benzodiazepine

Therapeutic effects: anxiolytic effect (relieve anxiety), sedative-hypnotic effect, anticonvulsant effect, muscle relaxation

MoA: enhance inhibitory GABA-A receptors (associated with opening chloride channels), this decreases neuronal firing. Needs GABA also to open channel

ADR: sedation, drowsiness, lightheadedness, mental clouding, confusion, psycomotor impairment, slurred speech, ataxia, memory impairment-anterograde amnesia, disinhibition of suppressed behavior (prounounced in elderly pt), euphoria, hangover, rebound anxiety, respiratory depression, tolerance (partiularly sedative/hypnotic), dependence, possible teratogenicity (avoid during pregnancy, esp 1st trimester)

Regarding sleep: decreased sleep latency (time to fall asleep), decrease in duration of REM sleep

ADME: metabolized by hepatic microsomal enzyme system, do not induce drug metabolizing enzymes

USE: anxiety, sedative/hypnotic, acute alcohol withdrawal,  convulsive sz, status epilepticus, skeletal muscle spasm relief, pre-anesthetic meds, induction of anesthesia

Drug interactions: additvie with alcohol/CNS depressants, cross tolerance/dependence

benzodiazepine antagonist (competitive) used to reverse CNS depressant effects of benzodiaepines (esp. surgical anesthesia, or benzodiazepine poisoning)

ADR: trigger sz (esp in pt with epilepsy or already currently dependent), ppt s/sx in addicted individuals

intermediate/ short acting barbiturate

USE: sedative-hypnotic mainly

MoA: facilitating action of GABA at GABA-A receptor-chloride channel (interact on site distinct from GABA/benzodiazepine site), can cause opening of Cl channel without GABA

Effects: sediatve/hypnotic, anxiolytic (suppress REM more than benzodiazepines, more likely to produce hangover), anesthetic effect (surgical anesthesia), depression of respiration, anticonvulsants, euphoria

ADME: cross BBB, induces microsomal enzymes, metabolized by liver

ADR: sedation, drowsiness, lethargy, confusion, ataxy, hanover, too much respiratory depression, disinhibition of suppressed havior, nausea/GI upset, allergic reactions

Drug interactions: additive with CNS depressants

Tendency of abuse. 

ultra short acting barbiturate

USE: induction of surgical anesthesia

MoA: facilitating action of GABA at GABA-A receptor-chloride channel (interact on site distinct from GABA/benzodiazepine site), can cause opening of Cl channel without GABA

Effects: sediatve/hypnotic, anxiolytic (suppress REM more than benzodiazepines, more likely to produce hangover), anesthetic effect (surgical anesthesia), depression of respiration, anticonvulsants, euphoria

ADME: cross BBB, induces microsomal enzymes, metabolized by liver

ADR: sedation, drowsiness, lethargy, confusion, ataxy, hanover, too much respiratory depression, disinhibition of suppressed havior, nausea/GI upset, allergic reactions

Drug interactions: additive with CNS depressants

Tendency of abuse. 

centrally acting muscle relaxant

MoA: related to TCAs, acts at brainstem to inhibit gamma and alpha motor systems

USE: muscle spasms of local origin

ADR: CNS depression, anticholinergic effects

centrally acting muscle relaxant

generally similar to cyclobenzapine

centrally acting muscle relaxant

MoA: alpha-2 adrenergic agonist

USE: skeletal muscle relaxant

ADR: hypotension, very sedating

miscellaneous anxiolytics and sedative hypnotices (non-barbiturates, non-benzodiazepines)

ADME: passive diffusion, oxidized in liver, follows zero order kinetics (metabolism independent of time/concentration), goes through alcohol dehydrogenase pathway (ethanol to acetaldehyde in the liver, acetaldehyde is toxic), microsomal ethanol oxidizing system (MEOS, high doses/chronic: induces which may lead to alcohol tolerance, raises possibility of numerous drug interactions), aldehyde metabolism (acetaldehyde to aceteate to water and carbon dioxide through aldehyde dehydrogenase) 

Effects: depression of CNS (release inhibitions, anxiolytic, sedation, hypnosis, anesthesia, respiratory depression, coma, death), anterograde amenesia, reduces  sleep latency, reduces time spent in REM, decreases overall quality of sleep. Hangovers from: acetaldehyde buildup, alcohol analogs in beverages, meatgic changes/dehydration, pharmcodynamic changes in the brain

