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
Treatment of amphetamine intoxication
Rehydrate
Correct electrolyte balance
Treat hyperthermia
Effects and physiology of phencyclidine (PCP)
PCP or “angel dust”
Dissociative, hallucinogenic drug that:
- Antagonizes N-methyl-D-aspartate (NMDA) glutamate receptors
- Activates dopaminergic receptors
Can have stimulant or CNS depressant effects, depending on dose taken
PCP can be smoked as “wet” (sprinkled on cigarette) or as a “joint” (sprinkled on marijuana)
Effects and physiology of ketamine
Ketamine is similar to PCP, but is less potent
Sometimes used as a “date rape” drug as it is odorless and tasteless
Clinical presentation of ketamine intoxication
Tachycardia
Tachypnea
Hallucinations
Amnesia
Clinical presentation of PCP intoxication
RED DANES:
- Rage (assaultiveness)
- Erythema (redness of skin)
- Dilated pupils
- Delusions
- Amnesia (memory impairment)
- Nystagmus (rotary, horizontal, or vertical; rotary nystagmus is very suggestive for PCP intoxication)
- Excitation (hypertension, tachycardia, muscle rigidity)
- Skin dryness
Synesthesia (one sensory stimulation evokes another = hearing a sound producing a color)
Impaired judgment
Ataxia
High tolerance to pain
Clinical presentation of PCP overdose
Seizures
Delirium
Coma
Death
Treatment of PCP intoxication
Monitor vitals, temp, and electrolytes
Minimize sensory stimulation
Use benzodiazepines (lorazepam) to treat agitation, anxiety, muscle spasms, and seizures
Use antipsychotics (haloperidol) to control severe agitation or psychotic symptoms
Clinical presentation of PCP withdrawal
No withdrawal syndrome
“Flashbacks” (recurrence of intoxication symptoms due to release of drug from body lipid stores)
What drugs are tactile and visual hallucinations seen with?
Cocaine
PCP
Agents in sedative-hypnotics category
Benzodiazepines
Barbiturates
Zolpidem, Zaleplon
Gamma-hydroxybutyrate (GHB)
Meprobamate
And others
These agents, especially benzos, are highly abused in US as they are more readily available than other drugs such as cocaine or opioids
Physiology and effects of gamma-hydroxybutyrate (GHB)
Dose-specific CNS depressant
Commonly used as a date-rape drug
Clinical presentation of GHB
Confusion
Dizziness
Drowsiness
Memory loss
Respiratory distress
Coma
Physiology and effects of benzodiazepines (BDZs)
Potentiate the effects of GABA by modulating receptor, thereby increasing frequency of chloride channel opening
Use of BDZs
Commonly used in treatment of anxiety disorders
Easily obtained via prescription from physician offices and EDs
Physiology and effects of barbiturates
Potentiate the effects of GABA by modulating receptor, thereby increasing duration of chloride channel opening
At high doses, act as direct GABA agonists, therefore have lower margin of safety relative to BDZs
Synergistic in combo w/ BDZs (and other CNS depressants such as alcohol)
- Respiratory depression can occur as complication
Use of barbiturates
Used in treatment of epilepsy and as anesthetics
Clinical presentation of sedative-hypnotics intoxication
Produces:
- Drowsiness
- Confusion
- Hypotension
- Slurred speech
- Incoordination
- Ataxia
- Mood lability
- Impaired judgment
- Nystagmus
- Respiratory depression
Symptoms are synergistic when combined w/ EtOH or opioids / narcotics
Long-term sedative use may cause dependence and depressive symptoms
Clinical presentation of sedative-hypnotics overdose
Coma/death
Which drug withdrawal has the highest mortality rate?
Barbiturates
Treatment of sedative-hypnotics intoxication
Maintain airway, breathing, and circulation
Monitor vital signs
Activated charcoal and gastric lavage to prevent further GI absorption (if drug was ingested in prior 4-6 hours)
BARBITURATES only: alkalinize urine w/ sodium bicarbonate to promote renal excretion
BENZODIAZEPINES only: flumazenil in overdose
Supportive care:
- Improve respiratory status
- Control hypertension
What is flumazenil?
Very short-acting BDZ antagonist used for treating BDZ overdose
Use w/ caution when treating overdose as it may precipitate seizures
Clinical presentation of sedative-hypnotics withdrawal?
