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Addiction is a brain disease: Meanings for the anesthesia community

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Presentation on theme: "Addiction is a brain disease: Meanings for the anesthesia community"— Presentation transcript:

1 Addiction is a brain disease: Meanings for the anesthesia community
Art Zwerling, DNP, CRNA, DAAPM AANA PAAC April 2013

2 Grateful Acknowledgements
Diana Quinlan, CRNA, MA Heather Hamza, CRNA, MS Greg Ramplemann, CRNA Linda Stone, CRNA, MSN Tony Chipas, CRNA, PhD Gary Clark, CRNA, EdD Saundra Dockins, CRNA Terry Wicks, CRNA, MSHS Michael Lords, SRNA Julie Rice, AANA Don Bell, CRNA, DNSc Steven D. LaRowe, Ph.D. AANA BOD

3 In December, 2008, “The New Republic” magazine ran a cover story on the anesthesia profession’s struggle with drug addiction, bringing attention to fatalities associated with anesthesia provider addiction. The gunshots you hear during this presentation represent , in real time, a life lost to substance abuse in the United States… 19,102 deaths per year… 1,591 per month… 367 per week… 52 per day… 2 per hour… (If you play this in slideshow with your volume up you will hear a powerful gunshot sound effect that leads the slide transition… this shot occurs at three later points in the presentation)

4 Learning Objectives Inform communities of interest regarding the antecedents, risks and consequences of chemical dependency Promote awareness of the impact of CD on the anesthesia community Review the basic neurobiology of chemical dependency as a chronic brain disease. Reduce the incidence of chemical dependency and the impact of CD on the nurse anesthesia profession

5 History/Background Diana Morgan, Minnesota President
1983 Annual Business Meeting Resolved: That the American Association of Nurse Anesthetists form a task force to study the impact of chemical dependency upon our profession and to be a source of positive public relations concerning chemical dependency information as it affects our members.

6 Pioneers in the AANA’s Peer Assistance and Recovering Community
Rusty Ratliff, Diana Quinlan and many other worked to support and find acceptance for the recovering CRNA community TW: Clark 1993 Fitzhugh McDonough, , 1999 Waugaman Norris

7 A Rude Awakening… Death of Jan Stewart in 2002
Jan Stewart Memorial Lecture Series 2004 Virginia Trotter Betts 2004 AANA Blue Ribbon Wellness Panel and establishment of the Wellness Program 2005 Presidential Wellness TF 2010 TW AANA President

8 Chemical Dependency Substance related disorders characterized by chronicity and progression that threaten wellness.. Propensity for relapse Transition to a chronic disease, chronic care model Subversion of primitive reward and anti-reward systems Neuroplasticity Art prevention, identification  intervention 15 min (4:05 – 4:20pm)

9 CRNA Statistics Approximately 1 in 10 CRNAs becomes addicted during their career (Clark & Stone, 1999) 15.8% of CRNAs found to be dependent on alcohol, drugs or both (Berry, 2000) Male CRNAs with 6 to 10 years of clinical experience are most at risk for addiction (Bell, 1999) 66.7% of SRNAs with substance abuse problems were ranked in the upper third of their graduating class (Clark & Stone, 1999) The statistics have reached staggering levels, resulting in a call to action by related professions to monitor anesthesia providers for signs of impairment (American Society of PeriAnesthesia Nurses, 2004). Our hope is that by noting the risk factors, which we touch upon here and will discuss in this presentation, we can prepare ourselves for success and avoid the downward spiral of substance abuse. These statistics show that approximately 1 in 10 CRNAs becomes addicted during their career… and that 15.8% of CRNAs are found to be dependent on alcohol, drugs or both. Male CRNAs with 6 to 10 years of clinical experience are the most at risk for addiction… and… of note… 66.7% of SRNAs with substance abuse problems were ranked in the upper third of their graduating class.

10 Drugs of Choice Opioids such as fentanyl and sufentanil are the most commonly cited abused substances by anesthesia providers (Booth, 2002) CRNA studies have shown midazolam is the most misused controlled drug among providers (Bell, 1999) It is often said that the first sign that an anesthesia provider is suffering from chemical dependency is when they are found dead in the on call room.  The recently reported rise in abuse of propofol and inhalation anesthetics supports this shocking reality, with high mortality rates associated with abuse of each of these drugs. Fentanyl, sufentanil and midazolam are reported in the literature as the most prominent drugs of choice. 