MoA: disordering of membrane lipids, NT/receptor/channel/signal transduction system changes, enhance effects of GABA at receptor chlroide channel

Other effects: CV (flushing), inhibits secretion of ADH (diuretic effect), inc conce of HDL, decrease conc of LDL, stimulates gastric acid secretion, may stimulate appetite (large amounts supppress), chronic use: hepatic function increased initially, then depletes, accumulation of fat in the liver: hepatitis/cirrhosis, teratogenic (fetal alcohol syndrome), anemia, folic acid deficiency, electrolyte imbalances, endocrine disturbances, increased risk of cancer, organic brain dysfunction

Tolerance: pharmacodynamic, cross tolerance

Managing withdrawal: prevent sz, delirium, arrhythmias, benzodiazepines suppress s/sx

miscellaneous anxiolytics and sedative hypnotices (non-barbiturates, non-benzodiazepines)

USE: alleviates mild-moderate anxiety with minimal sedative-hypnotic, muscle relxant, or respiratory depressant effects, low abuse potential (drug of choice for tx o anxiety for pt with history of alcohol/sedative abuse)

MoA: does not act through GABA mecchanisms, evidence suggests may act as partial agonist at serotonin (5-HT1A) receptors

ADR: dizziness, HA, irritability, tachycardia,n/d, high doses: CNS depression

miscellaneous anxiolytics and sedative hypnotices (non-barbiturates, non-benzodiazepines)

USE: newer sedative-hypnotic, less anxiolytic, anticonvulsant, muscle relaxant than benzodiazepines

MoA: enhances effects of GABA at benzodiazepeine receptor (omega-1 site)

ADME: metabolized by liver, long acting

ADR: CNS depression, abuse/dependence less likely than benzodiazepine

miscellaneous anxiolytics and sedative hypnotices (non-barbiturates, non-benzodiazepines)

USE: newer sedative-hypnotic, less anxiolytic, anticonvulsant, muscle relaxant than benzodiazepines

MoA: enhances effects of GABA at benzodiazepeine receptor (omega-1 site)

ADME: metabolized by liver, shorter acting

ADR: CNS depression, abuse/dependence less likely than benzodiazepine

miscellaneous anxiolytics and sedative hypnotices (non-barbiturates, non-benzodiazepines)

USE: newer sedative-hypnotic, less anxiolytic, anticonvulsant, muscle relaxant than benzodiazepines

MoA: enhances effects of GABA at benzodiazepeine receptor (omega-1 site)

ADME: metabolized by liver, long acting

ADR: CNS depression, abuse/dependence less likely than benzodiazepine

miscellaneous anxiolytics and sedative hypnotices (non-barbiturates, non-benzodiazepines)

MoA: agonist at melatonin receptors

USE: quantitatively different from other sedative/hypnotics

little potential for abuse/dependence, use with caution in pt with impaired hepatic function, may inc levels of prolactin, decrease levels of testosterone

miscellaneous anxiolytics and sedative hypnotices (non-barbiturates, non-benzodiazepines)

MoA: hormone produced by pineal gland

USE: OTC sleep aid, may help with jet lag (circadian sleep problems), qualitatively different from other sedative/hypnotics 

tx alcoholism

USE: decrease craving for alcohol (maintain abstinence)

MoA: unclear, may involve both glutamate, GABA receptors, block NMDA receptors, partially stimulate GABA-A receptors

ADR:  diarrhea, anxiety, insomnia, depression, less potential of hepatotoxicity (may be most effective when combined with naltrexone) 

tx alcoholism

USE: reduce craving for alcohol

ADR: hepatotoxic 

phenothiazine

USE: tx schizophrenia

Effects: antipsychotic (effects perceived as unpleasant), sedation (tolerance develops), inhibition of conditioned avoidance response in animals, lowering of sz threshold, anti-emetic, poikilothermic, anticholinergic, antihistaminic, CV (orthostatic hypotension, tachycardia, EKG changes, cardiac arrest), sexual dysfunction, endocrine (increased prolactin), weight gain (appetite stimulation), inhibition of Ca/calmoduline-depependned processes, teratogenic effects

Toxic effects: 

phenothiazine

phenothiazine

"second gen" or "atypical" antipsycotic

"second gen" or "atypical" antipsycotic

"second gen" or "atypical" antipsycotic

"second gen" or "atypical" antipsycotic

"second gen" or "atypical" antipsycotic