Abrupt abstinence after chronic use can be life-threatening
While physiological dependence is more likely w/ short-acting agents, longer-acting agents can also cause dependence and withdrawal symptoms
Signs and symptoms of withdrawal are the same as those of EtOH withdrawal
Tonic-clonic seizures may occur and can be life-threatening
What is a good general rule in terms of drug withdrawal symptoms?
Drugs that are sedating (e.g. alcohol, barbiturates, benzos) are life-threatening
Drugs that are stimulants (e.g. cocaine, amphetamines) are not
Physiology and effects of opioids
Stimulate mu, kappa, and delta opiate receptors (normally stimulated by endogenous opiates)
Involved in analgesia, sedation, and dependence
Have effects on dopaminergic system which mediates their addictive and rewarding properties
Examples of opioids
Heroin
Oxycodone
Codeine
Dextromethorphan
Morphine
Methadone
Meperidine (Demerol)
Prescription opioids are the most commonly used opioids:
- Oxycodone (OxyContin)
- Hydrocodone/acetaminophen (Vicodin)
- Oxycodone/acetaminophen (Percocet)
- Not heroin
Behaviors such as losing medication, “doctor shopping”, and running out of meds early should alert clinical of possible misuse
What drug is a common ingredient in cough syrup?
Dextromethorphan (opioid)
What is a common cause of morbidity from street heroin use?
Infection secondary to needle sharing
Clinical presentation of opioid intoxication
Drowsiness/sedation/decreased pain perception
Nausea/vomiting
Constipation (decreased GI motility)
Slurred speech
Constricted pupils (except meperidine) - " Demerol Dilates pupils"
Seizures
Respiratory depression (can be fatal) - May progress to coma or death in overdose
Meperidine and MAOIs taken in combo may cause serotonin syndrome:
- Hyperthermia
- Confusion
- Hyper- or hypotension
- Muscular rigidity
What is the classic triad of opioid overdose?
Rebels Admire Morphine:
- Respiratory depression
- Altered mental status
- Miosis
Treatment of opioid intoxication/overdose
Ensure adequate airway, breathing, and circulation
In overdose, administration of naloxone (opioid antagonist) will improve respiratory depression, but may cause severe withdrawal in an opioid-dependent patient
- Rapid recovery of consciousness following administration of IV naloxone is consistent w/ opioid overdose
Ventilatory support may be required
What is the treatment of choice for opiate overdose?
Naloxone
Treatment of opioid use disorder
PHARMACOTHERAPY:
- Methadone
- Buprenorphine
- Naltrexone
Methadone treatment of opioid use disorder
Long-acting opioid receptor agonist
Pros:
- Administered once daily
- Significantly reduces morbidity and mortality in opioid-dependent persons
- “Gold standard” treatment in pregnant opioid-dependent women
Cons:
- Restricted to federally licensed substance abuse treatment programs
- Can cause QTc interval prolongation (screening ECG is indicated)
Buprenorphine treatment of opioid use disorder
Partial opioid receptor agonist
Pros:
- Sublingual preparation that is safer than methadone
- Its effects reach plateau and make overdose unlikely
- Comes as Suboxone (buprenorphine + naloxone) = prevents intoxication from IV injection
Cons:
- Available by prescription from office-based physicians
Naltrexone treatment of opioid use disorder
Competitive opioid antagonist
- Precipitates withdrawal if used within 7 days of heroin use
Pros:
- Either daily orally or monthly depot injection
- Good choice for highly motivated patients (e.g. health care professionals)
Cons:
- Compliance is an issue
What everyday food can result as positive for opioids in a urine drug screen?
Large amounts of poppy seed bagels or muffins
Clinical presentation of sedative-hypnotics withdrawal
Not life-threatening
Abstinence in opioid-dependent individual leads to unpleasant withdrawal syndrome:
- Dysphoria/anxiety
- Insomnia
- Lacrimation
- Rinorrhea
- Yawning
- Weakness
- Sweating
- Piloerection
- Nausea/vomiting
- Fever
- Dilated pupils
- Abdominal cramps
- Arthralgia/myalgia
- Hypertension
- Tachycardia
- Craving
Treatment of sedative-hypnotics withdrawal
MODERATE symptoms:
- Symptomatic treatment w/ clonidine (for autonomic signs/symptoms of withdrawal)
- NSAIDs (for pain)
- Dicyclomine (for abdominal cramps, etc.)