11 Drug Misuse by Preference Inside the OR

12 Triad of Contributing Factors© Drug Misuse by CRNAs
AVAILABILITY Genetics Stress Burnout Fatigue Terminal uniqueness & pharmacologic optimism a deadly combination Invulnerability Prior Experimentation ACCESSIBILITY ACCOUNTABILITY Adapted from Bell 2007

13 Warning Signs At work during off hours Isolation Frequent breaks
Tardy or Absent Signing out more drugs than peers Inappropriate dosages, drug choices Problematic alcohol use at social functions Difficulty with authority Forgetful, confused Freq. Illness, physical complaints Dishonesty (trivial matters) Elaborate excuses Tremors Long sleeves, alcohol on breath Source: AANA Website

14 Causes of Addiction: Disease Model
Alcoholism and other addictions represent diseases for which a certain proportion of the population is genetically predisposed Developed by Dr. Benjamin Rush, late 1700’s Scientific credence in 1960 Jellinek’s “Disease Concept of Alcoholism” Originally rejected by AMA, but now accepted Framework for AA and other 12 step groups Burgeoning support from bench research in the neurobiology of addictions

15 Why Do People Take Drugs in The First Place?
To feel good To have novel: feelings sensations experiences AND to share them To feel better To lessen: anxiety worries fears depression hopelessness Research has shown that people generally take drugs to either feel good (sensation seekers, or anyone wanting to experiment with feeling high or feeling different) or to feel better (self-medicators, or individuals who take drugs in an attempt to cope with difficult problems or situations, including stress, trauma, and symptoms of mental disorders).

16 Natural Rewards Elevate Dopamine Levels DA Concentration (% Baseline)
FOOD SEX 200 200 NAc shell 150 150 DA Concentration (% Baseline) 100 100 15 5 10 Copulation Frequency % of Basal DA Output Empty 50 Box Feeding Natural rewards increase dopamine neurotransmission. For example, eating something that you enjoy or engaging in sexual behavior can cause dopamine levels to increase. In these graphs, dopamine is being measured inside the brains of animals, its increase shown in response to food or sex cues. This basic mechanism has been carefully shaped and calibrated by evolution to reward normal activities critical for survival. 60 120 180 Female Present Time (min) 1 2 3 4 5 6 7 8 Sample Number Mounts Intromissions Ejaculations Di Chiara et al., Neuroscience, 1999. Fiorino and Phillips, J. Neuroscience, 1997.

17 Effects of Drugs on Dopamine Release
100 200 300 400 500 600 700 800 900 1000 1100 1 2 3 4 5 hr Time After Amphetamine % of Basal Release DA DOPAC HVA Accumbens AMPHETAMINE 100 200 300 400 1 2 3 4 5 hr Time After Cocaine % of Basal Release DA DOPAC HVA Accumbens COCAINE 100 150 200 250 1 2 3 hr Time After Nicotine % of Basal Release Accumbens Caudate NICOTINE 100 150 200 250 1 2 3 4 5hr Time After Morphine % of Basal Release Accumbens 0.5 1.0 2.5 10 Dose (mg/kg) MORPHINE Drugs of abuse increase dopamine neurotransmission. All the drugs depicted in this slide have different mechanisms of action; however, all increase activity in the reward pathway by increasing dopamine neurotransmission. Because drugs activate these brain regionsusually more effectively than natural rewardsthey have an inherent risk of being abused. Di Chiara and Imperato, PNAS, 1988

18 Why do some people become addicted while others do not?
Vulnerability Why do some people become addicted while others do not? What makes some people more vulnerable to drug addiction? Many people try drugs without getting addicted, while others do become addictedsome quickly and easily.

19 Big Genetic Contribution to Drug Abuse and Addiction…
We Know There’s a Big Genetic Contribution to Drug Abuse and Addiction… ….Overlapping with Environmental Influences that Help Make Addiction a Complex Disease.

