substance abuse1
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Substance Abuse
Substance abuse – Use of drug interferes with ability to function
Fails to meet work or family obligations – No physiological dependence
Substance dependence (addiction) – Involves either tolerance or withdrawal – Tolerance
Greater and greater amounts of substance are needed to produce
the desired effect – Withdrawal
Physiological and psychological consequences when individual
discontinues or reduces substance use – Restlessness, anxiety, cramps, death
Alcohol-Related Disorders Discontinuation of alcohol in heavy user: – Anxiety – Depression – Weakness – Restlessness – Difficulty sleeping – Muscle tremors • Face, fingers, eyelids, other small
musculature – Elevated BP, pulse, temperature
Management of Alcohol Withdrawal
General Measures Seizure precautions with h/o Sz Hydration Thiamine 100mg IM/IV prior to
glucose Correct electrolytes—Mg, Ca, K, PO4
Treat concurrent illnesses
Management of AWS
Benzodiazepines (BDZ) Treatment of choice Reduce symptoms and decrease risk of
Seizurezs Phenobarbital
Narrow therapeutic index Carbamazepine
Effective alternative, less sedation
Mayo-Smith JAMA 1997;278:144-51
Choice of Benzodiazepine All seem effective for AWS
Limited comparative data All metabolized by liver Differences
Onset of action, half life, routes 1 or 2 step metabolism; active
metabolites Long vs shorter acting
Long-acting Benzodiazepines
Chlordiazepoxide (Librium®) Oral dosing only Intermediate onset Long-acting parent compound and metabolites Smoother withdrawal, less sz, better cognitive
fxn Potential accumulation in elderly and patients
with liver disease [Diazepam]
Shorter-acting BDZs
Lorazepam (Ativan®) Versatile dosing—PO, IV, IM, SL Fast to intermediate onset Intermediate half-life, no metabolites Less likely to accumulate in elderly or
with liver disease Breakthrough sx, met. acidosis, delirium [Oxazepam]
Benzodiazepines
Chlordiazepoxide generally preferred
Indications for Lorazepam Elderly Established liver disease NPO Severe w/d requiring frequent or high
doses
Benzodiazepines
Route of administration Oral preferable
Ease of administrationMore consistent blood levels
Sublingual if NPO (e.g., surgical patients)
IntravenousSevere w/d requiring rapid titration or NPO
Amphetamine Related Disorder DSM IV
Amphetamine induced Anxiety disorder Mood disorder Psychotic disorder with delusions Psychotic disorder with hallucinations Sexual dysfunction
Amphetamine Related Disorder Treatment
None established Treat specific symptoms Comorbid conditions such as
depression may respond to antidepressants Bupropion (Wellbutrin)
Used after patients withdraw from amphetamines
Caffeine-Related Disorder Caffeine is an methylxantine More potent than other known
methylxantines Theophyline (Primatene)
Half-life- 3-10 hrs Peak 30-60 minutes Crosses BBB Adenosine-receptor antagonist
Amount of Caffeine Consumption
Beverages / Food: Cup of coffee: 65-120 mg caffeine
Espresso 1oz shot: 40 mg Cup of tea: 40-60 mg Can of soda: 30-60 mg Red Bull (8.3oz): 80 mg Hershey’s milk chocolate almond bar (6oz): 25mg
Over the counter medicines: No-Doze: 100 – 200 mg Midol: 20-100 mg Excedrin: 30-65 mgBenowitz, 1990
Total consumption of caffeine per person per day is estimated at 210 to 238 mg (Barone and Roberts, 1996)
Mechanism of Action
Three main hypotheses:1. Mobilization of intracellular calcium Biphasic effect on intracellular calcium levels *Toxic amounts of caffeine2. Inhibition of phosphodiesterase Inhibition of enzyme that breaks down cyclic adenosine
monophosphate (cAMP) *Toxic amounts of caffeine3. Antagonism of inhibitory presynaptic adenosine
receptors Caffeine blocks adenosine receptors Resulting in the inhibition of the breakdown of cAMP Blocking the inhibitory effects of adenosine Nehlig et al., 1992
Pharmacodynamics
CaffeineCaffeineCentral Nervous SystemCentral Nervous System Enhances neurotransmitter releaseEnhances neurotransmitter release
Stimulates locomotor activityStimulates locomotor activityDecreases cerebral blood flowDecreases cerebral blood flow
