Art Zwerling DNP CRNA DAAPM AANA PAAC atozcomcastnet April 2013 Grateful Acknowledgements Diana Quinlan CRNA MA Heather Hamza CRNA MS Greg Ramplemann CRNA Linda Stone CRNA MSN ID: 658615
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Slide1
Addiction is a brain disease: Meanings for the anesthesia community
Art Zwerling, DNP, CRNA, DAAPMAANA PAACa.to.z@comcast.net
April 2013Slide2
Grateful Acknowledgements
Diana Quinlan, CRNA, MAHeather Hamza, CRNA, MSGreg Ramplemann, CRNALinda 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 BODSlide3Slide4
Learning Objectives
Inform communities of interest regarding the antecedents, risks and consequences of chemical dependencyPromote awareness of the impact of CD on the anesthesia communityReview 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 professionSlide5
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.Slide6
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 communitySlide7
A Rude Awakening…
Death of Jan Stewart in 2002Jan Stewart Memorial Lecture Series 2004Virginia Trotter Betts 2004AANA Blue Ribbon Wellness Panel and establishment of the Wellness Program 2005Presidential Wellness TF 2010
AANA President
1999-2000Slide8
Chemical Dependency
Substance related disorders characterized by chronicity and progression that threaten wellness..Propensity for relapseTransition to a chronic disease, chronic care modelSubversion of primitive reward and anti-reward systems
NeuroplasticitySlide9
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)Slide10
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)Slide11
Drug Misuse
by PreferenceInside the OR
OPIOIDS
Fentanyl & Sufenta (Nasal)
BENZODIAZEPINES
Midazolam (Nasal)
N
2
O
PROPOFOL
DISSOCIATIVE DRUGS
AGONIST/ANTAGONISTS
BARBITURATES
Bell 2007Slide12
Triad of Contributing Factors©
Drug Misuse by CRNAs
Genetics
AVAILABILITY
ACCESSIBILITY
ACCOUNTABILITY
Stress
Fatigue
Invulnerability
Burnout
Prior Experimentation
Adapted from Bell 2007Slide13
Warning Signs
At work during off hoursIsolationFrequent breaksTardy 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 WebsiteSlide14
Causes of Addiction:
Disease ModelAlcoholism 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 addictionsSlide15
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
Slide16
0
50
100
150
200
0
60
120
180
Time (min)
% of Basal DA Output
NAc shell
Empty
Box
Feeding
Di Chiara et al., Neuroscience, 1999.
FOOD
Mounts
Intromissions
Ejaculations
Fiorino and Phillips, J. Neuroscience, 1997.
Natural Rewards Elevate Dopamine Levels
100
150
200
DA Concentration (% Baseline)
15
0
5
10
Copulation Frequency
Sample
Number
1
2
3
4
5
6
7
8
SEX
Female PresentSlide17
0
100
200
300
400
500
600
700
800
900
1000
1100
0
1
2
3
4
5 hr
Time After Amphetamine
% of Basal Release
DA
DOPAC
HVA
Accumbens
AMPHETAMINE
0
100
200
300
400
0
1
2
3
4
5 hr
Time After Cocaine
% of Basal Release
DA
DOPAC
HVA
Accumbens
COCAINE
0
100
150
200
250
0
1
2
3
4
5hr
Time After Morphine
% of Basal Release
Accumbens
0.5
1.0
2.5
10
Dose (mg/kg)
MORPHINE
0
100
150
200
250
0
1
2
3 hr
Time After Nicotine
% of Basal Release
Accumbens
Caudate
NICOTINE
Di
Chiara
and
Imperato
, PNAS, 1988
Effects
of Drugs on Dopamine ReleaseSlide18
Why do some people become
addicted while others do not?
VulnerabilitySlide19
We Know There’s a
Big Genetic Contribution to
Drug Abuse and Addiction…
….Overlapping with Environmental Influences that Help Make Addiction a Complex Disease.Slide20
Biology/genes
Environment
Biology/
Environment
InteractionsSlide21
Biology/genes
Environment
Biology/
Environment
Interactions
Anesthesia
Applicant genome
Stress Accessibility
Accountability
PotencySlide22Slide23
high
low
High DA
receptor
Low DA receptor
DA Receptors and the Response to
Methylphenidate (MP)
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.
Dopamine receptor level Slide24
Adaptations to reward & anti-reward systems lead to chronic diseaseSlide25
Dancing with the white rabbit: A break from the neuroscience Slide26
EMERGING THREAT: PROPOFOLSlide27
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: 1082-6084 print / 1532-2491 onlineSlide28
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 outcomesMust read for every anesthesia educator
*The Drug Seeking Anesthesia Care Provider
Ethan O. Bryson, MD, Heather Hamza, MS, CRNA
Int
Anesthesiol
Clin
. 2011 Winter;49(1):157-71Slide29
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.Slide30
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.Slide31
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.Slide32
The Neurobiology of Addiction
Steven D. LaRowe, Ph.D.Center for Drug and Alcohol ProgramsMedical University of South Carolina
Substance Abuse Treatment Center
Ralph H. Johnson VAMCSlide33
Addictive Behavior = Survival Behavior Gone Awry
Over the course of evolution, we have developed circuitry in our brains that have promoted our survivalDrugs of addiction activate this “survival circuitry” and with chronic use, essentially take it overIn the late stages of addiction, an individual is basically a “survivalist” doing whatever it takes to acquire and use drugs regardless of the costsSlide34
Addiction: Hijacking the Basic Survival Circuitry
Food!
