Substance-Related & Addictive Disorders Flashcards
Diagnosis and DSM-V criteria of substance use disorders
Cognitive, behavioral, and physiological symptoms indicating continuous use of a substance despite significant substance-related problems
Characterized by problematic pattern of substance use –> impairment or distress manifested by at least 2 of the following within a 12-month period:
- Using substance more than originally intended
- Persistent desire or unsuccessful efforts to cut down on use
- Significant time spent in obtaining, using, or recovering from substance
- Craving to use substance
- Failure to fulfill obligations at work, school, or home
- Continued use despite social or interpersonal problems due to substance use
- Decrease social, occupational, or recreational activities because of substance use
- Use in dangerous situations (e.g. driving car)
- Continued use despite subsequent physical or psychological problem (e.g. drinking alcohol despite worsening liver problems)
- Tolerance
- Withdrawal
It is possible to have substance use disorder without having physiological dependence (i.e. without having withdrawal or tolerance)
Epidemiology of substance use disorders
1-year prevalence of any substance use disorder in US: approx. 8%
Men > women
Alcohol and nicotine are most commonly used substances
Psychiatric symptoms of substance use disorders
Mood symptoms are common among persons w/ substance use disorders
Psychotic symptoms may occur w/ some substances
Personality disorders and psychiatric comorbidities (e.g. major depression, anxiety disorders) common
Often challenging to decide whether psychiatric symptoms are primary or substance-induced
Substance-induced mood symptoms improve during abstinence, whereas primary mood symptoms persist
What is withdrawal in terms of substance use disorders?
Development of substance-specific syndrome due to cessation (or reduction) of substance use that has been heavy and prolonged
Withdrawal symptoms of drug are usually opposite of its intoxication effects
- Ex. Alcohol is sedating, but withdrawal can cause brain excitation and seizures
What is tolerance in terms of substance use disorders?
Need for increased amounts of substance to achieve the desired effect or diminished effect if using the same amount of substance
Acute intoxication and withdrawal of substance use disorders
Both intoxicated and withdrawing patient can present difficulties in diagnosis and treatment
Common for persons to abuse several substances at once
- Clinical presentation can be confusing
- Signs/symptoms may be atypical
Always be on the lookout for multiple substance use
Direct testing for alcohol
Stays in system for only a few hours
Breathalyzer test, commonly used by police enforcement
Blood/urine testing more accurate
Direct testing for cocaine
Urine drug screen positive for 2-4 days
Direct testing for amphetamines
Urine drug screen positive for 1-3 days
Most assays are not of adequate sensitivity or specificity
Direct testing for phencyclidine (PCP)
Urine drug screen positive for 4-7 days
Creatine phosphokinase (CPK) and aspartate aminotransferase (AST) are often elevated
Direct testing for sedative-hypnotics
In urine and blood for variable amounts of time
Barbiturates:
- Short-acting (pentobarbital): 24 hours
- Long-acting (phenobarbital): 3 weeks
Benzodiazepines:
- Short-acting (e.g. lorazepam): up to 5 days
- Long-acting (diazepam): up to 30 days
Direct testing for opioids
Urine drug test remains positive for 1-3 days, depending on opioid used
Methadone and oxycodone will come up negative on general screen
- Must order a separate panel
Direct testing for marijuana
Urine detection:
- After single use, about 3 days
- In heavy users, up to 4 weeks (THC released from adipose stores)
Treatment of substance use disorders
PSYCHOTHERAPY
- Behavioral counseling should be part of all
- Psychosocial treatments are effective (include motivational intervention (MI), CBT, contigency management, individual and group therapy)
- 12-step groups (Alcoholics Anonymous [AA], Narcotics Anonymous [NA]) should be encouraged
PHARMACOTHERAPY