20 Biology/genes Environment Biology/ Environment Interactions
It is clear today that addiction is the result of complex interactions not only among many genes but also between genes and a host of environmental factors. Environment

21 Anesthesia Biology/genes Environment Applicant genome
Interactions It is clear today that addiction is the result of complex interactions not only among many genes but also between genes and a host of environmental factors. Environment Stress Accessibility Accountability Potency


23 DA Receptors and the Response to
Methylphenidate (MP) High DA receptor high Dopamine receptor level low Low DA receptor The level of dopamine receptors in the brain can influence whether a person likes or dislikes the effects of a drug. Dopamine is one of many chemicals normally found in the brain and is involved in the perception of pleasure. Most abused drugs directly or indirectly increase dopamine in brain regions related to reward and motivation. Dopamine receptors are the sites on nerve cells where dopamine attaches to regulate their function. The graph on the right side of this slide shows that individuals with a lot of dopamine receptors (top picture on the left; dopamine receptors are in yellow/red) tend to experience methylphenidate (a stimulant) as unpleasant, whereas persons with lower numbers of dopamine receptors (bottom picture on the left) find it pleasurable. This biological difference can influence the chances of re-exposure to a drug, and thus the risk of abuse or addiction. As a group, subjects with low receptor levels found MP pleasant while those with high levels found MP unpleasant Adapted from Volkow et al., Am. J. Psychiatry, 1999.

24 Adaptations to reward & anti-reward systems lead to chronic disease

25 Dancing with the white rabbit: A break from the neuroscience
Dancing with the white rabbit CSA Connie Ward

The standard dose of propofol is 2–2.5 mg/kg body weight for the induction of anaesthesia within 1–2 min and arousal after 5– 10 min.5 After a bolus injection, patients lose consciousness at blood concentrations of 1.3–6.8 tg/ml and regain it through fast redistribution at concentrations of 1–2.5 tg/ml. The onset of unconsciousness and CNS depression are also known to be related to the speed of injection.4 The mechanism of action is not com­pletely known, however, the drug probably exerts its pharmaco­logical effects by enhancing the function of the GABA-activated chloride channel.7 In CNS propofol has euphoric feelings, sexual hallucinations and has sedative and relaxing effects.8–11 Its eupho­ric effects are clinically known and have also been demonstrated in a double blind randomized study in healthy volunteers using pro­pofol in subanaesthetic dosages (0.2–0.6 mg/kg). The authors of this study concluded that use of propofol may be rewarding in some people without history of drug abuse.12

27 The Misuse and Abuse of Propofol *
Another must read The Misuse and Abuse of Propofol * Todd Monroe, Heather Hamza, Greg Stocks, Paula Davies Scimeca and Ronald Cowan *Substance Use & Misuse, Early Online:1–7, 2011 ISSN: print / online

28 Seminal Review Article: Concise, Clear & Comprehensive*
Critical review of the current state identification, intervention and monitoring. There are areas with an incredible paucity of data such as CRNA specific outcomes Must read for every anesthesia educator AZ: Cites Dr. Bell Extensively *The Drug Seeking Anesthesia Care Provider Ethan O. Bryson, MD, Heather Hamza, MS, CRNA Int Anesthesiol Clin Winter;49(1):157-71 *The Drug Seeking Anesthesia Care Provider Ethan O. Bryson, MD, Heather Hamza, MS, CRNA Int Anesthesiol Clin Winter;49(1):157-71

29 Evolution of the concept of the high-jacked cortex
For millennia we have grappled with the perverse polymorphic nature of addictive processes and the behaviors exhibited. Addictive behavior appears to defy logical analysis at many levels. By exposing how primitive (midbrain) reward & anti-reward system dynamics supersede higher cognitive processes (orbitofrontal) allows us a different perspective on the powerful, cunning, & baffling nature of addiction.

30 The high jacked cortex It certainly can look like demonic possession
The behavior is puzzling, baffling, perplexing and frightening. Once complete abstinence is achieved an effective denialectomy is possible.

31 Addictive Thinking Revisited
Normal Logic: All trees have leaves, this has leaves, this may be a tree. Neurotic Logic: All trees have leaves, this has leaves, this may be a tree and when fall comes I’m going to pick up each leaf. Psychotic Logic: All trees have leaves, this has leaves therefore I am a tree. Addictive Logic: All trees have leaves, this has leaves therefore I need a drink/drug.

