final

Question 1

substances of abuse act ___

Answer 1

directly or indirectly on GPCRs
directly - opioids (mu), LSD, mushrooms (5HT), marijuana, K2, spice (CB1), GHB (GABA), caffeine (adenosine)
indirectly -
-Cocaine/ amphetamines: block dopamine transporter = increased dopamine in synapse
-MDMA/ Ecstasy: monoamine transporter: dopamine, serotonin
-Alcohol: Release of endogenous opioids
on ion channels - nicotine (ACh), PCP, ketamine (NMDA), benzos, barbituates (GABA)

Question 2

dangerous withdrawal symptoms

Answer 2

alcohol and tranquilizers

grand mal seizures, heart attacks, strokes, hallucinations, delirium tremens

Question 3

positive vs. negative reinforcement

Answer 3

positive - feels normal, takes drug to feel good

negative - feels bad, takes drug to feel normal

Question 4

DEA schedules

Answer 4

I: no medical use, marijuana, THC, LSD
II: high abuse, cocaine, PCP
III: moderate abuse
IV: low abuse

Question 5

dopamine

Answer 5

drugs or pleasurable events cause a release of dopamine - leads to high and establishes addiction
abuse replaces normal dopamine release that tells our brain what we need to do (eat, sex, school) - instead we only care about getting the drug
dissociation between liking and wanting

Question 6

incentive salience

Answer 6

salience = state or quality of an item that stands out relative to neighboring items
“diving into used toilet for opium suppositories”

Question 7

synaptic strength

Answer 7

increases after long term stimulation

Question 8

DSM5

Answer 8

mild 2-3
moderate 4-5
severe 6+

Question 9

psychological dependence

Answer 9

mental urge to take drug - mind is telling you you want it

Question 10

physical dependence

Answer 10

body needs more drug - tolerance - and withdrawals without the drug
cellular adaptations

Question 11

emotional withdrawal

Answer 11

anxiety, depression, restlessness, insomnia, irritability, HAs, poor concentration

Question 12

physical withdrawal

Answer 12

sweating, racing heart, goose bumps, muscle spasms, tremors, NV, diarrhea

Question 13

glutamate

Answer 13

can increase dopamine activity in NAcc
Destruction of this pathway reduces reward
Rewarding substances cause relative increase in glutamatergic AMPA receptors (NMDA numbers stay relatively the same)
Cellular Memory: all rewards increase AMPA/NMDA ration, but synaptic plasticity endures for unnatural rewards (cocaine, heroin, alcohol)

Question 14

Describe the therapeutic uses of psychostimulants, which
psychostimulants are used in treatment, and what their
primary target is

Answer 14

therapeutic use - ADHD, narcolepsy, suppress appetite, migraine
used in treatment - caffeine, nicotine, amphetamine, methylphenidate, armodafinil (DAT), sodium oxybate, lisdexamphetamine (prodrug), atomoxetine (NET selective), guanfacine, benzphetamine, phentermine, amfepramone
primary targets - DAT, NET

Question 15

Describe mechanism of action of nicotine. Explain how

nicotine differs from acetylcholine. List smoking cessation drugs and describe MOA

Answer 15

MOA - nicotine activates nicotinic acetylcholine receptor (Na/K transporters) = Na enters and K+ leaves = action potential
GABA = inhibitory
First neuron releases more GABA onto GABA receptors = inhibition of second neuron to release GABA
Less GABA release = less inhibition of dopamine release = more dopamine release after nicotine
Nicotine is not degraded by acetylcholinesterase

Question 16

Describe mechanism of action of cocaine and explain how it

differs from that of amphetamines and ecstasy

Answer 16

MOA - blocks dopamine transporters, Da gets trapped in synapse and has longer to bind to receptors, DAT > SERT > NET
amphetamines - do not block the transporter, but are taken up by the transporter, compete with uptake of dopamine, they are MAOi’s which can enter into VMAT and increase Da conc in synapse. They can also bind to TAAR1 which phosphorylates DAT, induces reverse transport function

Question 17

Explain the health effects associated with psychostimulant
use, psychostimulant withdrawal, risks of dependence and
overdose when used alone or in combination with other drugs
of abuse

Answer 17

health effects- increase BP, HR; euphoria; agitation/restlessness/nervousness, Heightened alertness and awareness, increased energy and
motivation, euphoria, Increased sociability and talkativeness, Reduced appetite, Heart palpitations, cardiac arrest, Anxiety, self-destructive behavior, violence, Insomnia, seizures, hyperthermia*, Paranoid delusion, Can last for days, Kidney and liver failure
withdrawal- Anxiety, Depression, Pain and body aches, Exhaustion, Tremors, Increased appetite, Vivid and unpleasant dreams

Question 18

Explain the legal status ( including scheduling) of natural and synthetic cannabinoids.

