Substance Use

Interventions

Therapeutic Use of Self Introspective "Know Thyself" Maintain nonjudgmental approach During detoxification Monitor vital signs Administer medication Monitor intake and output Fluids, nutrition Seizure precautions Teach pt and family about substance abuse Symptoms Dependence Relapse Dangers Encourage verbalization, expression of feelings Stress management and coping skills

pharm tx acute sxs of alcohol withdrawal benzos - function, 3 meds PRNs (3) B vitamins (2) Mg Sulfate LONG TERM NON ACUTE DRUGS (4) LT version of naltrexone -naltrexone be off of what for how long -what doesn't it do? -risk of OD acamprosate decreasses (3)

To Treat Acute Symptoms of Withdrawal Benzodiazepines: sedate and reduce anxiety diazepam (Valium) 5-10 mg Q 2 - 4 hours chlordiazepoxide (Librium) 25-100 mg Q 4 hours lorazepam (Ativan) 2-10mg Q 4 - 6 hours Other PRNs: antidepressants, sleep meds, antipsychotics Nutrition and vitamins B vitamins Thiamine (vitamin B1) Folic Acid (vitamin B9) Magnesium Sulfate Mg is usually decreased Want to increase it reduced Mg can contribute to the seizures ******************************************************************************** LONG TERM/NON ACUTE: To help sustain AWS recovery: Disulfiram (Antabuse) This + alcohol = makes patient really sick Anything with alcohol!!!!! = ex: Nyquil !!!! Need to educate patient Inhibits the breakdown of alcohol (acetyl dehydrogenase) Get effect such as Asian flush Usually low compliance Naltrexone (ReVia, Depade, Vivitrol) Reduces alcohol craving = not actually, just makes alcohol less desirable Opioid blocker = block euphoric and pain reliever effect Have to be off opioids for 1-2 weeks Acamprosate (Campral) Topiramate (Topamax) They are meant for AFTER withdrawl syndrome For long term

Use Moderate, "at risk" "hazardous", Binge, Heavy Abuse Dependence Intoxication Withdrawal Tolerance Addiction Detoxification Relapse Overdose

Use: ingestion, smoking, sniffing, or injection of mind-altering substance Abuse: use for purposes of intoxication or beyond intended use Dependence: psychologically or physiologically needing a drug after long term use Intoxication: the effect of the drug Withdrawal: symptoms occurring when substance no longer used Tolerance: decrease in effect at a given dose or needing more to obtain an effect Addiction: continued use despite adverse consequences Detoxification: process for safe withdrawal Relapse: recurrence Overdose: use of greater than recommended dose of substance Know the effects, what intoxication looks like, what withdrawal looks like, is it a sedative or stimulant

antabuse (disulfiram)

Usual dose is 250mg a day=prevents breakdown of etoh=person who drinks =very sick=flushed, weak, n/v Teach about monitoring for use of Etoh in food products Can elevate live enzymes Disulfiram (Antabuse®) interferes with degradation of alcohol, resulting in the accumulation of acetaldehyde, which, in turn, produces a very unpleasant reaction that includes flushing, nausea, and palpitations if a person drinks alcohol. The utility and effectiveness of disulfiram are considered limited because compliance is generally poor. However, among patients who are highly motivated, disulfiram can be effective, and some patients use it episodically for high-risk situations, such as social occasions where alcohol is present. It can also be administered in a monitored fashion, such as in a clinic or by a spouse, improving its efficacy. No longer in widespread use.

Coke withdrawal and tx Withdrawal - depeletion of what causes/is caused by what chemical what neurotransmitter causes post coke blues? tx - (2)

Withdrawal Depletion of neurotransmitters causes ↑ sleep → "crash" Specifically depletion of norepinephrine Dopamine depletion causes "post-coke blues" Anxiety, depression, sleep disturbances with rebound REM, anergia, decreased libido, suicidality, anhedonia, poor concentration and cocaine craving Treatment Presently, there are no FDA-approved medications to treat cocaine addiction Antidepressants = depression Dopamine agonists = trying to add dopamine back a cocaine vaccine that prevents entry of cocaine into the brain holds great promise for reducing the risk of relapse

opiate tx withdrawal sxs detox opioid subs (2) opioid antagonist (2) - fast vs short acting why at increased risk of overdose with relapse?

