Benzodiazepines:Alprazolam, Diazepam, Oxazepam

Antidepressants: TCAs and SSRIs

Barbiturates: phenobarbital

Hydoxyzine: Atarax, Visatril

Buspirone: Buspar

Enhances the effects of GABA-A receptor, an inhibitory enzyme of the CNS

various types, subunits and locations

With BZD, Cl- intake increases and the CNS is inhbited

Anxiolytic (a2-GABA-A)

Muscle Relaxant (a2-GABA-A) - Diazepam

Sedation/Hypnotic (a1-GABA-A)

Anterograde Amnesia (a1-GABA-A) - Versed

Anticonvulsant

anxiolytic

Intermediate Acting (10-20 hours)

anxiolytic

muscle relaxer

anticonvulsant

Long acting (1-3 days)

A: lipophilic, equally distributed

D: short, intermediate and long

M: metabolized by liver, most have active metabolites

E: urinary

anxiolytic

Short acting (3-8 hours)

Tolerance

Dependence (psych and phys)

Withdrawal symptoms: confusion, anxiety, agitation, restlessness, insomnia, seizures

CNS Depression: drowsiness, ataxia, confusion and impaired cognition

DO NOT Rx. with Liver disease

Alcohol and CNS depressants act synergistically

Flumazenil (Romazicon)

-GABA receptor antagonist

-rapid onset, short duration

adverse effects: dizziness, n/v, agitation

Anxiolytic (non BZD)

Slow onset of sedation

Uses CYP450

Will not prevent BZD withdrawal but will help with anxiety

Hydroxyzine (Vistaril)

antihistamine, anxiolytic, antiemetic

less addictive

side effects: sedation (good), drowsiness, dry mouth, blurred vision

TCAs

SSRIs (Paxil, Prozac)

For chronic use

Phenobarbital (anticonvulsant)

also: anesthesia, anticonvulsant, anxiolytic, hypnotic, CNS depression and Respiratory depression

-CNS (dizziness, mental and phys slowing, concentration probs)

-GI (nausea)

Overdose = fatal with no antagonist

Also induces CYP450

Zolpidem (Ambien)

zaleplon (Sonata)

Eszopiclone (Lunesta)

Ramelteon (Rozerem)

MoA: acts on BZD receptors but non BZD

few withdrawal effects, little tolerance

use for 2-4 weeks top (not chronic use)

adverse effects: nightmares, agitation, GI upset, dizziness, daytime, drowsiness, amnesia

Hypnotic

Better for patients who experience daytime drowsiness on Ambien

Non BZD hypnotic but acts on BZD receptor

Effective for up to 6 months continuous use

Adverse effects: unpleasant taste, dry mouth, Headache (HA), peripheral edema, somnolence (drowsiness)

Melatonin agonist

Promotes sleep with circadian sleep-wake cycle

Use: insomnia

Adverse effects: dizziness, fatigue, somnolence, increased prolactin levels

No abuse, withdrawal or dependence

TCAs

Warfarin (Coumadin)

Theophylline

Caffeine

TCTC  

NSAIDs

Oral hypoglycemics

Warfarin (coumadin)

Proton Pump Inhibitors

Antiepileptic drugs

"PA"

Antidepressants

Antipsychotics

Beta Blockers

Codeine

AABC

Acetaminopen (Tylenol)

Anesthetic

Alcohol (ethanol)

AAA

Calcium Channel Blockers

Hormones

Antibiotics (macrolides)

Benzodiazepines (BXD)

 Immunosupressants

Statins

HIV antivirals

CHABISH

Utilized for sleep due to side effects

Use only for short term and mild insomnia

Ex: Benadryl (Diphenhydramine)

Adverse effects: daytime drowsiness, anticholenergic side effects

CNS Depressant: anxiolytic, hypnotic, sedative

Chronic use: liver disease, gastritis, nutritional deficiences and cardiomyopathy

Withdrawal = life threatening

Uses zero order kinetics

Uses liver metabolism (CYP450 2E1) and urinary excretion

Drug interactions: synergism with other CNS depressants (BZDs, antihistamines, barbituates)

Disulfram (Antabuse): intferes with ethanol metabolism and causes flushing, tachycardia, hyperventilation, n/v

Acamprosate (Campral): new medication used in alcohol rehab

Naltrexone: long-acting opiate antagonist but used for alcohol dependence (better than Disulfram)

Work on opiate receptors, which regulate pain response

Pain: an unpleasant subjective sensory or emotional experience

Take the form of neurotransmitters: enkephalins, dynorphins, endorphins

Opiod = synthetic form of an opiate (poppy)

Mu: major receptor involved in pain

Kappa: sedative actions

Delta: pain relief and sedative

Throughout the body

Brainstem - inspiration, cough, n/v, BP, pupil diameter, stomach secretions

Medial Thalamus - deep, poorly localized pain (emotional)

Spinal Cord

Hypothalamus

Limbic System

Peripheral NS: sensory, via Ca+ dependent release of pro-inflammatory substances (ex. substance P)

Binds to opiate receptors in the CNS and

-inhibits ascending pain pathway

-general CNS depressant

     ▪Hypersensitivity to opioids

• Analgesia
• Mood changes: Euphoria
• Somnolence
• Nausea/Vomiting (chemoreceptor stimulation)
• Respiratory depression (decreased RR and response to CO2)
• decreased GI tract motility: possible constipation
• increased sphincter tone: biliary spasm, urinary retention
• Histamine release: Pruritis and Urticaria
• Possible Tolerance and Dependence

An OPIOD

MoA: binds to opiate receptors and caused hyperpolarization of cells. Decreases release of SubstanceP

Uses: Analgesia and Acute Pulmonary Edema (relieves dyspnea)

Kinetics: slow absorption, low F, liver metabolism, urinary excretion

Adverse effects: increased intracranial pressure,urinary retention

An Opiod - moderate agonist

Less euphoria

An Opiod - weak agonist

Buprenorphine

An Opiod - Partial Agonist

An Opiod - Mixed Agonist / Antagonist

Agonist on Kappa

Antagonist: Mu and Delta

MoA:  Provides analgesia for moderate pain by acting on receptors in the spinal cord

An Opiod - antidiarrheal

Less addictive than other opiates