CardiovascularCardiovascular Release of epinephrine (adrenaline) Release of epinephrine (adrenaline) whichwhichIncreases heart rateIncreases heart rateIncreases blood pressureIncreases blood pressureIncreases blood flow to the musclesIncreases blood flow to the musclesDecreases blood flow to skin and inner Decreases blood flow to skin and inner organsorgans
RenalRenal Diuresis; stimulates renal releaseDiuresis; stimulates renal releaseVasculatureVasculature Peripheral: DilationPeripheral: Dilation
Central: ConstrictionCentral: ConstrictionGastrointestinalGastrointestinal Increases gastric secretionsIncreases gastric secretionsRespiratoryRespiratory BronchodilationBronchodilation
Increases respiratory rateIncreases respiratory rateGarrett and Griffiths 1997Garrett and Griffiths 1997
Pharmacokinetics
Absorption Gastrointestinal tract and stomach Rapid rate, peak blood level in 30-60 min. Crosses lipid-membrane (not water soluble)
Distribution Diffuses throughout the organism and
crosses BBB Including placenta and placental BBB
Nehlig et al., 1999; Fredholm et al., 1999
Pharmacokinetics
Metabolism Metabolized through liver biotransformation initially by
demethylation into dimethylxanthines. *Dimethylxanthines are pharmacologically active and may add
to the effects of caffeine consumption in humans. This process is unique to humans, no other animal species
metabolizes caffeine in a similar way Half life of caffeine
Three to eight hours; varies with age and other external factors Newborns cannot metabolize caffeine, mainly eliminated by
excretion Half life 80 +/_ 23 hours
Smokers, half life is reduced up to 50% Pregnant women and those taking oral contraceptive, half life
up to 15 hours longer
Nehlig et al., 1999; Fredholm et al., 1999
Treatment of Caffeine-Related Disorders Reducing or eliminating caffeine
consumption ASA
Headaches, muscle aches from withdrawal
Benzodiazepines-rarely required
Cannabis-Related Disorders
Major active ingredient – THC (delta-9- tetrahydrocannabinol) • Psychological – Feelings of relaxation and sociability – Rapid shifts of emotion – Interferes with attention, memory, and thinking – Heavy doses can induce hallucinations and panic – Impairment of skills needed for driving • Impairment present for several hours after ‘high’ has worn off
Physiological – Bloodshot & itchy eyes – Dry mouth and throat – Increased appetite – Reduced pressure within the eye – Reduced BP – Abnormal heart rate • May exacerbate preexisting cardiovascular problems – Damage to lung structure and function – Tolerance may develop
Cannabis Withdrawal
No specific treatment Abstinence and support
Anxiolytics Short-term withdrawal symptoms relief If depressive disorder is present, treat
with antidepressants
Cocaine-Related Disorder
Alkaloid obtained from coca leaves – Reduces pain – Produces euphoria – Heightens sexual desire – Increases self-confidence
and indefatigability Blocks reuptake of
dopamine in mesolimbic areas of brain
Overdose – Chills, nausea, insomnia,
paranoia, hallucinations, and other psychotic symptoms
– Can cause heart attack and death because drug causes
blood vessels to narrow • Not all users develop
tolerance – Some become more sensitive
• May increase risk of OD • Usage increased in 70s and
80s – Dropped late 80s; rose mid
90s In 2003, 2.3 million users
over the age of 12 (SAMHSA, 2004)
Cocaine-Related Disorder
Crack – Form of cocaine that become popular
in the 80s
– Rock crystal that is heated, melted, & smoked
– Increased popularity because it is cheaper than cocaine
Cocaine-Related Disorder
Treatment No pharmacological treatments produce
decreases in cocaine use comparable to the decreases in opioid use when heroin users are treated with methadone, levomethadyl and buprenorphine.
Methylphenidate (Ritalin),Lithium (Eskalith) Cocaine users presumed to have preexisting
ADHD and mood disorders Those drugs are useless in patients
without the disorders
Cocaine-Related Disorder
Treatment, cont. Many different treatments have been
use with little or no effects TCAs MAOIs SSRIs Antipsychotics Etc.