32 The Neurobiology of Addiction
Steven D. LaRowe, Ph.D. Center for Drug and Alcohol Programs Medical University of South Carolina Substance Abuse Treatment Center Ralph H. Johnson VAMC AANA Presentation 8-09

33 Addictive Behavior = Survival Behavior Gone Awry
Over the course of evolution, we have developed circuitry in our brains that have promoted our survival Drugs of addiction activate this “survival circuitry” and with chronic use, essentially take it over In the late stages of addiction, an individual is basically a “survivalist” doing whatever it takes to acquire and use drugs regardless of the costs

34 Addiction: Hijacking the Basic Survival Circuitry
Food! Food! Martini!

35 Basic Neurobiology Acquisition Progression Neuroplasticity
Chronicity & relapse

as other diseases it affects the tissue function Control Cocaine Abuser Decreased Brain Metabolism in Drug Abuse Patient High Low Decreased Heart Metabolism in Heart Disease Patient Healthy Heart Diseased Heart Sources: From the laboratories of Drs. N. Volkow and H. Schelbert


38 Addiction Changes Brain Circuits
Stop & Go Systems Awry Drive Saliency Memory Control Non-Addicted Brain NOT GO Addicted Brain AZ: Addiction changes brain circuitry making it hard to “apply the brakes” to detrimental behaviors. In the non-addicted brain, control mechanisms constantly assess the value of stimuli and the appropriateness of the planned response, applying inhibitory control as needed. In the addicted brain, this control circuit becomes impaired through drug abuse, losing much of its inhibitory power over the circuits that drive response to stimuli deemed salient. Source: Adapted from Volkow et al., Neuropharmacology, 2004.


40 Dopamine and Glutamate Revisited

41 Addictive Thinking Revisited
Normal Logic: All trees have leaves, this has leaves, this may be a tree. Neurotic Logic: All trees have leaves, this has leaves, this may be a tree and when fall comes I’m going to pick up each leaf. Psychotic Logic: All trees have leaves, this has leaves therefore I am a tree. Addictive Logic: All trees have leaves, this has leaves therefore I need a drink/drug. This is the apparent change in orbitifrontal processing from a functional perspective.

42 Neurobiological Basis   • Addiction: a condition in which behavior that can function both to produce pleasure and to reduce painful effects is employed in a pattern that is characterized by two key features: (1) recurrent failure to control behavior and (2) continuation of the behavior despite significant harmful consequences (Goodman,2007). • Dependence: Emergence of a negative emotional state produced by negative reinforcement mechanisms (e.g. dysphoria, anxiety, irritability) when access to the drug is prevented (Koob, 2009). • Salience: Prioritization of a stimulus in the environment based on its relative importance to the organism’s overall well being or survival. Readily influenced by long-term memory stores or anticipatory mechanisms. *important concept • Hedonism: Intrinsic value of pleasure. The only value is how much good is produced and how little pain is experienced (Encyclopedia Britannica, 11th ed., 1911). In the past decade there has been a tremendous amount of research on the subject of addiction and dependence. Clearer understanding and specific definitions have been sought while employing a framework deep rooted in neurobiology. What was once considered a disease of personality disorder, lack of will and/or dysregulated emotional states with uncontrolled coping mechanisms has now been proven to have a pathogenesis founded in neuronal pathways, hyperplasticity of reward centers in the cerebral cortex and neurotransmitter mediated messenger pathways which render the addict a prisoner to his or her own neurobiology. If we define addiction with a behavioral syndrome and dependence as an emotional state characterized by negative feedback loops that are based in organic structures dependent on the activation and transmission of specified neurotransmitters… it makes good sense that this divergent disease process can be ultimately described as behavioral and emotional sequelae derived from an organic dysfunction of negative feedback loops rooted in neurobiological dysplasia and neurotransmission.

43 Allostasis    • A state of chronic deviation of the regulatory system from its normal operating level (homeostasis) (Koob et al. 2008). • A continuous readjustment of all parameters toward a new set point illustrates the construct of this mechanism as “stability through change” (Koob et al. 2008). • Repeated challenges, such as the case with drugs of abuse, lead to attempts of the brain via molecular, cellular and neurocirciutry changes to maintain stability (Koob et al. 2008). • The residual deviation from normal brain reward systems threshold is termed the allostatic state (Koob et al. 2008).   In defining allostasis we see that it is a chronic deviation from normalized functioning. This is probably the most important concept to understand because this is where the rubber meets the road in illustrating the causative interplay of neurophysiology and the behavioral paradigm associated with addiction. The chronic elevation of a reward set point is fueled from opponent processes inducing a regulatory dysplasia in the neurobiological structures. The motivational perspective by way of a decreased function of reward circuits and the recruitment of anti-reward systems ultimately lead to the compulsivity of drug seeking behavior (Koob et al. 2008).

