterone, ↑prolactin)
Drugs SE: similar to diazepam but w/ minimal muscle relaxing & anticonvulsant effects as well as less development of tolerance & dependence. Reduced alteration in normal sleep arch
Drug P-kinetics: oral, IM, IV, t1/2 15-50 hrs. Long acting (1-2 days)
Drug Use: Anxiety disorders, status epilepticus & seizure disorders including drug induced, skeletal muscle relaxation, anesthetic premedication, ETOH withdrawal
Side effects: Persistent effects during waking hours. Resp: hypnotic doses = similar to resp. during sleep (unless with COPD, OSA, impaired liver function, or child); preanesthetic
Drug P-kinetics Intermediate-acting: Peak levels 1-6 hrs, 1/2 life 10-20 hrs, no active metabolites, non-liver metabolism
Drug P-kinetics: oral, IM, IV, t1/2 15-50 hrs, only Na+ salt for parenteral. Short acting (3-8 hours).
Phenobarbital class
Temazepam class
Drug use: Anxiety disorders, preanesthetic med, seizure disorders, insomnia
Lorazepam class
Drug use: anxiety disorders, muscle relaxant
Drug use: insomnia & anxiety
Drug P-kinetics: Long-acting: peak levels in 1-2 hrs. 1/2 life 20-60 hrs, active metabolites with long t1/2s; erratic bioavailability from IM injection
Drug P-kinetics: Short-acting: Peak levels 1-2 hrs, 1/2 life 12-15 hours, rapid oral absorption, no active metabolites
Class P-kinetics: Rapid oral absorption (form of Na+ salts). IV: induction of anesthesia & SE). Plasma PRO binding is extensive for both groups. Distributed widely, crosses placent
Drug MOA: unclear
Class P-kinetics cont: Cumulative effects at multiple dosing. Hepatic oxidation (except one drug) of groups attached at C5 --> pharmacokinetic or metabolic tolerance: repeated dose
Class drug interactions: Additive effects with other sedative-hypnotics (ethanol, many general anesthetics, many drugs to tx insomnia, benzodiazepines, barbituates, opiod analgesic
Drug P-kinetics: Liver CYP1A2 & CYP2C9
Drug P-kinetics: oral, t1/2 2-3 hrs
Drug use: delirium tremens in hospitalized pts
Drug P-kinetics: oral, t1/2 14-34 hrs, excreted unchanged
Butabarbital sodium class
Drug use: insomnia (efficacy similar to that of hypnotic benzodiazepines), BDZ1Subclass specific. Decreases sleep latency and REM -- induces & maintains sleep.
Midazolam class
Drug Use: Induction and/or maintenance of anesthesia, preop sedation, emergency management of seizures
Flumazenil class
Drug effect: Melatonin receptors may be involved in circadian rhythms & sleep-wake cycles.
Zaleplon class
Drug P-kinetics: intermediate-acting: Peak levels 1-2 hrs (nordiazepam), 1/2 life 2-3 hrs. Prodrug; hydrolyzed to active form in stomach. Active metabolites w/ long t1/2s
Clonazepam class
Estazolam class
Ramelteon class
Drug P-kinetic: Intermediate-acting: Peak levels 2 hrs, 1/2 life 10-24 hrs, no active metabolites
Drug P-kinetics: oral, t1/2 10-20 hrs, redistribution shortens duration
Chlordiazepoxide class
Drugs interactions: inducers of cyt P450 decrease half life & inhibitors increase half life
Drug MOA: Agonist of melatonin receptors MT1 and MT2 (suprachiasmatic nuclei)
Drug use: sedation in children
Drug Use: Seizure disorders (second line), daytime sedation
Drugs effects: decrease in firing rate of specific neurons that contain the BZ1 subtype of the GABA-A channel
Drug P-kinetics: oral, t1/2 6-17 hrs
Drug effect: Reverses effects of BZDs zolpidem, zaleplon, eszopiclone
Thiopental class
Class SE: Therapeutic doses: persistent drowsiness, residual effects inc. vertigo, n/v, or diarrhea. Paradoxical excitement. Enhancement of porphyrin synthesis (contraindicated in
Drug interactions: enhances hepatic metabolism of other drugs like oral anticoagulants
Class MOA: Dose dependent effects: Low doses--binds to GABA-A channels separate from GABA binding & BDZ binding site & prolongs duration of opening of GABA bound GABA-A channels --
Drug P-kinetics: Short-duration: rapid first pass effect, IV admin. Very short t1/2 0.7-1.3 hrs (fast hepatic clearance). Rapid IV action. Repeated injections often necessary since
Drug P-kinetics: IV, Rectal, sodium salt, t1/2 8-10 hrs. Ultra short acting (20 minutes)
Class MOA: Binds to GABA-A channels separate from GABA binding site, allosterically increases the ability of GABA to bind its GABA binding site --> increased frequency of opening o
Drug SE: acute use: epigastric distress, n/v (taste bad). Hangover symptoms. Hepatic damage (chronic use), severe withdrawal syndrome
Benzodiazepines safe to use in liver failure pts are those metabolized
Paraldehyde class
Chloral hydrate class
Oxazepam class
Drug SE: OD can cause severe hypotension, resp depression & death
Drug MOA: Competitively inhibits binding of BDZs on the GABA-a receptor at the BDZ binding site (specific to BDZs, does not block barbituates)
Drug Use: Seizure disorders, adjunctive tx in acute mania & certain movement disorders
Class Drug interactions: Severe depression in combo w/ other CNS depressants (like ETOH, opiods, anticonvulsants, phenothiazines, & to a lesser degree antihistamines, antihypertens
Class effects: Dose dependent decrease in firing rate of critical neurons throughout the brain. GABAergic activation --> sedation, decreased anxiety, and pharmacologic hypnosis
Class Pharmacodynamics: GABA-A Receptor: pentamer of α, β, and γ subunits. GABA binds at α/β, benzodiazepines bind on γ. Cl- current hyperpolarizing (inhibitory). Sedative hy
Drug Use: Anxiety disorders, management of ETOH withdrawal, anesthetic premedication
Drug use: Preanesthetic & intraoperative med.
Side effects cont: Paradoxical psych effects: disinhibitory reactions, delirium, aggression, violence, garrulousness, anxiety, irritability, paranoia, suicidal ideation, & physiolo
Drug Use: BDZ for Insomnia
Drug P-kinetics: Long-acting: Peak levels in 2-4 hrs. 1/2 life 15-40 hrs, otherwise similar to diazepam, active metabolites with long t1/2s
Drug P-kinetics: Intermediate-acting: Peak levels 2-3 hrs, 1/2 life10-40, slow oral absorption, no active metabolites, non-liver metabolism
Class MOA cont.: No effect of the GABA-A channel alone. Will not produce profound anesthesia
Drug P-kinetics: oral, IM, IV, rectal, t1/2 15-40 hrs, only sodium salt available. Short acting (3-8 hours).
Drug Use: generalized anxiety disorders (non-acute)
Zolpidem class
Mephobarbital class
Drug SE: N/V & rash. Idiosyncratic excitement, fever, thrombocytopenia
Flurazepam class
Drug use: Anxiety disorders, ETOH withdrawal
Triazolam class
Drug MOA: unclear (GABA-a binding)
Drug P-kinetics: Intermediate-acting: t1/2 18 to 28 hours
Drug use: DOC for anxiety disorders & agoraphobia
Drug P-kinetics: Short-acting: Peak levels 1 hr, 1/2 life 2-3 hrs, rapid onset (most rapid); short DOA

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