Miscellaneous Quiz / Sedative Hyponotic Drugs

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Can you name the Sedative Hyponotic Drugs?

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Drug Use: Induction and/or maintenance of anesthesia, preop sedation, emergency management of seizures
Drugs effects: decrease in firing rate of specific neurons that contain the BZ1 subtype of the GABA-A channel
Zaleplon class
Chlordiazepoxide class
Drug use: delirium tremens in hospitalized pts
Drug use: Decreases sleep latency -- induction of sleep, BDZ1Subclass specific. Used in those who have difficulty falling asleep or going back to sleep
Drug SE: N/V & rash. Idiosyncratic excitement, fever, thrombocytopenia
Drug use: sedation in children
Drug P-kinetics: oral, t1/2 10-70
Clonazepam class
Eszopiclone class
Drug SE: Agitation, confusion, dizziness, and nausea, also induce seizure in BDZ dependent pts, abstinence syndrome in BDZ dependent pts.
Class effects: Dose dependent decrease in firing rate of critical neurons throughout the brain. GABAergic activation --> sedation, decreased anxiety, and pharmacologic hypnosis
Drug P-kinetics: Intermediate-acting: Peak levels 2-3 hrs, 1/2 life10-40, slow oral absorption, no active metabolites, non-liver metabolism
Class P-kinetics cont. Excretion - mostly glucuronides in the urine. Factors affecting 'biodisposition' - liver function (increased or decreased microsomal enzymes); pharmacokineti
Class SE: Therapeutic doses: persistent drowsiness, residual effects inc. vertigo, n/v, or diarrhea. Paradoxical excitement. Enhancement of porphyrin synthesis (contraindicated in
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
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
Oxazepam class
Drug use: Anxiety disorders, seizure disorders, ETOH withdrawal
Hydroxyzine class
Drug P-kinetics: Short-acting: Peak levels 1 hr, 1/2 life 2-3 hrs, rapid onset (most rapid); short DOA
Alprazolam class
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 effect: Melatonin receptors may be involved in circadian rhythms & sleep-wake cycles.
Estazolam class
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 MOA: antihistamine
Benzodiazepines safe to use in liver failure pts are those metabolized
Drug use: Preanesthetic & intraoperative med.
Drug MOA: unclear (GABA-a binding)
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 SE: acidosis, hepatitis, bleeding gastritis & nephrosis
Drug interactions: enhances hepatic metabolism of other drugs like oral anticoagulants
Drug Use: Anxiety disorders, status epilepticus & seizure disorders including drug induced, skeletal muscle relaxation, anesthetic premedication, ETOH withdrawal
Drug P-kinetics: oral, t1/2 10-20 hrs, redistribution shortens duration
Drug use: 'Chronic insomnia. Note: does not interact with GABA receptors. Reduces sleep latency with little effect on sleep architecture. '
Drug P-kinetics: Intermediate-acting: t1/2 18 to 28 hours
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
Butabarbital sodium class
Ethchlorvynol class
Drug P-kinetics: oral, rectal, t1/2 5-10 hrs, converted to trichloroethane (active metabolite)
Ramelteon class
Flurazepam class
Drug P-kinetics: Short-acting: Peak levels 1-2 hrs, 1/2 life 12-15 hours, rapid oral absorption, no active metabolites
Drug effect: Reverses effects of BZDs zolpidem, zaleplon, eszopiclone
Flumazenil class
Drug Use: Insomnia, preop sedation, emergency mgmt of seizures
Aprobarbital class
Drug MOA: unclear
Drug Use: Insomnia, preop sedation
Drug P-kinetics: Long-acting: peak levels 2 hrs, 1/2 life 39 hrs, Active metabolites with long 1/2 life
Thiopental class
Triazolam class
Meprobamate class
Drug Use: Seizure disorders, adjunctive tx in acute mania & certain movement disorders
Temazepam class
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 P-kinetics: Short-acting: t1/2 2hrs, most rapidly metabolized benzo. For anesthesia, not active metabolites
Drug P-kinetics: effects may take weeks to establish, extensive first pass, active metabolites, t1/2 2-4 hrs
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: 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
Drug Use: Anxiety disorders, management of ETOH withdrawal, anesthetic premedication
Drug use: insomnia & anxiety
Diazepam class
Drug P-kinetics: oral, IM, IV, t1/2 15-50 hrs, only Na+ salt for parenteral. Short acting (3-8 hours).
