Intermediate acting benzodiazepine

Benzodiazepines has all of the following effects: (1) anxiolytic effect (limbic system) (2) sedative-hypnotic effect (reticular activating system ↓ arousal/wakefulness) (3) Anticonvulsant effect - ↓ activity/spread of seizures (4) muscle relaxant (modify internuncial polysynpatic reflexes in brainstem)

MOA: ↑ GABA interaction with GABA_A receptor = ↑ Cl^- into neuronal cell hyperpolarizing membrane = ↓ neuronal firing

Alprazolam is used as an anxiolytic

Side effects are innumberable: Sedation, Confusion, Impaired movement/speech, memory impairment, disinhibition of behavior (you do dumb shit), euphoria, hangover, rebound anxiety, respiratory depression, tolerance, dependance, and possible teratogenicity

Benzos cause ↓ sleep latency and ↓ time in REM sleep

Stopping benzos can cause REM rebound, which characterized by bizzarre dreams

Benzos are metabolized by hepatic MEOS, but they don't seem to induce drug metabolizing enzyme (different then barbiturates)

Cross tolerance and cross dependance does seem to develop with benzos and alcohol/barbiturates

Long acting benzodiazepine

Benzodiazepines has all of the following effects: (1) anxiolytic effect (limbic system) (2) sedative-hypnotic effect (reticular activating system ↓ arousal/wakefulness) (3) Anticonvulsant effect - ↓ activity/spread of seizures (4) muscle relaxant (modify internuncial polysynpatic reflexes in brainstem)

MOA: ↑ GABA interaction with GABA_A receptor = ↑ Cl^- into neuronal cell hyperpolarizing membrane = ↓ neuronal firing

Chlordiazepoxide is used as anxiolytic, anticonvulsant, and withdrawal suppressant

Side effects are innumberable: Sedation, Confusion, Impaired movement/speech, memory impairment, disinhibition of behavior (you do dumb shit), euphoria, hangover, rebound anxiety, respiratory depression, tolerance, dependance, and possible teratogenicity

Benzos cause ↓ sleep latency and ↓ time in REM sleep

Stopping benzos can cause REM rebound, which characterized by bizzarre dreams

Benzos are metabolized by hepatic MEOS, but they don't seem to induce drug metabolizing enzyme (different then barbiturates)

Cross tolerance and cross dependance does seem to develop with benzos and alcohol/barbiturates

Long acting benzodiazepine

Diazepam is used as an anxiolytic, anticonvulsant, anesthesia supplement, withdrawal suppressant, and muscle relaxant

Benzodiazepines has all of the following effects: (1) anxiolytic effect (limbic system) (2) sedative-hypnotic effect (reticular activating system ↓ arousal/wakefulness) (3) Anticonvulsant effect - ↓ activity/spread of seizures (4) muscle relaxant (modify internuncial polysynpatic reflexes in brainstem)

MOA: ↑ GABA interaction with GABA_A receptor = ↑ Cl^- into neuronal cell hyperpolarizing membrane = ↓ neuronal firing

Side effects are innumberable: Sedation, Confusion, Impaired movement/speech, memory impairment, disinhibition of behavior (you do dumb shit), euphoria, hangover, rebound anxiety, respiratory depression, tolerance, dependance, and possible teratogenicity

Benzos cause ↓ sleep latency and ↓ time in REM sleep

Stopping benzos can cause REM rebound, which characterized by bizzarre dreams

Benzos are metabolized by hepatic MEOS, but don't seem to induce drug metabolizing enzymes (different than barbiturates)

Cross tolerance and cross dependance does seem to develop with benzos and alcohol/barbiturates

Intermediate acting benzodiazepine

Benzodiazepines has all of the following effects: (1) anxiolytic effect (limbic system) (2) sedative-hypnotic effect (reticular activating system ↓ arousal/wakefulness) (3) Anticonvulsant effect - ↓ activity/spread of seizures (4) muscle relaxant (modify internuncial polysynpatic reflexes in brainstem)

MOA: ↑ GABA interaction with GABA_A receptor = ↑ Cl^- into neuronal cell hyperpolarizing membrane = ↓ neuronal firing

Lorazepam is used as a hypnotic, anxiolytic, anesthesia supplement, and withdrawal supplement

Side effects are innumberable: Sedation, Confusion, Impaired movement/speech, memory impairment, disinhibition of behavior (you do dumb shit), euphoria, hangover, rebound anxiety, respiratory depression, tolerance, dependance, and possible teratogenicity

