Pharm - Stimulants and Abuse

What is the Controlled Substances Act of 1970?

Federal legislation that categorized potentially addictive substances into five categories: Schedule I – V
 To prescribe controlled drugs, prescribers need DEA licenses

Schedule 1

Highest abuse potential, no approved medical use

Schedule 2

Rx must be typed or inked and signed, single Rx, no refills

Schedule 3 + 4

Oral, written, electronic prescriptions; limited refills

Schedule 5

Rx not needed, dispensed by PharmD with record of tx: limited amount, age > 18 y/o

What do CNS Stimulants do?

Most act by increasing the activity of CNS neurons
 Some enhance neuronal excitation
 Some suppress neuronal inhibition

CNS Stimulants uses:

ADD/ADHD, narcolepsy, increased alertness

CNS Stimulants drugs:

-amphetamine
-methylphenidate
-modafinil
-methylxanthine

amphetamine and methylphenidate MOA:

 Increased release of norepinephrine & dopamine
 Also inhibits reuptake in the CNS and peripheral nervous system

amphetamine and methylphenidate pharmacokinetics:

 Available PO
 Short and long-duration forms

amphetamine and methylphenidate are what schedule drug?

schedule 2

amphetamine and methylphenidate therapeutic effects:

 increased alertness
 increased initiative
 reduced fatigue
 elevated mood

amphetamine and methylphenidate tolerance and dependence:

 Tolerance develops to mood elevation, appetite suppression and CV effects
 High dependence & abuse potential

amphetamine and methylphenidate adverse effects:

 Excess CNS stimulation (→ nervousness, insomnia)
 Reduced appetite (→ weight loss)
 Vasoconstriction (→ HTN)
 Cardiac excitation (→ dysrhythmias, angina)
 Psychosis (with excessive use/excess dosage)
 Overdose can cause seizures/coma
 Tolerance develops to mood elevation, appetite suppression, and CV effects
 High dependence & abuse potential

Amphetamines & Methylphenidate Interactions

 Other stimulants
 HTN meds
 MAOIs
 Tricyclic antidepressants

Amphetamines & Methylphenidate nursing interventions:

 Daytime dosing reduces sleep disturbance
 Monitor weight, especially in children
 Education on provider- approved drug “holidays”
 Monitor for tolerance
 Monitor vital signs

What is the Non-Amphetamine Stimulant?

Modafinil

What schedule is Modafinil?

4

Modafinil MOA:

 Blocks norepinephrine reuptake?
 Longer effect

Modafinil administration:

 PO, timed to awake period
 Taking with food reduces GI upset

Modafinil uses:

 Narcolepsy
 Daytime sleepiness due to obstructive sleep apnea
 Night-shift workers

Modafinil adverse effects:

 Nausea/diarrhea
 Minor CNS effects
 Stevens-Johnson syndrome (rarely)
 Dependence and abuse potential, less than amphetamines

Modafinil interactions:

 Reduces levels of OCPs
 Can increase levels of warfarin, phenytoin, propranolol, or TCAs

What is Methylxanthine?

Caffeine

CNS stimulant

Methylxanthine MOA:

blockade of adenosine receptors appears responsible for most effects

Methylxanthine therapeutic effects:

 Decreased drowsiness
 Decreased fatigue
 Headache relief (vasoconstriction)
 Mild diuretic

Methylxanthine less desirable effects:

 Nervousness
 Insomnia
 Convulsions (extreme doses)

Substance abuse

very common
 causes significant health problems
 affects nursing care for other diseases

Knowledge of substance abuse enables nurses to:

 recognize abuse and toxicity
 participate in treatment and withdrawal
 educate patients who are struggling with addiction and recovery

What Leads to Substance Abuse?

 Highly situation-dependent
 Acceptable use vs. abuse is socially and culturally defined
 Exists on a spectrum from occasional use to compulsive use
 Reinforcing qualities of substances
 Physical dependence
 Psychological dependence
 Social factors
 Availability
 Individual vulnerability

Addiction

 a state of psychological and/or physical dependence on the use of drugs or other substances (APA Dictionary of Psychology)
 a chronic, relapsing brain disease/illness

Tolerance and cross tolerance:

smaller response from same dose of a substance

tolerance to one drug confers tolerance to another

Psychologic dependence

an intense, subjective need for a psychoactive drug

Substance Use Disorder:

a cluster of physiological, behavioral, and cognitive symptoms associated with the continued use of substances despite substance-related problems, distress and/or impairment

Alcohol two main CNS effects:

1) GABA receptor activation
2) Glutamate inhibition

widespread CNS depression

What does alcohol cause:

 Reflexes diminish, impaired consciousness
 Depressant effect is dose-dependent → as concentration increases, “deeper” levels of the brain are affected
 High doses = state of general anesthesia