Answer 18

synthetic cannabinoids are schedule I

marijuana is schedule I, decriminalized for use in many states, legalized in others, federally still illegal

Question 19

Describe the physical effects associated with marijuana use and summarize the abuse potential of marijuana.

Answer 19

Sedation
Red eye (conjunctival injection)ƒ
Tachycardia - Tolerance development
ƒCause angina in patients with Hx of coronary insufficiency
ƒReduction in pulmonary vitality- Deep inhalation, prolonged retention, Chronic bronchial irritation
ƒAnxiety, panic attack with potent marijuana
Low dependence potential, Overdose (non fatal) uncommon, tolerance, Cannabinoid hyperemesis syndrome (NV, relieved by hot shower)

Question 20

Describe the pharmacology of cannabinoid receptors and the pharmacokinetics of marijuana and other cannabinoids at the CB receptors

Answer 20

THC - Quick absorption from lungs into blood, Metabolized in liver (CYP2C9), agonist of cannabinoid receptors - CB1 and CB2, inhibit GABA

Question 21

stimulants

Answer 21

cocaine, amphetamine, meth, bath salts, ecstasy, nicotine

Question 22

depressants

Answer 22

opioids, alcohol, cannabis, GHB, inhalants

Question 23

psychadelics

Answer 23

LSD, psilocybin, PCP, mescaline, ketamine

Question 24

pathway to addiction

Answer 24

Therapeutic use (opioid being used to relieve pain) -> Positive reinforcement (pain is being relieved = user feels better) -> Negative reinforcement (baseline pain is worse = user takes medication to not feel pain)
Recreational use = positive reinforcement (cocaine feels good) -> negative reinforcement (cocaine prevents bad feelings)
Self Medication = user feels bad so they take heroin (only negative reinforcement) - Need to function (alcohol to mask withdrawal symptoms), Reduce anxiety, mental pain, depression, Escapism

Question 25

narcolepsy

Answer 25

Excessive sleepiness, sudden sleep attack, atypical sleep pattern, cataplexy Options: amphetamine or methylphenidate Non-stimulant Options: Armodafinil, Modafinil, Sodium Oxybate (GHB)

Question 26

ADHD

Answer 26

Inattention and/or hyperactivity impulsiveness | Options: amphetamines or methylphenidate

Question 27

anorectic

Answer 27

Stimulate release of NE, DA in lateral hypothalamus Options: benzphetamine, diethylpropion, phentermine Weight is often regained when discontinuing drug, chronic use can exacerbate HTN, tolerance, and abuse potential

Question 28

smoking cessation treatment

Answer 28

Replacement: gum, nicotine patch, e-cigarette? Drugs: Varenicline: partial agonist at nAchR = blocks nicotine effect but less withdrawal incurred; Bupropion: nAchR antagonist = could precipitate withdrawal in heavy smoker

Question 29

cocaine mechanism

Answer 29

Antagonist of amine transporters (DAT > SERT > NET) = prevents dopamine uptake = increased dopamine concentration and duration of action

Question 30

meth, ecstasy, bath salts MOA

Answer 30

Resembles endogenous DA/NE so they compete with reuptake (substrates) - Block DA reuptake at VMAT-> push out dopamine from vesicles = increased extra-vesicular dopamine (considered intracellular) and reverses gradient to push dopamine into synapse - Activate trace amine-associated receptor (TAAR1) = phosphorylated DAT = reverse transport function = more dopamine in synapse

Question 31

methamphetamine and amphetamine MOA

Answer 31

inhibitors of monoamine oxidase (contraindicated with anti-depressant use d/t risk of serotonin syndrome)

Question 32

cocaine and crack cocaine

Answer 32

Add ammonia to cocaine to get free base precipitate for smoking = crack Local anesthetic effect Increase in HR, vasoconstriction, BP

