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ADDICTIONS 101 A Refresher Course The Brain and Addiction Neuroanatomy William J. Lorman, PhD, MSN, PsyNP, CARN-AP Neurophysiology V. P. & Chief Clinical Officer, Livengrin Foundation, Inc. Agonist Spectrum Ass’t Clinical Professor, Graduate Nursing Dept., Drexel University [email protected]

mesolimbic pathway Drug Categories

û Alcohol û Canabis û Cocaine û CNS depressants û CNS stimulants û Opioids û Hallucinogens û Inhalants û Anabolic-androgenic steroids û Synthetic û OTC û Club drugs

Stahl S M, Essential Psychopharmacology (2000)

Addicting Molecules Is there a single pathway to addiction?

Nicotine Alcohol ó Drugs of abuse have very different structures and neurotransmitter targets in the brain, but they all exhibit: ◦ acute reward ◦ chronic reward Cocaine Heroin ◦ sensitization ◦ negative withdrawal symptoms ◦ associative cue learning ◦ incentive motivation (relapse) ó A progression from impulsive to compulsive drug use (which defines the progression from abuse into addiction).

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The Body’s Own Psychotropics

cannabis GABA amphetamine ó The brain makes its own morphine (beta

alcohol endorphin) and its own marijuana DA (anandamide) opioid ó The brain may even make its own antidepressants, anxiolytics, and cocaine hallucinogens ACh

nicotine PCP ó Drugs often mimic the brain’s natural alcohol neurotransmitters 5HT Glu ó Often, drugs are discovered prior to the hallucinogen natural neurotransmitter

Stahl S M, Essential Psychopharmacology (2000)

Exogenous vs. Endogenous Drugs We knew about : TRANSITION TO ó Morphine before the discovery of β- ADDICTION endorphin ó Marijuana before the discovery of cannabinoid receptors and anandamide ó Valium and Xanax before the discovery of benzodiazepine receptors Taking drugs may begin as a voluntary choice ó to seek a pleasant stimulus, but for addicts, that Elavil & Prozac before the discovery of choice is no longer volitional, even in the face the serotonin transporter site of terrible personal consequences.

ó During the initial stages of addiction Types of Craving ◦ The pleasure derived from various drugs’ activation of the brain’s natural reward system promotes continued ó Cue-based craving drug use ◦ Response to environmental cue ó Repeated exposure to drugs induces the brain ◦ Cue creates internal state which is recognized as mechanism of dependence craving ó Dependence leads to daily drug use to avert the ◦ Most notable in cocaine & nicotine unpleasant symptoms of drug withdrawal ó State or stress-based craving ó Further prolonged use of drugs lead to more ◦ Emotional tone, level of perceived stress, state of long-lasting changes in the brain that may self care set the state underlie the compulsive drug-seeking behavior ◦ Craving appears to emerge out of difficult and related adverse consequences that are the emotional states hallmarks of addiction. ◦ Most notable in alcohol & sedatives

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ó Stressors can trigger drug craving in addicts. THE IMPORTANT ñ Sinha R, Catapano D & O’Malley S. (1999). Stress-induced craving and stress response in cocaine dependent individuals. Psychopharmacology , 142, 343-351. ROLE OF STRESS ◦ One explanation is that abused drugs raise levels of cortisol which plays a primary role in stress responses. ◦ Cortisol raises the level of activity in the mesolimbic reward system. ñ Kreek MJ & Koob GF. (1998). Drug dependence: Stress and dysregulation of brain reward pathways. Drug & Alcohol Dependence , 51(1-2), 23-47. ◦ By these mechanisms, stress may contribute to the abuser’s desire to take drugs in the first place, as well as the subsequent compulsion to keep taking them.

The Anatomy of the Nervous System

ó A complex wiring diagram, carrying electrical impulses to wherever the ‘wire’ is plugged in – at the synapse. ó There are an estimated 100 billion neurons, which make over 100 trillion synapses in the human brain.

Stahl, S., Essential Psychopharmacology

The Anatomy of the Nervous System Fast-Onset vs. Slow-Onset Signals

ó Neurons send electrical impulses from ó Some neurotransmitter signals are very one part of the cell to another part of the fast in onset cell. ◦ Rapidly change the flux of ions, thus ó At the presynaptic terminal, chemicals are altering the excitability of the neuron released to any of a variety of sites on a second postsynaptic neuron or to other ◦ Glutamate: universally stimulates almost sites distant to the synapse by diffusion. any neuron ó The postsynaptic neuron can also “talk ◦ GABA: universally inhibits almost any back” to the presynaptic neuron with neuron chemical messengers of its own.

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Fast-Onset vs. Slow-Onset Signals Neurotransmitters

ó Some neurotransmitter signals take ó The known or suspected longer to develop neurotransmitters in the brain already ◦ Called neuromodulators number several dozen. ◦ Examples are the monoamines norepi- ó Based on theoretical considerations of nephrine and serotonin as well as the amount of genetic material in various neuropeptides neurons, there may be several hundred to several thousand unique brain chemicals.

Categories of Neurotransmitters Co-Transmitters

1. Cholinergic – Acetylcholine ó Each neuron was originally thought to use 2. Monoamines one neurotransmitter only and to use it 1. Catecholamines – Norepinephrine, at all of its synapses. Dopamine ó It is now known that many neurons have 2. Indoleamines - Serotonin more than one neurotransmitter 3. Amino acids – GABA, Glutamate ó Co-transmission often involves a 4. Neuropeptides – Substance P, Enkephalin monoamine coupled with a neuropeptide 5. Lipids - Anandamide

Chemical Neurotransmission: Co-Transmission A Team of Molecular Players ó Under some conditions, the monoamine is ó Neurotransmitter released alone; under other conditions, both are ó Specific ions that interact with ion channels released ó Various enzymes ó The rationale behind the use and action of ó Transport carriers Each molecule is: many drugs arose in the era of thinking about ó Active transport pumps • a known or potential site one neuron using only one neurotransmitter, so ó Second messengers of drug interactions that the more selective a drug, the better it ó Receptors • a theoretical site of mal- could modify neurotransmitters. ó Transcription factors function that could possibly contribute to a nervous or ó It is now believed in order to replace or ó Genes mental disorder influence abnormal neurotransmission, it may be ó Gene products necessary to use multiple drug actions.

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Opening/Closing of Ion Channels

ó Ions: Sodium, Potassium, Chloride, Calcium ó Regulation of opening/closing: ◦ Electricity ñ Called voltage-gated ◦ Neurotransmitter binding to a receptor ñ Called ligand-gated

Transport Carriers

ó Bind to molecules that need to shuttle into cells that otherwise would not be able to get into the cell through the membrane. ó If a transport carrier is coupled with an energy-providing enzyme such as ATPase , it is called an active transport pump . ó Example: reuptake of neurotransmitter into its presynaptic neuron

Stahl S M, Essential Psychopharmacology (2000)

Active Transport Pump Reuptake Inhibition

Stahl, S., Essential Psychopharmacology Stahl, S., Essential Psychopharmacology

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Regulation of Receptors Regulation of Enzymes

ó Drugs can cause: ó The enzymes most important in the ◦ A decrease in the rate of receptor synthesis neurotransmission process are those that ñ Down-regulation or desensitization make and destroy the neurotransmitters ñ Takes days to occur ó ñ Diminishes the sensitivity of neurotransmission There are very few drugs that are enzyme ◦ Immediate desensitization by activating an enzyme inhibitors. (Most drugs target the that makes the receptor immediately insensitive. receptors) ◦ An increase in the rate of receptor synthesis ó The binding of inhibitors can be either ñ When receptors are blocked by a drug reversible or irreversible ñ Increases sensitivity of neurotransmission ñ May also produce a disease (e.g., Tardive dyskinesia)

Special Properties of Receptors Pharmacological Subtyping

ó They are organized into multiple subtypes ó Each neurotransmitter can act on more ó Their interactions with drugs define the than one neurotransmitter receptor. type of drug (i.e., agonist, antagonist, ó There are multiple subtypes of receptors partial agonist, etc.) for every neurotransmitter ó Allosteric modulation ◦ Serotonin: 1A, 1D, 2C ◦ Norepinephrine: α1, α2 ◦ Dopamine: D2, D4

There is a spectrum of degree to The Agonist Spectrum which a receptor can be stimulated ó Naturally occurring neurotransmitters stimulate receptors ◦ Agonists ó Various drugs acting at a receptor exist in a spectrum from full agonist to antagonist to inverse agonist

No longer considered

Stahl, S., Essential Psychopharmacology

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AGONIST ANTAGONIST

ó Stimulates receptors ó Blocks the actions of everything in the ó Function Example agonist spectrum ◦ Turns on the synthesis of the second ó By themselves, antagonists have no messenger to the greatest extent possible intrinsic activity ◦ Opens ion channel column completely ó Function Example ◦ Neither opens nor closes ion channels

INVERSE AGONIST PARTIAL AGONIST

ó Does the opposite of agonists ó Exerts an effect similar to but weaker than that of the full agonist ó Function Example ó Example ◦ Causes ion channel to close completely ◦ Opens the ion channel to a certain extent but only partially as compared with the full agonist ó Note: An antagonist will also block the ◦ ‘Light & Dark’ as an analogy action of an inverse agonist just as it ó Can appear as net agonists or as net would an agonist. antagonists depending on the amount of naturally occurring full agonist that is present

A Modern Formulation of Psychiatric & Substance Use The The PARTIAL PARTIAL AGONIST causes AGONIST the channel to Disorders At left, the causes the close partly; in channel in its channel to this case the resting state. open partly. Partial Agonist is The AGONIST having an opens the ANTAGONISTIC channel fully. effect. Stahl S M, Essential Psychopharmacology (2000) 42

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Integration of at least four key elements Genetic Vulnerability

1. Genetic vulnerability to the expression ó People do not inherit a mental of a disease illness/SUD; they inherit a 2. Life event stressors that come that vulnerability to it . individual’s way (divorce, legal problems) ó Factors are poorly understood, multiple in 3. The individual’s personality, coping skills, number, and very complicated and social support available from others ó Different genes may be abnormal in 4. Other environmental influences on the individual (e.g., viruses, toxins, other different families with the same diseases) psychiatric illness

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The Two-Hit Hypothesis of Psychiatric & SUD Disorders SUBSTANCE USE DISORDER , TOLERANCE, ó In order to manifest an overt disorder, one must not only sustain the first hit, namely INTOXICATION AND all the critical genetic vulnerabilities, but WITHDRAWAL one must also sustain a second hit of some type from the environment. DRUGS OF ABUSE

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SUBSTANCE USE DISORDER Essential Features (DSM-5) ó A cluster of cognitive, behavioral, and (Dependence – DSM-IV-TR) physiological symptoms indicating that the individual continues using the substance “A problematic pattern of substance use, despite significant substance-related leading to clinically significant problems. ó An underlying change in brain circuits that impairment or distress, as manifested may persist beyond detoxification, particularly in individuals with severe by at least 2 of 11 criteria, occurring in disorders the same 12-month period.” ◦ Behavioral effects may be exhibited in the repeated relapses and intense drug craving when exposed to drug-related stimuli.

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SUD Criteria SUD Criteria IMPAIRED CONTROL

Pathological Pattern of Behaviors ó (1) The substance is often taken in larger amounts or over a longer period than was intended. • Impaired Control ó (2) There is a persistent desire or unsuccessful • Social Impairment efforts to cut down or control use. ó (3) A great deal of time is spent in activities • Risky Use necessary to obtain, use or recover from the effects. •Pharmacological Criteria ó (4) Craving, or a strong desire or urge to use.

SUD Criteria SUD Criteria

ó IMPAIRED CONTROL: Commentary SOCIAL IMPAIRMENT ◦ In some instances of more severe substance use disorders, virtually all of the individual’s ó (5) Recurrent use resulting in a failure to fulfill daily activities revolve around the substance. major role obligations at work, school, or home. ◦ Craving is manifested by an intense desire or ó (6) Continued use despite having persistent or urge for the drug that may occur at any time recurrent social or interpersonal problems caused but is more likely when in an environment or exacerbated by the effects of the drug. where the drug previously was obtained or ó (7) Important social, occupational or recreational used. activities are given up or reduced because of use. ñ Current craving is used as a treatment outcome ó Commentary: measure because it may be a signal of impending ◦ The individual may withdraw from family activities and relapse. hobbies in order to use the substance.

SUD Criteria SUD Criteria RISKY USE PHARMACOLOGICAL CRITERIA

ó (8) Recurrent use in situations in which it is ó (10) Tolerance physically hazardous. ó (11) Withdrawal ó (9) Use is continued despite knowledge of having a persistent or recurrent physical or ◦ Commentary: psychological problem that is likely to have ñ The drug (or a closely-related substance) may be been caused or exacerbated by the drug. taken to relieve or avoid withdrawal symptoms. This now counts as the presence of withdrawal. ◦ Commentary: ñ The key issue in evaluating this criterion is not the ó NOTE: existence of the problem, but the individual’s failure to ◦ Neither tolerance nor withdrawal is necessary abstain despite the difficulty it is causing. for a diagnosis of a substance use disorder.