Benzos cause ↓ sleep latency and ↓ time in REM sleep

Stopping benzos can cause REM rebound, which characterized by bizzarre dreams

NOTE: Lorazepam can be used in patient with impaired liver function b/c it is NOT meatbolized in liver

Cross tolerance and cross dependance does seem to develop with benzos and alcohol/barbiturates

Short acting benzodiazepine

Benzodiazepines has all of the following effects: (1) anxiolytic effect (limbic system) (2) sedative-hypnotic effect (reticular activating system ↓ arousal/wakefulness) (3) Anticonvulsant effect - ↓ activity/spread of seizures (4) muscle relaxant (modify internuncial polysynpatic reflexes in brainstem)

MOA: ↑ GABA interaction with GABA_A receptor = ↑ Cl^- into neuronal cell hyperpolarizing membrane = ↓ neuronal firing

Induction or supplement for anesthesia (respiratory depression side effect of midazolam can be concering for anesthiologist - something to be aware of)

Side effects are innumberable: Sedation, Confusion, Impaired movement/speech, memory impairment, disinhibition of behavior (you do dumb shit), euphoria, hangover, rebound anxiety, respiratory depression, tolerance, dependance, and possible teratogenicity

Benzos cause ↓ sleep latency and ↓ time in REM sleep

Stopping benzos can cause REM rebound, which characterized by bizarre dreams

Benzos are metabolized by hepatic MEOS, but don't seem to induce drug metabolizing enzymes (different than barbiturates)

Cross tolerance and cross dependance does seem to develop with benzos and alcohol/barbiturates

Intermediate acting benzodiazepine

Benzodiazepines has all of the following effects: (1) anxiolytic effect (limbic system) (2) sedative-hypnotic effect (reticular activating system ↓ arousal/wakefulness) (3) Anticonvulsant effect - ↓ activity/spread of seizures (4) muscle relaxant (modify internuncial polysynpatic reflexes in brainstem)

MOA: ↑ GABA interaction with GABA_A receptor = ↑ Cl^- into neuronal cell hyperpolarizing membrane = ↓ neuronal firing

Ozazepam is used as a hypnotic and anxiolytic

Side effects are innumberable: Sedation, Confusion, Impaired movement/speech, memory impairment, disinhibition of behavior (you do dumb shit), euphoria, hangover, rebound anxiety, respiratory depression, tolerance, dependance, and possible teratogenicity

Benzos cause ↓ sleep latency and ↓ time in REM sleep

Stopping benzos can cause REM rebound, which characterized by bizzarre dreams

Note: Ozazepam is not oxidized by the liver and thus can be used in patients with impaired hepatic function

Cross tolerance and cross dependance does seem to develop with benzos and alcohol/barbiturates

Intermediate acting benzodiazepine

Benzodiazepines has all of the following effects: (1) anxiolytic effect (limbic system) (2) sedative-hypnotic effect (reticular activating system ↓ arousal/wakefulness) (3) Anticonvulsant effect - ↓ activity/spread of seizures (4) muscle relaxant (modify internuncial polysynpatic reflexes in brainstem)

MOA: ↑ GABA interaction with GABA_A receptor = ↑ Cl^- into neuronal cell hyperpolarizing membrane = ↓ neuronal firing

Termazepam is used as hypnotic

Side effects are innumberable: Sedation, Confusion, Impaired movement/speech, memory impairment, disinhibition of behavior (you do dumb shit), euphoria, hangover, rebound anxiety, respiratory depression, tolerance, dependance, and possible teratogenicity

Benzos cause ↓ sleep latency and ↓ time in REM sleep

Stopping benzos can cause REM rebound, which characterized by bizzarre dreams

Benzos are metabolized by hepatic MEOS, but don't seem to induce drug metabolizing enzymes (different than barbiturates)

Cross tolerance and cross dependance does seem to develop with benzos and alcohol/barbiturates

Benzodiazepine

Benzodiazepines has all of the following effects: (1) anxiolytic effect (limbic system) (2) sedative-hypnotic effect (reticular activating system ↓ arousal/wakefulness) (3) Anticonvulsant effect - ↓ activity/spread of seizures (4) muscle relaxant (modify internuncial polysynpatic reflexes in brainstem)

MOA: ↑ GABA interaction with GABA_A receptor = ↑ Cl^- into neuronal cell hyperpolarizing membrane = ↓ neuronal firing