Withdrawal → Detoxification → Maintenance Withdrawal symptoms yawning, insomnia, irritability, rhinorrhea, panic, diaphoresis, cramps, nausea, vomiting, diarrhea, fatigue, severe dysphoria, muscle aches, bone pain(long bones), piloerection, dilated pupils Detoxification - tapering with methadone or buprenorphine - discontinuing opioids and administering oral clonidine to ameliorate symptoms of withdrawal Opioid substitutes = controlled sub, narcotics Buprenorphine Methadone Opioid Antagonist = block receptor Naloxone (Narcan) Fast acting. But last short time (injected or nasal form) Naltrexone Also used with alcohol Short acting. But long acting (tabs) Note: Whereas mortality from opioid withdrawal is negligible, mortality rate for persons who resume opioid use is significant Increased risk of fatal overdose resulting from the loss of opioid tolerance associated with even a short period of abstinence, as occurs in most detoxification attempts

WERNECKIE'S ENCEPHALOPATHY definition sxs (4) tx - mg, route, time, duration sxs cont (5)

acute rxn to severe deficiency of thiamine secondary to alcohol abuse ataxia, vestibular dysfunction, confusion, ocular motility abnl (lateral rectal palsy, horizontal nystagmus, gaze palsy) tx: large doses of parenteral thiamine that prevents progression into korsakoff's syndrome -100mg oral 8-12hr for 1-2wks inability to form new memories loss of memory, can be severe confabulation - making up stories hallucinations vision changes: abnl eye movements, double vision, nystagmus *not all sxs have to be present

Korasokoff's syndrome definition what kind of memory amenesia in what pt associated with tx dose, how often, duration

chronic condition that follows wernicke's encephalopathy organic amnestic syndrome - esp recent memory amnesia is an alert and responsive pt usually associated with confabulation tx - thiamine 100mg oral 8-12h for 3-12mos

alcoholic dementia definition improvement?

long term complication fo alcohol abuse characterized by global decrease in cognitive fx - decreased intellectual fx and memory tends to improve w abstinence, but most have permanent disabilties Impaired abstract thinking and judgment, personality changes, impaired memory. Decrease IQ , decreased in pre-frontal cortex effects abstract thinking, impaired memory, and personality These changes CAN BE PERMANENT. Can improve with abstinence but more likely than not it is permanent It is a long term complication od Alcohol Abuse, Charaterized by global decrease in cognative functioning Decreased intellectual functioning and memory This disorder tends to improve with abstinence But most of the pts may have permanent disabilities

Progressive effects of alcohol

slide 25 .01-.05 = relaxing .06 - .10 = sleepy, nausea, .11-.20 = mania, aggressive, mood swings .21-.30 = depression, reduced sensations .31-.40 = coma, unconscious >.41 = death

Acute coke toxicity

slide 55 Phase 1 - increased respiratory Phase 2- decreased respiratory Phase 3 - respiratory failure

Coke high duration short term bio effects (3) long term bio effects CNS stimulant - dopamine (2), NE (4), 5Htn (2)

"Cocaine rush"-high lasts ~ 15-30 mins Followed by a let down = irritability, depression, tiredness, craving more now Biologic effects Short-term: increase levels of dopamine (gives immediate high) increased neural activity in the nucleus accumbens constricted blood vessels dilated pupils; and increased body temperature, heart rate, and blood pressure Long-term Depletion of dopamine effect on reward system CNS stimulant ↑ dopamine euphoria, psychotic symptoms ↑ norepinephrine tachycardia, hypertension, dilated pupils, rising body temperature ↑ serotonin sleep disturbances, anorexia

Addiction Severity Index (ASI) how many problem areas?

7 potential problem areas measures problem severity in each of 7 areas: alcohol medical health employment/self-support illegal activity drug use psychiatric health family relations semi-structured This is another type of cage

SUD (11)

A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by 2 or more of the following, occurring within a 12 month period: Recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home Recurrent use in situations in which it is physically hazardous Ex: drinking while driving Continued substance use despite having persistent or recurrent social or interpersonal problems cause or exacerbated by the effects Tolerance, as defined by either of the following: Need for markedly increased amounts to achieve intoxication/desired effect Markedly diminished effect with continued use of same amount Withdrawal, as manifested by either: Characteristic withdrawal syndrome Same substance is taken to relieve or avoid withdrawal Substance is taken in larger amounts or over a longer period that was intended There is a persistent desire or unsuccessful efforts to cut down or control use a great deal of time is spent in activities necessary to obtain substance Important social, occupational, or recreational activities are given up or reduced b/c of use Use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance Craving or strong desire or urge to use

acamprosate

Acamprosate (Campral®) acts on the gamma-aminobutyric acid (GABA) and glutamate neurotransmitter systems and is thought to reduce symptoms of protracted withdrawal, such as insomnia, anxiety, restlessness, and dysphoria. Acamprosate has been shown to help dependent drinkers maintain abstinence for several weeks to months, and it may be more effective in patients with severe dependence. Reducing anxiety, restlessness, and euphora