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Pseudoaddiction TOLERANCE

ó Symptoms of tolerance and withdrawal ó Dopamine release Stimulation of occurring during appropriate medical receptor treatment with prescribed medications ó Stimulation of receptor Activation of cAMP ó Symptoms related to undermedication ó cAMP enters nucleus Activation of CREB ◦ cAMP Response Element Binding protein ó CREB activates Dynorphin ó Dynorphin desensitizes Dopamine Receptor ó Resensitization (Reverse Tolerance) ◦ Activation of ∆ fos B

Intoxication Syndrome Heroin/Opiates

ó General Effects “Clinically significant problematic behavioral ◦ Analgesia, control coughing & diarrhea or psychological changes (e.g., inappropriate ó Effects of Intoxication sexual or aggressive behavior, mood lability, ◦ Decreased TPR, BP; confusion, miosis, impaired judgment) that developed during slurred/slowed speech, severe constipation or shortly after use of the substance.” ó Effects of Overdose ◦ Respiratory insufficiency/failure, clammy skin, seizures, coma, death

Depressants Stimulants (Barbiturates, Benzos, Alcohol) (Cocaine/Crack, Amphetamines, Nicotine) ó General Effects ó General Effects ◦ Decreased anxiety/restlessness, dysinhibition ◦ Increased alertness, energy, assertiveness, HR, BP ◦ Skeletal muscle relaxant ◦ Decreased fatigue, appetite ó Effects of Intoxication ◦ Manic presentation, dilated pupils ◦ Slurred/slowed speech, disorientation, change ó Effects of Intoxication in sensorium, sedation/violence, memory ◦ Increased TPR, BP, diaphoresis, N/V, hyperactive impairment, trauma/accidents reflexes, repetitive compulsive behaviors, biting/self-mutilation ó Effects of Overdose ó Effects of Overdose ◦ Respiratory failure, stupor, coma, death ◦ Cardiac arrhythmias, Seizures, Hallucinations, ◦ Status epilepticus Death

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Hallucinogens Cannabis (LSD, PCP, MDMA, Ketamine etc.) ó General Effects ó General Effects ◦ Mild hypnotic; exaggerates mood & personality ◦ Altered perceptions, intensifies sensations ◦ Relaxation, increased appetite ó Effects of Intoxication ó Effects of Intoxication ◦ Delusions, impaired judgment/distorted ◦ Blood shot eyes, coughing, loss of motor reasoning coordination, confusion ó Effects of Overdose ó Effects of Overdose ◦ Intense ‘trip’ experience, Psychosis, Death ◦ Dissociation/depersonalization, poor concentration, psychosis, anxiety reaction, ◦ MDMA: malignant hyperthermia, seizures, N/V paranoia

Inhalants Withdrawal Syndrome

ó Effects of Intoxication ◦ Lethargy/restlessness, slurred speech “The development of a substance-specific ◦ Tremors, headache, N/V syndrome due to the cessation of (or ◦ Ataxia, confusion, depression reduction in) substance use that has been ó Effects of Overdose heavy and prolonged. The syndrome ◦ Renal/liver failure causes clinically significant distress or ◦ Peripheral neuropathy impairment in social, occupational, or ◦ Coma/Death other important areas of functioning.”

WITHDRAWAL STATES Heroin/Opiates

ó Withdrawal syndrome is the predictable constellation of signs and symptoms following abrupt discontinuation of, or rapid decrease in, intake of a substance that has been used ó Rhinorrhea • Cramps consistently for a period of time. ó Yawning • Nausea ó Usually the opposite of a substance’s direct • Chills pharmacologic effects. ó Loss of appetite ó Substances in a given pharmacologic class ó Irritability • Diaphoresis produce similar withdrawal syndromes ó Tremors • Body aches ó The onset, duration, and intensity are variable, depending on the particular agent used, the ó Lacrimation • Panic duration of use, and the degree of neuroadaptation

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Depressants Stimulants

ó Anxiety ó Apathy ó Insomnia ó Hypersomnia ó Tremors ó Irritability ó ó Delirium Depression ó Disorientation ó Seizures ó Possible death

Cannabis Hallucinogens & Inhalants

ó Occasional reports of insomnia ó Unknown ó Hyperactivity ó Decreased appetite

Club Drug Facts Post-Acute Withdrawal Syndrome Name Class Street Name Desired Effect Risks

MDMA Stimulant Ecstasy Euphoria Tachycardia Adam Energy ↓ serotonin ó PAWS Rollies ó Anxiety GHB Sedative Georgia-Home Boy Relaxation and Post-use anxiety well-being Liquid XTC ó Depression EZ Lay Cannibi- Synthetic K2 Relaxation and well- akathisia, tremor, ó Autonomic Instability cyclohex- Cannabinoid being palpitations, headache, inol nausea, vomiting, Spice depression ó Insomnia/hypersomnia Kronic Ketamine NMDA Special K Vivid dreams & Dissociation Antagonist hallucinations ó Drug cravings “K” Cat Valium ó Poor concentration/attention deficits Mephadrone Synthetic Plant Food Euphoria Post-use depression and Stimulant violence Bath Salts Hyperactivity Teeth grinding

LSD Hallucinogen Acid Hallucinations Post-use flashbacks

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Responsibilities

ó Addictions nurses are concerned with the actual or potential responses of people to addictive substances or behaviors. These responses include: ◦ Conditions which increase vulnerability to or risk for addiction ◦ The consequences that occur when people use those substances or engage in those behaviors ◦ The responses of people to dependence on ADDICTIONS NURSING addictive substances/behaviors ◦ The conditions that affect recovery and PRACTICE rehabilitation

Facts About Addiction

ó Addiction affects 22 million Americans ó 75% of addicts are in the workforce PROBLEMS ó Only 9% of Americans who need ASSOCIATED WITH treatment receive it ADDICTION ó New medications can help control craving ó Relapse is a normal part of the disease ó Treatment can work

Physiological Problems

ó Altered levels of CNS responsiveness ◦ Hyperactivity, sedation, seizures ó Altered psychomotor patterns ó GI dysfunctions ó Cardiovascular dysfunctions ó Hepatic disorders ó Respiratory disorders ó Difficulty with pain management ó Increased risk of STDs

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Psychological Problems Family Problems

ó Impulse dyscontrol ó Family life disruption/crises ó Unmanageable feeling states ó Role model failure ◦ Mood symptoms, shame, guilt, anger ◦ Marital infidelity, nonsupport of dependents ◦ Hoplessness/helplessness/aggressiveness ó Enabling behaviors of family members ó Disruption in self-concept ó Children assume role of parents ó Excessive use of defense mechanisms ó Instability

Social/Community Problems Workplace Problems

ó Disturbed interpersonal relationships ó Stressful environments, maladaptive ó Altered productivity at work coping strategy ó Inability to behave/social inappropriateness ó Absenteeism, lateness ó Deterioration in social life ó Decreased morale ó Increased criminal activity, violence ó On the job accidents ó Transient domiciles ó Inconsistent behavior at work ó Risk factors: poverty, racism, unemployment ó Deterioration in work performance ó Homelessness

Legal Problems Spiritual Problems

ó DUI ó Disruption in spiritual connectedness ó Prostitution ó Diminished purpose in life ó Arrests for disturbing the peace ó Feelings of meaninglessness ó Increased criminal activity ó Loss of control over self ó Illegal drug sales/distribution ó Domestic violence

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Cognitive Problems

ó Problems in acquisition of new information ó Problems in learning new life skills/healthy patterns of living ó Altered states of consciousness/clouded The Progression sensorium of Addiction ó Impaired problem solving ó Dysfunctional views of the world and other people ó Lack of insight

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The Addicted Person During Periods of Abstinence:

ó The addict’s behavior creates a disturbed ó The addict feels lonely and isolated because he environment for those who live with him. no longer has meaningful relationships with ó As addiction progresses, the addict becomes people more preoccupied with the drug ó These feelings are compounded by additional ◦ Maintaining a supply feelings of shame, fear, and guilt ◦ Covering up ◦ Despairing about getting high again ó To survive, the addict denies these feelings and ◦ Though the family is loved, they take a back seat places the blame for them on others, family, friends, and co-workers

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The Family is Drawn in FAMILY RULES

ó Since the addict cannot bear to feel, he ó Every family has rules that keep family life cannot tolerate family members running smoothly. Some rules are spoken, expressing honest feelings others are unspoken but understood. ó As the addict loses control over his own life, he demands and gains control over the family’s life ó The family learns to plan its life around the addiction

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Rule #1 Rule #2

ó The addict feels he is not to blame for ó Everyone must protect the addict from using. The blame is placed on someone the consequences of using. else in the family, usually the spouse or a child who is acting out.

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Rule #3 What Can The Family Do?

ó Don’t talk to anyone about the family ó Hold the addict/alcoholic responsible for situation: his/her behaviors. ◦ To other family members ó Be consistent in enforcing consequences. ◦ To outsiders ó Acknowledge your anger and frustration ◦ Letting no information out or new with the addicted person. information into the family keeps the addict’s grip on family members ◦ A rigid insistence on family loyalty

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Initial Nursing Assessment THE NURSING ASSESSMENT ó Purpose: ◦ to determine the need for medication and medical management ó Includes: ◦ Evaluation of predicted withdrawal severity SCREENING TOOLS ◦ Presence of medical comorbidity LAB TESTS ◦ Presence of psychiatric comorbidity SUBSTANCE-INDUCED DISORDERS INFECTIOUS DISEASES

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Medical Perspectives Methods of Assessment

ó Persons with addictive disorders often do ó Interviews with the patient not receive regular health care. ó Interviews with collateral sources (family ◦ Medical care for acute and chronic conditions members, friends, other providers) can be fragmented and inefficient ó Observation of the patient ◦ They miss opportunities to receive preventive ó Structured interviews health care ó Self-report questionnaires and rating ◦ In addition to the direct effects of scales intoxication, overdose and withdrawal, abused ó Psychological tests substances can affect every body system ó Physical examination & laboratory tests

Collect Data in a Systematic and BEFORE YOU TREAT: Ongoing Way ó Obtain a detailed Drug & Alcohol ó Objective & subjective data regarding history current health status ◦ Including current/recent use history ó Past medical, psychiatric & addictions ó Urine Drug Screening history ◦ Screening tests have not been developed ◦ Review every body system or are not readily available for newer ◦ History of psychiatric symptoms ‘designer drugs’ ◦ SUD history ó Determine priority of data collection ó Family history, current family status ◦ Based on the client’s immediate physical needs. ó Mental status

Collect Data in a Systematic and Collect Data in a Systematic and Ongoing Way Ongoing Way ó Spiritual health ó Current use of addictive ◦ Concept of higher power substances/behaviors ◦ Source of hope and strength ◦ Duration, frequency, route ó Personal, developmental & social history ◦ Effect of the substance/behavior ó Work and/or school adjustment ◦ Consequences of the substance/behavior ◦ Presence of intoxication/withdrawal/tolerance ó Relationships with others ◦ Presence/absence of cognitive deficits ó Coping skills, ability to adapt ◦ Suicide risk assessment (include protective factors)

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Assess the Stage of Change Next Steps

ó Precontemplation ó Use standardized assessment forms, ó Contemplation techniques, tools that have been validated ó Preparation through research and clinical practice ◦ Screening Tools ó Action ñ Drug Abuse Screening Test (DAST) ó Maintenance ñ Alcohol Use Disorders Identification Test (AUDIT) ó Relapse/reoccurrence ñ Addictions Severity Index (ASI) ñ Substance Abuse Subtle Screening Inventory (SASSI) ◦ Withdrawal Assessment Tools ñ CIWA, CINA, COWS

Laboratory Management

ó CBC ó Breathalyzer or blood ó Electrolytes alcohol level ó Magnesium ó Skin test for tuberculosis ó Calcium SPECIAL ó ó Phosphate Chest x-ray ó ó Liver enzymes EKG ó POPULATIONS ó Urine drug screen Hepatic enzymes ó ó Pregnancy test Sexually transmitted diseases

Adolescent Use Child with FAS Prevention Strategies ó Provide positive role models. ó Reinforce dangers of use. ó Teach positive behaviors. ó Establish limits, structure. ó Anticipate pressures. ó Reinforce positive coping. ó Provide life skills training. ó Monitor media use.

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EFFECT OF Differential Diagnosis SUBSTANCE USE

Many disorders may mimic substance abuse and EUPHORIA DYSPHORIA Substance abuse may mimic (INTOXICATION) (WITHDRAWAL) many disorders (MANIA/IRRITABILITY) (DEPRESSION/ANXIETY)

Substance-Induced Mental Alcohol Intoxication Disorders BAL Consequences ó Nine substance-induced disorders in 0.02-0.05 Mildly impaired coordination DSM-IV Potential changes in behavior ◦ Organic brain syndrome disorders 0.08-0.1 Impaired driving, slurred speech, ñ Substance-induced delirium, persisting dementia and ataxia,  sensory function persisting amnestic disorder 0.1-0.15 Impaired balance, gross judgment ◦ Mimics of Axis I disorders and cognition impairment ñ Substance-induced psychotic, mood and anxiety 0.2-0.3 All sensory motor function impaired disorders 0.3 & up Potential cardiovascular and ◦ Substance-induced sexual dysfunction respiratory collapse ◦ Substance-induced sleep disorder Coma, death ◦ Hallucinogen persisting perceptual disorder

INFECTIOUS Challenges for the Clinician

DISEASES RELATED ó To differentiate the occult or incipient TO ALCOHOL AND infection from symptoms of intoxication OTHER DRUG USE or withdrawal ó To recognize an atypical presentation of an infection modified by defective host defenses (splenectomy or AIDS) or the patient’s self-medication with antibiotics or analgesics ó 60% of hospital admissions among IDUs are related to acute infections

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Skin & Soft Tissue Infections Respiratory Infections

ó Organisms most often seen: ó Pneumonia ◦ S. aureus ó Drug-induced bronchospasm ◦ Groups A, C, F & G beta-hemolytic streptococci ó ó IDUs who mix their drugs with saliva or Pulmonary edema who lick their needles before injecting are ó Development of various types of foreign pront to development of polymicrobial body granuloma from contaminants in infections with viridans streptococci injected materials (cotton, starch or talc) ó Repeated injection of nonsterile, potentially vasoactive opiates can cause ischemic ó TB necrosis at the injection site.