Question 33

risks of poly drug abuse

Answer 33

Stimulant with Depression: mask crash of stimulant with depressant (i.e. benzos and stimulants, alcohol and stimulants, cocaine and heroin) Dangers: increased risk of overdose, arrhythmias Treatment: biggest risk first

Question 34

synthetic cannabinoids

Answer 34

K2/spice Studies suggest higher risk of psychosis Often originated from scientists academic laboratories and publications Very potent overdose: panic attacks, convulsions Physical Effects: anxiety, sedation, red eye, tachycardia, angina Drug Dependence, OD, Withdrawal: -Low dependence -Overdose uncommon: anxiety/panic attacks -Psychoactive Tolerance: increase strength or use -Cannabinoid hyperemesis syndrome: N/V -Withdrawal lasts 1-2 weeks: dysphoria, anxiety, depression, decreased appetite

Question 35

THC

Answer 35

-Agonist to cannabinoid receptors CB1 and CB2 (GPCR) -Gi = inhibit cAMP , inhibit Ca channels, activate GIRK potassium channels = inhibit release of GABA Drug Interactions: CNS Depressants (opioids, benzo, barbiturates, alcohol, buprenorphine, GHB) Brain more CB1 receptors than CB2: Receptors not located in respiratory centers of brainstem = reduced risk of respiratory depression seen with other depressants; CB2 located on glia Cannabinoid binds to CB receptor on GABA-ergic neuron (neuron #1): THC = inhibit GABA release onto dopaminergic neuron (neuron #2), Less GABA on dopaminergic neuron (neuron #2) = no inhibition on release of dopamine on dopamine receptors = increased dopamine binding Periphery has more CB2 receptors than CB1: CB2 on lymphocytes, CB1 on liver

Question 36

endogenous cannabinoids

Answer 36

Quickly produced near site of action when needed and quick degraded Anandamide: broken down by fatty acid amide hydrolase 2-arachidonylglycerol -DAG lipase = synthesis -MAG lipase = degradation

Question 37

clinical use of cannabinoids

Answer 37

inc appetite, chemotherapy induced NV, glaucoma, MS, chronic pain

Question 38

cannabinoid use in increasing appetite

Answer 38

Stimulation of POMC neurons in hypothalamus Increases β-endorphin release over α-MSH (anoreigenic) = increased appetite Possibly a partial agonist could be use for an anorectic drug

Question 39

cannabinoid use in chemotherapy induced NV

Answer 39

Immediate Phase: CB1 presence in GI tract in the submucoasl plexus and myenteric plexus Delayed Phase: CB1 presence in brain stem in chemoactive trigger zone that controls vomiting

Question 40

cannabinoid use in glaucoma

Answer 40

Caused by increased fluid build-up because blocked drainage or increased contraction of ciliary muscles = increase intraocular pressure Activated CB1 inhibit function of ciliary muscles = relaxed and allow drainage of aqueous humor

Question 41

cannabinoid use in MS

Answer 41

Reduction in tremors and spasticity | Endocannabinoids activating shift towards anti-inflammatory T cells (TH2) similar to glatiramer acetate

Question 42

cannabinoid use in chronic pain

Answer 42

Substance P increases glutamate signaling and pain signals | CBs inhibit glutamate signaling to decrease central pain sensitization or expression of chronic pain

Question 43

alcohol metabolism

Answer 43

Limited by gastric emptying =slowed by food Men dilute alcohol more due to having more total body water Zero order kinetics: Above 20-mg/dL due to alcohol dehydrogenase (rate-limiting step), Essentially means that if your BAC doubles, it takes twice as long to metabolize Metabolism done by alcohol dehydrogenase, microsomal ethanol oxidizing system (MEOS), and aldehyde dehyrogenase - MEOS only at high alcohol concentrations Molecular Pharmacological Action: alcohol action at nicotinic receptors means varenicline could work for those addicted to smoking and drinking

Question 44

alcohol dehydrogenase

Answer 44

Metabolizes alcohol, ethanol, ethylene glycol, etc. Found in liver, brain, and stomach Men express higher levels of gastric ADH = start metabolizing sooner Fomepizole: ADH inhibitor used for ethylene glycol, MeOH poisoning - Alcohol can be used as well to outcompete enzyme, Slow formation of formaldehyde and toxic metabolites and allows more time for the liver to further metabolize toxic metabolites

