The Patient with Substance Abuse and Dependence

Denise Coe RN MSN HNC

Substance Use Disorders/Substance Induced Disorders

• Two groups:

• Substance use- abuse and dependence.

• Substance –induced disorders- intoxication,withdrawal, delirium,dementia, amnesia,, psychosis, mood disorders, anxiety disorders, sexual dysfunction, and sleep disorders.

• We will talk about substance abuse/dependence and intoxication/withdrawal.

Which ones will we talk about?

• Alcohol.

• Other CNS depressants- barbiturates,non-barbiturates and anti anxiety agents.

• CNS stimulants-amphetamines and cocaine.

• Opioids-morphine,codeine,heroin,dilaudid,percodan(oxycodone), demerol,Darvon, Talwin.

• Hallucinogens.

• Cannibinols.

Define terms

• Substance Abuse:

use of any psychoactive drug alone or in combination that poses problems to health and/or to the functioning in major role obligations at work, school,or home and the repeated use of it despite the adverse consequences.

• Substance Dependence:

The person continues to use the substance despite consequences and develops physical dependence which manifests in behaviors, thinking and physical symptoms.

Define Terms

• Tolerance develops with continued use, necessitating increasingly larger or more frequent doses to achieve the desired effects. Continued use necessitates continued use to avoid symptoms of withdrawal from lack of drug in the body.

• There is also psychological dependence- the person perceives the use of the drug as necessary to personal well being, performance or relationships.

Define terms

• Substance induced disorders:

Intoxication is the development of a reversible substance specific syndrome caused by the recent ingestion of a substance.

• Substance withdrawal:

The development of a substance specific maladaptive behavior change with physiological and cognitive symptoms due to reduction or stopping of using the substance. Usually indicative of dependence.

Etiological factors

• Genetics- especially evident with alcoholism. 50% incidence of alcoholism in the offspring.

• Biochemical Deficit of neuro-transmitters such as serotonin, “ feel good” chemical. When the person drinks get encoded in the limbic system and sets up a craving response.

Etiology….

• Developmental: Dependent personality, poor impulse control, difficulty with frustration, low self esteem, introversion. Once experience the a drug induced feeling of functioning, continue to crave it as a solution to problems on biochemical level.

• A learned response to anxiety. Kids more apt to use if parents do as an emotional way of coping.

• Modeling of peers in adolescents.

• Conditioning related to the use of the substance

Etiology

• Who gets it?

• Some people more susceptible than others.

• There seems to be a genetic connection.

• The body of the person who develops the disease of alcoholism reacts to mood altering chemicals differently.

• The liver metabolizes it differently. Alcoholics can drink more without getting drunk because of difference in metabolism.

Etiology

• Who gets it?

• Some scientists believe that the brain of the alcoholic has different brain chemistry. A lesser amount of the feel good chemicals, serotonin, and when they drink, it produces the same good effects as the natural brain chemicals would have. But continued use of the mood altering substance further depletes the brain of its chemicals.

Etiology

• Who gets it?

• A bio-psycho-social-spiritual illness.

• The psychological theory states that people have a preset disposition or personality: low self esteem, fear, shame, anxiety in social situations re: to the self worth.

• Most alcoholics say when they took the first drink something wonderful happened. Alcohol medicated the pain and anxiety.

• Tolerance develops as they want more of the feeling good.

Alcohol

• Considered a food because of the calories but no nutritional value. Alcohol content varies by type of beverage. The average drink all contain about the same amount of alcohol.

• It exerts a depressant effect on body. The effects on the CNS are proportionate to the amount in the blood.

Alcohol

• Legal standard of intoxication: 0.08 gr/dl in the blood .

• BAC- blood alcohol concentration

• The concentration of alcohol in the blood is measured in grams of alcohol per deciliter of blood. Ex. Ingesting one drink per hour( one beer, glass of wine, mixed drink) which contains about ½ oz of ethyl alcohol produces a BAC of .02 in a 150 lb. male. Thus, the average male who drinks about 5 drinks in an hr. has a blood alcohol of .10 which is illegal to drive.

Alcohol

Gender Differences:

Women have higher blood alcohol levels than men from the same number of drinks because:

• They usually weigh less

• They have more body fat than men( which does not absorb it as readily as muscle)

• They have sex hormones that increase alcohol absorption and decrease elimination.

• Women tend to absorb more from the stomach.

It is eliminated at the speed of ½ oz. Per hr. No faster.

Patterns of Use

• Can be traced back to Neolithic Age. Acceptance of it’s use has had to do with the prevailing mores of the country.