Food
!
Martini!Slide35
Basic Neurobiology
AcquisitionProgressionNeuroplasticityChronicity & relapseSlide36
Healthy Heart
Diseased Heart
Decreased Heart Metabolism in
Heart Disease Patient
ADDICTION IS A DISEASE OF THE BRAIN
as other diseases it affects the tissue function
Control Cocaine Abuser
Decreased Brain Metabolism in
Drug Abuse Patient
Sources: From the laboratories of Drs. N.
Volkow
and H.
Schelbert
High
LowSlide37Slide38
Source: Adapted from
Volkow
et al., Neuropharmacology, 2004.
Drive
Saliency
Memory
Control
Non-Addicted Brain
NOT
GO
Addicted Brain
Drive
Memory
Control
GO
Saliency
Addiction Changes Brain
Circuits
Stop & Go Systems AwrySlide39Slide40
Dopamine and Glutamate RevisitedSlide41
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.Slide42
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, 11
th
ed., 1911).Slide43
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).
Slide44
Opponent Processes
Reward system (s) involved in the acquisition of addictionsAnti-reward system (s) involved in the maintenance of addictionsNeuroplasticity appears to underpin the chronicity of addictions and propensity for relapseSlide45
Neurocircuitry of Addiction
George F. Koob, & Nora D. Volkow
Neuropsychopharmacology
REVIEWS (2010) 35
,
217–238 &
2010 Nature Publishing GroupSlide46
Neuroplasticity Progression
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
Green= Go Preoccupation Compulsivity
Blue= Binge Intoxication
Red= Withdrawal Stress
DysphoriaSlide47
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.Slide48
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)
Slide49
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)
Slide50
Common pathwaySlide51
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 recoverySlide52
Relapse Rates Are Similar for Drug
Addiction & Other Chronic Illnesses
Drug
Addiction
Type I
Diabetes
0
10
20
30
40
50
60
70
80
90
100
Hypertension
Asthma
40 to 60%
30 to 50%
50 to 70%
50 to 70%
Percent of Patients Who Relapse
McLellan
et al., JAMA, 2000. Slide53
Relapse and Relapse Triggers
Cue based- People Places ThingsExposure- Iatrogenic MediatedStress- Alterations in CRF ResponsivenessDefining the dysphoric experienceSlide54
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. Slide55
The Stress Hormone Cycle
Hypothalamus
Pituitary
Gland
Adrenal
Glands
Kidneys
CRF
ACTH
CORTISOL
CRF:
Corticotropin
Releasing
FactorSlide56
DRUG USE
(Self-Medication)
STRESS
CRF
Anxiety
CRF
Anxiety
What Role Does Stress Play
In
Relapse to Drug UseSlide57
Prolonged
DRUG
USE
Abstinence
RELAPSE
CRF
Anxiety
What Happens When A Person
Stops Taking A Drug?Slide58
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; 152:140-148Slide59
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. Slide60
Relapse Triggers: Stress
Stress appears to mediate reinstatement of drug seeking via CRF1 receptor activity in the BNSTThe 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; 152:140-148Slide61
Relapse Cycle and RecommendationsSlide62
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!Slide63
Case Study: Martin
Expert cardiothoracic CRNA
Voted favorite preceptor
Played viola in a string quartet
Adored husband and father
Drug of choice: FentanylSlide64
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!Slide65
People, Places, ThingsSlide66
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.Slide67
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 accessOnce 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.Slide68
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!
Slide69
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, 66:447-475.Gardner E - What we have learned about addiction from animal models of drug self-administration Am J Addict 2000;9:285-313Slide70
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, 2115-2125Fattore,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 2006Slide71
References
Kauer, J. A.: Learning Mechanisms in Addiction:Synaptic Plasticity in the Ventral TegmentalArea as a Result of Exposure to Drugs of AbuseAnnu. Rev. Physiol. 2004. 66:447–75
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, 101:5664-5669.Slide72
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 10:201-217, 2001 Nestler, E J, Malenka, R C: Biotechnology:
The Addicted Brain, Scientific American, April 2004, retrieved online on the WWW at:
http://www.sciam.com/article.cfm?articleID=0001E632-978A-1019-978A83414B7F0101&sc=I100322
on 7-20-06.Slide73
References
Sinha R et al Psychological stress, drug-related cues, and cocaine craving. Psychopharmacology 2000; 152:140-148Volkow 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 Slide74
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):6583-6588Slide75
Resources
AANA PEER ASSISTANCE: http://www.aana.com/peerassist.aspxAIR (Anesthetists in Recovery): a.to.z@comcast.net or 215-635-0183AANA Wellness:
http://tinyurl.com/6du96lj