- Available for some drugs
Physiology and effects of alcohol
Activates GABA (inhibitory), dopamine, and serotonin receptors in CNS
Inhibits glutamate receptor activity (excitatory) and voltage-gated Ca2+ channels
Potent CNS depressant
Metabolized by:
- Alcohol –> acetaldehyde (enzyme: alcohol dehydrogenase)
- Acetaldehyde –> acetic acid (enzyme: aldehyde dehydrogenase)
There is upregulation of these enzymes in heavy drinkers
Secondary to gene variant, Asians often have less aldehyde dehydrogenase –> result in flushing and nausea (reduce risk of alcohol use disorder)
Most common co-ingestant in drug overdoses
Prevalence of alcohol abuse
Lifetime prevalence in US is 5% of women and 12% of men
Spousal abuse is more likely in home in which male is involved in some kind of substance use disorder, especially alcoholism
Alcohol is most commonly used intoxicating substance in the US
Clinical presentation of alcohol intoxication
Absorption and elimination rates of alcohol are variable and depend on many factors:
- Age
- Sex
- Body weight
- Chronic nature of use
- Duration of consumption
- Food in stomach
- State of nutrition and liver health
Effects of EtOH depend on blood alcohol level (BAL):
- Decreased fine motor control
- Impaired judgment and coordination
- Ataxic gait and poor balance
- Lethargy, difficulty sitting upright, difficulty w/ memory, nausea/vomiting
- Coma in novice drinker
- Respiratory depression, death possible
Serum EtOH level or expired air breathalyzer can determine extent of intoxication
- Most adults will show some signs of intoxication w/ BAL >100 and obvious signs w/ BAL >150 mg/dl
- Effects/BAL may be decreased if high tolerance has been developed
Treatment of alcohol intoxication
MONITOR: airway, breathing, circulation, glucose, electrolytes, acid-base status
- Ethanol, methanol, and ethylene glycol can cause metabolic acidosis w/ increased anion gap
Give THIAMINE to prevent/treat Wernicke’s encephalopathy
Give FOLATE
NALOXONE may be necessary to reverse effects of co-ingested opioids
CT of head may be necessary to rule out subdural hematoma or other brain injury
Liver will eventually metabolize alcohol without any other interventions
Severely intoxicated patient may require mechanical ventilation w/ attention to acid-base balance, temp, and electrolytes while he/she is recovering
GI evacuation (e.g. gastric lavage, induction of emesis, and charcoal) is not indicated in treatment of EtOH overdose unless significant amount of EtOH was ingested within the last 30-60 mins.
Clinical presentation of alcohol withdrawal
Chronic alcohol use has depressant effect on CNS, and cessation of use causes compensatory hyperactivity
- Potentially lethal!
Signs/symptoms: insomnia, anxiety, hand tremor, irritability, anorexia, nausea, vomiting, autonomic hyperactivity (diaphoresis, tachycardia, hypertension), pscyhomotor agitation, fever, seizures, hallucinations, and delirium
- Earliest symptoms begin between 6-24 hours after cessation of drinking and depend on duration and quantity of EtOH consumption
- Generalized tonic-clonic seizures usually occur between 12-48 hours after cessation of drinking w/ peak around 12-24 hours
- About 1/3 w/ seizures develop delirium tremens (DTs)
- Hypomagnesemia may predispose to seizures = need to be corrected promptly
Treatment of seizures seen during alcohol withdrawal
Benzodiazepines
Long-term treatment w/ anticonvulsants is not recommended
What is delirium tremens (DTs)?
Most serious form of EtOH withdrawal
Usually begins 48-96 hours after last drink, but may occur later
Only 5% of alcohol withdrawal develop DTs
5% mortality rate (up to 35% if left untreated)
Physical illness predisposes to condition
Age >30 and prior DTs increase risk
Symptoms: disorientation, delirium, hallucinations (most commonly visual and tactile), agitation, gross tremor, autonomic instability (high RR, HR, & BP), and fluctuating levels of psychomotor activity
It is medical emergency and should be treated w/ adequate doses of benzodiazepines
What is attempted suicide with?
Mental illness
Young females
Alcohol use
What are the severities of alcohol withdrawal?
