Substance abuse1
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Substance abuse1






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    Substance abuse1 Substance abuse1 Presentation Transcript

    • 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 AlcoholWithdrawal 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 administration More consistent blood levels  Sublingual if NPO (e.g., surgical patients)  Intravenous Severe w/d requiring rapid titration or NPO
    • Amphetamine RelatedDisorder DSM IV  Amphetamine induced  Anxiety disorder  Mood disorder  Psychotic disorder with delusions  Psychotic disorder with hallucinations  Sexual dysfunction
    • Amphetamine RelatedDisorder 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 ConsumptionBeverages / 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): 25mgOver the counter medicines: No-Doze: 100 – 200 mg Midol: 20-100 mg Excedrin: 30-65 mgBenowitz, 1990Total consumption of caffeine per person per day is estimated at210 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 caffeine 2. Inhibition of phosphodiesterase  Inhibition of enzyme that breaks down cyclic adenosine monophosphate (cAMP)  *Toxic amounts of caffeine 3. 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 Caffeine Central Nervous System Enhances neurotransmitter release Stimulates locomotor activity Decreases cerebral blood flow Cardiovascular Release of epinephrine (adrenaline) which Increases heart rate Increases blood pressure Increases blood flow to the muscles Decreases blood flow to skin and inner organs Renal Diuresis; stimulates renal release Vasculature Peripheral: Dilation Central: Constriction Gastrointestinal Increases gastric secretions Respiratory Bronchodilation Increases respiratory rateGarrett 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 BBBNehlig 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 longerNehlig et al., 1999; Fredholm et al., 1999
    • Treatment of Caffeine-RelatedDisorders Reducing or eliminating caffeine consumption ASA  Headaches, muscle aches from withdrawal  Benzodiazepines-rarely required
    • Cannabis-Related Disorders Major active ingredient  Physiological – THC (delta-9-  – Bloodshot & itchy eyes tetrahydrocannabinol)  – Dry mouth and throat • Psychological  – Increased appetite – Feelings of relaxation and  – Reduced pressure within the sociability  eye – Rapid shifts of emotion  – Reduced BP – Interferes with attention,  – Abnormal heart rate memory, and thinking  • May exacerbate preexisting – Heavy doses can induce  cardiovascular problems hallucinations and panic  – Damage to lung structure and – Impairment of skills needed  function for driving  – Tolerance may develop • Impairment present for several hours after ‘high’ has worn off
    • 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  Overdose leaves  – Chills, nausea, insomnia,  – Reduces pain paranoia, hallucinations, and  – Produces euphoria  other psychotic symptoms  – Heightens sexual desire  – Can cause heart attack and  – Increases self-confidence and death because drug causes indefatigability  blood vessels to narrow Blocks reuptake of dopamine in  • Not all users develop tolerance mesolimbic areas of brain  – 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 classes2. Solvents, glues and adhesives3. Propelants for aerosol sprays4. Thinners5. 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  Varenicline (Chantix)  Non-nicotine medications  Chantix is supplied in doses of 0.5 mg (white) and 1 mg (blue) tablets  Bupropion (wellbutrin) –  You may start with an initial Chantix dose of 0.5 mg once a day 150 mg/day for 3 days  You may increase the Chantix dose to 0.5  Increase to 150 mg twice a mg twice daily after 3 days day for 6 to 12 weeks  Chantix dosage is increased to 1 mg twice  300 mg/day doubles the daily after 7 days  Chantix is generally taken with a glass of quit rate in smokers with or water after food without depression  Dont skip doses and double dose for  Clonidine (Catapress) missed Chantix dose decreases sympathetic activity  Patch or orally 0.2 to 0.4 mg/day may cause drowsiness
    • 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 ideation SSRIs 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.