Eye Infections Other Common Infections

ó IDUs have an increased incidence of ó HIV/AIDS bacterial and fungal endophthalmitis ó Sexually transmitted infections ◦ C. albicans endophthalmitis as part of a ó Hepatitis syndrome of disseminated candidiasis in IDUs who inected ‘brown heroin’ (from fungal contamination of the lemon juice used to dissolve the drug) ◦ Most commonly reported bacterial causes include S. aureus and Bacillus cereus

Planning Care

ó Developed through collaboration among the addictions nurse, the multidisciplinary treatment team, the patient and significant others. ó The plan of care: ◦ Addresses priorities first ◦ Incorporates principles of appropriate treatment PLANNING, IMPLEMENTING ◦ Includes specific interventions that reflect current science and evidence of effectiveness & EVALUATING CARE ◦ Includes health education ◦ Designates a discharge plan ◦ Includes strategies for health promotion and restoration of health

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Implementation of Care Evaluating Care

ó Interventions are based on problem ó Document the patient’s responses to identification interventions ó Interventions include: ó Examine the patient’s progress toward ◦ Detoxification as needed attainment of outcomes ◦ Appropriate administration of pharmacologic ó Use ongoing assessment data to revise plan therapies of care as needed. ◦ Development of a therapeutic relationship ◦ Maintain safety ó Involve the patient, significant others, and ◦ Health teaching other healthcare providers in the evaluation ◦ Involvement of patient in goal setting of care. ◦ Attention to family issues ó Ensure that evaluation is an ongoing process. ◦ Referral for ongoing support

EARLY INTERVENTION

ó DUI Program ó Patients do not meet criteria for chemical dependency THE LEVELS OF CARE ó Program is designed to explore and address problems or risk factors that are related to substance use and to assist patients in recognizing the harmful consequences of inappropriate substance use.

GENERAL OUTPATIENT INTENSIVE OUTPATIENT

ó Patients come in once or twice a week ó Patients come in 3 times a week – either ◦ Weekly individual therapy session during the evening or during the day. ◦ Weekly group therapy session ◦ Three 1-hour lectures ◦ Three group therapy sessions ◦ Individual sessions as needed

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PARTIAL HOSPITALIZATION RESIDENTIAL REHAB

ó Patients come in Monday through Friday ó This is a therapeutic community designed from 8 a.m. to 4 p.m. to maintain recovery. ◦ Two individual therapy sessions per week ó Patients attend: ◦ Four group therapy sessions per week ◦ Individual therapy sessions ◦ Twenty hours of lectures per week ◦ Group therapy sessions ◦ Educational lectures ◦ Other activities

DETOXIFICATION ADDITIONAL SERVICES

ó Detoxification is the gradual safe ó Dual Diagnosis elimination of the drug from the body. ó Family Program ó Occurs over 3 to 5 days ó Gender-Focused Groups ◦ Depressants (alcohol & benzodiazepines) ó 12-Step Meetings (Support Groups) ◦ Opiates (heroin, Oxycontin, Vicodan, etc.) ó Aftercare Services/Case Management ó There is no detoxification for stimulants or hallucinogens (cocaine, PCP, LSD, Meth)

ó Motivation-based interventions have been found to be the most effective in treating co-occurring disorders ◦ Adapted to the patient’s motivation for change ó Changes in maladaptive behavior occur over a series of stages ó Stages of Treatment provides a framework MOTIVATION-BASED for assessing: ◦ Motivational states TREATMENT ◦ Setting goals ◦ Selecting stage-appropriate interventions

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Stages of Treatment Relationship between Stages of Treatment ó Treatment progresses through a series of four and Stages of Change stages: Stages of Treatment Stages of Change 1. Engagement 2. Persuasion ó Engagement ó Precontemplation 3. Active treatment 4. Relapse prevention ß Each stage is defined in terms of ó Persuasion ó Contemplation ◦ the patient’s AOD use, and ◦ the nature of the relationship with the DD Clinician ó Active treatment ó Action ó When a patient’s stage of treatment is determined, appropriate goals can be identified and a treatment ó Relapse prevention ó Maintenance plan formulated.

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Examples of Clinical Interventions for the ENGAGEMENT Engagement Stage ó Definition ó Outreach ◦ Patient does not have regular contact with ó Crisis intervention the clinician ó Support and assistance to social networks ó Stabilization of psych symptoms – ó Goal medication management ◦ To establish a working alliance with the ó Family meetings patient ó Close monitoring

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Examples of Clinical Interventions for the PERSUASION Persuasion Stage ó Definition ó Individual and family education ◦ Patient has regular contact with clinician, but ó Motivational interviewing does not want to work on reducing substance ó Social skills training abuse ó Safe housing (‘damp’ housing) ó ó Goal Medication management ◦ To develop the patient’s awareness that ó Psychological preparation for lifestyle substance use is a problem changes necessary to achieve remission ◦ Increase motivation to change

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Examples of Clinical Interventions for the ACTIVE TREATMENT Active Treatment Stage ó Definition ó Family and individual problem solving ó Active treatment groups ◦ Patient is motivated to reduce substance use, ó Social skills training as indicated by reduction for at least 1 month but less than 6 months ó Self-help groups ó Individual counseling ó Substituting activities (e.g., work, sports) ó Goal ó Pharmacological treatments to support abstinence ◦ To help the patient further reduce substance ó Safe housing (‘dry’ housing) use and attain abstinence ó Psychoeducation ó Stress management and coping skills

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Psychoeducational Groups

ó Educate and share knowledge about disease TYPES OF GROUPS ó Early in recovery ó Helps in precontemplative and contemplative stages ó Format ◦ Leader led ◦ Interactive ◦ May use slides or props

Skills Group/Focus Group Interpersonal Process Group

ó Cultivates skills needed to remain abstinence ó Examines developmental experiences as ó Practice is essential to improve functioning they relate to current situations ó Provides education specific to the skill or ó Discuss ‘here and now’ issues topic of the group ó Probing of individual and interactions ó Format ó Format ◦ Interactive ◦ psychotherapy ◦ Focus on specific topics (e.g., anger mgt, stress mgt) ◦ May give homework

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Support Groups

ó Make connections to community ó Support ongoing recovery ó 12-step or other format EXAMPLES OF TYPES ó Engage with sponsor/mentor OF THERAPY ó Format ◦ Peer support ◦ Education

Individual Therapy Family Therapy

ó Designed to bring about modifications of ó Focuses on examining and improving feelings, thoughts, attitudes, and behaviors ◦ Family processes that have caused problems for the person. ◦ Communication ó Used as a component of total treatment ◦ Decision-making plan ◦ Problem solving ó Evaluate response, side effects and adherence to medications prescribed. ó Discharge planning and coordination are an essential part of therapy.

Dialectical Behavior Therapy (DBT) Mindfulness

ó Developed to treat patients with ó Main theorist: Dr. Jon Kabat-Zinn Borderline Personality Disorder ó Defined as paying attention in a particular ó Has been adapted for use across many way: diseases including SUD. ◦ On purpose ó Treatment addresses the following ◦ In the present moment functions: ◦ Nonjudgmentally ◦ Improving patient motivation to change ó Engages the patient to be with their ◦ Enhancing patient capabilities thoughts, not to act on them. ◦ Generalizing new behaviors ó Promotes stress reduction & improve ◦ Structuring the environment mood

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Acceptance & Commitment Contingency Management Therapy ó Can be used for short term or long term ó Use of prizes or rewards for abstinence therapy and treatment adherence ó Emphasizes ó Based on principles of operant ◦ Values conditioning ◦ Forgiveness ó Reinforces positive outcomes ◦ Acceptance ◦ Compassion ◦ Living in the moment ó Goal: to create a rich and meaningful life

Community Support Management of Pain

ó Part of aftercare ó Pain management often becomes an issue. ó Continuous involvement with support in ◦ Fear of causing or worsening addiction the community improves abstinence and ñ This management style generally results in inadequate pain management and frustration for sustained recovery. patient and provider. ó Programs available ◦ With opiate dependence, pain control can be ◦ Twelve Step Programs – AA, NA achieved only with substantially higher doses ◦ Secular Organization for Sobriety (SOS) of opiates ◦ AlAnon & AlAteen ñ Once a dose is determined, pain meds should be given on a regular schedule rather than as needed. ◦ ACOA

Types of Pain Biological Pain Signals

ó Objective ó Aching ◦ Biological ó Sore ◦ Nociception ó Burning ◦ Pain ó Subjective ó Sharp ◦ Psychological ó Tingling ◦ Suffering ó Cramping ó Pounding ó “Pain is mandatory, suffering is optional.” ñ Dalai Lama

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Psychological Pain Signals

ó Awful ó Agonizing ó Torturing MEDICAL ó Dreadful CONSEQUENCES ó Distressing ó Excruciating ó Grueling

Alcohol Alcohol

ó Medical consequences seen in almost ó Neurologic Consequences every organ system ◦ Head trauma ◦ Women are more susceptible to many of the effects at lower doses because of less first- ◦ Alcohol can lower the seizure threshold in pass metabolism of alcohol and lower body epileptics and seizures may be the presenting sign weights. of an intracranial hemorrhage ó Withdrawal, Seizures and DTs ◦ Cognitive impairment (Wernicke-Korsakoff) ◦ Benzodiazepines are the only medications ñ From thiamine deficiency (confusion, ataxia, nystagmus) proven to ameliorate symptoms of ñ Treat with parenteral thiamine 100mg administered before glucose withdrawal and decrease the risk of seizures ◦ Alcoholic polyneuropathy and delirium.

Alcohol Alcohol

ó Gastrointestinal Consequences ó Other consequences: ◦ Gastritis ◦ Folate deficiency with megaloblastic anemia ◦ Hepatitis ó Predictors of death: ñ From an asymptomatic elevation of the hepatic transaminases to hepatic failure ◦ Hyperglycemia, anemia, hypoxemia, acidosis, ñ AST usually higher than ALT older age, leukocytosis, elevated blood urea ñ Higher ALT suggests another etiology (Hep C) nitrogen, elevated lactate dehydrogenase, ñ Classic alcoholic hepatitis presentation: hypocalcemia or hypovolemia ñ Fever, leukocytosis, RUQ pain & tenderness, elevation of AST ◦ Cirrhosis ◦ Pancreatitis

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Opiates, Cocaine & Other Drugs Opiates, Cocaine & Other Drugs

ó Complications are often related to route of ó Inhalation of Drugs administration ◦ Effects related to the size of the particles ñ Larger particles affect the airways ó Injection Drug Use ñ Smaller particles reach the alveoli ◦ Skin and soft tissue infections common ◦ Complications include: ◦ Cellulitis caused by staphylococci & streptococci ñ granulomatous responses to fibrogenic substances such ◦ False-positive screening for syphilis often found as talc ñ Bronchitis from inhaled smoke ◦ Bloodborne pathogens spread by injection or ñ Bronchospasm from inhaled cocaine risky behaviors ñ Pneumothorax or pneumomediastinum from prolonged ñ HIV, Hep B, Hep C breath holding or stimulant use ñ Hemoptysis from airway irritation

Co-Occurring Disorders EPIDEMIOLOGY

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SUBSTANCE RELATED 7 of the 10 Leading Causes of Disability PROBLEMS in the World ó Major Depressive Disorder ó Traffic accidents (often substance-related) ó 3rd leading cause of death in U.S. ó Alcohol Use ó Alcoholism causes 80% of cases of hepatic ó Self-inflicted injuries cirrhosis ó Aocholism increases the risk of pancreatitis ó Bipolar disorders ó Increased incidence of HIV/STD ó Violence ó Patients injured while under the influence ó Schizophrenia fill 50% of U.S. trauma beds

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Prevalence

ó General Population ◦ 26.6% have a substance use disorder ◦ 21.4% have a mental disorder ó Patients with Mental Disorders ◦ 51% have a substance use disorder Classification ó Patients with Substance Use Disorders ◦ 41-66% have a mental disorder Systems

National Comorbidity Study (1996)

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The Quadrants of Care Dichotomy of Care

ó If Substance Use Disorder Dominates: ◦ Patient enters the health care system through High Category III Category IV Severity Mental disorders less severe Mental disorders more severe a Chemical Dependency Program Substance disorders more severe Substance disorders more severe ◦ Usually, unless severe, any psychiatric Locus of Care Locus of care Substance Abuse System State hospitals, jails, ERs, etc. symptoms are not addressed. Category I Category II Mental disorders less severe Mental disorders more severe ◦ After discharge, the patient’s mood may Substance disorders less severe Substance disorders less severe remain low or feelings of anxiety persist Locus of Care Locus of Care Alcohol/Drugs Primary health care setting Mental health system which increases the potential for relapse Low High Severity Severity Mental Illness

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Dichotomy of Care

ó If Psychiatric Disorder takes priority: ◦ Patient seeks help through a mental health clinic or hospital MODELS OF CARE ◦ Counseling and medication are aimed at improving the psychiatric symptoms ◦ The Chemical Dependency issues are not addressed ◦ After discharge, the compulsion to use substances will remain & risk for relapse is high

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The Parallel Model The Sequential Model

ó The patient receives treatment for the psychiatric ó Focuses on stabilizing the most acute disorder in one system and treatment for the disorder first, then addressing the other substance use disorder in another system at the same time. disorder. ó This model can work, but increases the odds of ó Since psychiatric & CD symptoms often poor adherence since the patient has to: overlap, it is sometimes not easy to ◦ adjust to two different treatment philosophies distinguish between primary and ◦ Develop relationships with at least two different teams secondary disorders ◦ Attend services at different geographic locations ó Treatment expectations vary between agencies

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The Integrated Model ó Generally viewed as the most effective Relationships Between Chemical model and involves the dual-diagnosis patient receiving treatment by the same Dependency and Psychiatric treatment team that addresses both Illness disorders as well as related problems.