EtOH withdrawal symptoms usually begin in 6-24 hours and last 2-7 days
Mild: irritability, tremor, insomnia
Moderate: diaphoresis, hypertension, tachycardia, fever, disorinetation
Severe: tonic-clonic seizures, DTs, hallucinations
Treatment of alcohol withdrawal
Benzodiazepines (chlordiazepoxide, diazepam, or lorazepam)
- Should be given in sufficient doses to keep patient calm & lightly sedated, then tapered down slowly
Carbamazepine & valproic acid can be used in mild withdrawal
Antipsychotics
- Be careful of lowering seizure threshold
- Temporary restraints for severe agitation
Thiamine, folic acid, and multivitamin
- To treat nutritional deficiencies (“banana bag”)
Electrolyte and fluid abnormalities must be corrected
Monitor withdrawal signs/symptoms w/ Clinical Institute Withdrawal Assessment (CIWA) scale
Careful attention must be given to level of consciousness and possibility of trauma should be investigated
Check for signs of hepatic failure (e.g. ascites, jaundice, caput medusae, coagulopathy)
What symptoms are associated w/ Korsakoff’s “psychosis” or alcohol-induced neurocognitive disorder
Confabulations (inventing stories of events that never occurred)
- Patients are unaware that they are “making it up”
Screening for alcohol use disorder
AUDIT-C is used to screen for alcohol use disorder
Biochemical markers are useful in detecting recent prolonged drinking and ongoing monitoring can help detect relapse
- BAL
- LFTs (AST, ALT)
- GGT
- MCV
- AST:ALT ratio >=2.1 and elevated GGT suggest excessive alcohol use
- Alcohol can cause increase LFTs and macrocytosis (increased MCV)
At-risk or heaving drinking:
- Men: >4 drinks per day or >14 drinks per week
- Women: >3 drinks per day or >7 drinks per week
What is AUDIT-C?
Questionnaire used to screen for alcohol use disorder
Q1: How often did you have a drink containing alcohol in the past year?
Q2: How many drinks did you have on a typical day when you were drinking in the past year?
Q3: How often did you have 6 or more drinks on 1 occasion in the past year?
Scale of 0-12 (0 = no alcohol use)
Men: 4 or more is positive
Women: 3 or more is positive
Medications for alcohol use disorder
FIRST-LINE:
- Naltrexone (Revia, IM-Vivitrol)
- Acamprosate (Campral)
SECOND-LINE:
- Disulfiram (Antabuse)
- Topiramate (Topamax)
Naltrexone (Revia, IM-Vivitrol) treatment of alcohol use disorder
First-line
Opioid receptor blocker
Works by decreasing desire / craving and “high” associated w/ alcohol
Maybe greater benefit is seen in men w/ family history of alcoholism
In patients w/ physical opioid dependence, it will precipitate withdrawal
Acamprosate (Campral) treatment of alcohol use disorder
First-line
Thought to modulate glutamate transmission
Should be started post-detoxification for relapse prevention in patients who have stopped drinking
Major advantage is that it can be used in patients w/ liver diseasse
Contraindicated in severe renal disease
Disulfiram (Antabuse) treatment of alcohol use disorder
Blocks enzyme aldehyde dehydrogenase in liver and causes aversive reaction to alcohol (flushing, headache, nausea/vomiting, palpitations, shortness of breath)
Contraindicated in severe cardiac disease, pregnancy, psychosis
Liver function should be monitored
Best used in highly motivated patients, as med adherence is an issue
Topiramate (Topamax) treatment of alcohol use disorder
Anticonvulsant that potentiates GABA and inhibits glutamate receptors
Reduces cravings for alcohol and decreases alcohol use
Long-term complications of alcohol intake
Wernicke’s encephalopathy:
- Caused by thiamine (vitamin B1) deficiency resulting from poor nutrition
- Acute and can be reversed w/ thiamine therapy
- Features: ataxia (broad-based), confusion, ocular abnormalities (nystagmus, gaze palsies)
If left untreated, Wernicke’s encephalopathy may progress to Korsakoff syndrome:
- Chronic amnestic syndrome
- Reversible in only 20% of patients
- Features: impaired recent memory, anterograde amnesia, confabulation (unconsciously making up answers when memory has failed)
All patients w/ altered mental status should be given thiamine before glucose or Wernicke-Korsakoff syndrome may be precipitated
- Thiamine is coenzyme used in carbohydrate metabolism
Physiology and effects of cocaine
Blocks the reuptake of dopamine, epinephrine, and norepinephrine from synaptic cleft
- Causes stimulant effect
Dopamine plays a role in behavioral reinforcement (“reward”) system of brain
Overdose can cause death secondary to cardiac arrhythmia, MI, seizure, or respiratory depression
Clinical presentation of cocaine intoxication
GENERAL: euphoria, heightened self-esteem, increase/decreased BP, tachy/bradycardia, nausea, dilated pupils, weight loss, psychomotor agitation/depression, chills, sweating
DANGEROUS: respiratory depression, seizures, arrhythimas, hyperthermia, paranoia, hallucinations (especially tactile)
- Since cocaine is an indirect sympathomimetic, intoxication mimics fight-or-flight response
DEADLY: vasoconstrictive effects may result in MI, intracranial hemorrhage, or stroke
Management of cocaine intoxication
MILD-TO-MODERATE agitation & anxiety: reassurance of patient and benzodiazepines
SEVERE agitation or psychosis: antipsychotics (e.g. haloperidol)
Symptomatic support (i.e. control hypertension, arrhythmias)
Temp of >102 F should be treated aggressively w/ ice bath, cooling blanket, and other supportive measures
Treatment of cocaine use disorder
PHARMACOTHERAPY:
- No FDA-approved pharmacotherapy
- Off-label meds are sometimes used (disulfiram, modafinil, topiramate)
PSYCOTHERAPY:
- Psychological interventions are efficacious and mainstay of treatment:
- Contingency management
- Relapse prevention
- NA
- Etc.