• Socially acceptable as a drug. It’s use is only frowned upon when it manifests in symptoms which interfere with functioning of the person.

• Third major health problem in the US.

What is it?

• A primary, chronic disease with genetic, psychosocial, and environmental factors influencing who develops it and how it manifests.

• It is progressive and fatal.

• Characterized by use of the substance either in binges or continuously, and a loss of control over the use, getting into difficulty because of the use, using despite the problems and distortions in thinking and denial.

Stages of addiction

• Prealcoholic:

Drinks because of social motivations, finds alcohol relieves stress. Over time develops a tolerance and needs more to achieve the same effect, can be described as a heavy drinker. Other people may think the person is drinking too much. Body cells are changing to adapt to higher levels,

• Psychological dependence begins. Person gets used to using it to reduce anxiety and social problems. Use begins to be normal part of life.

Stages

• Early alcoholic

Earliest sign is blackouts, periods of amnesia during or immediately after the time of drinking. Has hangovers and may need to drink to chase away the hangover effect. The drinking becomes more important and the person becomes preoccupied with it. Drinks fast in order t get effect. Defensive about drinking. Rationalization.

• Friends who don’t drink are replaced by those who do. May have liquor hidden. DENIAL (blocks any motivation for help).

Stages..

• Also begins to have loss of control when drinking. It takes more to get high, but getting drunk is more frequent. Damage to body cells, brain, liver.

• The drug is used to control the pain created by not using it.

• Work, family, and physical problems may start.

Stages…

• Phase 3 True alcoholic:

Loss of control over whether to drink or not. Binges. Stops only when too sick to continue. Experiences feelings of isolation, aggression, loss of interest in anything that used to be pleasurable, lack of interest or ability in sex. Nutritionally compromised, loss of relationships, jobs, trouble with the law. Loss of self esteem. (Denial) Sickness. Drinking the total focus.

• Drink to avoid these feelings. Physiological dependence is evident.

Stages

• Phase 4 Chronic:

• Marked deterioration of physical, emotional, social, behavioral, and spiritual aspects of the persons life.

• Life is consumed by the relationship with the substance and the need to use. (Denial and impaired thinking) Drunk more than sober.

• Denial blocks the motivation for recovery by masking the pain of reality. Families play a part in this web, too.

Stages

• Implications to Health care practice:

The patient may come to you in any stage. It is difficult to tell in the early stages, but a careful history must be done so that a good data base is established. Can play a part in chipping away at the denial .

• Motivational Interviewing

• Must do a quality assessment and update the information. People may become more open as they develop a relationship with you.

Effects of Alcohol on the body

• Depression of the CNS which can be reversed.

• Peripheral neuropathy-nerve damage S/S burning, tingling or prickly sensations of the extremities. Probably due to deficiency of B vitamins, esp. thiamine.

• Nutritional deficiencies R/T insufficient intake of nutrients and the toxic effects of alcohol that result in malabsorption.

Effects on body..

• Alcoholic Myopathy- acute or chronic. Also due to Vitamin B deficit. Reversible.

• Acute- pain,edema, tenderness in the skeletal muscles of the extremities, pelvic muscles and shoulder girdle and of the thoracic cage following ingestion. ( elevated CPK<LDH AST)

• Chronic- wasting and weakness in the skeletal muscles.

Effects on Body

• Wernicke’s encephalopathy- most serious form of thiamine deficiency. Can be fatal if thiamine isn’t given. Paralysis of ocular muscles, diplopia,ataxia, somnolence and stupor.

• Korsakoff’s psychosis- A syndrome of confusion,loss of recent memory, and confabulation. Goes together with Wernicke’s. Tx. is thiamine.

Effects…

Alcoholic cardiomyopathy-enlargement of the heart and weakening of the heart muscle from accumulation of lipids in the heart cells. CHF or dysrhythmia. Sx of Chf. Elevated CPK,AST,LDH and EKG changes. Tx is abstinence and tx for the CHF.

Esophogitis-inflammation and pain in the esophagus from the toxic effects on the mucosa,or from frequent vomiting.

Effects

• Gastritis-inflammation of the stomach lining S/S nausea, vomiting,distention. ETOH breaks down the stomach’s protective mucosal barrier, allowing HCL to erode the stomach wall.

• Pancreatitis-acute or chronic- acute occurs 1-2 days after a binge. Severe epigastric pain,N/V, abdominal distention. Leads to pancreatic insufficiency and malnutrition, steatorrhea,wt. loss, and diabetes mellitus.