Triazolam used as hypnotic

Side effects are innumberable: Sedation, Confusion, Impaired movement/speech, memory impairment, disinhibition of behavior (you do dumb shit), euphoria, hangover, rebound anxiety, respiratory depression, tolerance, dependance, and possible teratogenicity

Benzos cause ↓ sleep latency and ↓ time in REM sleep

Stopping benzos can cause REM rebound, which characterized by bizzarre dreams

Benzos are metabolized by hepatic MEOS, but don't seem to induce drug metabolizing enzymes (different than barbiturates)

Cross tolerance and cross dependance does seem to develop with benzos and alcohol/barbiturates

Benzodiazepine Antagonist

Used to reverse the CNS depressant effects of Benzos

Effective against those used in surgery (midazolam) and benzo overdose

Can trigger seizures, particularly in patients with epilepsy or patients dependant on benzos, barbiturates, or alcohol

Can also precipitate withdrawal symptoms in dependant patients

Intermediate/short acting barbiturate

MOA: Act at an independant site of benzos, facilitating actions of GABA at GABA_A receptors (boards: ↑ duration Cl^- channel is open)

Barbiturates can also open Cl^- themselves, explaining their surgical anesthesia and CNS depression effects

Can be used for surgical anesthesia, induce coma, anticonvulsant, for tension headaches, and rarely now but as sedative hypnotics and anxiolytics

Barbiturates are abused due euphoric state, withdrawal from barbiturates can constitute medical emergency due to seizures, delirium, etc. - use benzos to control withdrawal seizures

Barbiturates have low therapeutic window, at levels just above normal dose, used often for suicide and causes decreased respirations.  Management is only supportive, no antedote. 

Pharmacological effects can cause a sedative-hypnotic effect (suppress REM sleep more than Benzos), anxiolytic effect, general anesthetic effect, depression of respiration (much more likely than benzos), anticonvulsant, and euphoria. 

Most barbiturates are metabolized in the liver and can cause drug-drug interactions via induction of microsomal enzymes (does not occur with benzos)

Tons of side effects and drug interactions (read in notes!)

Intermediate/short acting barbiturates

MOA: Act at an independant site of benzos, facilitating actions of GABA at GABA_A receptors (boards: ↑ duration Cl^- channel is open)

Barbiturates can also open Cl^- themselves, explaining their surgical anesthesia and CNS depression effects

Can be used for surgical anesthesia, induce coma, anticonvulsant, for tension headaches, and rarely now but as sedative hypnotics and anxiolytics

Barbiturates are abused due euphoric state, withdrawal from barbiturates can constitute medical emergency due to seizures, delirium, etc. - use benzos to control withdrawal seizures

Barbiturates have low therapeutic window, at levels just above normal dose, used often for suicide and causes decreased respirations.  Management is only supportive, no antedote. 

Pharmacological effects can cause a sedative-hypnotic effect (suppress REM sleep more than Benzos), anxiolytic effect, general anesthetic effect, depression of respiration (much more likely than benzos), anticonvulsant, and euphoria. 

Most barbiturates are metabolized in the liver and can cause drug-drug interactions via induction of microsomal enzymes (does not occur with benzos)

Tons of side effects and drug interactions (read in notes!)

Long acting barbiturate

MOA: Act at an independant site of benzos, facilitating actions of GABA at GABA_A receptors (boards: ↑ duration Cl^- channel is open)

Barbiturates can also open Cl^- themselves, explaining their surgical anesthesia and CNS depression effects

Phenobarbital is specifcally used as an anticonvulsant

Barbiturates are abused due euphoric state, withdrawal from barbiturates can constitute medical emergency due to seizures, delirium, etc. - use benzos to control withdrawal seizures

Barbiturates have low therapeutic window, at levels just above normal dose, used often for suicide and causes decreased respirations.  Management is only supportive, no antedote. 

Pharmacological effects can cause a sedative-hypnotic effect (suppress REM sleep more than Benzos), anxiolytic effect, general anesthetic effect, depression of respiration (much more likely than benzos), anticonvulsant, and euphoria. 

Most barbiturates are metabolized in the liver and can cause drug-drug interactions via induction of microsomal enzymes (does not occur with benzos)

Tons of side effects and drug interactions (read in notes!)