Question 45

aldehyde dehydrogenase

Answer 45

ALDH1B1 and ALDH2 Having less ALDH2 (Asians have 50% less) limits ability to convert acetaldehyde into acetic acid Genotype for *2 allele: -Heterozygous: reduced activity, can still consume alcohol -Homozygous: deficient in ability to metabolize acetaldehyde = essentially intolerant and similar to disulfiram reaction Disulfiram: inhibitor of aldehyde dehydrogenase = accumulation acetaldehyde = hangover feeling Treatment with disulfiram is difficult as it requires the patient to choose to take the medication and they likely won’t have great compliance

Question 46

pharmacological actions of alcohol

Answer 46

Euphoria, disinhibition: 30-60mg/dL Analgesia: 60-90mg/dL CNS stimulation (mood swings aggression): 80-120mg/dL CNS depression (slurred speech, ataxia, sedation, loss of motor control): 100-120mg/dL Coma, Death: 300-500mg/dL

Question 47

effects of alcohol

Answer 47

Acute: vasodilation (warm, flush), reduce blood pressure, increase HR Heavy/chronic use: reduce risk of coronary disease; cardiomyopathy, arrhythmias, hypertension, hemostasis Thermoregulation: hypothermias GI: Increased HCl secretion -> chronic gastritis, appetite stimulant, depressant Long-Term -Liver: cirrhosis, vitamin deficiencies -Blood: mild anemia, folic acid deficiency -Cancer: liver, along route of ingestion

Question 48

drug interactions w alcohol

Answer 48

CNS Depressants: Opioids antipsychotics, antidepressants, anti-histamines Aldehyde Dehydrogenase Inhibitors: disulfiram, metronidazole, some cephalosporins, tolbutamide Acetaminophen: increases toxic metabolite NAPQI; alcohol upregulates this pathway

Question 49

intoxication

Answer 49

prevent respiratory depression, aspiration of vomit, metabolic alterations

Question 50

fetal alcohol syndrome

Answer 50

facial dysmorphology, low birth weight, decreased brain size, mental retardation

Question 51

alcohol withdrawal

Answer 51

anxiety, insomnia; seizures; N/V; hallucination -> delirium tremens -Treatment: benzos, phenytoin for seizures, electrolytes

Question 52

alcoholism

Answer 52

Disulfiram: causes flushing, throbbing, headache N/V, sweating, hypotension, confusion - Patients should be alcohol free for 24 hours Acamprosate: NMDA receptor antagonist/ GABA agonist - Reduced relapse and prolong abstinence Naltrexone: opioid receptor antagonist - Prevents relapse Topiramate: inhibits glutamate signaling and enhances GABA signaling (works more like methadone, not a partial agonist like buprenorphine) Baclofen: stimulates GABA receptors Varenicline: weakly activates nicotinic Ach receptors

Question 53

psychadelics

Answer 53

psychoactive drugs whose primary function is to alter cognition and perception - Hallucinogen: give illusion of perception of sensory cues in external space (LSD) - Dissociatives: distort perception of self and environment (PCP) - Deliriants: induce delirium (confused state) (salvia)

Question 54

dangers of psychadelics

Answer 54

generally non-addicting and typically do not cause excessive CNS stimulation -Principal danger: psychological changes they can produce and users may injure themselves accidentally

Question 55

MOA of psychadelics

Answer 55

action thought to be on the 5HT2c and 5-HT2a serotonin receptors (GPCR) Mescaline: Increase dopamine and serotonin = more hallucinogenic; cross tolerance to LSD Dissociatives: NMDA receptor antagonist -Ketamine: fast and short acting -Dextromethorphan: serotonin reuptake inhibitor PCP: NMDA antagonist and dopamine agonist

Question 56

medical use of ketamine

Answer 56

Anesthesia: non-depolarizing NMDA antagonist for dissociative anesthesia Chronic pain analgesia: palliative for opioid tolerant Anti-depressant: Anti-depressants reduce glutamate transmission, could be useful in treatment resistant patients

Question 57

psychadelics and psychosis

Answer 57

Psychosis: abnormal condition of the psyche observed in bipolar disorder, schizophrenia, major depressive disorder treated with anti-psychotics Psychedelics and certain stimulants can induce short term, drug induced psychosis

