substance addiction
a chronic medical condition w/ roots in environment, neurotransmission, genetics & life experiences -> a strong craving of substance & person has desire to cut down w/o success
what is the biggest barrier towards treatment of addiction
stigma
countertransference
unconscious feelings that the healthcare worker has toward the pt
risk factors for addiction
Biologic: genetic predisposition, inc extracellular dopamine, immature brain dev., function of acetate, having another mental health disorder, being male
neurobio: neurotransmitters associated w/ substance use disorder (dec dopamine)
environment: chronic stressors, anxiety, abuse or trauma, etc
starting alc, nicotine or other drug use at an early age
increased extracellular dopamine in brain leads to
excess of dopamine causing the person to feel high
substances like cocaine, amphetamines, heroin & alc increase extracellular dopamine
front vs back of brain
back: emotion, memory, impulse, psychomotor activity
front: area of executive function, planning, problem solving, judgment, impulse control, organization
if given oxy before front is developed, will develop memory that the drug made me feel good and I don’t have the judgement to not use drugs
alcohol craving & acetate
alcohol breaks down into acetate -> acetate triggers a craving for more acetate -> in normal person acetate moves through system quickly and exits but a person w/ addiction processes alcohol at 1/3 to 1/10 the rate of a normal pancreas and liver -> the slow metabolism from 1 drink causes the acetate to barley be processed out and it makes the body crave more -> loss of control
reasons for continued used (of alc?)
what metabolizes down into acetate
alcohol and nicotine
substance intoxication
recent overuse/excessive use of a substance, such as an acute alcohol intoxication, that results in a reversible substance specific syndrome
tolerance
occurs when a person no longer responds to the drug or substance in the way that the person initially responded
blackouts
not the same as passing out, caused excessive consumption of alcohol followed by episodes of amnesia. during these periods of time, a person actively engages in behaviors, can perform complicated tasks and appears normal
relapse
the recurrence of alcohol - or drug - dependent behavior in an individual who has previously achieved and maintained abstinence for a significant time beyond the period of detox
dual diagnosis
co occurring mental illness and substance use or addictive disorder
substance withdrawal
a set of physiological symptoms that occur when a person stops using a substance
estimated timing of symptom appearance followign alc intake
6-12: insomnia, tremulousness, mild anxiety, GI upset, headache
12-24: alcoholic hallucinosis, visual, auditory or tactile hallucinations
24-48: w/draw seizures (gen tonic clonic)
48-72: alcohol w/draw delirium, hallucination, disorientation, tachycardia, htn, low grade fever, agitation, diaphoresis
peaks at 48hrs, use CIWA assessment q4
people can die from alc & benzo w/draw
CIWA symptoms of sedative hypnotic / alc withdrawal that need to be asked about
goal for alc w/draw mgt
to control agitation, decrease the risk of seizures and decrease morbidity and mortality
what drugs can be given for alc w/draw if pt scores 8+ on the CIWA
what vitamin needs to be given daily during alc w/draw
thiamine -> critical to give and should be given prior to IV dextrose support to prevent precipitation of Wernicke’s syndrome
delirium tremens (DTS)
DTS sx
agitation, inc anxiety, gross confusion & disorientation, coarse tremors, seizures, delusions, hallucinations, paranoia, autonomic hyperactivity (tachycardia, diaphoresis, fever, anxiety, insomnia & htn)
danger of misdiagnosis as psychiatric disorder
best ways to treat DTS
DTS medications for treatment