Ecstasy adverse effects (11) withdrawal increase what 2 neurotransmitters

Adverse Effects Serotonin syndrome Malignant hyperthermia → muscle breakdown, cardiovascular and renal failure Confusion, depression, sleep disturbance, drug craving, severe anxiety, paranoia and psychosis Memory impairments, difficulty concentrating Withdrawal - fatigue, loss of appetite, depressed feelings, difficulty concentrating MDMA (Ecstasy) ↑ serotonin and excess dopamine release hallucinations, confusion, depression, sleep problems, drug craving, severe anxiety, and paranoia; possible malignant hyperthermia Rohypnol, GHB, ketamine Aka : methylenedioxyMethanphetamine

Assessment

Age of regular use. Changes in use patterns. Periods of abstinence. Previous withdrawal symptoms. Last use. Type of substance. Type of compulsive behavior. Pattern and frequency. Amount. Onset age. Nursing History should include: Blackouts/ LOC/DTs (delirium tremors). Changes in bowel functions. Are they drinking and not eating Weight changes. Sleep problems. Stress. Chronic pain. Family history. Skin changes - rosacea, rhinophima, bruises, spider angiomata Lungs - associated COPD changes Heart - arrhythmias, tachycardia, cardiomegaly Abdomen - liver enlargement, tenderness, ascites Extremities - vascular changes, nicotine stains

Effects of alcohol alcohol withdrawal syndrome - onset/duration, sxs peak when, sxs improve when sxs (8) - which is mild and which are mod-severe following acute withdrawal what sxs (3) can persist for how long when is AWS likely to occur? early signs (6) what happens to sxs with each withdrawal HAVE AWS if (7) physiological effects of long term use (5)

Alcohol Withdrawal Syndrome Delirium Tremens Physiological Effects of Long Term Use Tolerance Alcohol-induced amnestic disorders (permanent brain disorder) Wernicke's encephalopathy Korsakoff's amnestic syndrome Wernicke-Korsakoff syndrome Other effects Alcohol Withdrawal Syndrome Onset/Duration: within 4-12 hours symptoms of AWS usually peak in intensity during 2nd day of abstinence And improve by 4th/5th day Symptoms: BP, HR, Temp Diaphoresis Mild anxiety/restlessness (mild AWS) Hand tremors or "shakes" Adverse GI effects Disorientation, Confusion, Seizures (moderate-severe AWS) Can be Mild, Moderate, Severe/Delirium Tremens* Following acute withdrawal symptoms of anxiety, insomnia, autonomic dysfunction persist for up to 3-6 months When alcohol is consumed in large quantities for a prolonged period (greater than two weeks) and then abruptly discontinued, withdrawal symptoms are likely to occur. Alcohol withdrawal affects the central nervous system, autonomic nervous system, and cognitive function. Early= irritable, anxiety;, insomnia, tremors, sweating, tachycardia. Sx peak on day 2 and improve by day 4 or 5. With repeated withdrawal sx worsen each time. Legal level of intoxication= 0.08-0.10.(percentage of etoh in blood) These sx progess in stages Patients have AWS if 2 of the following symptoms are present after the reduction or discontinuation of alcohol use: 1.autonomic hyperactivity (sweating, tachycardia) 2. increased hand tremor 3. insomnia 4. nausea or vomiting 5.transient visual, tactile, auditory hallucinations or illusions 6. psychomotor agitation; anxiety 7. tonic-clonic seizures.

Amphetamine effects (4) withdrawal (4)

Alertness, euphoria, self-confidence, increased sex drive. With increased use=hyper vigilant, agitated, irritable. Complications inc. increased heart rate bp, motor disturbances, memory deficits, CVA Withdrawal= fatigue, depression, increased appetite, suicide. Cocaine: dilated pupils AND Amphetamines: dilated pupils

slide 46

All contraindicated in pregnancy Know what med is used for Know effect of dissulfram (the sickness related to it) Don't really need to know adverse effects

Other CNS depressants barbituates (3) nonbarb hypnotics (3)

Barbiturates Nembutal (phenobartital) amytal sodium (amobarbital sodium) secobarbital sodium pentobarbital sodium Nonbarbiturate hypnotics Chloral Hydrate, methaqualone Qualudes/ludes Benzodiazepines: Xanax, Klonipin, Valium Street names "Benzos": Jellies, eggs, moggies, vallies, "Mother's Little Helper" All life threatening with withdrawal = can cause coma or death With overdose = also coma or death Need a medical detox!