MANY POSSIBLE PATTERNS OF INTERACTION

◦ Drake, RE & Meuser, KT (Eds). Dual Diagnosis of Major Mental Illness and Substance Abuse: Vol. 2. (1996) San Francisco. Jossey-Bass

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1. Chemical Dependency Increases the Risk of Developing 2. Psychiatric Illness Increases the Risk of Developing a a Psychiatric Illness Chemical Dependency

ó The odds of a chemically dependent ó Patients receiving psychiatric care show individual having a psychiatric illness are higher than expected rates of chemical higher than would be expected among dependency (2.7 times). the the general population (4.5 times). ó Rates of substance use disorders are especially high among clients with antisocial personality disorder, borderline personality disorder, bipolar disorder, or

-Epidemiologic Catchment Area Survey (1990) schizophrenia.

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3. Psychiatric Symptoms May Affect the Onset, Duration, 4. Chemical Dependency affects Adherence to Psychiatric or Response to Treatment of Chemical Dependency Treatment and Clinical Outcome

ó Psychiatric impairment has a strong ó Psychiatric patients with an additional correlation with relapse to drug use chemical dependency disorder show among opiate addicts. much worse treatment adherence rates ó Patients who have both chemical and higher rates of relapse and dependency and antisocial personality hospitalization in a psychiatric facility. As disorder drop out of treatment at a a result, clinical outcome is worse. higher rate and have a poorer prognosis than other diagnostic groups.

5. Psychiatric Symptoms may Arise as a Direct Result of 6. Symptoms of Psychiatric Illness may Result as the Chronic Substance Misuse or Withdrawal Indirect Consequences of Chemical Dependency

ó Drugs and alcohol may directly impair ó Depression and/or anxiety can result mood, cognitive functioning, or behavior. from: ◦ Disturbed family and interpersonal ó Depression, mania, anxiety, panic, paranoia, relationships delusions, and hallucinations are some of ◦ Increased health problems the specific symptoms that may result ◦ Job problems/loss of dignity from chronic use of substances or as part ó Chemical Dependency can produce of an acute or protracted withdrawal Antisocial Behavior syndrome. ◦ Selling drugs, stealing to support an addiction, aggressiveness

7. Over time, Symptoms of Chemical Dependency and 8. The Dual Disorders Can Develop Psychiatric Illness may Become Linked or Interrelated Independently at Different Times

ó In some cases, it may be difficult to ó Alcoholics or drug addicts who have been sober for many months or years can still develop an episode of distinguish which disorder is primary and psychiatric illness such as MDD. which is secondary. ó Individuals with a psychotic or anxiety disorder may abuse or become dependent on alcohol or other drugs ó Many of those with chronic disorders while their psychiatric symptoms are in remission. come to treatment with a very complex ó A psychiatric disorder can mask chemical dependency, and chemical dependency can mask a psychiatric set of symptoms and problems. disorder. ó Specific symptoms may vary from one episode of an illness to another.

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1. Employ a Recovery Perspective

ó Main Features ◦ Recovery is a long-term process of internal change ◦ These internal changes proceed through various stages Six Guiding Principles in Treating ó Principles for Practice ◦ Develop a treatment plan that provides for Patients With Co-Occurring continuity of care over time. ◦ Devise treatment interventions that are Disorders specific to the tasks and challenges faced at each stage of the recovery process.

2. Adopt a Multi-Problem Viewpoint 3. Develop a Phased Approach to Treatment ó Patients have an array of mental health, medical, substance abuse, family, and social ó Engagement problems ó Stabilization ó Treatment should address immediate and ó Treatment long-term needs for housing, work, health care, and a supportive network. ó Aftercare

4. Address Specific Real-Life Problems Early 5. Plan for the Patient’s Cognitive and in Treatment Functional Impairments ó Co-occurring disorders arise in a context ó Patients often display cognitive and other of personal and social problems, with a functional impairments that affect their corresponding disruption of personal and ability to comprehend information or social life. complete tasks. ◦ E.g., housing, legal matters, family problems, ó Use relatively short, highly structured work treatment sessions that are focused on practical life problems.

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6. Use Support Systems To Maintain and Extend Treatment Effectiveness ó Self-help groups ó Family ó Faith community TREATMENT GUIDELINES

Practice Guidelines Practice Guidelines

1. Establish & maintain a therapeutic alliance with the 5. Develop an overall treatment plan patient 6. 2. Manage the patient’s psychiatric &/or substance use Enhance adherence to the treatment symptoms and monitor the status of these over time plan 3. Provide education regarding the disorder(s) and 7. Help the patient and family adapt to the treatment psychosocial effects of the disorder(s) 4. Determine the need for medications and other specific treatments 8. Promote early recognition of new Practice Guidelines for the Treatment of Psychiatric Disorders (Am. Psychiatric Assoc) episodes and help identify factors that precipitate or perpetuate these episodes

Practice Guidelines

9. Initiate efforts to relieve and improve family functioning 10. Facilitate access to services and coordinating resources among different service providers PROFESSIONAL ENABLING

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Professional Enabling Professional Enabling

ó Professionals who lack knowledge or skill, or who carry 1. Failure to gather an accurate and negative attitudes and perceptions about certain detailed history of alcohol and other conditions or patients, may directly or indirectly perpetuate or exacerbate a person’s chemical drug use, as well as of psychiatric dependency or psychiatric illness symptoms ó Passive Enabling 2. Failure to address the chemical ◦ Ignoring a problem (CD or MH) dependency or the psychiatric illness in ó Active Enabling the treatment plan ◦ Giving inappropriate advice or treatment 3. Waiting for the person with a chemical dependency to “hit bottom” or to ask for treatment

Professional Enabling Professional Enabling

4. Assuming that the patient must acknowledge a 6. Assuming that major or multiple problems must exist psychiatric illness in order to benefit from treatment before the patient can be considered chemically dependent or psychiatrically ill. (There is a range of 5. Giving oversimplified advice, such as telling a severity) substance abuser to stop drug use without suggesting 7. Viewing the chemical dependency as merely a professional treatment program, or advising a symptomatic of a psychiatric illness or viewing patient with serious depression to attend meetings psychiatric symptoms as merely caused by chemical without considering other options such as medication dependency or psychotherapy 8. Excluding the family from the assessment or treatment processes when their involvement is indicated

Professional Enabling

9. Assuming recovery is in motion simply because a patient stops using alcohol or TREATMENT other drugs ADHERENCE 10. Assuming that each of the dual disorders requires treatment by ISSUES separate clinicians or in separate programs 11. Taking a rigid stance against the use of medications to treat psychiatric illness

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Difficulty Engaging & Maintaining Treatment Consequences of Poor Adherence

ó Time in treatment is one of the best ó Worsening of psychiatric symptoms predictors of successful treatment ó Return to substance use outcome ó Increased risk of rehospitalization ó Common Problems: ó Increased risk of adverse medical or ◦ Failure to attend the initial assessment psychosocial consequences ◦ Early dropout ◦ Inconsistent attendance ◦ Failure to take medications as prescribed

Strategies to Improve Adherence

1. Prepare the patient for treatment participation Strategies to • Discuss expectations and hopes for Improve treatment • Pros, cons, and limitations of treatment Treatment Adherence • Internal barriers or external roadblocks to participation • Types of treatment (group, individual, etc) • Negotiating a contract that patient agrees to follow

Strategies to Improve Adherence Strategies to Improve Adherence

2. Focus on enhancing the patient’s motivation to change 3. Attend to the therapeutic relationship • Motivation is best viewed as a “state” that can be changed rather than a “trait” that cannot be changed • Express empathy and concern • Normalize the ambivalence to change • Convey a genuine desire to help the patient • Accept varying levels of readiness to change • Encourage discussions of your counseling • Anticipate motivational problems at various phases of treatment and your relationship with the patient in • Help the patient learn from previous motivational struggles order to identify and work through impasses

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Strategies to Improve Adherence Strategies to Improve Adherence

4. Facilitate the transition between levels 5. Focus on the treatment process of care • Intensity of treatment may need to be changed • Many patients fail to follow through with based on: ñ Response of the patient next level of care ñ Changes in motivation to engage in the work of • Discuss differences between levels of care recovery ñ New problems that develop • Identify barriers for the patient’s continued ñ Positive changes that occur participation • Provide feedback & explore reactions to feedback • Use motivational strategies • Find out what the patient likes or dislikes about treatment

Strategies to Improve Adherence Strategies to Improve Adherence

6. Elicit the support of the family or 7. Monitor major symptoms of psychiatric illness significant others or chemical dependency • Discuss family or relationship issues that • Symptoms such as low motivation, anhedonia, concern the patient depression, poor impulse control, poor judgment, • Discuss ways to engage the family in mood impairment, or psychosis can impact on the treatment patient’s ability to adhere to treatment • Discuss ways to contain negative emotions • Strong cravings or obsessions to use substances, or repeated close calls due to exposure to high-risk during joint sessions people, places, or events impact treatment. ñ While families can be a great source of support, they can also add to the patient’s stress • Catching ‘early’ warning signs can lead to reducing the risk of relapse to either disorder

Strategies to Improve Adherence Strategies to Improve Adherence

8. Monitor medication use, side effects, and 9. Incorporate systems changes in clinical care potential problems • Provide easy entry and re-entry for dropouts • Elicit an agreement that medications will not be • Offer flexible appointment times stopped without first discussing with prescriber or counselor • Call or send a written note to remind patient of • Facilitate medication changes when they are scheduled sessions or med checks ineffective or only partially effective • Reach out as soon as patient misses sessions • Prepare the patient to deal with pressures from • Facilitate the use of other services (case others to stop taking medications management, social services, housing, etc.) • Discuss the potential interactions between alcohol, • Develop a philosophy to address adherence illicit drugs, nonprescribed drugs, herbal problems supplements, and medications

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Overview

ó Many chemical dependency and psychiatric disorders are chronic, persistent, and relapsing or RELAPSE recurrent illnesses ó Relapse to alcohol and drug use can precipitate or PREVENTION exacerbate a psychiatric relapse ó Patients may use alcohol or drugs to relieve psychiatric symptoms, and when they stop, the psychiatric symptoms reemerge ó Impaired judgment associated with certain psychiatric symptoms, such as mania or psychosis, can result in relapse to alcohol or drugs

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Factors Associated with Poor Outcome Positive Effects of Treatment

ó Low acceptance of illness ó Cessation or reduction in substance use ó Reduced medical costs following treatment ó Low desire to change ó Reductions in violent and nonviolent criminal behaviors, re-arrests, and re-incarcerations ó High severity of the disorder(s) ó Improved psychological functioning, including ó Poor adherence to medications or other reduced suicidal thoughts and behaviors types of treatments ó Improved family functioning ó Decreased dependence on welfare ó Lack of social or family supports ó Reduction in high-risk behaviors associated with ó Poor coping skills HIV transmission and acquisition ó Improved employment rates

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Relapse Risk Factors Relapse Risk Factors

ó Affective variables (mood states) ó Cognitive variables ◦ For example, anger, anxiety, boredom, ◦ Faulty beliefs about one’s ability to manage depression, emptiness, loneliness high-risk relapse factors ◦ It is not necessarily the mood in and of itself, ◦ Lack of awareness and acceptance of one’s but the patient’s inability to cope with it that illness contributes to relapse ◦ Lack of knowledge and understanding of one’s ó Behavioral variables illnesses and treatment ◦ Poor coping, stress management, or problem- ◦ Poor decision-making skills solving skills

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Relapse Risk Factors Relapse Risk Factors

ó Environmental variables ó Lifestyle factors and health care practices ◦ Availability of substances ◦ Persistent problems or symptoms ◦ Social pressures to engage in substance use or ◦ Lack of structure or regularity in daily life stop psychiatric medications ◦ Lack of goals or direction ◦ Lack of a support network ◦ Smoking cigarettes (nicotine can decrease the ◦ Homelessness blood level of many psychotropics thus raising ◦ Poverty the patient’s risk of becoming symptomatic) ◦ Stress associated with major life changes

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Relapse Risk Factors Relapse Risk Factors

ó Personal vulnerability ó Psychiatric and psychological variables ◦ Some individuals are more sensitive to stress ◦ Psychiatric illness or symptoms and ordinary life experiences than others ◦ Personality traits ◦ because of their biological/psychological Poor motivation ◦ Failure to comply with a treatment program makeup ó Relationship variables ó Physiological variables ◦ Loss of a significant relationship ◦ Post-acute withdrawal symptoms ◦ Experiencing rejection or severe criticism ◦ Intense cravings for substances ◦ Family problems ◦ Physical pain and illness ◦ Lack of a social support system or one that is a negative influence

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Relapse Risk Factors

ó Spiritual variables ◦ Excessive guilt and shame ◦ Lack of meaning or purpose in life CLINICAL ◦ Lack of a belief in the need for help and support from others or a Higher Power INTERVENTIONS TO ó Treatment participation and related variables ◦ Poor adherence to treatment REDUCE RELAPSE RISK ◦ Insufficient or wrong type of medications ◦ Inappropriate advice or interventions ◦ Lack of access to proper treatment ◦ Failure to respond to early warning signs of relapse

