Addiction

Slide 1: Unit 12: Addiction “The only way to get rid of a temptation is to yield to it.” Oscar Wilde

Slide 2: Progression to Addiction Initial use: peer pressure, self  medication, curiosity, etc. Transitional use: changes in thinking  and behavior Addiction: 

Slide 3: Mental Mechanisms in Addiction Denial: insistence that there is no problem  despite evidence to the contrary--$ crisis, effect on family, job Rationalization: explanations of use—self  imposed rules that legitimize use, statements like” everyone needs___” Therapeutic Confrontation: meaningful people  present reality in a receivable way.

Slide 4: Family Dynamics in Addiction Anger, Loss of Control, Anxiety,  Hopelessness Codependent behaviors: enabling, over-  functioning, controlling, lonely, hypervigilant, self esteem, not realistic Rescuer/victim relationship 

Slide 5: Child Roles in Addiction Parentified child “hero”  Scapegoat  Clown, mascot  Lost Child, loner 

Slide 6: Common Nursing Diagnoses Health Maintenance, ineffective  Defensive Coping  Family Process, Dysfunctional 

Slide 7: Nursing Strategies and Issues Aware of your own biases—  countertransference Develop trust and rapport before  confronting Then present reality and confront  discrepancies in thinnking Educate on all aspects of the illness 

Slide 8: Specific Interventions: assist client to: Catalogue use to Identify critical   decrease denial triggers for relapse Avoid situations that Set achievable goals   trigger use Increase self worth  Identify positive Building a non using   coping strategies if support network craving “HALT” 

Slide 9: Types of Treatment: 12 Step Programs Self diagnosis  Lifetime process  Cyclic recovery pattern  Social Network  No Fee  Higher Power 

Slide 10: Types of Treatment: Group Therapy Members find out they are not alone  Group is effective in challenging  distortions Group members understand  Been there, share pain 

Slide 11: Behavioral Treatment Part of the disease is avoidance of  responsibility for life tasks Decreases repression of feeling  Developmental arrest issue: don’t move  beyond psychosocial tasks at time of beginning of addiction

Slide 12: Other Intervention Strategies Social Skills Training: stress  management, assertiveness, feeling expression Cognitive restructuring—for denial and  underlying negative self beliefs Family therapy 

Slide 13: Epidemic of Alcohol Addiction Legal if over 21 in most states  Cheap  Socially acceptable/sometimes required  Family modeling—culture  Genetic predisposition to addiction 

Slide 14: How serious is the alcohol epidemic? 20 million Americans have a serious  problem 40% of the population of US have at  least one alcoholic family member Contributes to leading causes of death  in most age groups Involved in MVAs, homelessness,  domestic violence, ER admits

Slide 15: Behaviors at Increasing Blood Alcohol Levels (general) 0.1% -- euphoria, flushing, relaxation, slowed  reaction time (legally intoxicated) 0.2% -- narcosis, slow voluntary mvmnt.,  poor comprehension 0.3% -- little control of voluntary movement,  0.4% -- loss of consciousness (pass out)  0.5% -- coma/death 

Slide 16: Characteristics of Alcohol Small molecule  Absorption: 10-20% wall of stomach  80-90% duodenum Excretion: 10% unchanged through  lungs/kidneys; 90% metabolized in liver at usual rate of ½ oz per hour 1 beer = 1 oz hard liquor = 1 glass  wine

Slide 17: Alcohol in the Body C2H3OH –crosses blood brain barrier,  concentrates in areas with high blood concentration. Irritating to gastric mucosa, vomiting  protects from overdose at times Provides empty calories 

Slide 18: Alcohol is a CNS Depressant Synergism with other CNS depressants  Chronic use = nervous system metabolism  adapts Inhibits production of RNA (protein  synthesis), inhibits new learning and memory function Suppresses synaptic activity – increases the  inhibitory action of GABA and Decreases the excitatory activity of Glutamate receptors

Slide 19: Alcohol in the Liver First metabolized by alcohol  dehydrogenase to acetaldehyde (noxious) If drink a lot, this enzyme becomes  more available Acetaldehyde metabolized by  acetaldehyde dehydrogenase to acetate, which is excreted

Slide 20: More about alcohol in the liver Alcohol is a preferential fuel, leaving fat  to accumulate, fatty deposits Prolonged alcohol use stimulates  pathway that results in high levels of acetaldehyde, damaging cells over time Fatty deposits alter structure and  function of liver – cirrhosis Portal hypertension 

Slide 21: Stages of Alcohol Withdrawl Stage 1 – Tremulous: increased vital  signs, tremor, sweating Stage 2 – Minor DT: auditory and visual  hallucination, illusion, isolated convulsion 12 – 48 hours post last drink Stage 3 – Major DT: All of above, plus  severe motor agitation, after 48 hour

