Demystifying Drug Interactions with

Combined Analgesics Across Various

Therapeutic Classes

September 19, 2017

Jeffrey Fudin, PharmD, DAIPM, FCCP, FASHP

President & Director, Scientific & Clinical Affairs,Remitigate, LLC, Delmar, NY

Adjunct Associate Professor,Western New England University College of

Pharmacy, Springfield, MA

Adjunct Associate Professor of Pharmacy Practice & Pain Management,

Albany College of Pharmacy & Health Sciences,

Clinical Pharmacy Specialist & Director,PGY2 Pain & Palliative Care Residency,Stratton VA Medical Center, Albany, NY

Larry C. Driver, MD

University of Texas Distinguished Teaching Professor,

Professor, Department of Pain Medicine,

Professor, Section of Integrated Ethics,

The University of Texas M.D. Anderson Cancer Center,

Houston, TX

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Accreditation and

Credit Designation

• Accreditation:

The American Academy of Pain Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

• Credit Designation:

The American Academy of Pain Medicine designates this live activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Dr D

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Speaker and Planning Committee

Disclosures

Speakers:

AstraZeneca: Speakers BureauClarity: Consultant Collegium: Consultant Daiichi Sankyo: Advisory Board Depomed: Advisory Board, Speakers Bureau Egalet: Consultant, Advisory BoardEndo: Consultant, Speakers BureauIroko Pharmaceuticals: Speakers BureauPernix Therapeutics: Consultant Quest Labs: Advisory Board Remitigate, LLC: Owner

Jeffrey Fudin, PharmD, DAIPM, FCCP, FASHPPresident & Director, Scientific & Clinical Affairs, Remitigate, LLC Adjunct Associate Professor, Western New England

University College of Pharmacy, Adjunct Associate Professor of Pharmacy Practice &

Pain Management, Albany College of Pharmacy & Health Sciences, Clinical Pharmacy Specialist & Director, PGY2 Pain & Palliative Care Residency, Stratton VA Medical Center

Larry C. Driver, MDUniversity of Texas Distinguished

Teaching Professor,Professor, Department of Pain Medicine,Professor, Section of Integrated Ethics,The University of Texas M.D.

Anderson Cancer CenterNo relevant financial relationships

Reviewer:

Michael Harned, MD

University of Kentucky

Medtronic: Honorarium,

Speaker & Fellow

Education

St. Jude: Honorarium,

Speaker & Fellow

Education

Planners:

Jennifer Westlund, MSWDirector of Education, AAPMNo relevant financial relationships

Angela CaseyVP, Medical Director, PharmaCom GroupNo relevant financial relationships

Stephanie LeeMeetings Manager, PharmaCom GroupNo relevant financial relationships

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Target Audience

• The overarching goal of PCSS-O is to offer evidence-based trainings on the safe and effective prescribing of opioid medications in the treatment of pain and/or opioid addiction

• Our focus is to reach providers and/or providers-in-training from diverse healthcare professions including physicians, nurses, dentists, physician assistants, pharmacists, and program administrators

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Educational Objectives

• At the conclusion of this activity, participants should be able to:

1. Classify cytochrome P450 (CYP450) system nomenclature and describe role of CYP450 and p-glycoprotein in pharmacokinetics

2. Recognize key CYP450 mediated drug-drug interactions

3. Identify potential drug-drug interactions and important considerations when prescribing various analgesic classes and adjuvants

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Common Mechanisms for

Drug-Drug Interactions

• Similar or overlapping pharmacological activity

Opioids / Benzodiazepines and sedation

Opioids / TCAs and constipation

NSAIDs / SNRIs / Steroids and bleed risk

• Protein binding and free drug

NSAIDs and albumin

Amitriptyline and alpha-glycoprotein

• CYP450 induction, inhibition, autoinduction, substrates

Carbamazepine/methadone, codeine or tramadol/sertraline

• P-glycoprotein

Morphine/rifampin, methadone/telaprevir

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Adverse Outcomes Due to Drug-Drug

Interactions in Stable Patients

• Often occur after the addition of a new drug that increases or decreases the effect of a drug a patient is already taking

• Time course varies depending on the pharmacokinetics of the drugs involved

Most adverse outcomes manifest themselves within the first week or two of starting therapy with a new drug

Adverse outcomes can also occur in patients who have been stabilized on interacting drugs for weeks or months

Horn JR, Hansten PD. Pharmacy Times. March 20, 2017.