Clinical presentation of cocaine withdrawal
Abrupt abstinence is not life-threatening
Produces post-intoxication depression (“crash”): malaise, fatigue, hypersomnolence, depression, anhedonia, hunger, constricted pupils, vivid reams, psychomotor agitation, or retardation
- These patients can become suicidal
With mid/mod cocaine use, withdrawal symptoms resolve within 72 hours
With heavy, chronic use, they may last for 1-2 weeks
Treatment of cocaine withdrawal
Treatment is supportive
Severe psychiatric symptoms may warrant hospitalization
Physiology and effects of classic amphetamines
Block reuptake and facilitate release of dopamine and norepinephrine from nerve endings
- Cause stimulant effect
Examples and use of classic amphetamines
Ex.: Dextroamphetamine (Dexedrine), Methylphenidate (Ritalin), Methamphetamine (Desoxyn, “ice”, “speed”, “crystal meth”, “crank”)
Methamphetamines are easily manufactured in home labs using OTC medications (e.g. pseudoephedrine)
Used medically in treatment of narcolepsy, ADHD, and occasionally depressive disorders
Physiology and effects of substituted (“designer”, “club drugs”) amphetamines
Release dopamine, norepinephrine, and serotonin from nerve endings
Examples and use of substituted (“designer”, “club drugs”) amphetamines
Ex.: MDMA (“ecstasy”), MDEA (“eve”)
These substances are associated w/ dance clubs and raves
Have both stimulant and hallucinogenic properties
Serotonin syndrome is possible if designer amphetamines are combined w/ SSRIs
What can heavy use of amphetamines cause?
My cause amphetamine-induced psychosis (psychotic state that may mimic schizophrenia)
What are the symptoms of amphetamine abuse?
Euphoria
Dilated pupils
Increased libido
Tachycardia
Perspiration
Grinding teeth
Chest pain
Clinical presentation of amphetamine intoxication
Causes symptoms similar to those of cocaine
GENERAL: euphoria, heightened self-esteem, increase/decreased BP, tachy/bradycardia, nausea, dilated pupils, weight loss, psychomotor agitation/depression, chills, sweating
DANGEROUS: respiratory depression, seizures, arrhythimas, hyperthermia, paranoia, hallucinations (especially tactile)
- Since cocaine is an indirect sympathomimetic, intoxication mimics fight-or-flight response
DEADLY: vasoconstrictive effects may result in MI, intracranial hemorrhage, or stroke
MDMA and MDEA may induce sense of closeness to others
Chronic amphetamine use –> accelerated tooth decay (“meth mouth”)
Use is associated with increased tolerance, but can also induce seizures
Clinical presentation of amphetamine overdose
Hyperthermia
Dehydration (especially after prolonged period of dancing in club)
Rhabdomyolysis
Renal failure
Complications of amphetamine intoxication
Complications of long half-life can cause ongoing psychosis even during abstinence
Clinical presentation of amphetamine withdrawal
Prolonged depression
