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what is the criteria for substance use d/o
pt is using a substance more than what is intended and for longer.
there is intention and failed attempts to dec their use.
extra time is used to get the substance or recover after taking them.
strong craving
you can’t fulfil your typical responsibilities
continued use after social impairment.
you give up other activities
using it in a high risk setting like driving a car
using it w/o considering the harmful effects
developing a tolerance to it
withdrawal after the substance is d/c
how many of the criteria do you need to hit in order to have a substance use d/o
2-3 mild, 4-5 mod, >6 severe
priority of drug seeking over other behaviors while trying to maintain dysfunctional drug use
dependence syndrome
how does someone develop a substance use disorder
long term exposure to substances causing mental and physical dependence.
4 c’s of addiction
Compulsive use, loss of Control, Craving, Continued use even w negative consequences
what is the most prevalent substance misused in the US
alcohol
presentation varies widely. pt is intoxicated, withdrawing, or with physical/psych conseq of chronic alc consumption. can have hx of another drug or nic addiction. can can primary psych illness, abuse/trauma, and +FHx of this d/o
substance use d/o
Cardiovascular signs of alc use d/o
HTN, cardiomyopathy, inc Tg
GI sx of alc use d/o
cirrhosis, vomit, pancreatitis, duodenal ulcers
endocrine sx of alc use d/o
feminine appearing men
hematologic sx of alc use d/o
anemia, B1 def, thrombocytopenia, macrocytosis
oncology sx of alc use d/o
inc ca risk, liver, stomach, esophageal, pancreatic ca
neuro sx of alc use d/o
cognitive impairment, paresthesias, ataxia
MSK sx of alc use d/o
presence of an injury, inc fall risk, car accidents, fights
sexual sx of alc use d/o
ED in men
AUDIT screening for alc use d/o is
identifying at risk drinking and detect harmful drinking behavior. 0-4 rating for each question. 8+ score = serious alc use. AUDIT-C is used more. Limit is that it’s not good at detecting AUD in older pops
CAGE questionairre
have you ever felt the need to cut down on drinking? have people around you been annoyed by you drinking? have you ever felt bad or guilty about your drinking? have you ever had a drink first thing in AM to steady your nerves or rid a hangover (eye opener)? >/=2= AUD. limitation is that it can’t distinguish b/w past and current d/o
what labs are helpful to determine alc use d/o
BAL >35 in an alert pt shows a high tolerance. GGT if >35 = heavy drinking (false pos in pregnancy, smokers, and obesity). alanine and aspartate aminotransferase ratio, carb deficient transferrin test, MCV >100 = heavy drinker, also inc in B12/folate acid def
what does a brain CT show in a person with AUD
volume loss, shrinkage of brain tissue. shrinkage of frontal lobe, ventricular enlargement, widening of cortical sulci. shrinkage thalamus, inferior colliculus, mallillary bodies = wernicke/korsakoff dz.
a pt with alc intox can have similar sx to
lithium tox, medical conditions like hypoglycemia, hypothyroidism, CVA, head injuries, hepatic encephalopathy, DKA, metabolic derangements.
a pt with alc withdrawal can have similar sx to
stimulant intox, med conditions like thyroid storm, essential tremor
reduction or stopping alc in pt who depends on it leads to
imbalance of excitatory and inhibitory neurotransmission = excessive NMDA pathway activity and dec GABA activity.
a score of >15 on the CIWA-Ar scale indicates what for a pt with alc withdrawal
severe withdrawal, inpt, close monitoring
a score of 8-15 on the CIWA-Ar scale indicates what for a pt with alc withdrawal
moderate withdrawal. outpt, monitoring
a score of <8 on the CIWA-Ar scale indicates what for a pt with alc withdrawal
mild withdrawal. outpt, monitoring
pt has hand tremor, HA, anorexia, n/v, sweating, insomnia, tachy, HTN, psychomotor agitation, craving, anxiety. also seizures, hallucinations, delirium. sx began 2-6 hrs after reducing consumption of alc persisting for 2 weeks. this dz is
alc withdrawal
pt presents with/out hand tremors and flu like sx. they report seeing tactile and visual and auditory hallucinations, like it looks like insects are everywhere. they know it isn’t actually real. this is a
withdrawl hallucination
tonic clonic seizures can occur between what time frame of alc withdrawal
6-48 hrs later. half assoc with underlying epilepsy, brain lesions, or substance use. some develop delirium tremens
acute and fluctuating disturbances in consciousness, confusion, agitation, inattention, impaired cognitive function. hallucinations, life threatening fluid, metabolic, an electrolyte imbalances. autonomic instability. this is
delirium tremens
gold standard tx for alc withdrawl and delirium tremens
long acting benzos (inhibits GABA, relieves sx and prevents delirium tremens and seizures. chlordiazepoxide and diazepam).