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Adverse Outcomes Due to Drug-Drug

Interactions in Stable Patients

• Pharmacodynamic DDIs Risk may continue as long as a patient receives the 2 drugs; eg,

increased risk of bleeding when SSRIs are given with warfarin

• Addition of third drug Sometimes a patient is on long-term therapy with 2 interacting

drugs with no adverse outcomes, but a reaction occurs when a third drug is added

• Stopping a drug If a drug is titrated to effect in the presence of an inhibitor or

inducer, when the inhibitor or inducer is stopped, the drug concentrations may become subtherapeutic or excessive

• Change in renal function Some DDIs are more likely to result in adverse outcomes in

patients with impaired renal function

Horn JR, Hansten PD. Pharmacy Times. March 20, 2017.

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Cytochrome P450 Review

Dr F

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CYP450 Nomenclature

• Cytochrome is designated CYP

• CYP (#) - # identifying the enzyme family

• CYP (#) (A,C) - subfamily designation

• CYP (#) (A,C) (#) - individual enzyme(based on when enzyme was discovered)

• Examples:

CYP3A4

CYP2D6

CYP1A2

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Cytochrome P450 Enzyme Tree

1 2 3 4 5 7 11 17 19 21 27

1A 1B

1A1 1A2

1B1

2F2D2C2B 2E2A

2A6 2A7

2B6 2B7P

2C8 2C9 2C18 2C19

2D6 2D7P 2D8P

4A 4B 4F

4B1

4F2 4F3

11A 11B

11A1

11B1 11B2

21A

21A1P 21A2

4A9 4A11

3A

3A3 3A4 3A5 3A5P 3A7

2E1

2F1

Adapted from: Riddick DS. Drug biotransformation. In: H Kalant, W Roschlau (Ed), Principles of Medical Pharmacology, 6th ed, Oxford University Press: NY, 1997.

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Terminology

• Inducer

3 weeks

• Inhibitor

48 hours

• Substrate

• Genetic polymorphism

Poor metabolizer

Intermediate metabolizer

Extensive metabolizer*

Ultrarapid metabolizer

• Autoinducer

Carbamazepine

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Warfarin Metabolism by CYP2C9

© RxPrep/Dr Jeffrey Fudin

Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.

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Rifampin Induces CYP2C9

Metabolism of Warfarin

© RxPrep/Dr Jeffrey Fudin

Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.

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Amiodarone Inhibits CYP2C9

Metabolism of Warfarin

Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.

© RxPrep/Dr Jeffrey Fudin

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Paroxetine Inhibits CYP2D6 Conversion

of the Prodrug Codeine to Morphine

Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.

© RxPrep/Dr Jeffrey Fudin

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p-Glycoprotein (pGP) Efflux Pumps

• pGP efflux pumps “pump” drugs (pGP substrates) back into the gut

Decreases movement of some drugs across biological barriers, which decreases the amount of drug available in the blood

• pGP pumps located in the liver, gut wall, brain, and kidney

pGP inducerCauses creation of more pGP: blood drug levels go down. pGP inducers also reduce amount of some toxin ingestion, by pumping them back into the gut.

pGP inhibitorInhibits the drug-pump-inhibitor and, consequently, blood drug levels increase.

Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.

© RxPrep/Dr Jeffrey Fudin

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Polling Question

Drug A is a substrate of enzyme X.

Drug B is an inducer of enzyme X.

A patient has been using Drug A with good results.

The patient has now started therapy with Drug B. What will happen to the concentration of Drug A?

a) Increase

b) Decrease

c) Stay the same

d) Not enough information is given

e) None of the above

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Polling Question

Drug A is a substrate of enzyme X.

Drug B is an inhibitor of enzyme X.

A patient has been using Drug A with good results.

The patient has now started therapy with Drug B. What will happen to the concentration of Drug A?

a) Increase

b) Decrease

c) Stay the same

d) Not enough information is given

e) None of the above

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Opioid Pharmacokinetics and

Drug-Drug Interactions

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Opiates and Opioid Metabolism

Shown in red are the major CYP450 enzymes involved in phase I metabolism; patterns of drug metabolites may reflect the metabolic profile of the patient. Actual proportions of individual metabolites will vary.