SEVERE symptoms:
- Detox w/ buprenorphine or methadone
Monitor degree of withdrawal w/ COWS (Clinical Opioid Withdrawal Scale)
- Uses objective measures (i.e. pulse, pupil size, tremor) to assess withdrawal severity
Physiology and effects of hallucinogens
Pharmacological effects vary, but LSD is believed to act on the serotonergic system
Do not cause physical dependence or withdrawal, though users can rarely develop psychological dependence
Examples of hallucinogens
Psilocybin (mushrooms)
Mesacaline (peyote cactus)
Lysergic acid diethylamide (LSD)
What is an LSD flashback?
Recurrence of symptoms mimicking prior LSD trip that occurs spontaneously and lasts for mins. to hours
Clinical presentation of hallucinogen intoxication
Effects:
- Perceptual changes (illusions, hallucinations, body image distortions, synesthesia [1 sensory stimulation evokes another])
- Labile affect
- Dilated pupils
- Tachycardia
- Hypertension
- Hyperthermia
- Tremors
- Incoordination
- Sweating
- Palpitations
Usually lasts 6-12 hours, but may last for several days
May have “bad trip” that consists of marked anxiety, panic, and psychotic symptoms (paranoia, hallucinations)
Treatment of hallucinogen intoxication
Monitor for dangerous behavior and reassure patient
Use benzodiazepines first-line if necessary for agitated psychosis
- Can use antipsychotics
Clinical presentation of hallucinogen withdrawal
No withdrawal syndrome is produced
With long-term LSD use, patients may experience “flashbacks” later in life
Physiology and effects of marijuana
Main active component is THC (tetrahydrocannabinol)
Cannabinoid receptors in brain inhibit adenylate cyclase
Examples and uses of marijuana
Cannabis (“marijuana”, “pot”, “weed”, “grass”)
- Dronabinol is pill form of THC that is FDA-approved for certain indications
Most commonly used illicit substance in the world
Has shown some efficacy in treating:
- Nausea and vomiting in chemotherapy patients
- Increase appetite in AIDS patients
- Chronic pain (from cancer)
- Decrease intraocular pressure in glaucoma
Clinical presentation of marijuana intoxication
Causes:
- Euphoria
- Anxiety
- Impaired motor coordination
- Perceptual disturbances (sensation of slowed time)
- Mild tachycardia
- Anxiety
- Conjunctival injection (red eyes)
- Dry mouth
- Increased appetite (“the munchies”)
Cannabis-induced psychotic disorders w/ paranoia, hallucinations, and/or delusions may occur
- No overdose syndrome
Clinical presentation of chronic use of marijuana
May cause respiratory problems (e.g. asthma, chronic bronchitis)
Suppression of immune system
Cancer
Possible effects on reproductive hormones
Prevalence of cannabis use disorder
Approx. 10% of those who use
Up to 50% of daily users
Treatment of marijuana intoxication
Supportive
Psychosocial interventions:
- Contingency management
- Groups
- Etc.
Clinical presentation of marijuana withdrawal
Symptoms:
- Irritability
- Anxiety
- Restlessness
- Aggression
- Strange dreams
- Depression
- Headaches
- Sweating, chills
- Insomnia
- Decreased appetite
Treatment of marijuana withdrawal
Supportive and symptomatic
Physiology and effects of inhalants
Generally act as CNS depressants
Prevalence of inhalant use
Typically preadolescent or adolescent
Rate of use is similar between boys and girls (but rare in adult females)
Examples of inhalants
Solvents
Glue
Paint thinners
Fuels
Isobutyl nitrate (“huff”, “laughing gas”, “rush”, “bolt”)
Clinical presentation of inhalant intoxication
Effects:
- Perceptual disturbances
- Paranoia
- Lethargy, dizziness
- Nausea/vomiting
- Headache
- Nystagmus, tremor
- Muscle weakness, hyporeflexia, ataxia
- Slurred speech
- Euphoria, clouding of consciousness
- Hypoxia
- Stupor, coma
Acute intoxication: 15-30 mins.