Question 58

synthetics/designer drugs

Answer 58

o New psychoactive drugs to avoid existing drug laws Synthetics: Opioids: Krokodil- codeine derivative -> can cause gangrene, necrosis Cannabinoids: K2/spice Stimulants: bath salts, designer steroids Psychedelics: PCP, NBOMe -NBOMe: full 5-HT2a agonist -Reports of lethal overdose (no reported ODs on LSD)

Question 59

inhalant psychadelics

Answer 59

Volatile solvents, aerosols, gases, sprays, nitrites, hydrocarbons, ketones Pharmacology: highly lipophilic = fast entrance to CNS; inhibition of excitatory neurotransmission (NMDA antagonism) and activation of inhibitory neurotransmitters: GABA agonism Nitrous Oxide: Inhibits NMDA currents, no effect on GABA, release of endogenous opioids = mild analgesia -Activate dopamine = euphoria

Question 60

heroin

Answer 60

cheaper and more available than prescription opioids Pro-drug High lipid solubility and rapidly crosses BBB Active metabolites: 6-monoacetylmorphine, 3-monoacetylmorphine, morphine Black Tar: incomplete acylation of morphine - Can lead to venous sclerosis: clots form around repeated injected sites = more turbulence and rate of clotting -> eventually clots force vein to collapse

Question 61

Rx opioid dependence

Answer 61

Can start in the hospital with opioids to treat pain Can lead to hyperalgesia -> physical and/or psychological dependence on opioids Can start at home: pills left over and used for positive reinforcement -> may need to switch to heroin as its cheaper Opioids can be prescribed with proper awareness, monitoring, communications, with the patient

Question 62

depressants can cause ___ release

Answer 62

Depressants can cause dopamine release like stimulants: disinhibition of GABA leads to dopamine in nucleus accumbens -Stimulants are not identical: stimulants can be used to deal with environment, while depressants, like heroin, may be used in a safer environment

Question 63

opioid withdrawal syndroms and treatments

Answer 63

8-12 hours: tearing, sweating, yawning, runny nose 12-14 hours: tossing, restless sleep; awake 24-72 hours: dilated pupils, anorexia, goosebumps, restless, irritability, tremor 48-72 hours: anorexia, irritability, insomnia, sneezing, muscle weakness, depression, N/V, intestinal spasm, diarrhea Naltrexone, naloxone, buprenorphine may precipitate withdrawal if on opioids

Question 64

diarrhea from opioid withdrawal

Answer 64

Opioid agonists: Inhibitory actions on the peristaltic reflex on the intestine Diphenoxylate with Atropine: Schedule V; atropine to discourage overdose Loperamide: substrate for PGP = kicked out of CNS; reduced tolerance; OTC

Question 65

opioid tolerance

Answer 65

Tolerance: analgesic effects, nausea, urinary retention, respiratory depression, euphoria No tolerance: constipation, itch, miosis

Question 66

constipation

Answer 66

Start management early Senna (stimulant laxative): cause fluid secretion and colonic contraction PEG: stool softener; osmotic increase in GI water content Docusate: stool softener Mu opioid receptor antagonists: Methylnaltrexone, Nalmefene, Alvimopan, Naloxegol, Naldemedine

Question 67

neonatal abstinence syndrome

Answer 67

problems the baby may experience due to maternal drug use Newborn will not exhibit psychological dependence: requires memories associated with taking the medication; the child is born with physical dependence Treatment: Non-Pharm: swaddling, hypercaloric formula, frequent feedings, observation, rehydration Pharmacological: morphine sulfate, methadone, Opium tincture, Phenobarbital, chlorpromazine, diazepam

Question 68

opioid dependence treatment

Answer 68

Methadone: full mu receptor agonist; provides relief from withdrawal, Slow pharmacokinetics, Racemic mixture: (+) is NMDA antagonist and can be used for chronic pain, Cross Tolerance, Pro: requires more heroin to overcome, Con: Need more opioid if required for pain Buprenorphine: mu receptor partial agonist, Blocks full agonist effect by antagonism, Provides some activation by agonism = less withdrawal , Subutex – abuse potential, Suboxone – partially blocks agonist effects (Oral administration = only buprenorphine reaches bloodstream, IV administration = naloxone action = withdrawal), Should not be taken within 24 hours of heroin ingestion Naltrexone: antagonist, Intramuscular injection once monthly Naloxone: rapid onset, used for overdose short term