Effects of CNS depressants Behavioral and psych effects (7) Clinical signs and sxs (7) Withdrawal - rebound anxiety (4), autonomic rebound (4), sensory excitement, motor excitation (4), cognitive excitation (3)

Behavioral & Psychological Effects: Antianxiety effects initially Mood lability Impaired judgment Impaired social/occupational functioning Confusion, stupor, coma Clinical Signs & Symptoms: Slurred speech Lack of coordination Unsteady gait Nystagmus Impaired attention and memory Stupor or coma Withdrawal: Rebound Anxiety tension, agitation tremors, insomnia, anorexia Autonomic Rebound HTN, tachycardia, sweating, hyperpyrexia Sensory Excitement paresthesias, Motor Excitation: hyperreflexia, myoclonus, fasciculations, convulsions Cognitive Excitation nightmares, delirium, hallucinations Sx = similar to alcohol Monoclonus - effects the whole muscle. Rhythmic swinging movement. Ex: hiccups, hypnic jerk fasciculations twitching of fibers, over use of a muscle, not whole body part Convulsions - full body contraction of muscles

Heavy alcohol use, binge AU, functional AU

Binge Alcohol Use 5 or more drinks on the same occasion on at least 1 day in the past 30 days Ex: every staurday, once a month binge drinking Heavy alcohol use 5 or more drinks on the same occasion on 5 or more days in the past 30 days. Every weekend + an additional day Still a binge pattern but more often Functional alcohol use: drink on the weekends but functional during the week

Etiology - biologic (5)

Biologic Genetic predisposition Low levels of MAO enzymes Low levels of dehydrogenase Increased extracellular DA Inadequate self care abilities Social Environmental factors Peer influence Dysfunctional family dynamics Deviance or social maladaptation Consequences of abuse Psychological Depressed mood Low self-esteem Self-derogatory Excessive dependency Increased need for success or power Inability to cope with overwhelming feelings PD or hyperactivity Not entirely a brain disorder, it is also a mood disorder

amphetamine effects -what does it do to 2 neurotransmitters? -effects what parts of NS? -how is NE released?

Block reuptake of norepinephrine and dopamine Effect central and peripheral nervous systems Indirect catecholamine agonists release of newly synthesized norepinephrine

Buprenorphine / Subutex / Suboxone

Buprenorphine In 2002, the FDA approved the use of the unique opioid buprenorphine (Subutex, Suboxone) for the treatment of opioid addiction in the U.S. Buprenorphine has numerous advantages over methadone and naltrexone. As a medication-assisted treatment, it suppresses withdrawal symptoms and cravings for opioids, does not cause euphoria in the opioid-dependent patient, and it blocks the effects of the other (problem) opioids for at least 24 hours. Success rates, as measured by retention in treatment and one-year sobriety, have been reported as high as 40 to 60 percent in some studies. Treatment does not require participation in a highly-regulated federal program such as a methadone clinic. Since buprenorphine does not cause euphoria in patients with opioid addiction, its abuse potential is substantially lower than methadone. A 'partial opioid agonist' such as buprenorphine is an opioid that produces less of an effect than a full opioid when it attaches to an opioid receptor in the brain. Oxycodone, hydrocodone, morphine, heroin and methadone are examples of 'full opioid agonists. People who are opioid dependent do not get a euphoric effect or feel high when they take buprenorphine properly. Buprenorphine tricks the brain into thinking that a full opioid like oxycodone or heroin is in the lock, and this suppresses the withdrawal symptoms and cravings associated with that problem opioid.

Substance intoxication (3)

Development of a reversible substance-specific syndrome due to recent ingestion or exposure to a substance Clinically significant maladaptive behavioral or psychological changes d/t effect of substance on CNS Symptoms not due to a medical condition or are not better accounted for by another mental disorder

Withdrawal (3)

Development of a substance-specific syndrome due to the cessation of or reduction in substance use that has been heavy/prolonged Substance-specific syndrome causes clinically significant distress or impairment in social, occupational functioning Can't function because withdrawal is so strong Symptoms not due to a medical condition or are not better accounted for by another mental disorder