44 Opponent Processes Reward system (s) involved in the acquisition of addictions Anti-reward system (s) involved in the maintenance of addictions Neuroplasticity appears to underpin the chronicity of addictions and propensity for relapse

45 Neurocircuitry of Addiction
George F. Koob, & Nora D. Volkow Neuropsychopharmacology REVIEWS (2010) 35, 217–238 & 2010 Nature Publishing Group

46 Neuroplasticity Progression
Green= Go Preoccupation Compulsivity Blue= Binge Intoxication Red= Withdrawal Stress Dysphoria Figure 5. Neurocircuitry schematic illustrating the combination of neuroadaptations in the brain circuitry for the three stages of the addiction cycle that promote drug-seeking behavior in the addicted state. Note the activation of the ventral striatum/dorsal striatum/extended amygdala driven by cues through the hippocampus and basolateral amygdala and stress through the insula. The frontal cortex system is compromised, producing deficits in executive function and contributing to the incentive salience of drugs compared to natural reinforcers. Dopamine systems are compromised, and brainstress systems such as CRF are activated to reset further the salience of drugs and drug-related stimuli in the context of an aversive dysphoric state

47 Dark Side of Addiction The transition to a progressive, chronic and relapsing begins with the euphoric effects of these potent intoxicants on primitive reward systems that underpin basic biological survival drives. Ultimately maintenance of the addiction cycle is mediated by persistent Neuroplasticity in the reward and anti-reward systems. Avoidance of dysphoric states/withdrawal symptoms become the most powerful drivers of persistent addictive behavior.

48 The Dark Side of Addiction    • Development of an aversive emotional state that drives negative reinforcement of addiction (Koob et al. 2008). • Consists of key motivational elements: chronic irritability, emotional pain, difficulty identifying feelings (alexithymia), malaise, dysphoria, loss of motivation for natural rewards (Koob et al. 2008). • Two processes involved: –Loss of reward systems –Recruitment of brain stress or anti-reward systems (Koob et al. 2008)   The key elements of the motivational factors have all been explained through the science of neurobiology. Anti-reward systems are a construct based on the belief that brain systems are in place to limit reward. As dependence and addiction develop brain stress system such as CRF, Norepinephrine, and dynorphin an opiate receptor agonist are recruited (Koob al. 2008) (Allostasis). These systems produce aversive or stress like responsive states (Koob et al. 2008). At the same time the stress states develop, motivational systems in the ventral striatum of the extended amygdala decrease. The combination of a decreasing reward system with an increasing recruitment of anti-reward neurotransmitters provides a powerful source for negative reinforcement that contributes to the compulsivity of drug seeking behavior and addiction (Koob et al. 2008). I am going to hand the presentation over to one of my esteemed peers and we will look a bit closer at some of the stress motivators that drive this neurophysiologic mechanism.

49 Neurobiological Basis    • There are two key areas of brain arousal and stress mechanisms in the development of dependence: –Neuropharmacological actions of corticotropin-releasing factor (CRF) –Norepinephrine in the extrahypothalamic systems in the extended amygdala • Central nucleus of the amygdala • Bed nucleus of the stria terminalis • Transition area in the shell of the nucleus accumbens (Koob, 2009)   CRF is released from two different regions within the brain… which function as separate but connected stress systems (Goodman, 2007). The HPA axis, which is the mediator of hormonal stress response, activates CRF transmission within the neural pathways… We’ll look at this in the next few slides (Koob, 2009) .

50 Common pathway CREB is a transcription factor, a protein that regulates the expression, or activity, of genes and thus the overall behavior of nerve cells. When drugs of abuse are administered, dopamine concentrations in the nucleus accumbens rise, inducing dopamine-responsive cells to increase production of a small signaling molecule, cyclic AMP (cAMP), which in turn activates CREB. After CREB is switched on, it binds to a specific set of genes, triggering production of the proteins those genes encode. Chronic drug use causes sustained activation of CREB, which enhances expression of its target genes, some of which code for proteins that then dampen the reward circuitry. For example, CREB controls the production of dynorphin, a natural molecule with opiumlike effects. Dynorphin is synthesized by a subset of neurons in the nucleus accumbens that loop back and inhibit neurons in the VTA. Induction of dynorphin by CREB thereby stifles the brain's reward circuitry