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Interventions Interventions

ó Identifying and Coping with Relapse Risk ó Identifying and Managing Relapse Warning Factors Signs ◦ Some patients have so many relapse risk ◦ Usually appear as changes in client attitudes, factors that addressing each is impossible. emotions, thoughts, and feelings ◦ Global approaches such as social skills ñ Missed sessions training, cognitive reframing, assertiveness ñ Decreased participation in 12-step program training, and stress management may be ñ Poor adherence to taking medications with needed to teach skills that can be generalized subsequent symptoms of psychiatric disorder to address any potential problem

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Interventions Interventions

ó Clinical Aids for High-Risk Factors and ó Managing Emotions Warning Signs ◦ Difficulty managing negative emotional states such as anxiety, anger, depression, loneliness, ◦ Client manuals on recovery or boredom is the most common relapse ◦ Relapse Prevention Workbooks precipitant ◦ Dual diagnosis workbooks ó Building a Social Support Network ◦ Lists of warning signs or dangerous situations ◦ Patients who have supportive family and social support systems are more likely to experience a better recovery than those who do not

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Interventions Interventions

ó Resisting Social Pressures to Use ó Managing Pressures to Stop Taking Chemicals Psychiatric Medications ◦ Avoiding high-risk situations in which social ó Coping with Cravings or Desires to Use pressure will be strong or in which the patient Substances feels especially vulnerable ◦ Teach patients to identify cues or precipitants ◦ Developing and practicing refusal skills ó Using an Inventory or Symptom Review ◦ Challenging faulty beliefs such as “I can’t have fun unless I use alcohol or drugs with these ó Building Structure into Daily Life people; they won’t accept me” ó Coping with Emergencies

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Continuum of Treatment

Medications Used ó Management of Overdose In Addiction Treatment ó Management of Withdrawal Through the Continuum ó Relapse Prevention: MAT

Benzodiazepine Overdose Benzodiazepine Overdose

ó Romazicon (Flumazenil) 0.2 mg IV ó Rare cases pt. has only partial response may administered slowly over 30 seconds-wait require additional doses up to 5 mg. 30 seconds- If desired LOC is not ó Caution: Do not use (except in cases of obtained further dose of 0.3 mg IV to be imminent death) in mixed overdoses involving BZ’s and cyclic antidepressants due to potential given over 30 seconds. for emergence of seizures. If seizures do occur ó Further doses of 0.5 mg can be treat with IV BZ’s, Dilantin, or Barbiturates. administered over 30 second intervals up to cumulative dose of 3 mg.

Opiate Overdoses DETOXIFICATION

ó Narcan (Naloxone) 0.4 mg IV (preferred), ó The term ‘detoxification’ implies a SC, or IM q 2-3 minutes until desired clearing of toxins. improvement is achieved. ó However, for individuals with physiologic ó If no response by 10 mg diagnosis needs substance dependence, detoxification is to be questioned. defined as the management of the ó May need to be repeated every 1-2 hrs. withdrawal syndrome depending on type of opiate used. ◦ It is the process by which a substance on which an individual is physically dependent is gradually eliminated from the body

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GOALS OF DETOXIFICATION

1. To provide a safe withdrawal from alcohol or other drug(s) of dependence and enable the patient to become free of GENERAL PRINCIPLES nonprescribed medications 2. To provide a withdrawal that is humane and OF MANAGEMENT that protects the patient’s dignity 3. To prepare the patient for ongoing treatment of his or her dependence

ñ Center for Substance Abuse Treatment (CSAT) (1995) TIP#19

Initial Nursing Assessment Helpful Information to Predict ó Purpose: ◦ to determine the need for medication and Severity of Withdrawal medical management ó Includes: ó Amount and duration of alcohol or other ◦ Evaluation of predicted withdrawal severity drug use ◦ Presence of medical comorbidity ó The severity of the patient’s prior ◦ Presence of psychiatric comorbidity withdrawal experiences (if any) ó The patient’s medical and psychiatric history

Strategies for Pharmacologic Management

ó Two general strategies (either or both may be used): ◦ Suppress withdrawal through use of a cross- tolerant medication MANAGEMENT OF ñ A longer acting medication typically is used to provide a milder, controlled withdrawal ALCOHOL WITHDRAWAL ñ Examples: Methadone, buprenorphine, chlordiazepoxide ◦ Reduce signs and symptoms of withdrawal through alteration of another neuropharmacological process ñ Examples: clonidine, propranolol, ibuprofen

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Clinical Picture Clinical Picture

ó The clinical manifestations of alcohol ó Alcohol withdrawal seizures can occur at withdrawal begin 6 to 24 hours after the last various times, but most occur within 48 drink, sometimes arising before the blood hours alcohol level has returned to zero. ó Alcohol withdrawal delirium (DTs) typically ó Early withdrawal signs: begins 48 to 72 hours after the last drink ó Anxiety, sleep disturbances, vivid dreams, ◦ Signs of sympathetic hyperactivity (tachycardia, anorexia, nausea, headache hypertension, fever, diaphoresis) often are ó Tachycardia, elevation of blood pressure, profound and are hallmarks of delirium hyperactive reflexes, diaphoresis, hyperthermia ◦ Mortality rate is 1% - 5% and increases with ó Tremor – best brought out by extension of the delayed diagnosis, inadequate treatment, and hands or tongue concurrent medical conditions

Pathophysiology Pathophysiology

ó Dependency develops as a cell or organism ó Neurotransmitter systems affected: makes homeostatic adjustments to ◦ GABA compensate for the primary effect of a drug ñ Mediates effects such as sedation, muscle relaxation and a ñ Goldstein & Goldstein, 1961 raised seizure threshold ó The primary effect of alcohol on the brain is ñ Chronic alcohol intake leads to an adaptive suppression of GABA activity depressant ◦ Norephinephrine ◦ With chronic exposure, there are compensatory ñ Chronic alcohol intake leads to upregulation of receptors adjustments with down-regulation of inhibitory ñ Discontinuation of alcohol leads to rebound overactivity systems and up-regulation of excitatory systems of noradrenergic systems ñ The withdrawal symptoms last until the body readjusts to ñ Tachycardia, hypertension, tremor, diaphoresis & anxiety the absence of the alcohol and establishes a new ◦ Other systems affected: Calcium channels, equilibrium glutamate receptors, cAMP systems

Hallucinations Withdrawal Seizures

ó In mild withdrawal, patients may experience ó Usually begin within 48 hours and may perceptual distortions of a visual, auditory, and occur before the blood alcohol level has tactile nature returned to zero. ó Lights may seem too bright or sounds too loud ó Paresthesias may be experienced ó Most are generalized major motor ó In severe cases of withdrawal, these misperceptions seizures may develop into frank hallucinations ó Risk appears to be in part genetically ó Visual hallucinations are most common (hallucinosis) ó Frequently involve some type of animal life determined ó Auditory hallucinations begin as unformed sounds ◦ Increased in patients with a history of prior (clicks or buzzing) and may progress to accusatory withdrawal seizures voices of friends or relatives ó Tactile hallucinations: bugs/insects crawling on the skin

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Alcohol Withdrawal Delirium Alcohol Withdrawal Delirium

ó In 90% of patients, withdrawal does not ó Duration is variable, but averages 2 to 3 progress beyond relatively mild symptoms. days. ó Delirium tremens (DTs) generally appear 48 ◦ In some cases, may last only a few hours to 72 hours after the last drink. ó The amount of daily intake and duration ◦ Development of tachycardia, tremor, of heavy drinking have not been diaphoresis, fever correlated consistently with the severity ◦ Global confusion and disorientation to place & time of withdrawal delirium. ñ Believes himself to be in a location other than the hospital ñ Misidentifies staff as personal acquaintances

PHARMACOLOGIC Alcohol Withdrawal Severity Scales MANAGEMENT ó Clinical Institute Withdrawal Assessment – ó The cornerstone of pharmacologic Alcohol (CIWA) management of withdrawal is the use of ◦ Most extensively studied and best known benzodiazepines (Mayo-Smith et al, 1997) ◦ Shortened version: ñ CIWA-A Revised or CIWA-Ar ñ Well documented reliability, reproducibility, and validity ñ Requires two to five minutes to complete ñ A score of 9 or less indicates mild withdrawal ñ A score of 10 to 18 indicates moderate withdrawal ñ A score above 18 suggests severe withdrawal ñ High scores are predictive of the development of seizures and delirium

Benzodiazepines Benzodiazepines

ó Are pharmacologically cross-tolerant with ó Trials of different benzos indicate that all are alcohol and have the similar effect of similarly efficacious in reducing signs and symptoms of withdrawal. enhancing the effect of GABA-induced ó Longer acting agents may be more effective in sedation. preventing seizures ◦ A specific benzodiazepine receptor site has been ó E.g., chlordizepoxide, diazepam, clonazepam ó May also contribute to an overall smoother withdrawal identified on the GABA receptor complex. course, with a reduction in breakthrough or rebound ó The provision of benzodiazepines alleviates symptoms ó May also pose a risk of excess sedation in elderly and the acute deficiency of GABA significant liver disease neurotransmitter activity that occurs with ó Shorter acting agents are preferrable (lorazepam or oxazepam) sudden cessation of alcohol intake. ó Phenobarbital is still used by some programs ó Long-acting barbiturate with well-documented anti- convulsant activity, inexpensive, & low abuse liability

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Benzodiazepines Other Agents

ó Should be administered orally or, when ó Beta adrenergic blocking agents necessary, intravenously ◦ E.g., atenolol & propranolol ◦ For most agents, IM absorption is extremely ó Centrally acting alpha adrenergic agonists variable ◦ E.g., clonidine ◦ Lorazepam can be administered IM or SL ó Both these agents reduce the autonomic ñ Has good absorption by these routes nervous system manifestations of withdrawal ó These agents do not have known anticonvulsant activity

Carbamazepine Neuroleptic Agents

ó Has been shown to be equal in efficacy to ó Less effective than benzos in preventing benzodiazepines delirium ◦ No significant toxicity ◦ Actually increases the rate of seizures ◦ Associated with less psychiatric distress and a ◦ Haloperidol has least effect on seizure faster return to work threshold ◦ Does not potentiate the CNS and respiratory ó Widely used to calm agitated patients depression ◦ Does not inhibit learning ◦ Has no abuse potential

Thiamine Thiamine

ó Alcoholics are at risk for thiamine deficiency. ó Delay in provision of thiamine increases ◦ Leads to Wernicke’s Disease and the Wernicke- the risk of permanent memory damage. Korsakoff Syndrome ó The provision of intravenous glucose ó Wernicke’s: illness of acute onset solutions may exhaust a patient’s reserve characterized by the triad of of B vitamins, acutely precipitating ◦ mental disturbance ◦ paralysis of eye movements (weakness or paralysis Wernicke’s disease. of abduction [CN-VI]) ñ Invariably is bilateral, but rarely symmetric ñ Accompanied by diplopia, strabismus and nystagmus ◦ ataxia ñ Affects gait and stance

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Agents No Longer Recommended Management of the Patient With Delirium

ó Magnesium ó Admission to ICU ó Management of fluids and electrolytes ó Phenytoin ó Use of cross-tolerant sedative-hypnotics ◦ No evidence of effectiveness in preventing ◦ Have not been shown to reverse the delirium or recurrent withdrawal seizures reduce its duration ◦ The goal is to sedate the patient to a point of light sleep ñ To control agitation ◦ Massive doses may be needed ñ Hundreds or even thousands of milligrams of diazepam or its equivalent over the course of treatment ( Kasser, 1998)

Benzodiazepine Detox

ó Past treatment approach has been to slowly MANAGEMENT OF taper patient off the benzodiazepine over a 4-12 BENZODIAZEPINE week time period. ó This approach appears to be effective if the WITHDRAWAL patient has a physical dependence only. ó Patients who are chemically dependent on BZs however, are rarely able to tolerate this approach.

Benzodiazepine Detox Benzodiazepine Detox

BZ withdrawal has the potential for ó New approach: Use of Anticonvulsant serious medical complications and can be medication combined with substituted long lethal: acting benzodiazepine. 1. Withdrawal Seizures ó Taper Benzodiazepine (Klonipin or Librium) 2. Withdrawal Delirium over a 3 to 5 day period. Starting dosage Need to develop a detox protocol which depends on amount of BZ being abused. can safely get pts. off BZ’s in a short ó Start anticonvulsant medication ( Depakote ER period of time. 500 mg hs or bid, Tegretol 200mg bid or tid) and continue on med for 4-8 weeks.

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Overview

ó Methadone (Dolophine) was commonly MANAGEMENT OF used for detox beginning in 1970’s. OPIOID ó As heroin potency began to decline in the 1990’s withdrawal symptoms began to WITHDRAWAL decrease in intensity. ó Clonidine ( alpha 2 noradrenergic agonist) was then useful in treating withdrawal.

Overview Overview

ó Over the last 10 years the potency of ó In addition there has been an increase in street heroin has progressively been the abuse of high potency delayed increasing and in many areas the release/long acting opiate preparations concentration is over 50%. (i.e. Oxycontin, MS Contin etc). ó At this concentration the heroin can be Prescription Opiate abuse has become a inhaled or smoked to produce a high. major problem in the US. Resulted in a significant increase in heroin ó These factors have resulted in an increase use-especially in young people. in the severity of opiate withdrawal symptoms.