Alcohol Interactions

 Other CNS depressants
 NSAIDs
 Acetaminophen
 Disulfiram

Alcohol Use Disorder

 MAJOR public health problem
 Chronic use builds significant tolerance, but not to respiratory depression
 Withdrawal syndrome can be drastic
-GI distress, SNS over-activation, hallucinations, tonic-clonic seizures, disorientation, delirium tremens (rare)

Drugs to Treat Alcohol Abuse

 Naltrexone
 Blockage of opioid receptors can reduce ETOH cravings
long-term
 Start once detox has been achieved
 Acamprosate – can reduce cravings long-term, mechanism unclear
 Disulfiram – aversion therapy to encourage abstinence

What does disulfiram do?

blocks the second step of alcohol metabolism, resulting in accumulation of acetaldehyde

disulfiram unpleasant effects:

 GI upset
 Flushing/sweating/palpitations
 HA/chest pain/weakness/hypotension
 Potentially life-threatening

Nicotine & Smoking

 Cigarette smoking is the #1 preventable cause of death in the United States (obesity is closing in)
 Secondhand smoke concerns
 Public health measures such as changes in regulation of cigarette sales, advertising, and smoking ordinances are gradually reducing smoking rates

Nicotine MOA:

at low doses, activates nicotine receptors in the reward center which stimulate dopamine release
 The delivery system of inhalation through smoking is particularly addictive

Nicotine adverse effects:

cardiovascular stimulation, nausea, appetite suppression, fetal harm
 Long-term increased risk of CVD, several cancers, COPD

Nicotine Replacement Therapy - Patches

 Nicotine is absorbed into the skin & blood- producing steady blood levels
 Applied daily to a clean, non-hairy in the upper body
 Encourage patient not to smoke

Nicotine Replacement Therapy - Gum or lozenges

 Avoid eating or drinking 15 mins before
 Duration is around 20 mins
 Should not be taken longer than 6 months

Nicotine Replacement Therapy - Nasal spray

 Should not be taken longer than 4-6 weeks

Nicotine Replacement Therapy - Inhaler

 Not be taken longer than 2-3 months

What is Bupropion SR?

An atypical antidepressant (Wellbutrin)

Reduces cravings for nicotine and eases withdrawal symptoms

Bupropion SR MOA:

blocks uptake of NE and DA?

Bupropion SR common side effects:

dry mouth, insomnia, decreased appetite

When is Bupropion SR started:

before quit date, take 7-12 weeks

What is Varenicline?

Most effective aid for smoking cessation – reduced cravings and intensity of symptoms

When is Varenicline started:

one week before quit date, take for about 12 weeks

Varenicline MOA:

a partial nicotinic receptor agonist, it prevents most of the nicotine in cigarettes from binding to nicotine receptors

Varenicline adverse effects:

nausea & psychologic changes
 Screen for pre-existing depression or suicidal ideation

Psychostimulant Drugs of Abuse

 Includes cocaine and methamphetamines
 Schedule II because there are therapeutic uses
 Highly addictive drugs
 Cause stimulation of CNS and cardiovascular system

Cocaine MOA:

prevents dopamine reuptake in CNS neurons

Onset and duration depend upon route of administration

Cocaine two forms:

base and HCl

Cocaine HCl:

white powder usually diluted, taken intranasally

Cocaine base:

“crack” smoked, fast absorption in lungs

Cocaine two main adverse effects:

 Angina pectoris/MI from coronary vasospasms
 Nasal mucosa atrophy & septum perforation

Methamphetamine MOA:

increases levels of norepinephrine and dopamine in the CNS

Methamphetamine causes what:

arousal, improved mood, euphoria, decreased pain perception, decreased appetite
and need for sleep

Methamphetamine admin =

snorted, injected, or smoked

Methamphetamine adverse effects:

 Psychosis (delusions, paranoia, hallucinations)
 Cardiac stimulation and vasoconstriction (HTN, angina, dysrhythmias)
 Weight loss (appetite suppression)
 Tooth decay
 Pregnancy complications

Cannabis

 Mind-altering effects derive from THC compound in the plant
 Although now partially or fully legal in some states, remains a schedule I drug
 May 2024, the DOJ recommended downgrading to schedule III
 Widespread use among young adults (18-25 yos)
 Usually smoked in some form, or be ingested in food or tea
 Risk of long-term addiction
 Synthetic versions often have higher THC concentrations and/or contaminated with other substances (such as fentanyl)

Cannabis short term effects:

 A mellow euphoria
 Altered sense of time
 Impaired movement, cognitive function, memory
 Hallucinations and delusions (at high doses/concentrations)

Cannabis long term effects:

 Changes in brain development, possible loss of IQ
 Similar pulmonary effects as tobacco smoking
 Increased heart rate
 Significant effects on the fetus when used during pregnancy