- May be sustained w/ repeated use
Clinical presentation of inhalant overdose
May be fatal secondary to respiratory depression or cardiac arrhythmias
Effects of long-term use of inhalants
- Permanent damage to CNS (e.g. neurocognitive impairment, cerebellar dysfunction, Parkinsonism, seizures)
- Peripheral neuropathy
- Myopathy
- Aplastic anemia
- Malignancy
- Metabolic acidosis
- Urinary calculi
- Glomerulonephritis
- Myocarditis
- MI
- Hepatotoxicity
Treatment of inhalant intoxication
Monitor airway, breathing, and circulation
May need oxygen w/ hypoxic states
Identify solvent because some (e.g. leaded gasoline) may require chelation
Clinical presentation of inhalant withdrawal
Withdrawal syndrome does not usually occur
Symptoms may include:
- Irritability
- Sleep disturbance
- Anxiety / depression
- Nausea / vomiting
- Craving
Physiology and effects of caffeine
Acts as adenosine antagonist, causing increased cAMP and stimulating release of excitatory neurotransmitters
Most commonly used psychoactive substance in US, usually in form of coffee or tea
Clinical presentation of caffeine overdose
> 250mg (2 cups of coffee):
- Anxiety / insomnia / restlessness / excitement
- Muscle twitching
- Rambling speech
- Flushed face
- Diuresis, GI disturbance
- Tachycardia
> 1g:
- Tinnitus
- Severe agitation
- Visual light flashes
- Cardiac arrhythmias
> 10g:
- Death may occur secondary to seizures and respiratory failure
Treatment of caffeine overdose
Supportive and symptomatic
Clinical presentation of caffeine withdrawal
Symptoms occur in 50-75% of caffeine users if cessation is abrupt
Symptoms:
- Headache
- Fatigue
- Irritability
- Nausea/vomiting
- Drowsiness
- Muscle pain
- Depression
Usually resolves within 1 1/2 weeks
Physiology and effects of nicotine
Stimulates nicotinic receptors in autonomic ganglia of sympathetic and parasympathetic nervous systems
Smoking –> tolerance and physical dependence (i.e. prominent craving and withdrawal)
Nicotine is derived from tobacco plant
What does cigarette smoking cause?
Leading cause of preventable morbidity and mortality in US
Poses many health risks:
- COPD
- Cardiovascular disease
- Various cancers
During pregnancy - associated w/ low birth weight, SIDS, and variety of postnatal morbidities
Prevalence of cigarette smoking
21% of US adults
Clinical presentation of nicotine intoxication
- Restlessness
- Insomnia
- Anxiety
- Increased GI motility
Clinical presentation of nicotine withdrawal
- Intense craving
- Dysphoria
- Anxiety
- Poor concentration
- Increased appetite, weight gain
- Irritability / restlessness / insomnia
Treatment of nicotine dependence
FDA-approve PHARMACOTHERAPY:
- Varenicline (Chantix)
- Bupropion (Zyban)
- Nicotine replacement therapy (NRT) - transdermal patch, gum, lozenge, nasal spray, inhaler
PSYCHOTHERAPY:
- Behavioral support / counseling (should be part of every treatment)
Relapse after abstinence is common
Varenicline (Chantix) treatment of nicotine dependence
Alpha-4-beta-2 nicotinic cholinergic receptor (nAChR) partial agonist that mimics action of nicotine
Reduces rewarding aspects and prevents withdrawal symptoms
Bupropion (Zyban) treatment of nicotine dependence
Antidepressant that is inhibitor of dopamine and norepinephrine reuptake
Helps reduce craving and withdrawal symptoms
Diagnosis and DSM-V criteria of gambling disorder
Persistent and recurrent problematic gambling behavior, as evidenced by 4 or more of the following in 12-month period:
- Preoccupation w/ gambling
- Need to gamble w/ increasing amount of money to achieve pleasure
- Repeated and unsuccessful attempts to cut down on or stop gambling
- Restlessness / irritability when attempting to stop gambling
- Gambling when feeling distressed (depressed, anxious, etc.)
- Returning to reclaim losses after gambling (“get even”)
- Lying to hide level of gambling
- Jeapordizing relationships / job because of gambling
- Relying on others to financially support gambling
Epidemiology / etiology of gambling disorder
Prevalence: 0.4-1.0% of adults in US
Men represent most of cases
More common in young adults and middle-aged
- Lower rates in older adults
Similar to substance use disorders
- Course is marked by periods of abstinence and relapse
Increased incidence of mood disorders, anxiety, disorders, substance use disorders, and personality disorders
Etiology may involve: genetic, temperamental, environmental, and neurochemical factors
1/3 may achieve recovery without treatment
Treatment of gambling disorder
Participation in Gamblers Anonymous (12-step program) is most common treatment
CBT has been shown to be effective
- Particularly when combined w/ GA
Important to treat comorbid mood, anxiety, and substance use disorders as appropriate