51 Addiction is Similar to Other Chronic Illnesses Because:
Recovery from it--protracted abstinence and restored functioning--is often a long-term process requiring repeated treatments Relapses to drug abuse can occur during or after successful treatment episodes Participation in self-help support programs during and following treatment can be helpful in sustaining long-term recovery

52 Relapse Rates Are Similar for Drug Addiction & Other Chronic Illnesses
Type I Diabetes 10 20 30 40 50 60 70 80 90 100 Hypertension Asthma 40 to 60% 30 to 50% 50 to 70% Percent of Patients Who Relapse Relapse rates are similar for drug addiction and other well-characterized chronic illnesses. This slide compares relapse rates for drug-addicted patients and those suffering from diabetes, hypertension, and asthma. Relapse is common and similar across these illnesses (as is adherence to medication). Thus, drug addiction should be treated and evaluated like any other chronic illness. McLellan et al., JAMA, 2000.

53 Relapse and Relapse Triggers
Cue based- People Places Things Exposure- Iatrogenic Mediated Stress- Alterations in CRF Responsiveness Defining the dysphoric experience

54 Stress Susceptibility Model of Addictions
Certain people, due to a variety of biologically-based factors: genetics, neurocognitive functioning, stress response may be predisposed to developing an addiction to something, be it alcohol, heroin, gambling, sex or other process addictions if the right stressor, or combination of stressors, affects the person at a critical time, the person may be more inclined to develop an addiction.

55 The Stress Hormone Cycle
Hypothalamus CRF Pituitary Gland CORTISOL ACTH CRF: Corticotropin Releasing Factor Adrenal Glands Kidneys

56 DRUG USE (Self-Medication) What Role Does Stress Play
Anxiety DRUG USE (Self-Medication) CRF CRF The antireward system involved in fight flight response STRESS Anxiety What Role Does Stress Play In Relapse to Drug Use

57 What Happens When A Person
Stops Taking A Drug? RELAPSE Anxiety Prolonged DRUG USE CRF Abstinence

58 Relapse Triggers: Distinctions
Stress appears to mediate reinstatement of drug seeking via CRF1 receptor activity in the BNST. Contextual relapse appears to be mediated via prefrontal and extended amygdala Glutaminergic afferents to NAC shell. Priming (drug exposure) induced relapse appears to be mediated via direct increases in Dopaminergic tone via the VTA to the NAC core. Sinha R et al Psychological stress, drug-related cues, and cocaine craving. Psychopharmacology 2000; 152:

59 Relapse Triggers: Limbic Kindling of Craving
Glutaminergic prefrontal afferents from the prefrontal cortex appear to mediate the experience of craving induced by contextual exposure as evidenced by fMRI. Susceptibility to exaggerated responsiveness on exposure to drug related cues appears to persist.

60 Relapse Triggers: Stress
Stress appears to mediate reinstatement of drug seeking via CRF1 receptor activity in the BNST The mediation of cue associated reinstatement appears to be via Glutaminergic prefrontal inputs into the NAC Drug (priming) induced reinstatement appears to induce direct Dopaminergic release between the VTA and NAC. Sinha R et al Psychological stress, drug-related cues, and cocaine craving. Psychopharmacology 2000; 152:

61 Relapse Cycle and Recommendations
This figure represents the cycle of drug abuse and how relapse is inherently incorporated. This cycle shows how drug use leads to positive reinforcement and symptomology relief, which further leads to acute withdrawal symptoms leading to further drug use and abuse. After primary treatment for the chemically dependent, stress exposure during their abstinent time frame leads to a maladaptive stress response that includes increased conditioned emotional and drug craving responses, compounded with a decrease in adaptive coping, all leading to relapse. Recommendations for those at an increased risk for relapse include standard protocol, with an emphasis on increased workplace monitoring, more frequent random urine testing with observed micturation, and more intensive longterm followup and group therapy. Obviously, remaining abstinent from substance abuse is a two way street, and ultimately, the responsibility lies within each individual. Timed: 1 minute

62 Chronic Disease Models
DM as a model a. We know medication or diet non compliance can lead to relapse. b. We know that physiologic stressors such as a infective process can lead to an exacerbation. c. We know that compliance with treatment regimen is the key to disease management!