Pharmacogenetics testing is available for CYP2D6

Phase II reactions (eg, glucuronide conjugation) are not shown but are prominent for most compounds.

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Medication Metabolism

Phase of

metabolismKey enzymes involved

Examples of opioid

medication metabolized

Phase I

• CYP450

• Examples:

CYP2D6, CYP2C19,

CYP2B6, CYP2C9,

CYP3A4, and CYP3A5

Codeine, hydrocodone,

oxycodone, tramadol,

fentanyl, methadone,

buprenorphine

Phase II

• Uridine 5’-diphospho-

glucuronosyltransferase

(UDP-

glucuronosyltransferase, UGT)

• Examples:

UGT2B7 and UGT2B15

Morphine,

oxymorphone,

hydromorphone,

tapentadol, levorphanol

Smith HS. Mayo Clin Proc. 2009;84:613-24.

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Tramadol Metabolism

• 6,000 X weaker binding affinity to mu opioid receptors compared to morphine

• Serotonin and norepinephrine activity

Tramadol

CYP2D6

O-desmethyltramadol (M1)(active)

N-desmethyltramadol (M2)(inactive)

CYP2B6CYP3A4

N,N,-didesmethyl

tramadol (M3)

N,O-didesmethyl tramadol (M5)

CYP2B6CYP3A4

CYP2B6CYP3A4

CYP2D6

O-desmethyl tramadol

glucuronide (M5)

UGT2B7UGT1AB

Gong L, et al. Pharmacogenet Genomics. 2014;24:374-80.

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Common CYP3A4

Inhibitors and Inducers

CYP3A4 Inhibitors CYP3A4 Inducers

Aprepitant Grapefruit juice Armodafinil Griseofulvin

Amiodarone Indinavir Barbiturates Nafcillin

Atazanavir Itraconazole Bicalutamide Oxcarbazepine

Cimetidine Ketoconazole Carbamazepine* Phenobarbital

Clarithromycin Nefazodone Dexamethasone Phenytoin

Diltiazem Ritonavir Efavirenz Primidone

Erythromycin Telithromycin Etravirine Rifabutin

Fluconazole Verapamil Fosamprenavir Rifampin

Fosamprenavir Voriconazole Fosphenytoin St. John’s Wort

Horn JR, Hansten PD. Pharmacy Times. September 1, 2008.Horn JR, Hansten PD. Pharmacy Times. December 16, 2015.

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Polling Question

Oxycodone is metabolized by CYP3A4.

A patient has been using oxycodone with good results.

The patient has now started therapy with clarithromycin, which is a CYP3A4 inhibitor.

What is the likely result?

a) The patient could suffer fatal respiratory depression

b) The patient experiences a subtherapeutic analgesic response

c) Not enough information is given

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CASE: JB

• 45-year-old Caucasian male

History of cervical stenosis at C5-6 with myelopathy

Has been on tramadol for a number of years, but comes to you for assistance with optimal control of neuropathic pain

You initiate carbamazepine 100 mg PO daily x 7 days, then 200 mg PO daily

• 3 weeks later: JB calls the clinic in distress

Reports being in the worst pain he has experienced in years

• Why is JB suddenly in pain?

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Polling Question

JB has been on tramadol for several years.

Tramadol is metabolized by CYP3A4 and CYP2B6 to the inactive metabolite and by CYP2D6 to the active metabolite.

You add carbamazepine to treat JB’s neuropathic pain.

What is the likely cause of JB’s sudden pain?

a) Carbamazepine is a CYP3A4 inducer. It increases metabolism of tramadol by CYP3A4 to an inactive metabolite

b) Carbamazepine is a CYP2D6 inducer. It increases metabolism of tramadol by CYP2D6 to an active metabolite

c) Not enough information is given

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Common CYP2D6

Inhibitors

CYP2D6 Inhibitors CYP2D6 Inducers

Amiodarone Haloperidol • There are no known

CYP2D6 inducers

• Genetics, rather than drug

therapy, accounts for most

ultrarapid CYP2D6

metabolizers

Bupropion Imatinib

Celecoxib Paroxetine

Cinacalcet Quinidine

Diphenhydramine Terbinafine

Fluoxetine Thioridazone

Horn JR, Hansten PD. Pharmacy Times. July 1, 2008.

