Pharmacologic Treatment Options for Alcohol Dependency
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Transcript of Pharmacologic Treatment Options for Alcohol Dependency
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Pharmacologic Treatment Options for Alcohol Dependency
Damon Landreau, D.O.LCDR/USPH/USCG Flight Surgeon
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Objectives
• Review basic neurobiology• Review “road ahead” views of Alcohol
Dependency• Review treatment options• Look at a few Coast Guard Pictures
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Neurobiology 101
• Neurons are the functional unit of the nervous system
• They release neurotransmitters(NT) via electrical impulses – we currently know of about 60
• Neurotransmission occurs in 3 basic stages– Sending neuron releases NT via electrical impulses via
flow of Na and K– Receiving neuron binds the NT at a receptor– Chemical changes happen that are similar to the
process of the sending neuron
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Understanding this process is the key to understanding dependency
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Implications
The process for neurotransmission is highlyregulated on the molecular level.
1. Dysregulation is the core molecular problem of dependency
2. Symptoms of dysregulation may be overcome with treatment.
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Mesolimbic Dopamine System (MDS)
• Primal emotional center of the brain• Components
– Anterior cingulated cortex – autonomic nervous system, cognition, decision making
– Ventral tegmental area – primary site of drug actions
– Nucleus accumbens - pleasure center– Frontal/prefrontal cortex – executive functions– Amygdala – emotional center
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Drug Dysregulation
• Down/Up regulates production of NT• Depletes NT stores• Blocks release of NT• Inhibits NT transport systems• Binds to receptors blocking NT• Blocks the second messenger - electrical and
chemical impulses caused by NT
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USCG Medical Mission
• Provide Healthcare to active duty and reserve personnel to support USCG missions
• Maintain medical and dental readiness for world wide deployment
• Oversight of occupational and preventative services
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USCG Clinics
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Alaska Hawaii
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Drugs Effects - Molecular LevelDrug Effects
Nicotine Acetylcholine
Amphetamine , Cocaine Dopamine
Marijuana Endocannabinoids
Opiates Endorphins
Benzo’s Gamma-aminobutyric Acid (GABA)
LSD Serotonin
Note – very specific actionsThe Neurobiology of Addiction, Erickson, C.K. , 2009 pg 33
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AlcoholNeurotransmitter system Effects of alcohol
Gamma-aminobutyric acid (GABA) Enhance
Glycine Enhance
Acetylcholine Enhance
Serotonin Enhance
Adenosine triphosphate (ATP) Inhibit
Glutamate Inhibit
Voltage-gated (several) Enhance + inhibit
Principles of addiction medicine, 3d ed, 2003, page 104 [ISBN = 1-880425-08-4].Compliments of Dr David Franz
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Genetic PredispositionDrugs % Dependency Over Time
Nicotine 32%
Heroine 23%
Crack 20%
Cocaine 17%
ETOH 15%
Stimulants 11%
Opiates 9%
Sedatives 9%
Marijuana 9%
The Neurobiology of Addiction, Erickson, C.K. , 2009 pg 47
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47’ Motor Life Boat22 knot cruising speedTwin 435 HP diesel enginesSelf rights in 10-30 seconds
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Road Ahead
• Approaching Dependency as a Chronic Disease– Expect relapse– Success greatly depends on behavioral changes – Medications may help
• Disease Management Systems• Exploring Medications as more Neurobiology
is understood• More research and doing away with the
untreatable stigmata
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25’ Defender Class Boat
45 knotTwin 225 HP motorsSecurity and River patrols
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Medications
• Will not cover alcohol detox• FDA and non-FDA options• Much is expert opinion
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Clev Clin J Med 2006;73:641 [PMID = 16845975]. Compliments of Dr David Franz
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Naltrexone
• Opioid Antagonist• Decreases the acute pleasure of drinking by
blocking endogenous opioids that reinforce the pleasure
• Reduces relapse frequency in ~ 50% of alcoholics
• More effective when there is a strong Family History of ETOH
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Naltrexone
• Dosage• Oral 50-100 mg/day for 12 weeks
– Some advocate 6-12 months of treatment
• Depot naltrexone – 380 mg IM (gluts) q 4 weeks.– Monitor for local injection site complications
• FDA approved
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Naltrexone
• Contraindications– Opioid Use – consider drug testing– Acute Hepatitis– Acute liver failure
• Side Effects– Nausea, headache, dizziness – most common
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210’ Medium Endurance Cutter
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Acamprosate (Campral)
• Exact mechanism is unknown, but it targets the glutamate system
• May helps in decreasing the amount of ETOH used
• Renal clearance – consider with liver disease• FDA approved
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Disulfiram (Antabuse)
• Increases amount of acetaldehyde after ETOH• Causes a noxious reaction• Not very effective – it has shown to decrease
the amount ETOH but not abstinence• FDA approved
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H-65 "Dolphin" - Short Range Recovery Helicopter
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Ondansetron (Zofran)
• Affects the corticomesolimbic dopamine pathway and effects the reward pathways that are activated by alcohol
• Most effective for early onset alcohol dependence.
• Not FDA approved
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Topiramate (Topamax)
• Increases GABA and decreases glutamate function (opposite of ETOH)
• Reduces # of heavy drinking days• Increased # abstinent days• Not FDA approved
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Baclofen
• Alcohol alters the balance between gamma-aminobutyric acid (GABA) and glutamate
• Baclofen increases GABA function• May reduces alcohol cravings and leads to a
higher rate of abstinence• Not FDA Approved
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NationalMaritime
Center
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Varenicline (Chantix)
• Antagonizes nicotinic acetylcholine receptors• May reduce the rewarding properties and
cravings • Not FDA approved
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SSRI
• May be more effective when:– Co-Morbid depression– Older age with onset of ETOH– Not a strong family history
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Pharmacologic Strategies to Reduce Drinking Behavior
• Reduce ETOH seeking and craving– Naltrexone, ondansetron, topiramate
• Reduce dysphoria and sxs of acute and protracted withdrawal– Acamprosate, sedatives, baclofen, anti-epileptics
• Reduce ETOH bioavailability– Kudzu, alpha 2 antag (clonidine)
• Reduce impulsivity/attention deficits– Dopamine agonist and antagonist, ondansetron
• Treat comorbid psychiatric disease– TCA, SSRI, antipsychotics, buspirone
Adapted from Pharmacologic Interventions for the Treatment of Addiction – Dr. Marvin Seppala
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Questions?