what AUD tx causes respiratory depression and isn’t really used
barbiturates
what AUD tx is as effective as benzos for mild-moderate withdrawal
anticonvulsants like carbamazepine and valproic acid
what AUD tx is used to dec psych sx like agitation and hallucinations, but does NOT tx the progression or reversal of delirium tremens or withdrawal seizures
neuroleptics
what AUD tx is used to replenish nutrient stores and is protective against Wernicke-Korsakoff (encephalopathy and dementia)
thiamine
what AUD tx is helpful in highly motivated pts committed to abstinence bc it’s an aversive agent. will cause face flushing, dizziness, blurred vision, n/v, palpitations, weakness, HoTN, tachy.
disulfiram
AE for using disulfiram to tx AUD
seizures, respiratory depression, MI, and death. pts o this drug feel bad when they drink alc, so if they stop using the meds they’ll feel fine.
what AUD tx blocks effects of alc related release of endogenous opioids triggering the good effects of alc?
naltrexone
adverse effects of using naltrexone for AUD tx
GI/sedative, precipitates opioid withdrawal and blocks analgesic effects of opioids
this AUD tx is an NMDA glutamate receptor antagonist and is a good option for pt with a compromised liver.
acamprosate
this AUD tx is an anticonvulsant with efficacy in dec alc consumption.
topiramate
what are the adverse effects of topiramate tx for AUD
anorexia, cog impairment, paresthesias, taste perversion
what are psychotherapeutic interventions that can be used for AUD
CBT identifies triggers and refusal skills. AA meetings provide a social support network
what is the typical prognosis of pts with AUD
they usually age out of it. pts who are heavy drinkers can have a motor vehicle accident, cirrhosis, ca, homicide/suicide, hemorrhagic stroke. organ damage from alc is irreversible
principal psychoactive constituent of cannabis is
dleta-9-tertrahydrocannabinol (THC)
euphoria, relaxed, inc appetite, cog impairment, impaired motor coordination after taking cannabis is what type of sx
acute effects
pt took weed, they have dry mouth, conjunctival injection, tachy, orthostatic hypotension. these types of sx are
physiological effects
pt stopped taking weed and now they have sx of anger, aggression, appetite change, weight loss, irritability, anxiety, restlessness, altered sleep, strange dreams, cravings, physical discomfort.
withdrawal sx
chronic use of cannabis leads to what sx
amotivational syndrome. cannabinoids produce a full range of schizophrenia like pos, neg, and cognitive sx
THC can be detected in what screenings
plasma, saliva, nails, and hair. synthetic cannabis is undetectable in utox
MRI studies show what in chronic cannabis use
glutamatergic and GABAergic abnormalities
how to tx cannabis use d/o
rarely anxiolytics and/or antipsychotics are used to tx anxiety or psych sx.
what are the type sof hallucination mechanisms
serotonergic, NMDA antagonist, other.
pt explains that they took something and they have heightened/diminished sensory inputs (colors, textures, sounds, tastes, touch), sensory inputs immerse person so they disregard all else, illusions (distortions perceived as real objects), frank hallucinations, synesthesia, distorted time perception, depersonalization, derealization. what did they take
hallucinogen
what hallucinogens can be found in utox
ketamine and PCP
what is seen on neuroimaging of a pt who chronically uses ecstasy
reduced serotonin transporter in midbrain, thalamus, and cortical region.