63 Case Study: Martin Expert cardiothoracic CRNA Voted favorite preceptor
Played viola in a string quartet Adored husband and father Drug of choice: Fentanyl Let‘s call him Martin… to protect the family’s privacy… (and to perpetuate the stigma) He was a nurse anesthetist with an enviable expertise in cardiothoracic anesthesia… always at the top of his game. His was voted favorite preceptor by his students. He loved music… and played viola in a well-recognized string quartet. His wife is a PACU nurse. His daughter is graduating from medical school this year. His drug of choice was fentanyl… He overdosed. He’s dead.

64 Failed Re-entry Often it is a unfortunate confluence of circumstances combining stress, failed recognition of place preference and or exposure to kindling cues that leads to relapse. Recognition of potential relapse triggers and scenarios are critical to successful re-entry. Timing and assessing for readiness for reentry in addition to relapse prevention strategies and resources is also critical to success. Emphasis should be on getting it right the first time!

65 People, Places, Things

66 Effectiveness of Treatment & Relapse Prevention
Recovery According to the Betty Ford Institute, recovery is defined as a voluntary maintained lifestyle characterized by sobriety, personal health, and living with respect for yourself and those around you. Recovery is an ongoing process… …NOT a cure. Read from slide…

67 Over-riding principles
Our primary focus needs to be on prevention: a. screening of applicants and identifying and educating those at high risk b. toxicology screening c. increased accountability/decreasing ease of access Once we have identified the SRNA/CRNA with a CD the focus is: First we save lives and then downstream when and where appropriate we may cautiously help resurrect careers.

68 Take Homes CD is a chronic disease with similar compliance and relapse issues to other chronic diseases such as DM and HTN. Chronicity and relapse potential can be explained by persistent neuroplastic alterations in the CNS. New pharmacotherapy strategies may assist as a part of a multimodality approach to increase long term recovery in some cases. We need to take the long view and focus on relapse prevention! AZ

69 References Auer JA: Learning mechanisms in addiction: synaptic plasticity in the ventral tegmental area as a result of exposure to drugs of abuse. Annu Rev Physiol 2004, 66: Gardner E - What we have learned about addiction from animal models of drug self-administration Am J Addict 2000;9:

70 References Faleiro LJ, Jones S, Kauer JA: Rapid synaptic plasticity of glutamatergic synapses on dopamine neurons in the ventral tegmental area in response to acute amphetamine injection. Neuropsychopharmacology, 2004, 29, Fattore,L., Spano, S., Deiana,S., Melis, V. Cossu, G., Fadda,P. & Fratta, W. An endocannabinoid mechanism in relapse to drug seeking: A review of animal studies and clinical perspectives Brain Research Reviews, In Press, Corrected Proof, Available online 12 July 2006

71 References Kauer, J. A.: Learning Mechanisms in Addiction: Synaptic Plasticity in the Ventral Tegmental Area as a Result of Exposure to Drugs of Abuse Annu. Rev. Physiol :447–75 Kim JA, Pollak KA, Hjelmstad GO, Fields HL: A single cocaine exposure enhances both opioid reward and aversion througha ventral tegmental area-dependent mechanism. Proc Natl Acad Sci USA 2004, 101:

72 References Nestler, E J: Molecular basis of long-term plasticity underlying addiction. Nat Rev Neurosci 2001; 2:119–128; Nestler, E J: Molecular Biology of Addiction. Am J of Addictions 10: , 2001 Nestler, E J, Malenka, R C: Biotechnology: The Addicted Brain, Scientific American, April 2004, retrieved online on the WWW at: on

73 References Sinha R et al Psychological stress, drug-related cues, and cocaine craving. Psychopharmacology 2000; 152: Volkow ND, Wang G-J, Ma Y, Fowler JS, Zhu W, Maynard L, Telang R, Vaska P, Ding Y-S, Wong C, Swanson JM: Expectation enhances the regional brain metabolic and the reinforcing effects of stimulants in cocaine abusers. J Neurosci 2003; 23:11461–11468

74 References Volkow ND, Fowler JS, Wang GJ, Swanson JM: Dopamine in drug abuse and addiction: results from imaging studies and treatment implications. Mol Psychiatry, 2004, 9:557–569. Volkow ND, Wang GJ, Telang F, Fowler JS, Logan J, Childress AR, Jayne M, Ma Y, Wong C: Cocaine cues and dopamine in dorsal striatum: mechanism of craving in cocaine addiction. The Journal of Neuroscience, June 14, 2006, 26(24):

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