Assessment

Drug History When you were growing up, did anyone in your family drink alcohol or take any other kinds of drugs? If, so how did the the substance use affect the family situation? When did you have your first drink/drugs? How long have you been drinking/taking drugs on a regular basis? What is your pattern of substance use? When do you use substances? What do you use? How much do you use? Where are you and with whom when you use substances? When did you have your last drink/drug/ What was it and how much did you consume? Does using the substances cause problems for you? Describe. Include family, friends, job, school, other. Have you ever experienced injury as a result of substance use? Have you ever been arrested or incarcerated for drinking/using drugs? Have you ever tried to stop drinking/using drugs? If so, what was the result? Did you experience any physical symptoms? Have you ever experienced loss of memory for times when you have been drinking/using drugs? Describe a typical day in your life. Are there any changes you would like to make in your life? If so, what? What plans or ideas do you have for seeing that these changes occur? Laboratory Tests Blood alcohol, toxicology screen, LFTs Skin changes - rosacea, rhinophima, bruises, spider angiomata Nicotine - nails change Alcohol - skin changes jaundice Lungs - associated COPD changes Heart - arrhythmias, tachycardia, cardiomegaly Abdomen - liver enlargement, tenderness, ascites Extremities - vascular changes, nicotine stains What common findings (physical and psychosocial) with Intoxication Withdrawal Defense Mechanisms Denial Projection Motivation for treatment Key predictor Voluntary vs. Involuntary Motivation is a key factor - If they are not ready to give it up, you will have little progress

nicotine

Effects mental stimulation, muscle relaxant 46% of people with psychiatric disorders smoke (National Comorbidity Study) Adverse effects chronic lung disease, cardiovascular disease, stroke, cancer, tolerance, addiction adverse pregnancy outcomes Withdrawal cravings, irritability, anxiety, difficulty concentrating, increased appetite/weight gain, headaches, insomnia, decreased heart rate Treatment NRT Nicotine replacement therapy (NRT) : patches, gum, lozenges, meds Gum = need to deposit it between cheek and gum line to be able to be released Avoid anything acidic before chewing the gum (at least 15 min) beer, coffee, orange juice Psychiatric meds Wellbutrin Antidepressant effects Chantix Eases withdrawal because it blocks the nicotine from binding BUT can cause psychosis, hallucinations, paranoia, anxiety, changes in mood don't want to give to someone with schizophrenia Monitor cardiac effects E cigs Not sure if they are really working Nortriptyline and (something else)

Alcohol: effects a standard drink in grams - how much of beer, wine, 80 proof metabolized by, excreted through (3); metabolize how much per hour without intoxication intoxication and BAC BAC affected by (3)

Effects: Sedative anesthetic Chart next page A standard drink is equal to 14.0 grams (0.6 ounces) of pure alcohol. Generally, this amount of pure alcohol is found in: 12-ounces of beer; 5-ounces of wine1.5-ounces or a "shot" of 80-proof distilled spirits or liquor (e.g., gin, rum, vodka, or whiskey Metabolized by liver (95%) and excreted through lungs, kidneys and skin Skin = why you can smell it on them Metabolize 1 oz of liquor per hour without intoxication Intoxication = blood alcohol level (BAL)= ≥ 0.08% = intoxicated What affects BAC? Food. Absorption of alcohol is faster when the stomach is empty Water would also dilute it Body weight and build. Greater body weight provides a greater volume in which alcohol can be distributed. Smaller BMI = intoxicated faster Sex. Females, on average, have a smaller body mass and a higher proportion of body fat than do males.

LSD severe rxns (6)

Effects: euphoria or dysphoria, altered body image, distorted or sharpened visual and auditory perception, confusion, incoordination, and impaired judgment and memory Severe reactions: paranoia, fear of losing one's mind, depersonalization, illusions, delusions, hallucinations More than 100 different hallucinogens Psilocybin (mushroom) D-lysergic acid diethylamide (LSD) Mescaline Numerous amphetamine derivatives

weed adverse effects (9)

Effects: euphoria, relaxation, altered consciousness, increased sociability Adverse effects amotivational syndrome, memory impairments, coordination problems, slows reaction time, increased appetite, paranoia, social withdrawal, visual hallucinations, suicide attempts Withdrawal: Restlessness, irritability, insomnia, loss of appetite, depressed mood CBT, contingency management, gabapentin, Wellbutrin, N-sephetalsystine

Labs in alcohol abuse (7)