Question 69

DSM 5 criteria applied to

Answer 69

alcohol, caffeine, cannabis, hallucinogens, inhalants, opioids, sedative/hypnotics/anxiolytics, stimulants, tobacco, other

Question 70

Problematic patterns of substance use leading to clinically significant impairment or distress, as manifested by two of the following, occurring in a 12 month period

Answer 70

Larger amounts than intended Persistent desire to control use Great deal of time spent in activities necessary to obtain substance Craving, strong desire, or urge to use Recurrent use results in failure to fulfill major obligations Continued use despite social/interpersonal problems Important activities are given up or reduced Recurrent use in situation in which it is physically hazardous Continued use despite knowledge of having a problem Tolerance Withdrawal

Question 71

clinical course of substance use disorders

Answer 71

Difficult to determine who will develop substance abuse or dependence Chronic course with periods of partial or complete remission Relapse risk: greatest during first years of treatment -> majority will be able to maintain complete or partial remission Treatment: always recovering, never recovered, patient must be engaged in treatment, includes pharmacotherapy and psychotherapy

Question 72

stages of alcohol withdrawal

Answer 72

Stage 1: 6-8 hours: moderate autonomic hyperactivity Stage 2: 24 hours: autonomic hyperactivity with hallucinations Stage 3: 1-2 days: can develop seizures Stage 4: 3-5 days: risk for delirium tremens –> mortality associated with arrhythmias, shock, infection, trauma, aspiration

Question 73

DT risk factors

Answer 73

Prior history = top predictor of future DTs Number of detoxifications Consumption of 1 pint of whiskey/day for 10 of 14 days prior to admission Early symptoms of withdrawal Hepatic dysfunction

Question 74

CIWA

Answer 74

validated scale – used clinical settings to assess withdrawal severity

Question 75

treatment of alcohol withdrawal with benzos

Answer 75

No liver dysfunction = diazpepam or chlordiazepoxide | Alcoholic Liver Disease =lorazepam

Question 76

other treatments for alcohol withdrawal

Answer 76

Thiamine: always recommend if any suspicion of alcohol use Carbamazepine: may be effective for mild/moderate symptoms Valproic Acid: may reduce severity of alcohol withdrawal symptoms, including seizures Phenytoin: not effective for withdrawal seizures

Question 77

wernicke-korsakoff snydrome

Answer 77

Wernicke’s encephalopathy -Result of thiamine deficiency -Thiamine 100mg IM or slow IV push -Give before dextrose-containing fluids -Can switch to oral therapy after 24-48 hours IV Korsakoff’s psychosis -Chronic condition -> treat with antipsychotics

Question 78

alcohol use disorders

Answer 78

Drug therapy should be accompanied by psychotherapy

Question 79

disulfram

Answer 79

Aversive therapy = unpleasant effects if alcohol is used; monitor LFTs; reaction can last for up to 14 days after discontinuation

Question 80

acamprosate

Answer 80

Maintenance of abstinence Suicidality warning Take regardless of relapse

Question 81

naltrexone for alcoholism

Answer 81

Show best response to naltrexone over acamprosate in combination with psychotherapy Decreases binge drinking, helps to increase time between drinking days Elevated LFTs common, must monitor

Question 82

treatment for opioid withdrawal

Answer 82

Clonidine: reduces autonomic symptoms - Consider if comorbid cardiovascular disorders, Don’t use in patients with sedative withdrawal (alcohol, benzos), Monitor BP Antidiarrheals, analgesics, antiemetics

Question 83

maintenance treatment for opioid disorders

Answer 83

Methadone and buprenorphine are the oral drugs used for maintenance Methadone must be given in a licensed treatment program Buprenorphine is usually given in combination with naloxone - Must be written by a prescriber who is certified by DATA 2000

Question 84

methadone

Answer 84

Long half-life; once daily dosing is appropriate for use in methadone clinic Witnessed dosing or may earn take home doses P450 3A4 substrate QTc prolongation is a serious concern - EKG recommended

Question 85

bupronorphine

Answer 85

Given with naloxone in the same dosage for to decrease abuse; if injected – naloxone will block opiate effect Should wait at least 4 hours since last opioid use

Question 86

naltrexone in opioid disoders

Answer 86

FDA approved to treat opiate dependence disorder | Concern about any pain management that may be required while taking