Hallucinogen-Related Disorders Natural and synthetic substances
Psychedelics or psychomimetics Induce hallucinations or disconnection
with reality Schedule 1 drugs
Hallucinogen-Related Disorders Naturally occurring
Psilocybin Mushroom
Mescaline Peyote cactus
Other Harmine, harmaline, ibogaine,
dymethyltriptamine (DMT)
Hallucinogen-Related Disorders LSD
Synthesized in 1938 Classic synthetic hallucinogen MDMA- erroneously classified as a
hallucinogen, vstructirally related to amphetamines
Hallucinogen-Related Disorders Treatment
Symptom specific Psychological support Hallucinogen intoxication can be treated
with diazepam 20 mg Stops LSD effect and associated panic to a
stop within 20 minutes
Inhalants-Related Disorders Volatile hydrocarbons
Tolouene n-Hexane Methyl butyl ketone Trichloroethylane Dichloromethane Gasoline Butane
Inhalants-Related Disorders 4 commercial classes1.Solvents, glues and adhesives2.Propelants for aerosol sprays3.Thinners4.Fuels
Inhalants-Related Disorders Inhalant-induced pathological
conditions Intoxication Delirium Persisting dementia Psychotic disorder Mood and anxiety disorders Disorder not otherwise specified
Inhalants-Related Disorders Intoxication requires no medical
attention Effects of intoxication may require
attention Coma, bronchospasm, laryngospasm,
cardiac arrhythmias, or burns Sedation is contraindicated Confusion, panic or psychosis
Severe agitation Haloperidol 5mg IM/70 kg bw
Nicotine-Related Disorders One of the most highly addictive
drugs in the US. Known to cause conditions such as:
Cancer, emphysema and CV disease Secondhand smoke is associated with
lung cancer in adults and respiratory disease in children
Nicotine-Related Disorders According to the DSM IV TR, there is a
diagnosis of nicotine dependence and withdrawal but not of nicotine abuse or intoxication.
Nicotine dependence occurs very quickly due to activation of the ventral tegmental area dopaminergic system. It is enhance by social factors that encourage or
promote smoking
Nicotine-Related Disorders Pharmacotherapy
Nicotine replacement therapies Considered to double cessation rates Can also be used to reduce withdrawal rates in
patients Maintenance period of 6-12 weeks followed by a
gradual withdrawal of another 6 to 12 weeks Nicotine palicrex gum (Nicorette)
Releases nicotine via chewing and buccal absorption 2 mg for patients who smoke less than 25 cigarretes a day 4 mg for patients that smoke more than 25 cigarretes a
day
Nicotine-Related Disorders
Pharmacotherapy Non-nicotine medications
Bupropion (wellbutrin) – 150 mg/day for 3 days Increase to 150 mg twice
a day for 6 to 12 weeks 300 mg/day doubles the
quit rate in smokers with or without depression
Clonidine (Catapress) decreases sympathetic activity Patch or orally 0.2 to 0.4
mg/day may cause drowsiness
Varenicline (Chantix) Chantix is supplied in doses of 0.5
mg (white) and 1 mg (blue) tablets
You may start with an initial Chantix dose of 0.5 mg once a day
You may increase the Chantix dose to 0.5 mg twice daily after 3 days
Chantix dosage is increased to 1 mg twice daily after 7 days
Chantix is generally taken with a glass of water after food
Don't skip doses and double dose for missed Chantix dose
Opioids-Related Disorders• Opioids– Narcotic antagonists• Naloxone (Narcan)• Naltrexone (ReVia)• Nalmefene (Revex)
– Methadone– Buprenorphine– Clonidine
Phencyclidine-Related Diorders Treatment
NO DRUG KNOWN TO FUNCTION AS A DIRECT PCP ANTAGONIST
Treatment of PCP intoxication aims at reducing systemic levels of PCP
Address significant, medical, behavioral and psychiatric issues
Sedative, Hypnotic or Anxyolitic-Related Disorders Sedatives and Anxiolytics
Drugs that reduce subjective tension and induce mental calmness
Hypnotics Drugs that induce sleep In low dosages instead of inducing sleep,
produce daytime sedation as do sedatives and anxiolytics
Benzodiazepines, Barbiturates, barbiturate-like substances
Sedative, Hypnotic or Anxyolitic-Related Disorders Withdrawal Treatment
Carbamazepine Useful in the treatment of benzodiazepine
withdrawal Refer to table 12.12-6 Guidelines for treatment
of Benzodiazepine withdrawal Barbiturate
Caution with sudden withdrawal to prevent sudden death. See table 12.12-7 pg 459
Anabolic-Androgenic Steroid Abuse Family of drugs composed the natural male hormone Testosterone
Psychiatric concerns AAS Withdrawal AS-induced mood disorders AS-induced Psychotic Disorder AS-related disorder not otherwise specified
Anabolic-Androgenic Steroid Abuse Treatment Abstinence
Withdrawal Supportive therapy and monitoring Hospitalization may be required if patient
presents suicidal ideationSSRIs recommended only in patients that present depressive symptoms weeks after discontinuation of AAS use
NSAIDs- may be useful in treating muscle aches and headaches caused by withdrawal.