Ultra short acting barbiturates

Thiopental specifically is use to rapidly induce surgical anesthesia

MOA: Act at an independant site of benzos, facilitating actions of GABA at GABA_A receptors (boards: ↑ duration Cl^- channel is open)

Barbiturates can also open Cl^- themselves, explaining their surgical anesthesia and CNS depression effects

Barbiturates are abused due euphoric state, withdrawal from barbiturates can constitute medical emergency due to seizures, delirium, etc. - use benzos to control withdrawal seizures

Barbiturates have low therapeutic window, at levels just above normal dose, used often for suicide and causes decreased respirations.  Management is only supportive, no antedote. 

Pharmacological effects can cause a sedative-hypnotic effect (suppress REM sleep more than Benzos), anxiolytic effect, general anesthetic effect, depression of respiration (much more likely than benzos), anticonvulsant, and euphoria. 

Most barbiturates are metabolized in the liver and can cause drug-drug interactions via induction of microsomal enzymes (does not occur with benzos)

Tons of side effects and drug interactions (read in notes!)

Centrally acting muscle relaxant

Analog of GABA that acts as an agonist at GABA_B receptors

Acts at spinal cord to inhibit the release of excitatory transmitters (glutamate/aspartate) and thereby inhibits spasmogenic reflexes

Used to treat spasticity resulting from MS, spinal cord injuries, etc.

Main side effect is CNS depression (sedation, ataxia, weakness), can also cause euphoria, hallucinations, tremors, and even seizures

Dependance can develop

Centrally acting muscle relaxant

Structurally similar to tricyclic antidepressants

Acts at brainstem to inhibit γ/α motor systems

Treats muscle spasms of local origin (strains, pulls)

Can cause CNS depression (sedation, ataxia, etc.) and anticholinergic effects

Centrally acting muscle relaxant

Used for treating spasticity and muscle spasms

Enhances presynaptic inhibition by facilitating the actions of GABA in the spinal cord

Centrally acting muscle relaxant

Similar to cyclobenzapine (description same below)

Structurally similar to tricyclic antidepressants

Acts at brainstem to inhibit γ/α motor systems

Treats muscle spasms of local origin

Can cause CNS depression (sedation, ataxia, etc.) and anticholinergic effects

Centrally acting muscle relaxant

α₂ adrenergic agonst approved as a skeletal muscle relaxant

Can cause hypotension

Very sedating

Blood alcohol levels are directly related to the amount of alcohol ingested AND the amount of body water

Blood alcohol levels directly determine brain alcohol concentration

90% of alcohol is metabolized in the liver via ZERO order kinetics (constant time/rate)

Average adult metabolized 7-10 g/hour (RJP metabolizes 70-100 kg/hour)

Can be metabolized by alcohol dehydrogenase pathway (normally used) or microsomal ethanol oxidizing system (used in chronic alcoholics), both pathways generating acetaldehyde

MEOS can be induced in chronic alcoholics, contributing to tolerance

Aldehyde dehydrogenase metabolizes acetaldehyde

Can cause graded depression of CNS resulting in release of inhibitions → anxiolytic effect → sedation → hypnosis → anesthesia → respiratory depression → coma → death

Everyone reading these should name every affect of EtOH without reading that whole section

Alcohol has a steep dose-response curve, slight increase in dosage can cause marked effects

Reduces the amount of time spent in REM sleep (when you pass out your quality of sleep is dogshit)

High doses can cause respiratory arrest

In massive alcohol consumption, manage patient by maintaining respiration and preventing aspiration of vomitus

Hangovers result from acetaldehyde buildup, metabolic changes and dehydration, pharmacodynamic brain changes

Alcohol causes enhanced effect of GABA at GABA receptor chloride channel complex - explains similarities/cross tolerance/dependance with EtOH, Barbs, and Benzos

Alcohol withdrawal symptoms - appear 6-24 hrs after last drink and resolve in 5 days, can be severe with autonomic and psychiatric (delireum tremens, seizures, hallucinations), can be life-threatening in some patients

In a patient with EtOH witdrawal symptoms, want to prevent seizures, delirium, and arrhythmias - usually treated with Benzos (generally), phenytoin (seizures), haloperidol (psychotic effects)

READ THIS SECTION (so many effects)

Anxiolytic (non-benzodiazepine, non-barbiturates)

Alleviates mild anxiety with minimal sedative-hypnotic, muscle-relaxant, or respiratory depressant effects

Evidence suggests it may have partial action at serotonin (5-HT_1A) receptors, NOT GABA mechanisms

Has very low abuse potential - no cross tolerance or cross depedance that occurs with benzos, barbs, and EtOH