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
Lorazepam class
Drug use: sedation
Midazolam class
Drug Use: Insomnia & anxiety disorders
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 Use: Barbituate for insomnia
Drug P-kinetics: oral, t1/2 2-3 hrs
Drug use: Anxiety disorders, preanesthetic med, seizure disorders, insomnia
Paraldehyde class
Drug MOA: Agonist of melatonin receptors MT1 and MT2 (suprachiasmatic nuclei)
Clinical use: BDZ OD
Drug P-kinetics: oral, t1/2 14-34 hrs, excreted unchanged
Zolpidem class
Drug P-kinetics: oral, IM, IV, t1/2 15-50 hrs. Long acting (1-2 days)
Drug P-kinetics: IV, Rectal, sodium salt, t1/2 8-10 hrs. Ultra short acting (20 minutes)
Side effects cont: Paradoxical psych effects: disinhibitory reactions, delirium, aggression, violence, garrulousness, anxiety, irritability, paranoia, suicidal ideation, & physiolo
Drug SE: dizziness, n/v, hypotension & facial numbness, Hangover. marked excitement w/ pain. Contraindicated in pts w/ intermittent porphyria
Quazepam class
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: Liver CYP1A2 & CYP2C9
Mephobarbital class
Drug SE: Unlike BDZs it has NO hypnotic, anticonvulsant or muscle relaxant effects. Less psychomotor impairment than diazepam. It may cause tachycardia, palpitations, nervousness,
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
Chloral hydrate class
Drug P-kinetics: oral, t1/2 35-50 hrs, redistribution reduces duration
Drug P-kinetics: oral, IM IV, t1/2 10-40 hrs, Na+ salts only for parenteral admin. Short acting (3-8 hours).
Drugs interactions: inducers of cyt P450 decrease half life & inhibitors increase half life
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 Use: Seizure disorders (second line), daytime sedation
Drug use: Decreases sleep latency, increases NREM, decreaseds REM (high doses) -- insomnia (efficacy similar to that of hypnotic benzodiazepines), BDZ1Subclass specific. Used to in
Clorazepate class
Class drug interactions: Additive effects with other sedative-hypnotics (ethanol, many general anesthetics, many drugs to tx insomnia, benzodiazepines, barbituates, opiod analgesic
Pentobarbital class
Drug use: insomnia (efficacy similar to that of hypnotic benzodiazepines), BDZ1Subclass specific. Decreases sleep latency and REM -- induces & maintains sleep.
Phenobarbital class
Drug SE: acute use: epigastric distress, n/v (taste bad). Hangover symptoms. Hepatic damage (chronic use), severe withdrawal syndrome
Buspirone class
Drug P-kinetics: oral, t1/2 6-17 hrs
Drug Effects: unclear, anxiolytic w/o sedative side effects
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 1-2 h, 1/2 life 40-100 hrs. active metabolites w/ 1/2 lives
Drug Effects: similar to barbituates
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 Use: generalized anxiety disorders (non-acute)
Drug SE: Dizziness, somnolence, fatigue, endocrine changes (↓testosterone, ↑prolactin)
Drug use: anxiety disorders, muscle relaxant
Drug Use: Seizure disorders, SE, daytime sedation
Drug MOA: may act as a partial agonist of the 5-HT 1A (maybe D2) receptor. Metabolite has α-2 activity.
Drug interactions: rifampin (inducer of CYP3A4) may decrease t1/2, inhibitors of CYP3A4 may increase t1/2
Drug P-kinetics: oral, IM, IV, rectal, t1/2 15-40 hrs, only sodium salt available. Short acting (3-8 hours).
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 SE: OD can cause severe hypotension, resp depression & death
Amobarbital class
Drug use: Anxiety disorders, ETOH withdrawal
Class Drug interactions: Severe depression in combo w/ other CNS depressants (like ETOH, opiods, anticonvulsants, phenothiazines, & to a lesser degree antihistamines, antihypertens
Drug P-kinetics: Intermediate-acting: Peak levels 2-4 hrs, 1/2 life 10-20 hrs. no active metabolites, non-liver metabolism
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
Drug interactions: inhibitors of CYP 1A2 (ciporfloxacin, fluvoxamine, tacrine, zileuton) & CYP2C9 (fluconazole)
Drug Use: BDZ for Insomnia
Drug use: DOC for anxiety disorders & agoraphobia
Secobarbital class
Drug P-kinetics Intermediate-acting: Peak levels 1-6 hrs, 1/2 life 10-20 hrs, no active metabolites, non-liver metabolism
Class MOA cont.: No effect of the GABA-A channel alone. Will not produce profound anesthesia
Drug P-kinetic: Intermediate-acting: Peak levels 2 hrs, 1/2 life 10-24 hrs, no active metabolites

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