GGT Liver enzyme that increases with alcohol intake AST/ALT ALP LD MCV Urine toxicology and blood screen LFTs: Liver Function Tests GGT-a liver enzyme that is increased by heavy alcohol intake Mean corpuscular volume (MCV), which measure the size of red blood cells- MCV also has been used as a marker of heavy alcohol consumption. It tends to be less sensitive than measurement of the GGT level, but an elevated MCV level combined with an elevated GGT level should raise suspicion about alcohol abuse. The GGT result is more useful than the MCV result as a "red flag" to raise the suspicion that the person is drinking too much. Both of these tests are relatively poor as either a screening or diagnostic test because conditions other than alcohol abuse or alcoholism can cause elevated levels.

tx

Group therapy Learn from others coping mechanisms and stories Individual therapy Trying to find your coping mechanisms Family therapy Can have a disrupted family process Possibly may steal to get money to keep addiction Harm-reduction strategies Reduce the amount of use Twelve-step programs

Harm reduction

Harm reduction: policies, programs and practices that aim to reduce harms associated with the use of psychoactive drugs in people unable or unwilling to stop. The defining features: focus on the prevention of harm, rather than on the prevention of drug use itself, and the focus on people who continue to use drugs. Trying to prevent harm that can occur to the patient Not promoting abstinence Ex: exchange needles Clients with multiple relapses, severe addiction may not have goal of immediate total abstinence; goal is to increase the number of sober days or reduce usage 1. Excessive behaviors occur along a continuum of risk from minimal to extreme. Addictive behaviors are not all or nothing. 2. Changing addictive behavior is a process of steps with complete abstinence being the final step. 3. Sobriety is not for everyone. Being unwilling or unable to stop is no reason to deny services. Meet clients where they are at, but don't leave them where they are at

other substances

Inhalants: Erasex, petrol, glue, paint thinner solvents Common household products Effects: euphoria, disinhibition Adverse effects: Dizziness, confusion, nystagmus, ataxia, respiratory depression, cardiac arrhythmias Chronic use: Dementia, coma, death

amphetamine intoxication (9) and withdrawal (7)

Intoxication Tachycardia, arrhythmias, agitation, aggression, psychosis, impaired judgment, elevated HR & BP, dilated pupils, diaphoresis Withdrawal anxiety, depression, irritability, cravings, insomnia/hypersomnia, psychosis, suicidal ideation

Physiologic Effects of Long-Term Alcohol Use

Long term abuse Tolerance - higher BAL before intoxification Need more and more to get sensation you want Cerebellar degeneration, impaired coordination, unsteady gait, fine tremor, sleep disorders Blackouts Don't remember events Alcohol-Induced Amnestic Disorders: Wernicke's encephalopathy: degenerative brain disorder caused by thiamine deficiency Symptoms reversible Ataxia, confusion, ocular motility abnormalities Korsakoff's amnestic syndrome: can't acquire new info or retrieve memories Confabulation Symptoms usually irreversible Follows Wernicke Cardiac myopathy, pancreatitis, esophagitis, hepatitis, cirrhosis, leukopenia, thrombocytopenia, ascites Other=Peripheral neuropathy, alcoholic sympathy, esophagitis, gastritis, pancreatitis, hepatitis, cirrhosis, ascities, esophageal varices, leukopenia, thrombocytopenia, sexual dysfunction.

tx modalities

Medical model. 12 Step model. Cognitive Behavioral model. Relapse Prevention model. Harm Reduction Model. Medical= detox, abstinence/meds=antabuse=prevents breakdown of etoh. Naltrexone=diminishes cravings/euphoria / antidepressants. Cognitive model=develop and use positive coping skills. Sill training. Identify and change behaviors associated with addictive behaviors. Relapse model= Id situations and factors that =relapse.

methadone

Methadone for the treatment of opioid dependence is only available from federally-regulated clinics which are few in number and unappealing for most patients. In addition, studies show that participation in a methadone program improves both physical and mental health, and decreases mortality (deaths) from opioid addiction. methadone suppresses opioid withdrawal, blocks the effects of other problem opioids and reduces cravings. Federal regulated clinic - given

bath salts what gives stimulant effects? formulation - synthetic chemicals r/t what, which is found in what plant? mode of use (5) effects (6) onset length

Methylenedioxypyrovalerone (MDPV), mephedrone and methylone are the chemicals most often found in Bath Salts. = gives stimulant effect Formulation: one or more synthetic chemicals related to cathinone, an amphetamine-like stimulant found naturally in the Khat plant Mode of Use: sniffing, snorting, orally, smoked, injection Short-term effects: Severe paranoia Suicidal thoughts, agitation, combative/violent behavior, confusion, hallucinations/psychosis, Increased HR, HTN, chest pain, death or serious injury Onset is 15 minutes; length of the high from these drugs is 4-6 hours.