Overview The Opioids

ó Clonidine’s effectiveness alone for opiate detox ó Drugs Derived Directly from the Opium Poppy treatment has diminished. ó Morphine ó Codeine ó Return to use of Methadone. Dosage: 20-40 mg ó The Semisynthetic Opioids to start tapered by 5 mg daily. Often combined ó Heroin (diacetylmorphine) with clonidine 0.1-0.2 mg to start and ó Hydromorphone (Dilaudid) Phenobarbital 30-45 mg to start tapered along ó Oxycodone (Percocet, OxyContin) with the Methadone. ó Hydrocodone (Loricet, Vicodin) ó The Synthetic Opioids ó New approach-Use of buprenorphine as detox ó Methadone agent in place of Metadone. ó Fentanyl ó Propoxyphene (Darvocet) ó Meperidine (Demerol)

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Opioid Withdrawal Acute Withdrawal

ó The opioid abstinence syndrome is characterized by two phases: ó The patient typically experiences a range of symptoms for various lengths of time. ◦ Acute Withdrawal ó Symptoms include: ◦ Protracted Abstinence Syndrome ó Vital Sign Changes ó Tachycardia, Hypertension, Hyperpyrexia ó Current pharmacotherapeutic strategies ó CNS Changes are based on this duality. ó Restlessness, Irritability, Insomnia, Craving, Yawning ó Eye & Nose Changes ó Opiate withdrawal alone is not life threatening. ó Pupillary dilation, Lacrimation, Rhinorrhea Exception: Withdrawal may be fatal to fetus in pregnant ó Skin Changes women going thru opiate withdrawal. ó Piloerection ó GI Changes ó N/V/D

Chronic Dependence & Protracted Abstinence Clinical Picture ó Clinical phenomena associated with opioid withdrawal include neurophysiologic rebound in ó The time required for return to baseline ranges from one week to about six months the organ systems on which opioids have their primary action (Jaffe, 1990) ó Symptoms include: ó The severity varies with the dose and duration of drug use. ◦ Changes in Vital Signs ó Route of administration is important. ◦ Decreased sensitivity of the respiratory center to ó Injection drug use is associated with significantly CO2 higher withdrawal symptom scores than with inhaled opioid use (Smolka & Schmidt, 1999) ◦ Irritability, insomnia, craving ó The time to onset depends on the half-life of the ó Treatment: clonidine 0.1 mg bid or tid, drug being used. trazodone/doxepin 50-150 mg hs for sleep, ó E.g., Withdrawal may begin 4 to 6 hours after the last and Seroquel 25 mg bid or tid for severe use of heroin, but up to 36 hours after the last use of anxiety. methadone

Clinical Picture Pharmacologic Therapies

ó Neuropharmacologic studies of opioid ó Slow Methadone Detoxification withdrawal have supported the clinical ◦ The strategy is to stabilize heroin addicts on picture of increased CNS noradrenergic methadone, then slowly decrease the hyperactivity (Jaffe, 1990) methadone dose. ó Therapies to alter the course of opioid ó Clonidine Detoxification withdrawal (e.g., clonidine) are designed ó Buprenorphine Detoxification to decrease this hyperactivity, which occurs primarily at the locus ceruleus.

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What is buprenorphine? Opiate Dependence, ó Partial μ-opioid agonist ó High receptor affinity and receptor occupancy: Detoxification and The ◦ 95% occupancy at 16 mg (Greenwald et al, 2003) Role of Buprenorphine - Blockade or attenuated effect of the use of additional opioids ó Lower intrinsic activity than full agonists: ◦ Favorable safety profile due to “ceiling” effect ◦ Lower street value ◦ Lower abuse potential

(Walsh and Eisenberg, 2003)

Bioavailability Pharmacologic benefits: “Less Bounce To The Ounce” ó Has poor oral bioavailability ó Slow receptor dissociation: ◦ Sublingual administration is the primary route ◦ Longer duration of action of administration ◦ Milder withdrawal ó High lipid solubility ó Lower physical dependence liability than ◦ Expected to be active by the intranasal route full agonists ó Limited development of tolerance ó Ceiling effect on respiratory depression ◦ Increased safety against overdose

Rapid onset of effect Interactions with other opioids?

ó Readily absorbed sublingually: ó Opioid antagonists: ◦ 5-10 min. for tablet to dissolve ◦ Incomplete reversal by naloxone ó Rapid onset of action: 30-60 min ó Opioid agonists: ó Peak plasma levels at 1-2 h ◦ Blockade effect, limiting the effects of additional opioid use ó Peak subjective/physiologic effect at 1-4 h ◦ Potential for precipitated withdrawal when ó Distribution taken too soon after a full agonist ◦ 96% protein bound ( α and β globulin) ó Due to mild antagonist properties of buprenorphine daily opiate use needs to be below 40 mg of Methadone, 320 mg of oxycodone (or equivalent of other opiates), or below 20 bags of street heroin daily.

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Getting started Benefits of buprenorphine

ó General approaches: ó Less severe physiologic withdrawal than ◦ Manage withdrawal syndrome and cravings: full μ-opioid agonists: ñ Provide a long-acting opioid and taper the dose ◦ Improves program completion ◦ Manage signs and symptoms: ◦ Forms positive patient alliances ñ Give symptomatic relief ◦ Encourages future patient return ñ E.g., clonidine, ibuprofen, immodium ◦ Can be used to withdraw from short-acting ñ Non-benzodiazepine sedative opioids or long-acting opioids ◦ Combination of the two approaches ó Allows a wide range of continuing treatment options

Objectives of medical withdrawal “Must haves” for medical withdrawal

ó Short-term interventions: ó Assessment ó Supportive care: ◦ To alleviate withdrawal discomfort ◦ Counseling ◦ To prevent complications ◦ Safe environment/patient trust ◦ To interrupt a pattern of heavy and regular ◦ Provision of patient information opioid use ó Monitoring ◦ To facilitate post-withdrawal treatment ó Medications linkages ó Post-withdrawal ongoing support ◦ Continuing counseling and psychosocial support ◦ Naltrexone treatment ◦ Maintenance treatment

Examples of ≤10 day inpatient medical Protocol for Detoxification from withdrawal schedules Opiates Using Buprenorphine Buprenorphine dose (mg) – sublingual tablet Day 10-day 7-day 3-day ó Day 1: No Buprenorphine schedule* schedule** schedule*** ó Day 2: 10 a.m. 4mg 1 8 8 4+8 4 p.m. 2mg 2 6 6 8 10 p.m. 2mg 3 4 4 8 ó Day 3: 6 a.m. 2mg 4 4 4 12 N 2mg 5 4 2 6 p.m. 2mg 6 2 2 ó Day 4: 6 a.m. 2mg 7 2 0 4 p.m. 2mg

8 2 *Adapted from Vignau, 1998 ó Day 5: 6 a.m. 2 mg 9 2 ** Adapted from Zhi-Min et al., 1997 *** Adapted from Cheskin et al, 1994 10 0 As seen in Drug and Alcohol Dependence Supplement, Volume -Livengrin Foundation – Medical Manual 70, Issue 2, Supplement S1-S104

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PHARMACOLOGIC Drugs Used To Deter Alcohol INTERVENTIONS FOR Consumption ALCOHOLISM

Use of Medications to Prevent Relapse in Alcoholics

Alcohol-Sensitizing Agents ó Major challenges in the months after cessation of drinking: ó Alter the body’s response to alcohol, making ó Prevention of relapse to drinking its ingestion unpleasant or toxic ó Management of persistent emotional and physiologic disturbances ◦ Disulfiram (Antabuse) & carbamide [not avail. in US] ó Alcohol-sensitizing drugs make the ingestion of alcohol aversive or hazardous ó Inhibits aldehyde dehydrogenase (ALDH) ó Some drugs appear to reduce alcohol intake by: ◦ If alcohol is ingested after this enzyme is inhibited, ó Reducing the reinforcing effects of alcohol blood acetaldehyde levels rise ó Reducing the urge or craving to ingest alcohol ñ The disulfiram-ethanol reaction (DER) ó The treatment of persistent psychiatric symptoms is ó The DER varies in intensity both with the postulated to reduce the risk of relapse by removing motivation to use alcohol as “self-medication” to dose of disulfiram and with the volume of control those symptoms alcohol ingested

Primary Route of Ethanol Metabolism Pharmacokinetics of Disulfiram ó Absorbed almost completely after oral Ethanol administration. ó Metabolized rapidly to diethyldithiocarbamate ADH (DDC) Acetaldehyde ◦ Active metabolite ó This is degraded to diethylamine and carbon ALDH Disulfiram inhibition disulfide ◦ Detection of carbon disulfide in breath provides a measure of compliance ó Acetic Acid CO 2 & H 2O Disulfiram & DDC inhibit ALDH by binding to it irreversibly. ◦ Renewed enzyme activity requires the synthesis of new protein

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Pharmacokinetics of Disulfiram Symptoms of DER Syndrome

ó Inhibits dopamine beta-hydroxylase (DBH) ó Warmness and flushing of the skin ◦ Results in increased dopamine levels ó Especially upper chest and face ◦ Exacerbation of psychotic symptoms in ó Increased heart rate, palpitations, decreased BP schizophrenics ó Nausea & vomiting ó Daily dose is 250 – 500 mg/d ó Shortness of breath ◦ Some patients require in excess of 1 Gm/d to ó Sweating, dizziness, blurred vision reach blood levels sufficient to produce DER ó Confusion ñ Faulty bioactivation in some individuals can yield too ó low a concentration of the active metabolite. MOST REACTIONS LAST ABOUT 30 MINUTES AND ARE SELF-LIMITED ó DDC is being studied as a transdermal and ó Occasionally, can be severe and include marked tachycardia, hypotension, sustained-released formulation bradycardia, cardiac arrest secondary to vagal stimulation associated with retching or vomiting

Measures to Enhance Compliance ó Essential elements in the evaluation of the ó Provide the patient with incentives efficacy of treatment include: ó Contract with the patient and a significant ◦ Measures of compliance other to work together to insure ◦ Adequate controls in the study compliance ó The efficacy of alcohol-sensitizing agents ó Provide regular reminders and other in the prevention or limitation of relapse information to the patient in alcoholics remains to be demonstrated. ó Use behavioral training and social support ó Warn about the side effects including the need to avoid OTC preparations containing alcohol.

Opioidergic Agents

ó Naltrexone (ReVia) & nalmefene (Revex) ◦ Opioid antagonists DRUGS THAT CAN ó Naltrexone was approved by the FDA in DIRECTLY REDUCE 1985 for the treatment of opioid dependence and in 1994 for the treatment ALCOHOL of alcohol dependence CONSUMPTION ó Nalmefene is approved in the US only as a parenteral formulation for the acute reversal of opioid effects (e.g., during surgery) Several neurotransmitter systems appear to influence ó Vivitrol (sustained-release [depot] the reinforcing or discriminative stimulus effects of formulation of naltrexone approved in 2005 ethanol

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Agents Affecting Other Neurotransmitter Systems Naltrexone/Acamprosate ó Acamprosate (Campral) Combination Treatment ó An amino acid derivative ó Affects both GABA and Glutamate neurotransmission ó Several studies lend support to the ó Glutamate being the one that is important for its therapeutic perspective that there may be a subset of effects in alcoholism ó Decreased the desire to drink alcoholic patients who do not respond to ó Decreased the degree of anxiety symptoms either medication alone but will respond ó May be more useful in combination with disulfiram. to combination treatment with both ñ Besson J, Aeby F, Kasas A et al. (1998). Combined efficacy of acamprosate and disulfiram in the treatment of alcoholism: A medications. controlled study. Alcoholism: Clinical & Experimental Research 22:573- 579.

Topiramate Topiramate

ó Topiramate potentiates GABA and ó Not FDA approved for use in alcohol inhibits excitatory glutamate dependence but may be used off-label. transmission-results in decreased ó Initiate dose of 25 mg daily and increase dopamine release in response to alcohol dose over several weeks to 300 mg daily consumption. in divided doses. ó Several studies have reported reduction ó Excreted renally-dosage may need to be in drinking and increased abstinence with reduced with impaired renal function. its use.

Factors in the Production of Mood Disturbances ó Heavy alcohol intake ó Acute and protracted withdrawal ó Alcohol-induced damage to the CNS PHARMACOTHERAPIES FOR ó Damage to the CNS from indirect effects POSTWITHDRAWAL of alcohol (e.g., head trauma or thiamine AFFECTIVE DISTURBANCES deficiency) ó Social, economic, and interpersonal losses ó Antecedent psychiatric disorders

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Medications ó Tricyclic Antidepressants (TCAs) ó Selective Serotonin Reuptake Inhibitors (SSRIs) PHARMACOLOGIC ó Benzodiazepines ó Alcoholics are vulnerable to the development of INTERVENTIONS FOR dependence on the benzodiazepines OPIOID ADDICTION ó Dependence on both alcohol and benzos can increase depressive symptoms ó The combination of alcohol and benzodiazepine dependence may be more difficult to treat than the alcoholism alone ó Other Anxiolytics ó Buspirone (BuSpar) ó Propranolol (Inderal) ó Dopaminergic Blockers: Atypical Antipsychotics

Naltrexone Naltrexone (continued)

ó Long-acting opioid antagonist ó Initiated following acute withdrawal from opioids ó Provides complete blockade of opioid ◦ Seven to 10 day opioid free period receptors when taken at least three times a ó Initial dose generally 25 mg (1 st day) – GI side week effects ◦ Then 50 mg daily or 100mg every other day or 350 ó Total weekly dose of about 350 mg. mg weekly (in 3 divided doses) ó Treatment retention rates are 20-30% over ó Most serious side effect is liver toxicity 6 months. ó If patient uses an opiate while on Naltrexone, it ó Factors for poor retention: will have no effect. ◦ Does not provide narcotic effect ó VIVITROL: Monthly injection – 350mg ◦ Cravings may continue during treatment ó Surgical implant also available

Naltrexone Naltrexone

ó Blockade produced is competitive. Can be ó Multiple studies have supported its overcome by using increasing amounts of the efficacy in opiate addiction treatment. opiate. ó Most common side effects are headache, ó Relatively fine line between the amount of mild nausea, and GI complaints. opiate it takes to overcome the blockade and the lethal dose. ó Duration of use is variable ( weeks to ó Usage has been most successful in populations months). who are highly motivated and are not likely to try to overcome the blockade (individuals with a good support system, professionals, etc.).