Slide 22: Nursing Care for Withdrawl Assess frequently Keep calm   (discuss tools) environment Know the high risk Hydrate, replenish   times (based on nutritionally (may time of last drink) give vitamins) Intervene early Encourage rest   Use CNS depressant, Seizure precautions   e.g. Librium

Slide 23: Lab findings in Alcoholism Anemia, low WBC,  Elevated liver function tests—SGOT, SGPT,  etc Elevated prothrombin time  Increased uric acid, decreased BUN,  Decreased magnesium, decreased calcium ECG—A fib, PVC’s, T and P wave  abnormalities; cardiomegaly

Slide 24: Factors that affect alcohol metabolism Sex, body weight  Food in stomach slows absorption  Dilution slows absorption  Presence of carbonation speeds  absorption Drinking experience 

Slide 25: Medication management Antabuse: disulfuram Works by blocking a step in the process  of alcohol breakdown in the liver: Tips: reaction occurs even with a small  amount of alcohol; be off alcohol before starting; can last up to 2 weeks after stop taking it; reaction involves headache, N/V, “sick”, and B/P change

Slide 26: Medication Management: Naltrexone Narcotic antagonist--Works by blocking  narcotic receptors; so that alcohol does not have an intoxicant effect Be aware that some alcoholics will take  in huge amounts of alcohol to try to over ride the medication and this can be very dangerous.

Slide 27: Hallucinogen abuse: PCP, mushrooms, mescaline, LSD Not a lot is known with certainty, some  effect on serotonin B receptors Intoxication: first nausea, jitters,  increased vital signs; then distorted sensory perception (vis), hallucinations, sense confusion (synesthesia) Not physically addicting, after effects  include flashbacks, psychosis

Slide 28: Stimulant Abuse: “uppers”—cocaine, amphetamines, methamphetamines, Ritalin They prolong activity of neurotransmitters:  dopamine, norepi, acetylcholine, serotonin Effect—energy, libido, euphoria  Pattern of abuse: tendency to binge and then  bottoming up, see nasal ulceration, cough, etc. Intoxication symptoms: anxiety, manicy,  combative, vigilant, increased VS, can have seizure,CVA, Cardiac arrest Withdrawl: “bottoming out” 

Slide 29: Marijuana/Hashish Commonly abused: 10 million regular users in  US/5% HS seniors abuse Intoxication effect: euphoria, calmness,  drowsiness, dreamlike state Dependence is insidious: leads to  amotivation, decreased persistence at tasks, anxiety, respiratory disease, decreased immune function, altered hormone balance

Slide 30: Opiate Abuse: Heroin, morphine, fentanyl, codiene, methadone In abuse: stimulates opiate receptors “”endorphins” in  brain Effects: respiratory depression, pulmonary edema,  pulmonary fibrosis, hepatitis, bacterial meningitis, constipation, lower immune function Intoxication looks like: pinpoint pupils, decreased  resps/coma, seizure=give narcotic antagonist Withdrawl looks like: Yawning, tearing, gooseflesh,  abdominal and muscle pain, tremors , nightmares

Slide 31: Inhalent Abuse: butyl nitrate, amyl nitrate, nitrous oxide, toluene, gas, paint thinner, hairspray, lighter fluid Legal, available, teens at risk, volatile  substances Effect: partly depends on substance, all  CNS toxic and starve brain of O2, Increase HR, cause lung damage; Drugs can be fatal even without long  addiction Hx—stroke, heart attack, brain damage

Slide 32: Ecstasy or MDMA MDMA started as an appetite  suppresant It is a combination of  methamphetamine and mescaline (a stimulant and a hallucinogen) Effects start in 30-60 minutes after  ingesting and can last 8 hours

Slide 33: Adverse Reactions to Ecstasy Long term cognitive impairment  Hyperthermia—can cause  rhabdomyolosis Tachycardia—can cause severe cardiac  Sx. Can cause “serotonin syndrome”  After the “high” person feels depressed,  achy, and downright terrible

Slide 34: Rohypol: Flunitrazepam “Roofies,” Date rape drug  Odorless and tasteless  A potent benzodiazepine, “like Valium  but 10x as strong.” Half life is 20 hours, but clinical effects  are more short lived

Slide 35: Ketamine “Vitamin K” – Ketamine is a legitimate  veterinary medicine It is a derivative of PCP, which is a  potent hallucinogen Serious cardiovascular effects 

Slide 36: GHB This is a naturally occurring fatty acid  derivative of GABA (the inhibitory neurotransmitter) It acts as a CNS depressant  At high doses, can cause coma/death. 