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Substance Use Disorders: Definition
chronic, relapsing medical conditions
involves dysregulation of brain reward, motivation, memory, and inhibitory control
key features: impaired control, craving, risky use, social impairment, physio;ogic dependence
Dopamine Reward Pathway Overstimualtion
reinforces the compulsion to seek the drug above all else
intense stimuli cause massive dopamine surges, overriding natural rewards
Glutamate Dysregulation
impaired learning and memory around cues and triggers
causes the brain to form powerful, long-lasting associations between environmental cues (triggers) and the substance
Reduced Prefrontal Cortex Activity
poor impulse control and decision-making
chronic use of substances physically weakens the area of the brain responsible for executive function
Dependence
physiological state where the body has adapted to the presence of a drug and requires it to function "normally" on a cellular level
Addiction
a behavioral and psychological condition characterized by a loss of control and compulsive use despite significant negative life consequences.
Withdrawal
physiologic response when substance is absent
the body struggles to recalibrate its baseline
CNS hyperactivity
Tolerance
the brain becomes less sensitive to a drug
requiring higher doses to achieve the original effect
Intoxication
acte effects of substances on CNS
often euphoric, sedated, impulsive, or altered sensorium
Opioid: Intoxication Patho
opioids target mu receptors
initially suppressing pain and triggering a surge of dopamine that reinforces the "highâ (CNS depression)
Opioid : Intoxication Signs
â LOC
pinpoint pupils
slow GI mobility â constipation
HoTN, bradycardia
Opioid: Withdrawal Patho
occurs when opioids removed after chronic use
â norepinephrine release
not usually fatal, but extremely uncomfortable
Opioid: Withdrawal Signs
rhinorrhea (runny nose)
sweating
goosebumps
tachycardia
yawning
bone pain
diarrhea
irritability
Harmful Reduction
approach that acknowledges that people may continue to use substances
goal: reduce negative health outcomes, not require abstinence
supports autonomy, dignity, and safety
Harmful Reduction: Core Principles
meet people where they are
focus on safety
prioritize engagement and trust
respect patient goals
promote, non-punitive, trauma-informed care
recognize substance use as a health issue, not a moral failure
Opioid Use: Harm Reduction in Practice
offer naloxone + education
encourage never using alone
discuss safe injection practices
encourage medication treatment
Chemsex
consuming drugs to enhance sexual activity
may lead to risky behaviors:
transmitting HIV, Hepatitis C, and other STIs
Opioid Agonist-Antagonist
buprenorphine (sublingual)
MOA: depress CNA and alter pain perception
Use: opioid dependence, opioid use disorder
Opioid Agonist-Antagonist (Buprenorphine) Considerations
decreases potential for abuse
safe during labor
possible liver or renal failure
dental problems
Buprenorphine: Nursing Priority
ensure the patient is in active, moderate withdrawal before first dose
COWS score
giving it too early while other opioids are still active will cause "precipitated withdrawalâ
Long-Acting Opioid Agonist Use
methadone
synthetic
Use: chronic pain management, treatment of opioid use disorder
prevents withdrawal, reduces cravings
Methadone: Safety
long half-life
risk of respiratory depression
risk of QT prolongation
monitor EKG in cardiac patients
high overdose risk if combined with benzodiazepines
no âceiling effectâ
Ceiling Effect
drug effects plateau at a maximum level
Opiod Antagonist
naloxone
MOA: attaches to the same receptors as opioids
Uses: opioid overdose, reversal of respiratory depression
Reactions: severe agitation/ delirium/ HTN
Naloxone: Warnings
drug works within 2 to 5 minutes
naloxone wears off quickly
monitor the patient closely for "re-narcotizationâ
the patient may stop breathing again once the naloxone levels drop
will cause immediate, intense withdrawal symptoms for opioid dependent patients
agitation, vomiting, â HR, HTN
Alcohol Intoxication
CNS depression, slowed cognition, ataxia, impaired judgment
High levels â respiratory depression, hypoglycemia, coma
Alcohol Withdrawal
6-48 hours since last drink
CNS becomes hyperexcitable
GI distress
"the shakes" (fine tremors)
anxiety/ palpitations
insomnia
Alcohol Withdrawal: Severe Stage
48-96 hours since last drink
delirium tremens
life-threatening instability
profound disorientation
visual or tactile hallucinations
hypertension
hyperthermia
tonic-clonic seizures
Chronic Alcohol Use: Hepatic Effects
steatosis â hepatitis â cirrhosis
(fatty liver disease) â (inflammation of liver) â (liver scarring)
Chronic Alcohol Use: Cardiovascular Effects
