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Addiction is a brain disease: Meanings for the anesthesia community Addiction is a brain disease: Meanings for the anesthesia community

Addiction is a brain disease: Meanings for the anesthesia community - PowerPoint Presentation

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Addiction is a brain disease: Meanings for the anesthesia community - PPT Presentation

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

addiction drug stress relapse drug addiction relapse stress leaves amp crna brain reward chronic disease drugs systems cocaine koob

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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 BODSlide3
Slide4

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

PotencySlide22
Slide23

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

LowSlide37
Slide38

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 AwrySlide39
Slide40

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