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Methadone Metabolism

Gerber JG, et al. Chirality. 2004;16:36-44.

CYP3A4R-methadone

parent drug

EDDP

inactive metabolite

S: Sorrowing outcome (cardiotoxic effects, QT prolongation with potential of Torsade de pointes

CYP2B6S-methadone

parent drug

EDDP

inactive metabolite

R: Responsible for analgesia

CYP2B6 selectively metabolizes S-enantiomerPotential risk?

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QTc Prolonging Drugs

QTc prolonging

drugs

Quinolone antibiotics

Macrolide antibiotics

Amiodarone/ Sotalol

Sertraline/ Citalopram

Venlafaxine

Fluconazole/ Ketoconazole

Ondansetron

Quetiapine

Buprenorphine

Methadone

Fudin J, Pratt Cleary J, Gottwald J. Pharmacy Times. Mar 22, 2016.

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QTc Prolonging Drugs:

Buprenorphine

• Buprenorphine buccal film

900 mcg Q12H (maximum dose)

− QTc 450-480 msec for 2% of patients

Up to 9.2 msec QT prolongation

• Buprenorphine transdermal patch

20 mcg/hour (maximum dose)

No QTc prolongation seen in trials at this dose

Fudin J, Pratt Cleary J, Gottwald J. Pharmacy Times. Mar 22, 2016.

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0 5 10 15 20 25 30 35 40

Haloperidol 15 mg/d

Buccal buprenorphine 3 mg/naltrexone 50 mg

Antidepressants (SSRI vs TCA)

Olanzapine 20 mg/d

Escitalopram

Buprenorphine transdermal patch 40 mcg/hr

Citalopram

Risperidone 16 mg/d

Moxifloxacin 400 mg

Quetiapine 750 mg/d

Ziprasidone 160 mg/d

Thioridazine 300 mg/d

QT prolongation (msec)

Fudin J, Pratt Cleary J, Gottwald J. Pharmacy Times. Mar 22, 2016.

• Note, these data are: Not meant for direct comparisons between the

various agents because of differences in study design, QT correction strategies, and population variations

Provided as context for the current landscape of QT-prolonging drugs

QT Prolongation of Various

Medications

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Methadone vs Levorphanol

Methadone Both Levorphanol

< kappa opioid agonist

Serotonin reuptake inhibitor

Mu opioid agonist

NMDA antagonist

Norepinephrine reuptake inhibitor

> kappa opioid agonist

Delta opioid agonist

CYP450 metabolism

pGP substrate

Phase II glucuronidation

Not a known pGPsubstrate

t1/2 = 15-60 hours

Up to 150 hours in polymorphic outliers

t1/2 = 11-16 hours

QTc prolongation No QTc prolongation

Pham TC, Fudin J, Raffa RB. Pain Med. 2015;16:1673-9.

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Pharmacogenetics

• Drug metabolism and variability among patients in terms of drug response can sometimes be explained by genetic variations within CYP450 enzymes

2 patients: same gender, weight, height, and race on oxycodone ER 10 mg Q12H

− Patient A’s serum oxymorphone level: as expected

− Patient B’s serum oxymorphone level: elevated

Patients A and B are genetically tested:

Gene

Predicted phenotype

Patient A Patient B

CYP3A4/3A5 Normal metabolizer Normal metabolizer

CYP2D6 Normal metabolizer Ultrarapid metabolizer

Naginewicz T, Archer K, Raouf M, Fudin J. Pharmacy Times. August 24, 2017.

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The Perfect Storm: Opioid Risks

and “The Holy Trinity”

• Opioids, benzodiazepines, and carisoprodol have overlapping side effects

Drowsiness, respiratory depression (opioid), confusion, tremor, and seizures risk

• Combined, these drugs are synergistic in causing respiratory depression

Could collectively result in death

Opioid

Wolf AA, Fudin J. Pharmacy Times. September 24, 2014.