cardiomyopathy (weakened heart muscle)
arrhythmias
increased risk of stroke
Chronic Alcohol Use: Neurological Effects
peripheral neuropathy
damage to the peripheral nerves (causes pain, weakness, tingling
Wenicke-Korsakoff syndrome - severe thiamine (vitamin B) deficiency
acute confusion (Wernickeâs encephalopathy)
permanent memory loss with confabulation (Korsakoffâs psychosis)
Chronic Alcohol Use: Hematologic Effects
folate deficiency
anemia
bone marrow suppression
Clinical Institute Withdrawal Assessment for Alcohol
CIWA-Ar
diagnostic scale used by nurses to objectively monitor the severity of alcohol withdrawal and guide medication dosing
Benzodiazepine
Uses:
first-line treatment for acute alcohol withdrawal
prevents seizures and delirium tremens
monitor for oversedation, respiratory depression, and ataxia (unsteadiness)
dosage based on the patient's CIWA-Ar score
Opioid Antagonist
naltrexone
MOA: blocks the mu-opioid receptors involved in the reward and pleasure circuits of the brain
Use: treats alcohol and opioid use disorders
Naltrexone: Nursing Priority
the patient needs been opioid-free for 7 to 10 days before starting naltrexone
opioid antagonist
will trigger immediate, severe withdrawal if opioid are still in their system
poor medication adherence = a long-acting IM injection (Vivitrol) can be given once every 4 weeks to provide steady coverage
Glutamate Modulator: Acamprosate
MOA: modulating the glutamate system and potentially the GABA system
Use: helping to "rebalance" brain chemistry that has been chronically disrupted by long-term alcohol use
reduce the "negative" symptoms of abstinence
insomnia, anxiety, and restlessness, which often lead patients to relapse
Aldehyde Dehydrogenase Inhibitor: Disulfiram
MOA: inhibiting the enzyme acetaldehyde dehydrogenase
Use: treats chronic alcoholism by creating an unpleasant sensitivity to alcohol
CAUTION: CANNOT have any alcohol with it
Disulfiram: Cautions
consuming even small amounts of alcohol will trigger a violent physical reaction
causes a toxic buildup of acetaldehyde in the blood
flushing, throbbing headache, nausea, vomiting, chest pain, palpitations, and dyspnea
avoid "hidden" alcohol sources
mouthwash, cough syrups, vanilla extract, aftershave
contraindicated in patients with severe cardiovascular disease, psychosis, or significant liver impairment
Nicotine Effect on the Brain
nicotine stimulates nicotinic acetylcholine receptors
massive dopamine release in reward pathway
nicotine also stimulates the adrenal glands
release epinephrine (adrenaline)
acutely â HR, BP, and blood glucose levels
Nicotine: Chronic Use
Up-Regulation: the brain compensates for the constant stimulation by increasing the number of receptors
creates tolerance
meaning the user needs more nicotine to achieve the same effect
Nicotine Withdrawal
leads to irritability, anxiety, restlessness, insomnia, difficulty concentrating, increases appetite
peaks 24-72 hours, lasts weeks
Nicotine Replacement Therapy
Uses: smoking cessation support, reduces withdrawal and cravings
provides a controlled, lower dose of nicotine without the harmful toxins and carcinogens found in tobacco smoke
The Transdermal Patch (Long-Acting)
provides a steady, continuous level of nicotine over 16 to 24 hours to prevent the "trough" that triggers morning cravings
instruct patients to rotate sites daily on a clean, hairless area above the waist
Nicotine Patch: Safety
if the patient experiences vivid dreams or insomnia, they should remove the patch at bedtime
the patch must be removed before an MRI to prevent skin burns from the metallic backing
Nicotine Gum
short-acting
Use: for breakthrough cravings
patients must use the "chew and park" method
chewing until a peppery taste or tingling occurs
then "parking" it between the cheek and gum to allow for mucosal absorption
Nicotine Gum: Patient Education
instruct patients not to drink acidic beverages (coffee, juice, soda) for 15 minutes before or during use
acidity prevents nicotine absorption in the mouth
Nicotine Lozenge
short-acting
lozenge is a transmucosal delivery system that should be allowed to dissolve slowly in the mouth
not to be chewed or swallowed
which would cause GI upset and poor absorption.
Partial Nicotinic Receptor Agonist
varencline
Use: most effective single agent for smoking cessation
Patho: reduces cravings + withdrawals
prevents the "reward" if a patient smokes
Varencline: Nursing Priority
monitoring for changes in behavior, hostility, agitation, depressed mood, or suicidal ideation
black box warning was removed
typically started one week before the patientâs actual quit date to allow the medication to reach steady-state levels in the brain
assess for new or worsening symptoms of cardiovascular disease
(like chest pain or SOB)