Focus is on safe withdrawal

Monitor vitals and withdrawal symptoms: Nausea/Vomiting Tremor Hands out test Sweating Anxiety/Agitation Auditory/Visual disturbances Hallucinations Disorientation Ask date and time DTs/ Psychosis/ Seizures Includes previous interventions plus withdrawal meds= Anticonvulsants benzos Anxiety, sleep, sedation vitamins-B1 All to help prevent confusion and mental status changes. OUTCOME= SAFE WD, ORIENTED TO REALITY, BEGIN TO DEVELOP MOTIVATION AND COMMITMENT.

naltrexone (reviva, vivitrol)

Naltrexone is an opioid blocker that is also useful in the treatment of opioid addiction. Naltrexone blocks the euphoric and pain-relieving effects of heroin and most other opioids. This type of medication-assisted treatment does not have addictive properties, does not produce physical dependence, and tolerance does not develop. It does not suppress withdrawal or cravings. Therefore, many patients are not motivated enough to take it on a regular basis. It cannot be started until a patient is off of all opioids for at least two weeks, though many patients are unable to maintain abstinence during that waiting period. Also, once patients have started on naltrexone the risk of overdose death is increased if relapse does occur. An extended release version, Vivitrol—administered once a month by injection—is also FDA-approved for treating alcoholism, and may offer benefits regarding compliance.

opiates 3 from natural origin opioid derivatives (4) synthetic (5) effects of opiates (6)

Opioids of natural origin Opium, morphine, codeine Opioid derivatives Heroin, hydromorphone (Dilaudid), oxycodone (Percodan, OxyContin), hydrocodone (Vicodin) Synthetic Meperidine (Demerol), methadone, propoxyphene (Darvon), fentanyl (Duragesic, Actiq), pentazocine (Talwin) Effects of opiates Relief of: pain, cough, diarrhea Sedation Euphoria, pleasure **** PIN POINT PUPILS - myosis = intoxicated During withdrawals pupils will be dilated why so addictive: Attach to opioid receptors in the brain Stimulate the release of amounts of dopamine = extreme pleasurable feelings Physiologic dependence So normal pleasure becomes nonpleasureable=anhedonia Increasing need for more drug to prevent wd and create euphoria

Rx and OTC

Opioids: oxycodone, hydrocodone, morphine, fentanyl, codeine are the most commonly abused Barbiturates and benzodiazepines OTC cough medicines containing dextromethorphan (similar effects as with ketamine or PCP)

Genetic influence

Polygenetic with complex inheritance pattern = ex: skin color No one marker Not simple Mendelian transmission! = punnet square No one marker is responsible=the more risk factors the greater the risk of developing the disease. SUDs are common, complex disorders that do not conform to a simple Mendelian transmission pattern and involve multiple genes and environment (G×E) interactions (Enoch & Goldman 199 Children of alcoholics are approximately four times as likely to become alcoholics as children of non-alcoholics, even when the children of alcoholics are separated from their biological parents at birth, and reared by non-alcoholic adoptive parents. Children of non-alcoholic parents have a low rate of alcoholism, even when adopted by alcoholic parents. There is a 25-50% lifetime risk of alcoholism among sons and brothers of severely alcoholic men. Alcoholics and their offspring show several neurobiochemical abnormalities, Polygenetic inheritence Polygenic=Genetic disorder resulting from the combined action of alleles-(any of several forms of a gene, usually arising through mutation, that are responsible for hereditary variation)- of more than one gene (e.g., heart disease, diabetes, and some cancers). Although such disorders are inherited, they depend on the simultaneous presence of several alleles; thus the hereditary patterns usually are more complex than those of single-gene disorders. Autism also polygenic

Alcohol effects - increases and decreases what neurotransmitters depression caused is stimulation is caused when and why

Potentiates GABA activity. Decreases Glutamate (Glu). Alcohol is a multiple-action depressor of the Central Nervous System, and the depression caused by it is dose-dependent. Although alcohol is mainly used because of its stimulating action, this action is only apparent and happens only with moderate doses. It results from the depression of inhibitory controlling mechanisms. Under the effect of alcohol the cortex is freed from its integrative role, thus resulting confuse and disorganized thinking, as well as disruption of adequate motor control. GABA=a major INHIBITORY neurotransmitter. Glutamate= major excitatory neurotransmitter. With both =CNS depression. Alcohol Increase GABA Decrease glutamate