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METHADONE METHADONE

ó May only be prescribed in the community for ó Rationale for long-term methadone maintenance: opiate addiction treatment by physicians’ ó Ability to relieve protracted abstinence syndrome ó Block heroin euphoria affiliated with an CSAT accredited Methadone ó Psychosocial stabilization Maintenance Treatment Program. ó Reduced criminal activity ó Federal and State regulations govern its ó No serious side effects utilization within these programs. ó Mainly constipation, sweating, drowsiness, decreased sexual interest/performance ó Specific criteria must be met in order to be ó Safe during pregnancy admitted to a program. ó Today’s high-purity street heroin has required even higher methadone doses to achieve cross- tolerance

Methadone-Benefits Methadone-Benefits

ó Produces tolerance to other opiates. ó Results in increased employment, ó Can be given in a single daily dose (24 improved physical and mental health, and hour half life). improved social functioning. ó Reduces opiate cravings. ó Pt’s involved in MM programs have a ó Prevents emergence of opiate physical significantly reduced rate of withdrawal symptoms. seroconversion to HIV disease. ó Requires patient to be involved in ongoing ó No long term physical or mental formal treatment. complications have been identified.

Methadone-Dosing Methadone-Issues

ó Initiation of medication. Most pt’s are started on ó Patients need to go to MM clinic daily to 30 mg daily with the dosage increased by 5-10 get their medication. May limit social mg per week until urine drug screens are activities. negative for other opiates. ó Patients remain physically dependent on ó Minimum effective Methadone dose (to produce Methadone. sufficient tolerance) is 60 mg per day. ó MM patients are often discriminated ó Most patients will require MM doses of 90-120 against in housing and other social mg daily, some even higher. programs.

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Methadone-Issues

ó Patients are often not welcomed at community self-help support groups (i.e. NA) due to their use of Methadone. Some Principles of Medical ó Side Effects: Most common problems are chronic constipation and excessive sweating. Management of Methadone ó Duration of treatment: Felt to be long term in Patients most cases.

Select Appropriate Patients Achieve Adequate Steady-State Dosing

ó Minimum age of 18 years (generally) ó Begin induction dosing phase ó At least one year of physiologic ó Establish maintenance-phase dosage dependence on a narcotic ó Avoid drugs that potentiate methadone ó Meets criteria for opioid dependence dose or induce withdrawal ó Evaluate need for detoxification or continued maintenance

Evaluate & Treat Medical Prevent Relapse Conditions ó Educate patient and family about potential ó Infectious Disease for relapse ◦ Reduce risk of contracting and transmitting ó Encourage involvement in Narcotics disease Anonymous and Nar-Anon ◦ Educate family and involve them in preventive efforts ó Monitor patient for symptoms of opioid intoxication or drug-seeking behavior ó Pain Management ◦ Consider non-narcotic agents first ó Adjust dosage according to needs ◦ Evaluate cross-tolerance in narcotic analgesia ◦ Avoid narcotics that induce withdrawal

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Drugs That Interact with Methadone

Induction Inhibition

ó Rifampin ó Fluconazole ó Cimetidine ó Pehnytoin ó Erythromycin ó Ethyl Alcohol ó Fluvoxamine ó Fluoxetine BUPRENORPHINE ó Barbiturates ó Ketoconazole ó Carbamazepine ó Nefazadone ó St. John’s Wart ó Ritonavir ó Clomipramine ó Haloperidol ó Paroxetine

Opioids bind to different receptors What determines opioid effects?

ó Opioids exert their effects by binding to the ó Receptor affinity opioid receptor ó Various receptor subtypes involved in different ◦ How tightly the drug binds to the receptor systems: ó Dissociation ◦ μ (mu), δ (delta), and κ (kappa) ◦ How fast the drug leaves the receptor ó μ-opioid receptor mediates: ◦ Analgesic effects ó Intrinsic activity ◦ Euphoria ◦ How much the drug stimulates the receptor ◦ Some side effects: ñ Respiratory depression ñ Sedation ñ Dependence

Receptor Pharmacology Receptor Pharmacology

ó Full agonists – bind to the μ receptor producing an almost linear increase in biologic effect: ◦ Methadone, morphine, heroin ó Partial agonists – bind to the μ receptor but have a ‘ceiling’ effect on receptor activation: ◦ Buprenorphine ó Antagonists – bind to the μ receptor and do not produce a biologic response but able to block agonist effects: ◦ Naloxone, naltrexone, nalmefene

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Opioid receptors – activity levels Pharmacologic benefits µ κ δ ó Slow receptor dissociation: ◦ Longer duration of action Agonist (+) ◦ Milder withdrawal Morphine +++ + Methadone +++ ó Lower physical dependence liability than LAAM +++ full agonists Buprenorphine ++ -- ó Limited development of tolerance Antagonist (-) ó Ceiling effect on respiratory depression Naltrexone ------◦ Increased safety against overdose Naloxone ------Nalmefene ------

Urine Testing Pharmacodynamic drug interactions

ó CNS depressants and sedatives (eg, ó Buprenorphine and its glucuronide benzodiazepines): metabolite appear in the urine for 1-2 days ◦ All opioids have additive sedative effects when used in combination with other sedatives ó Norbuprenorphine and its glucuronide ñ Increased potential for respiratory depression, metabolite appear for 1-4 days heavy sedation, coma, and death ó Urine testing for opiates typically screens ó Despite favorable safety, use caution with for morphine. concomitant psychotropics (eg., benzodiazepines) ◦ These tests do not cross-react with buprenorphine or norbuprenorphine

Understanding precipitated withdrawal ó Buprenorphine displaces full opioid Buprenorphine may interact with opioid agonists: receptors to act as an agonist (morphine- ◦ Higher receptor affinity like) or as an antagonist (naltrexone-like) ó Lower level of receptor activation ◦ Patients may experience some withdrawal symptoms

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How to prevent When does a buprenorphine- precipitated withdrawal precipitated withdrawal occur? ó Withdrawal more likely when: ◦ Level of physical dependence is high ó Generally commences ~30-90 min after 1 st dose ◦ Short time since last opioid use (short- vs ó Generally peaks with 90-180 min after 1 st dose long-acting opioids) ó Minor symptoms may continue after 2 nd or 3 rd ◦ Initial dose of buprenorphine too high dose ó Prevention: ó Symptoms may also persist with continued st ◦ Administer 1 buprenorphine dose heroin/opioid use when objective signs of withdrawal are present

Suboxone ó Disadvantage of buprenorphine: ◦ It can be abused because it is an opioid that is ó Combination buprenorphine/naloxone reinforcing. ◦ Naloxone has relatively poor sublingual ó Solution: bioavailability ◦ Combination product of buprenorphine and ◦ Results in a predominant buprenorphine naloxone (Suboxone) effect when tablet is taken by the therapeutic ñ By reducing the abuse liability of buprenorphine, it route (sublingually) can be made acceptable for use by clinicians outside ◦ Abuse via the parenteral route results in a of OTPs. predominant naloxone effect

Screening Patients for Outpatient Suboxone Buprenorphine Treatment ó The optimal combination is a 4:1 ratio of buprenorphine to naloxone Pros Cons ◦ Formulations available: ó Compliant ó In MMT ◦ Appointments ñ 2/0.5 mg buprenorphine/naloxone ó Extensive legal ◦ Medications for other problems ñ 8/2 mg buprenorphine/naloxone medical/psychiatric ó Non-compliant conditions ó Limited/no support ó Employed ó Extensive psychiatric ó Limited legal problems problems ó Multiple substance use ó Intact family/support system problems

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Selecting treatment modalities Objectives of Maintenance Treatment

ó To reduce mortality from overdose and ó Consider: infection ◦ Patient expectations of treatment ó To reduce opioid and other illicit drug use ◦ Patient goals ó To reduce transmission of HIV, HBV and HCV ◦ Stages of change ó To improve the general health and well-being of ◦ Current circumstances patients ◦ Available resources ó To reduce drug-related crime ◦ Past history of treatment outcome ó To improve social functioning and ability to stay ◦ Evidence regarding safety, efficacy and in work effectiveness ó Informed consent

Objectives of OBT with Choosing Maintenance Medications Buprenorphine ó Help to destigmatize opioid dependence treatment ó No evidence that certain patients respond better to buprenorphine/methadone ó Reduce barriers for patient entry into treatment ó The choice between methadone or buprenorphine depends upon: ó Move addiction treatment into ◦ Overall response to each treatment mainstream medicine ñ Many patients express a clear preference ◦ Access to treatment setting (e.g., doctors office vs Opioid Treatment Program) ◦ Ease of withdrawal ◦ Patient (and clinician) expectancy

Choosing Subutex or Suboxone Induction

ó It is expected that patients maintained on ó Accurate history buprenorphine will be given the tablet or ó Objective signs of withdrawal ó Day 1: strip containing the combination of ◦ Initial dose 4 mg buprenorphine and naloxone. ◦ Second dose of 4 mg after assessing initial ó For a patient taking a long acting full response ó Day 2: opioid agonist, monotherapy tablets could ◦ First day’s dose plus 2-4 mg as indicated by be considered for the first 2 days of patient’s response induction. ó Day 3: ◦ Target 16 mg according to patient’s response

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Methadone Buprenorphine Always dose to desired clinical effect Transfers ó Variability in patient metabolism of buprenorphine requires individualized dosing Generally not recommended in stable ó Majority respond to 4-24 mg daily patients ó No maximum recommended dose ◦ Use of illicit opioids decreases and treatment retention improves with increasing dose (Ling, 1998) ó No maximum or minimum duration of treatment

Reasons to transfer Avoiding Precipitated Withdrawal

ó Patient preference ó To reduce risk of precipitated withdrawal: ó Side effects from methadone ◦ Transfer from doses of methadone <30 mg ó Desire to stop additional heroin use ◦ Check patient has not used opioid since last ó Escalating doses of methadone methadone dose ◦ Rapid metabolizers ◦ Commence with low dose of buprenorphine ◦ Tolerance (2-4 mg) ó Patient wishes to reach abstinence ◦ Delay first dose of buprenorphine until mild- ◦ May be easier to stabilize on buprenorphine first and taper dose moderate objective signs of opioid withdrawal are evident ó Ease of dosing, easier access to treatment

Buprenorphine is generally well tolerated but… Not all patients are suitable ó Common side effects may include: ó Contraindication for buprenorphine treatment: ◦ Headache ó Hypersensitivity to buprenorphine or naloxone ◦ Constipation ó Age < 16 years ◦ Nausea ó Access to specialty treatment services may be ◦ Anxiety required: ◦ Rhinitis ó Pregnancy ◦ Sweating ó Unstable dual diagnosis/psychiatric co-morbidity ◦ Insomnia ó Unstable polydrug use (especially ◦ Pain benzodiazepines and CNS depressants) ó HIV/HCV with acute hepatic dysfunction

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Reducing/Discontinuing Buprenorphine Special populations- Pregnant women

ó Active opiate addiction can mimic the ó Abrupt discontinuation produces a mild early stages of pregnancy. to moderate withdrawal syndrome ó Screen all women for pregnancy. ◦ Subjective symptoms of withdrawal begin within the first 3 days, peak between days 3 ó MMT is the treatment of choice for and 5, and return to baseline in 10-14 days. pregnant opiate addicted women. ◦ Autonomic signs of opioid withdrawal (e.g., ó Neonates born to a mother maintained chills, gooseflesh, tremors, rhinorrhea, on methadone will be physically lacrimation) are generally less pronounced dependant on opioids. ó Taper dose over 5 – 10 days.

Special populations- Pain patients Special populations- MMT patients ó BUP is roughly equal to 60 mg methadone. ó BUP has analgesic properties like any ó Transfer from MMT to BUP is generally not mu agonist, but it must be dosed q. 6 recommended for stable patients. hrs. ó Transfer from methadone to BUP can be

ó Single day BUP dosing is not adequate difficult due to the long t 1/2 of methadone. analgesia for acute/chronic pain. ó Patients need to be on < 30 mg and wait at ó The role of BUP in chronic pain is still least 24 hours after last methadone dose. under investigation. ó Patients should be exhibiting objective signs ó Pain management for patients taking of opiate WD before induction. BUP ó Start with low BUP doses (4mg)

Patients who continue to use despite treatment

ó Inadequate Suboxone dose PHARMACOLOGIC ó Readiness to change INTERVENTIONS ó Living environment FOR COCAINE ó Comorbid psychopathology ADDICTION

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Cocaine Addiction Treatment Cocaine Addiction Treatment

ó Use of high dose vitamin preparations. Contain ó Tricyclic Antidepressants amino acid precursors to Dopamine, Desipramine 150-200 mg daily for 6 months Norepinephrine, and Seratonin to address ó Anticonvulsant Medications (Anti-kindling hypothesized Neurotransmitter depletion. effect) for 3-6 months. ó Cocaine Withdrawal (approx. 2 weeks) Depakote 500-1000 mg daily Use of Dopamine agonists: Tegretol 200 mg bid or tid Bromocriptine (2.5 mg qid then taper over 2 Topiramate 25 mg/d then increase by 25 mg/d weeks). weekly until 200 mg/d. Continue this dosage for Amantidine HCL 100 mg bid or tid for 14 days. weeks 8-12 then taper to zero on week 13.