Benzodiazepine

Carisoprodol

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Non-Opioid

Drug-Drug Interactions

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Acetaminophen

• Metabolism Pediatrics: sulfation

Adults: glucuronidation

CYP2E1: conversion to N-acetyl-p-benzoquinone imine (NAPQI)

− Hepatotoxic metabolite

• Drug-drug interactions Avoid concomitant hepatotoxic therapies

Imatinib, dasatinib, and sunitinib inhibit glucuronidation− Max acetaminophen dose: 1,300 mg/day

Warfarin− Possibly: CYP2C9, NAPQI, and/or hepatoxicity

− Increased anticoagulant effect: INR

McGill MR, Jaeschke H. Pharm Res. 2013;30:2174-87.Zhang Q, et al. Eur J Clin Pharmacol. 2011;67:309-14.Sasu-Tenkoramaa J, Fudin J. Practical Pain Management. 2013;13:50-64.

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NSAIDs

• Bleeding

COX-1 vs COX-2

• Renally cleared

Lithium

− Which NSAIDs are safest?

Methotrexate

ACE inhibitors/diuretics

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Arachidonic acid

Prostaglandins Prostaglandins

COX-1 COX-2

Inhibit gastric acid secretion

GI mucus

Renal perfusion

Platelet activation

Pain, inflammation

NSAID NSAID

GI side effectsUlceration

Water retentionHyperkalemia

Interstitial nephritis

Anti-coagulation AnalgesiaAnti-inflammatory

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Skeletal Muscle Relaxants

• CNS depressants

• Tizanidine

CYP1A2 inhibitors – increased exposure

− Ciprofloxacin

− Birth control

− Verapamil

• Cyclobenzaprine

Cardiac toxicity

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Antidepressants

• SNRIs Duloxetine

− CYP2D6 and CYP1A2

Venlafaxine− CYP3A4

• SSRIs CYP2D6 Fluvoxamine

− CYP1A2

• Bupropion CYP2B6

• Tricyclic antidepressants Cardiotoxic medications Cyclobenzaprine

Medication CYP activity

Duloxetine 2D6 inhibitor (weak)

pGP inhibitor

Venlafaxine 2D6 inhibitor (weak)

Desvenlafaxine 2D6 inhibitor (weak)

Bupropion 2D6 inhibitor (strong)

Cyclobenzaprine vs Amitriptyline

https://pubchem.ncbi.nlm.nih.gov

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Case Assessment

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CASE: MK

• 69-year-old African American male

Chronic low back pain s/p laminectomy

• Current medications:

− Acetaminophen 1000 mg PO TID

− Methadone 5 mg PO QID

− Dabigatran 150 mg PO BID

− Metoprolol tartrate 50 mg PO BID

− Lisinopril 10 mg PO daily

− Atorvastatin 40 mg PO daily

• What drug-drug interactions are you concerned about?

− Docusate/senna 4 tabs PO QHS

− Celecoxib 100mg PO BID

− Omeprazole 20mg PO QAM

− Venlafaxine 100mg PO BID

− Metformin 500mg PO TID

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CASE: MK

• MK reports to the ED with complaints of productive cough x 1 week with bright green sputum

Diagnosed with community-acquiredpneumonia

• Which of the following drug or dugs do you want to avoid and why?

Amoxicillin/clavulanic acid

Cefdinir

Sulfamethoxazole/trimethoprim

Levofloxacin

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Conclusions

• Considering drug-drug interactions is key in selecting the safest and most efficacious therapies

• Understanding pharmacology is essential to appropriately identify drug-drug interactions

• Pharmacogenetic differences among patients can highly impact efficacy, drug interactions, and ability to tolerate medications

Dr D

References

• Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. A Comprehensive Course for the NAPLEX and CPJE. 2014 ed.

• Fudin J, Pratt Cleary J, Gottwald J. A brief review of buprenorphine products. Pharmacy Times. Mar 22, 2016. www.pharmacytimes.com/contributor/jeffrey-fudin/2016/03/a-brief-review-of-buprenorphine-products

• Gerber JG, Rhodes RJ, Gal J. Stereoselective metabolism of methadone N-demethylation by cytochrome P4502B6 and 2C19. Chirality. 2004;16:36-44.

• Gong L, Stamer UM, Tzvetkov MV, Altman RB, Klein TE. PharmGKB summary: tramadol pathway. Pharmacogenet Genomics. 2014;24:374-80.