Coke effects

Powerful reward properties=creates obsessive users. Euphoria, increased energy, mental alertness, self-confidence, sexual arousal. Fatigue, shyness disappear. Intoxications due to excessive doses of cocaine are commonly fatal, with arrhythmias, respiratory depression, and convulsions Cardiovascular effects of cocaine are complex and dose-dependent. Noradrenalin increase makes total peripheral resistance greater, elevating arterial blood pressure. This vasoconstriction decreases skin heat loss, thus contributing to hyperthermia. Local anesthetic effects interfere with myocardial conduction, leading to cardiac arrhythmias and convulsions. Paranoid psychoses and bacterial endocarditic, due to contaminated syringes, are complications of the chronic use of cocaine. Avg high is 20 min for cocaine Dopamine and noradrenaline released Noradrenaline (increase HR and BP) Continued use of cocaine due to both positive and negative reinforcement Rebound dysphoria or crash=more cocaine to overcome the dysphoria. With prolonged use less positive effects and intensified negatives. Highs are not as high and the lows are lower. Rebound dysphoria and rebound euphoria?? Need more cocaine to overcome the dysphoria from coming down from the high The highs are not as high And the lowers are low Intoxication CNS stimulation followed by depression Increasing doses - restlessness tremors and agitation seizures respiratory depression cardiac arrest death (from intoxication)

Psychological, behavioral, social theories

Psychological Theories Personality traits Eg. self-centeredness, inner dishonesty Addictive personality Behavioral Theories Conduct problems of childhood Relationship between conduct problems, hyperactivity, impulsivity and future substance abuse Social Theories Family Peer use and affiliation Environmental

K2 effects (6)

Psychotic effects like extreme anxiety, paranoia, and hallucinations, increase BP, myocardial ischemia, heart attacks Acts on same cell receptors as THC

screening - CAGE

Simply asking about use can reduce use A form of brief intervention by itself Single question: When was the last time you had more than X drinks in one day? (men=5, women=4) Simple tools for brief visit: AUDIT for detailed direct screening CAGE, T-ACE for further assessment Important throughout the life cycle Some screening methods suggest beginning at age 9 Alcohol Screening and Brief Intervention for Youth http://pubs.niaaa.nih.gov/publications/Practitioner/YouthGuide/YouthGuide.pdf Standardized, Structured Questionnaires and Scales C.A.G.E. Have you ever felt you should Cut down on your drinking? Have people Annoyed you by criticizing your drinking? Have you ever felt bad or Guilty about your drinking? Have you ever had a drink in the morning as an Eye-opener to get rid of a hangover? One positive=concern, more than one=strong indication of etoh problem C = cut A =annoyed G= guilty E = eye-opener KNOW CAGE AND KNOW THE QUESTIONS

3 stages of AWS 1 (6) 2 (7) 3 (5)

Stage 1 Mild Anxiety, tremor, insomnia, headache, palpitations, gastrointestinal disturbances Stage 2 Moderate Mild symptoms and diaphoresis, increased systolic blood pressure, tachypnea (more difficulty breathing , tachycardia, confusion, mild hyperthermia Stage 3 DTs Moderate symptoms and disorientation, impaired attention, visual and/or auditory hallucinations, seizures Progression to stage 2 or 3 can occur quickly without treatment. Stage 2: confusion, more difficulty breathing

Meth routes (4) what kind of hallucinations? what happens to teeth?

Swallowed, inhaled, injected or smoked binge/crash pattern Adverse Effects Increased wakefulness, dry mouth, nausea, vomiting, diarrhea, loss of appetite, increased physical activity, increased respiration, irritability, confusion, tremors, anxiety, amphetamine psychosis, repetitive behaviors, sensation of insects crawling under the skin, obsessive scratching, violent behavior, CVA, arrhythmia, cardiac arrest, seizures, death, teeth decay Sensory somatic hallucinations Scratching or picking at skin insects crawling on them Tooth decay Tolerance Withdrawal - drug craving, depressed mood, disturbed sleep patterns, increased appetite Methamphetamine: release of excess dopamine; highly addictive; use in a "binge and crash" pattern

DTs

Tachycardia Diaphoresis Hypertension Confusion Tremor Disorientation Vivid hallucinations Seizures - life-threatening Resolves in 3 - 4 days DELIRIUM=DTs usually on day 2 or 3 but may appear as late as 14 days. Confusion, disorientation, hallucinations, tachacardia, hypertension, hypotension, tremors, agitation, fever, diaphoresis.