Effects…

• Alcoholic hepatitis- often follows a prolonged bout of drinking and superimposed on an already damaged liver. Inflammation and necrosis. S/S enlarged liver and spleen, abdominal. Pain,N/V, weakness, low grade temp. loss of appetite, fatigue,elevated WBC and jaundice. Most die or go on to cirrhosis, but can be reversed with abstention.

Effects

• Cirrhosis-end stage of alcoholic liver disease from toxic effect of alcohol on the liver. Destruction of liver cells and they are replaced by scar tissue. Liver shrinks. Tx. is abstention and correct malnutrition and prevention of complications: portal hypertension, ascites, esophageal varices, veins in the esophagus that become distended due to excessive pressure from bad blood flow thru a defective liver. Pressure increases and varices rupture.

Effects

• Hepatic encephalopathy-diseased liver can not convert NH3 to urea for excretion. Rise in serum NH3 results in progressively impaired mental functioning, apathy,mood changes, sleep disturbance, confusion,coma and death.Tx is abstention,elimination of protein from the diet, and reduction of intestinal NH3 using neomycin and/or lactulose.

Effects…

• Leukopenia-impaired function of WBC. The pt. is susceptible to infection.

• Thrombocytopenia-platelet production and life is impaired from the toxic effects of the ETOH. Reversible. Can be fatal from hemorrhage.

• Sexual dysfunction-long term gynnecomastia, sterility, impotence, and decreased libido.

Intoxication and Withdrawal

• Intoxication-disinhibition of impulses sexual and/or aggressive, impaired judgment, impaired social functioning,unsteady gait,slurred speech, flushed face. Usually at blood levels between 100-200. Death @ 400-700.

Withdrawal

• Within 4-12 hrs. after reduction or cessation of drinking may see:coarse tremor of hands, tongue,N/V,tachycardia,sweating, elevated B/P, anxiety, mood lability,irritability, hallucinations, insomnia. May progress to alcoholic delirium. (DTs). DTs is usually 2-3 days after stopping use. Tx by substitution therapy with Benzodiazpines.

Withdrawal

• Librium, Ativan, Valium, Serax and Xanax in larger than usual doses and taper down by 20-25 % each day until withdrawal complete. In cases of liver damage accumulation of the longer acting benzodiazapine may be a problem. Will use shorter acting ones. Also multivitamin therapy and thiamine. Replacement therapy prevents neuropathy, confusion and encephalopathy.

Assessment At risk Populations

• Obtain thorough information from all age levels of patients.

• Adolescents- About 50% have used drugs or alcohol by the time they graduate. Binge drinking and peer pressure play a part.

• Kids at more risk are: those in chaotic family situations, inconsistent rules, the family uses substances,kids who feel like they do not fit in.

• Easy accessibility and the need to belong

• An adolescent can become addicted faster than an adult (within 6 months of heavy drinking).

Assessment

• Adolescents- Talk to them, get their confidence, have literature (age leveled) in the waiting area.

• Women- About 40% of those diagnosed with substance abuse disorders.

• More hidden in women still caries more of a societal stigma.Women experience symptoms of alcoholism faster than men and there is a strong link with stress and use. Substance abuse in women is coupled with a high incidence of abuse and exploitation. Not diagnosed as S.A. as readily as men-might be diagnosed as depression.

Assessment

• The elderly- The hidden addiction. We don’t think of them being “alcoholic”. Common are alcohol and benzodiapines for sleep and relief of anxiety. The drugs are metabolized more slowly so their effects are more intense. They last longer in the body.

• The unborn child- all drugs cross the placenta and all have harmful affects on the fetus. About 5,000 kids a year are born with FAS. Is a cause of MR.

• Criteria for at risk alcohol use-MEN>14 drinks/wk 4 on any occasion.Women>7 a week 3 on one occasion.

Assessment – At Risk

• The impaired Professional:

• What would you do if one of your colleagues came in intoxicated or “hung over”?

• Our professional responsibility is to intervene. You may save her/his life. Protect the public. Must report. We are licensed. An organized intervention. Keep objective data about job performance.

Impaired Practice

• In nursing , report to Intervention Project for Nursing (IPN) 1-800-270-2420

• www.ipnfl.org for nurses

• All other health related professionals-PRN

– Professional Resource Network 1 (800) 8888776 or (904) 277-8004

Assessment

• Develop trust.

• Perform assessment all age levels. CAGE

• Ask question non-judgmentally, without hurry. (sometimes people want someone to find out because they feel so out of control- relieved).

• Ask about patterns of consumption, frequency and amount on an average day.

Assessment

• Any medical conditions that are suggestive of an alcohol related connection.

• Explain to the patient that you will be giving and prescribing medications that can be potentiated if the person drinks or uses other CNS depressants. Ask if self medicated prior to coming.