• Horn JR, Hansten PD. Get to know an enzyme: CYP2D6. Pharmacy Times. July 1, 2008. www.pharmacytimes.com/publications/issue/2008/2008-07/2008-07-8624

• Horn JR, Hansten PD. Get to know an enzyme: CYP3A4. Pharmacy Times. Sep 1, 2008. www.pharmacytimes.com/publications/issue/2008/2008-09/2008-09-8687

• Horn JR, Hansten PD. Drug interactions with CYP3A4: an update. Pharmacy Times. Dec 16, 2015. www.pharmacytimes.com/publications/issue/2015/december2015/drug-interactions-with-cyp3a4-an-update

• Horn JR, Hansten PD. Adverse outcomes in stabilized patients. Pharmacy Times. March 20, 2017. www.pharmacytimes.com/publications/issue/2017/march2017/adverse-outcomes-in-stabilized-patients

Dr D

References

• McGill MR, Jaeschke H. Metabolism and disposition of acetaminophen: recent advances in relation to hepatotoxicity and diagnosis. Pharm Res. 2013;30:2174-87.

• Naginewicz T, Archer K, Raouf M, Fudin J. Pharmacogenetics: medications do not have doses, people do. Pharmacy Times. Aug 24, 2017. www.pharmacytimes.com/contributor/jeffrey-fudin/2017/08/pharmacogenetics-medications-dont-have-doses-people-have-doses

• Pham TC, Fudin J, Raffa RB. Is levorphanol a better option than methadone? Pain Med. 2015;16:1673-9.

• Riddick DS. Drug biotransformation. In: H Kalant, W Roschlau (Ed), Principles of Medical Pharmacology, 6th ed, Oxford University Press: NY, 1997.

• Sasu-Tenkoramaa J, Fudin J. Drug interactions in cancer patients requiring concomitant chemotherapy and analgesics. Practical Pain Management. 2013;13:50-64.

• Smith HS. Opioid metabolism. Mayo Clin Proc. 2009;84:613-24.

• Wolf AA, Fudin J. The perfect storm: opioid risks and 'the holy trinity.' Pharmacy Times. Sep 24, 2014. www.pharmacytimes.com/contributor/jeffrey-fudin/2014/09/the-perfect-storm-opioid-risks-and-the-holy-trinity

• Zhang Q, Bal-dit-Sollier C, Drouet L, Simoneau G, Alvarez JC, Pruvot S, et al. Interaction between acetaminophen and warfarin in adults receiving long-term oral anticoagulants: a randomized controlled trial. Eur J Clin Pharmacol. 2011;67:309-14.

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PCSS-O Colleague Support

Program and Listserv

• PCSS-O Colleague Support Program is designed to offer general information to health professionals seeking guidance in their clinical practice in prescribing opioid medications.

• PCSS-O Mentors comprise a national network of trained providers with expertise in addiction medicine/psychiatry and pain management.

• Our mentoring approach allows every mentor/mentee relationship to be unique and catered to the specific needs of both parties.

• The mentoring program is available at no cost to providers.

• Listserv: A resource that provides an “Expert of the Month” who will answer questions about educational content that has been presented through PCSS-O project. To join email: pcss-o@aaap.org.

For more information on requesting or becoming a mentor visit:

www.pcss-o.org/colleague-support

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PCSS-O is a collaborative effort led by American Academy of Addiction Psychiatry (AAAP) in

partnership with: Addiction Technology Transfer Center (ATTC), American Academy of Neurology

(AAN), American Academy of Pain Medicine (AAPM), American Academy of Pediatrics (AAP),

American College of Physicians (ACP), American Dental Association (ADA), American Medical

Association (AMA), American Osteopathic Academy of Addiction Medicine (AOAAM), American

Psychiatric Association (APA), American Society for Pain Management Nursing (ASPMN),

International Nurses Society on Addictions (IntNSA), and Southeast Consortium for Substance

Abuse Training (SECSAT).

For more information visit: www.pcss-o.org

For questions email: pcss-o@aaap.org

Twitter: @PCSSProjects

Funding for this initiative was made possible (in part) by Providers’ Clinical Support System for Opioid Therapies (grant no.

5H79TI025595) from SAMHSA. The views expressed in written conference materials or publications and by speakers and

moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention of trade

names, commercial practices, or organizations imply endorsement by the U.S. Government.

Dr D

50Please type your questions into the text chat box

Dr D