Cocaine Addiction Treatment PHARMACOLOGIC ó Modafinil (Used to treat narcolepsy) ◦ Increases glutamate levels depleted by cocaine INTERVENTIONS FOR usage. 400 mg daily for 8 weeks. (Dr. Dackis at NICOTINE Penn). Reduced cocaine positive urines and increased abstinence. DEPENDENCE ó Cocaine Vaccine ( Dr. Kosten at Yale) ◦ Compound called TA-CD. ◦ Pts received weekly injections for 8-12 weeks. Produced significantly reduced euphoria following use.

Nicotine Dependence Nicotine Dependence

ó Nicotine Replacement Medications: ó Topiramate (Topamax) has recently been shown in several studies to be useful as an adjunctive medication Nicotine patch, gum, nasal spray, and inhaler. in smoking cessation. Side effects can include ó Other Medications: parasthesias and weight loss. Buproprion (Wellbutrin SR, Zyban) Dosage is ó Varenicline (Chantix) approved by FDA in 5/06. 300 mg daily and should be continued for at Reportedly acts by reducing the pleasure of smoking least 4-8 weeks following completion of and reducing withdrawal. Attaches to nicotine receptors in brain pleasure centers and blockades the nicotine substitution tapering. Approved by FDA binding of nicotine. Also slows the release of Dopamine in 1997. which may reduce craving.

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Varenicline Varenicline

ó Dosage titrated upward over a weeks period ó Some patients will experience problems of time to 1 mg twice daily. with ongoing severe nightmares as a ó FDA initiated Black Box warning in 2009. result of its usage which may necessitate Monitor patients for possible serious it being discontinued. neuropsychiatric events including behavioral changes, hostility, agitation, depression, suicidal ideations as well as worsening of psychiatric symptoms in patients with preexisting psychiatric conditions.

Nicotine Dependence

ó Nicotine Vaccine (Dr. Hatsukami -2005). NicVax-Triggers the production of antibodies that bind nicotine in the blood and keep it from reaching the brain. Countertransference : Initial study in 68 smokers showed The Source of Our Conflict and favorable results. Blunders When Working With Patients

HISTORY FREUD

ó Narrow definition The concept of ó Referred to the clinician’s transference to the patient or the clinician’s response to countertransference has the patient’s transference undergone considerable ó Caused by unresolved conflicts from the evolution since its inception clinician

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Contemporary Perspective Evolution of the Concept – 3 Stages

ó Countertransference is a jointly created 1. Countertransference is an obstacle to reaction in the clinician with two parts: treatment and a sign of possible ◦ Contributions of the clinician’s past professional incompetence. ◦ Feelings induced by the patient’s behavior 2. Countertransference is unavoidable but must be tightly controlled. The implication was, “It exists, but it shouldn’t.” 3. Acknowledgement of the ubiquity of CT but viewed as a potentially valuable clinical tool.

COUNTERTRANSFERENCE

ó All instances in which clinicians act out feelings toward patients that are unresolved characterological or cultural conflicts or biases within themselves, whether or not induced by corresponding DEFINITION feelings in the patient

Categories of Countertransference Clinician Errors

ó Objective Countertransference ó Technical ◦ Induced by the patient and which the clinician ◦ Usually occur in the first two or three years feels, without the temptation to act out on it. of a clinician’s practice ◦ Expected to be induced in any clinician ó Countertransference ó Subjective Countertransference ◦ Primary source of errors for the experienced ◦ An irrational response to the patient rooted clinician in the clinician’s fixations. ◦ A true transference based upon pathological configurations within the clinician.

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Some Caveats

ó All of the clinician’s emotional reactions to the patient should be internally treated Procedure for the and neutralized so that they are fully under control before any intervention is Communication of made. Countertransference Feelings ó When a negative feeling is induced, the patient’s interest is safeguarded when the clinician processes his feelings.

Processing of Clinician’s Feelings

1. Observe the full emotional impact the patient is having. 2. Be fully aware of counter-destructive impulses and wishes DIAGNOSIS AND 3. Reduce the intensity of feelings without attempting to eliminate them TREATMENT OF 4. Discover whether the main source is subjective or objective COUNTERTRANSFERENCE 5. Determine what the patient needs in the way of an intervention 6. Observe carefully the effects of the intervention

Resolving the Denial – Part 1

ó “What kind of countertransferences am I prone to?” ó “How can I categorize them so I will be forewarned and sensitized to certain The question is no longer, “Do I patients or certain kinds of material?” have countertransferences?” ó “Are they so strong that I should clearly avoid certain patients because I know that they will push buttons in me that will be counter-productive to a successful therapeutic outcome?”

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Resolving the Denial – Part 2

ó “What clues do I have to tell me when a countertransference is rearing its ugly head.” ó “What should I do when I discover such a clue?” Answering These Questions….

“What kind of countertransferences am I “What clues do I have to tell me when a prone to?” countertransference is rearing its ugly head.” ó To find the answer we look at the parts of ó A feeling of distaste about a patient’s our mothers, fathers, and siblings that we appearance did not like or caused us problems. ó Making a mistake in scheduling/forgetting ◦ Was your mother intrusive, passive, an appointment complaining? ó Becoming anxious during a session ◦ Was your father rejecting, angry, competitive? ó Finding your mind wandering ◦ Did you hate a sibling? ó Feeling drowsy

“What clues do I have to tell me when a countertransference is rearing its ugly head.” Categorizing Countertransference ó Having a dream about a patient ó Erotic ◦ A signal that the patient represents some ó Sadomasochistic figure from your past. ó Narcissistic ó Slips of the tongue made during a session ó Ending the session too early/too late ó Characterological ó Ignoring non-payment issues ó Cultural ó Giving the patient a great deal of extra time ó Socializing with a patient

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Erotic Countertransferences Sadomasochistic Countertransferences

ó Usually the most difficult for a clinician to ó The danger is always that the clinician will be aware of, manage, and utilize. become involved in a power struggle with the patient. ó It is common for patients of both sexes to be seductive toward their clinicians. ó Sometimes the clinician has a need to dominate, manipulate, or control the ó clinicians may fail to understand or patient. empathize with patients because of their ó Or the clinician may have an unconscious own unresolved erotic conflicts. need to be dominated, controlled, or manipulated by the patient. -MORE-

Sadomasochistic Countertransferences Sadomasochistic Countertransferences

ó A clinician may use the patient as a ó A patient’s hostility will often elicit a vehicle for proving his own skills and sadomasochistic CT reaction. powers as a clinician. ◦ It is a given that at some point in successful ◦ May conduct the treatment in a way that therapy all patients express hostility to their disregards their patients’ real needs and desires. clinicians. ◦ ó clinicians may insist that their patients Usually this is expressed through criticism of accept their interventions without their clinicians question, as though they were the law, and ñ Those clinicians who have not completely worked through their own feelings of anger at parental become irritated when their patients do figures will be unable to tolerate their patients’ not accept them as such. hostility. -MORE-

Characterological Narcissistic Countertransferences Countertransferences ó Involve the acting out of feelings of low ó Refer to being emotionally blocked in self-esteem, rage, depression, or some way or another. dependency. ◦ Narcissistic clinicians may be resistant to ◦ Have a need to be always right confronting their patients’ grandiosity or rage ◦ To be the “perfect” clinician ó The worst are those stemming from ◦ Try to impress patients character disorders in which symptoms ◦ Sometimes have the attitude that they are “gods” who are going to remold the patient in are ego-syntonic and never recognized their own image. and worked through. ñ They will have an agenda for the patient that will usually be in opposition to the patient’s needs.

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Cultural Countertransferences

ó One of the more prevalent and potentially harmful forms of cultural CT comes about when clinicians identify Countertransference Reactions themselves with a cause, a religion, or a mass movement. to Patients with ◦ They will often become self-righteous Antisocial Personality/Traits ◦ They will fell justified in transferring, resisting, and acting out aggressive feelings without feeling any guilt.

3 Common Reactions Disbelief

ó Disbelief ó May surface as denial that the patient is ó Collusion really “that bad.” ó Condemnation ó Rationalizing behaviors as being due to such problems as drug abuse or adolescent rebellion ◦ May cause clinician to deny the presence of psychopathic features ◦ May view the patient as depressed or misunderstood

Collusion Condemnation

ó One of the most problematic forms of ó Often manifested in expressions that a countertransference. patient is totally untreatable and that no ó In the belief that they are helping the effort should be made to establish a patient, clinicians’ acting out may commit treatment relationship. illegal acts or otherwise behave unethically ó Most often a knee-jerk reaction to ◦ Lie on behalf of the patient hearing some history of antisocial activity. ◦ Falsify records ◦ Seduced into sexual relationships ◦ Helped patients to escape

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ETHICS “Confronting and resolving our countertransferences can reduce their negative impact to a tolerable minimum. It is our way of healing ourselves so we can heal our patients.” -Richard C. Robertiello, MD

Confidentiality of Information Examples of Breaches

ó Clinicians do not communicate, directly or ó Talking about patients in public indirectly, information that a person has shared ó Calling out patients’ names when phone within the context of a professional relationship. calls for them come in ó If the clinician knows that he/she is unable to assure ó the patient of confidentiality of information, he/she Discussing patients in the waiting room must inform the patient of this fact before the ó Discussing patients with those without a patient has shared personal information. need to know.

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Code of Ethics Limit-Setting

ó Provides the clinician with guidelines ó A clinician should not offer professional about appropriate professional behavior services to a family member or friend ó Provides the patient with guidelines to ó A clinician should not treat patient recognize proper clinician behavior problems that are beyond his skill level ó At no time should a clinician meet with a patient on a personal/social basis ó A clinician should not initiate, encourage, or maintain an overt/covert relationship with a patient

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Other Ethical Concerns

ó The clinician must be aware of racial or sexual prejudices and act accordingly ó The clinician must confront a fellow clinician if he discovers that his/her CONFIDENTIALITY colleague has a drinking problem or a substance abuse problem ó A clinician must report patient abuse if observed in a colleague

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What Can Be Disclosed Confidentiality Issues (With Consent) ó Confidentiality means that statements, ó Whether the patient is or is not in actions, and communications of the treatment patient are kept private within the ó The patient’s diagnosis confines of the therapeutic relationship. ó The services offered to the patient ó Confidentiality is essential to the patient’s ó A brief description of the patient’s trust in the clinician. progress ó A short statement as to whether the patient has relapsed

Case Example Protecting the Patient You are chatting with a new patient and he informs you that he has decided to seek ó When patients enter treatment – no treatment at your facility on the matter who they are – we must respect recommendation of a friend who is their privacy and adhere to complete currently in outpatient. The new patient confidentiality tells you that he was motivated to begin ó Patients reveal very personal and private treatment because he has seen how much information which is documented in the his friend has been helped. Meaning to patient’s clinical chart. encourage the new patient, you mention ó The Federal Non-Disclosure Rule forbids that his friend has certainly made a lot of even identifying a person as a patient. progress and you have heard that he continues to be completely abstinent.

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What To Say Case Example While driving home, you realized that you still had a ó A good rule is to say nothing about any list of patients’ names in your pocket. Since it patient even when you know that the wasn’t part of a chart, you weren’t worried about person making an inquiry already knows it. You fold it and lay it on the seat next to you. As you’re driving, you see your neighbor who asks that the patient is in treatment. for a ride. She knows where you work and is ó The best response is to inform the always trying to find out who is in treatment. As inquiring party that federal law prevents you are driving, you hear her shriek as she exclaims, “I knew that boy was using drugs. His you from answering the question. mother told me he was on vacation with his father.” She was reading your list of patients.

Dual Relationships

ó Patients and staff can also be neighbors, co- workers, members of the same church or social club, etc. ó All dual relationships must be reported immediately to your supervisor as soon as you become aware that someone you know is in ETHICAL PRINCIPLES treatment. ó You are not permitted to make any contact or discuss any issue not relating to the patient’s treatment.

Ethical Principles Ethical Principles

4. You avoid relationships that may create a 1. You respect the dignity and worth of each conflict of interest. patient and strive to protect individual 5. You try to prevent distortion or misuse human rights. of your findings. 2. You do not permit patients’ skills to be 6. You present material objectively, fully, and misused. accurately. 3. You accept the responsibility for the 7. You know that your work bears a heavy consequences of your actions. When you responsibility because your are wrong, you promptly admit it. recommendations and actions may alter the lives of others.

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Ethical Principles Ethical Principles

8. You accurately represent your 11. You recognize that personal problems competence, education, training, and may interfere with your professional effectiveness. You refrain from becoming experience. engaged in an activity where your 9. You recognize the differences among personal problems may have an influence. people of different races, sexes, cultures, If you have serious problems, then you creeds, ethnic backgrounds, and have a responsibility to seek appropriate socioeconomic statuses. professional assistance. 10. You follow all guidelines and regulations 12. You do not condone practices that you of your profession and your facility. perceive as being inhumane or unjust.

Ethical Principles Ethical Principles

13. You respect the confidentiality of all 16. You ensure that appropriate provisions information obtained within the context of are made for maintaining confidentiality in your work. the storage and disposal of any patient 14. You reveal such information only with the records. written permission of the patient, except when the patient is a clear danger to self or others. 17. You recognize your own needs and are 15. You discuss information obtained in cognizant of your potential to influence professional relationships only for professional patients and other staff. purposes and only with persons clearly 18. You understand that sexual intimacies concerned with the case. with patients are unethical.

Ethical Principles

19. You make every effort to avoid relationships that could impair your professional judgment or increase the risk of exploitation. This includes QUESTIONS socializing with patients who you know outside the facility. AND 20. You cooperate fully with other professionals. COMMENTS 21. You do not condone or participate in any form of sexual harassment.

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