• Also explain that bleeding may be harder to control if they has a pattern of using alcohol. Need to know in order to provide safe care.

Assessment

• You also need to know if someone is in recovery. Ask their feelings about the use of pain meds. Some will not want them. Discuss options. May want something non-addictive. Some will not realize the potential for relapse and will take whatever is prescribed.Might set up a trigger mechanism.

Assessment

• Ask about any hospitalizations suggestive of alcohol related accidents.

• Ask about other meds. Often, there is usually poly drug use .

• Clinical observations along with a thorough medical history help you to provide safer care.

• Cage (see text book), AA (see handout) .

• Have information in the waiting room. Have info that lists local resources for help. Education is important for the patient and family.

Assessment

• Handout of the questions to ask in the substance abuse history.

• You are teaching while asking the questions. Point out that it is a disease.

Defense mechanisms in Alcoholism

• Denial.

• Rationalization- explains the behavior as appropriate. “ I’m not an alcoholic, because I don’t drink every day”.

• Projection- blaming of external events and people for stimulating the desire to drink.

• Minimization- not as bad as others say.

What can you do?

• Become more knowledgeable.

• Recognize it is not just the person with the disease who suffers.

• Fight your discomfort about talking about it. Talk with them.

• Accept that it is an illness and can be treated (no matter who you may know that has not been able to maintain sobriety).

• Maintain the high index of suspicion

What can you do

• Familiarize yourself with local tx. And recovery programs- Go to an open AA meeting to learn more about it.

• Nursing Diagnoses see page 251 of text.

• Care on the unit begins with detoxification and progresses to long term recovery with abstinence.

• Education of client and family is important. See page 254 of text.

Treatment

• Tell about AA. (1935) peer support, spiritually based program. See page 255.

• Familiarize yourself with the Steps if working with alcoholics.

• Staying sober and helping others to stay sober.

Treatment

• Disuffiram (Antabuse):

Deterrent to drinking in the pt. having a hard time staying sober. If take ETOH will get uncomfortable symptoms due to the accumulation of acetaldehyde in the blood. Flushed skin, throbbing in head and neck,N/V , difficulty breathing, sweating. tachy., weak , blurred vision.

Treatment

• If taking Antabuse must not do anything with alcohol: cough meds, after shave lotions, vanilla, mouthwash, nail polish remover.

• Teach to read labels and carry a card.

• Still needs AA and other help.

• Revia – to control craving (naltrexone). Originally used for heroin addiction, but works with ETOH.

Communication Techniques

• http://edtech.tennessee.edu/%7Edpatter2/MET/Start.htm

Sedative hypnotic or Anxiolytic abuse and dependence

• CNS depressants. See page 230 for names of drugs.

• All depressant are additive with each other, there is no blocking agent or something we can give to reverse an OD. Low doses produce euphoria and excitement.

• If the pt. has been taking and withdraws abruptly there can be hyperexciteablity and seizures and death. Physiological dependence.

CNS depressants

• Can produce psychological dependence-craving.

• Used to treat insomnia and anxiety-short term.

• Pattern of addiction usually begins with prescription use.The pt. increases the dose and develops tolerance. May go from MD to MD to get more RX. Or use with young kids who get high with it, use with other substances. Illegal use.

• Intoxication presents like ETOH intoxication. Withdrawal occurs depending on the short or long term half lives of the drug.

CNS Stimulants

• Behavioral stimulation and psychomotor agitation.

• Caffeine, nicotine, cocaine, amphetamines, non amphetamine like diet pills Ritalin, Pemoline.

• Cocaine can be snorted, crack- highly addicting, rapid onset but short acting.

CNS Stimulants

• Highly pleasurable but effects wear off followed by marked dysphoria and craving.

• Poly substance taking upper in the morning and downers at hs.

• Effects on body-excite the whole nervous system. Tremors, restlessness, anorexia, agitation,insomnia,alertness,elation,power. Chronic use can lead to paranoia, hallucinations, and aggression.

CNS stimulants

• Increased B/P, HR, Dysrhythmias,increased oxygen demand by heart and severe vasoconstriction, resulting in MI,VF, pulmonary hemorrhage, intracranial bleeding, diffculty, voiding, constipation, aphrodisiac effect.

• Intoxication p.236.

• Withdrawal-fatigue,dysphoria,bad dreams,increased appetite, sleeping problems, agitation motor retardation. Crash depression. May be suicidal

Opioid

• Pain meds,tx of diarrhea, relief of cough, Addictive. see p238

• Produce euphoria and decrease anxiety.

• Commonly abused by professionals.