MRI scans of pts who depend on ketamine show
dec frontal cortex gray matter volume and white matter abnl, cortical atrophy, dec white matter integrity
how to tx adverse emotional reactions to a hallucinogen
librium and valium
3 sx clusters for opioid related risoders
loss of control, prominent behavioral rep, craving
chronic hallucinogen use leads to
mood lability, cog deterioration, personality alterations
when determining opioid related d/o in a pt we must concentrate on the following 2sxs clusters
loss o control, prominence to behavioral rep, craving
how can you tell that someone is in opioid intox
hx of recent ingestion, euphoria, pupillary constriction, slowed respiratory rate, drowsiness, slurred speech, inattention.
how can you tell a pt is in opioid withdrawal
dysphoria, n/v/d, muscle aches, lacrimation/rhinorrhea, pupils dilated, piloerection (goosebumps), sweating, yawn, fever, insomnia. happens in minutes or day safter stopping or being given a reversal agent like naltrexone, buprenorphine.
what psych d/o is most commonly assoc with OUD
PTSD
what is the opioid risk tool (ORT)
5 question test to see what pt can get drug related d/o.
what is the current opioid misuse measure (COMM)
17 item self assessment tool to help clinicians identify if a pt has bad behaviors assoc with misuse of opioids
what is the drug abuse screening test (DAST)
28 tru or false ques that identify a current drug disorder
what is a clinical opioid withdrawlal Scale (COWS)
11 item questions used to assess presence of and extent of withdrawal
what labs show a pt has OUD
pos utox, leukocytosis during detox, test for HIV, syphilis, tuberculin skin test, ECG if you want methadone maintenance therapy, CXR rule out TB
what does neuroimaging show in a pt with OUD
neurovascular d/o, leukoencephalopathy, atrophy. ventricular enlargement and frontal lobe loss, autopsy shows hi cerebral edema
what is the mainstay therapy tx for OUD
CBT. same results as giving buprenorphine
first line of tx of acute opioid overdose
naloxone. might need repeat dose bc half life is short.
SE of using naloxone for opioid OD
flash pulmonary edema
how to tx opioid withdrawal
clonidine
how to tx GI sxs in opioid withdrawal
dicyclomine
how to tx insomnia with opioid withdrawal
antihistamines
to tx muscle aches in a tp with opioid withdrawal
NSAIDs
how to tx n/v in a pt in opioid withdrawal
promethazine or metoclopramide
how to tx muscle spasms in a pt with opioid withdrawal
methocarbamol
how to tx diarrhea in a pt with opioid withdrawal
loperamide
what are the 3 approaches to opioid relapse prevention
agonist, partial agonist, antagonist
what is the agonist you can give for opioid relapse prevention
methadone, a long acting med used long term. make sure to follow EKGs bc of QTc prolognation
what is the partial agonist you can give for opioid relapse prevention
buprenorphine, used w nalxone
what is the antagonist you can give for opioid relapse prevention
naltrexone, reserved for very motivated pts. removes the rewarding effects of using opioids
psychotherapeutic interventions and medically assisted detox programs have a worse outcome of successful opioid detox in comparison to
maintenance or detox coupled with CBT and individual counseling
what are positive prognostic indicators for opioid remission
shorter opioid use hx, only PO opioids, not using heroin, fewer prior tx attempts, inc social stability.
what is the most likely drug to be assoc with ED visits
a stimulant like cocaine, meth, or MDMA
enhanced energy, dec fatigue, euphoria, hyperalert, grandiosity, alert, sociability after taking a drug.
stimulant intox
adverse effects of stimulant consumption
dysphoria, anxiety, restlessness, stereotypical behavior, psychomotor agitation, impaired judgement.
agitation is a problem with what type of stimulant
meth
stimulant induced psychosis is sene in what type of stimulant users
high dose chronic users
what consists of stimulant induced psychosis
paranoia, stereotyped compulsive behavior.
LOC, disorientation, perceptual disturbances like auditory and visual hallucinations
stimulant delirium, indicative of OD
what stimulant drug shows psychotic sxs more
meth
what is seen on neuroimaging in a pt who takes stimualnts
poor white matter integrity, dec gray matter in frontal region
how are ADHD and stimulants related
we typically give pts stimulants to tx this condition.
how to tx acute intox of stimulants
put them in quiet safe environment,, give benzos for intense agitation, antipsychs for extreme paranoia or psychosis (dec seizure threshold and inc hypothermia).
what should you avoid in a tp with acute stimulant intox
BB bc of risk of coronary spasms. vasoconstrictors leading to MIs
how to tx stimulant withdrawal
can give benzos for intense agitation or bad sleep, if they’re depressed give antidepressant or psychotherapy.
how does contingency management help pts with stimulant addiction
dec substance behaviors thru alternate enforcers. give tangible reinforcers to maintain goals. 12 step program