Use it with a patient who has been brought through alcohol withdrawal and then develops anxiety (he talked about this for 20 mins, it'll be on the test)

Fairly safe, at high doses can cause CNS depression and GI effects

Newer non-benzodiazepine sedative-hypnotics

Enhances the effects of GABA at the benzodiazepine receptor-chloride channel complex by interacting with a subtype of benzo receptor (called omega-1 site)

Causes less anxiolytic, anticonvulsant, and muscle relaxant effects then benzos

Eszopiclone is longer acting (6-8 hours) so it's used to help patients STAY asleep (think: eSzoplicone for STAY asleep)

Some concerning side effects include CNS depression (sedation, amnesia, etc.) and there have been reports of performing complex behaviors with no memory of the event (mostly with Zolpidem)

Drugs can be abused and may interact with other CNS dperessents

Cause less REM depression and less rebound insomnia then other benzos

GABA analog (CAN cross BBB)

Has been claimed to have ergogenic effect (better balling - caid needs this) and has been used by athletes

Used primarily for CNS effects (sedation, euphoria, amnesia) as the "date-rape" drug

High dose chronic use leads to CNS depression with seizures, coma, and death

Can induce a state of physical dependance

Hormone produced by the pineal gland

Used as an OTC sleep aid

 Has little abuse potential

Melatonin receptor agonist

FDA approved sleep aid

Should be used with caution in patients with impaired hepatic function

Reports show that it can ↑ prolactin and ↓ testerone

Newer non-benzodiazepine sedative-hypnotics

Enhances the effects of GABA at the benzodiazepine receptor-chloride channel complex by interacting with a subtype of benzo receptor (called omega-1 site)

Causes less anxiolytic, anticonvulsant, and muscle relaxant effects then benzos

Zolpidem is longer acting (6-8 hours) so it's used to help patients STAY asleep

Zopidem has some concerning side effects include CNS depression (sedation, amnesia, etc.) and there have been reports of performing complex behaviors with no memory of the event

Drugs can be abused and may interact with other CNS dperessents

Cause less REM depression and less rebound insomnia then other benzos

Newer non-benzodiazepine sedative-hypnotics

Enhances the effects of GABA at the benzodiazepine receptor-chloride channel complex by interacting with a subtype of benzo receptor (called omega-1 site)

Causes less anxiolytic, anticonvulsant, and muscle relaxant effects then benzos

Zaleplon is shorter acting (2-4 hours) so it's used to help patients FALL asleep (think: Faleplon for Fall asleep)

Some concerning side effects include CNS depression (sedation, amnesia, etc.) and there have been reports of performing complex behaviors with no memory of the event (mostly with Zolpidem)

Drugs can be abused and may interact with other CNS dperessents

Cause less REM depression and less rebound insomnia then other benzos

Inhibitor of aldehyde dehydrogenase (which metabolizes acetaldehyde from EtOH metabolism)

Causes accumulation acetaldehyde which results in flushing, headache, nausea, and confusion

Goal is symptomology will cause patient to not consume alcohol

Biggest issue is patient won't keep taking drug

Can be potentially hepatotoxic, MAJOR issue seeing as it's use is in alcoholics who have shitty livers

New drug therapy for alcoholism

↓ cravings for alcohol and helps maintain abstinence

Mechanism unclear, acting at both GABA and glutamate receptors

Block NMDA receptors and partially stimulate GABA_A receptors

Main side effect are diarrhea, anxiety, insomnia, and depression

Less potential for hepatotoxicity than other drugs

Recent research suggests that naltrexone+acomprostate are more effective in combination

Long-acting opioid antagonist

Has been reported to reduce cravings for alcohol in alcoholics

Has been approved for treatment of alcoholism

Can cause hepatotoxicity which limits use in alcoholics

Recent research suggests that naltrexone+acomprostate are more effective in combination

Antihistamine

Used as a mild sedative

Also has anxiolytic activity with limited abuse potential (can be used as alternative in patient with anxiety and drug abuse history)

Antihistamine

Used as a mild sedative

Antihistamine

Present in OTC sleep aid products

β-adrenergic blocker

Anxiolytic activity and are useful in patiend with pronounced autonomic symptoms (tachycardia, HTN, etc.)

Used for treatment of stage fright

Centrally acting α-agonist

Can alleviate some of the autonomic effects of alcohol withdrawal; tachycardia, HTN, etc.