Substance Related Disorders Flashcards
What is the DSM-IV criteria for substance abuse?
Abuse is a pattern of substance use leading to impairment or distress for at least 1 year w/ one or more of the following manifestations:
- Failure to fulfill obligations at work, school or home
- Use in dangerous situations (driving a car)
- Recurrent substance-related legal problems
- Continued use despite social or interpersonal problems due to the substance use
What is the DSM-IV criteria for substance dependence?
Dependence is a substance us leading to impairment or distress manifested by at least 3 of the following w/i a 12 mo period:
- Tolerance
- Withdrawal
- Using substance more than originally intended
- Persistent desire or unsuccessful efforts to cut down on use
- Significant time spent on getting, using or recovering from substance
- Decreased social, occupational or recreational activities because of substance use
- Continued use despite subsequent physical or psychological problem (ex: drinking despite worsening liver problems)
A diagnosis of substance ________ supercedes a diagnosis of ________.
dependence, abuse
Substance dependence
- Lifetime prevalence
- Men vs. Women
- Most commonly used substances
- What symptoms are most common
- Lifetime prevalence: 17%
- Men >> Women
- Caffeine, alcohol, nicotine
- Depressive symptoms
What is the definition of withdrawal?
The development of a substance-specific symptom due to the cessation of substance use that has been heavy and prolonged
What is the definition of tolerance?
The need for increased amounts of the substance to achieve the desired effect or diminished effect if using the same amt of the substance.
______ is the most common co-ingestant in drug overdoses
Alcohol
____% of Americans are alcoholics
7-10%
Alcohol…
- ______ GABA receptors
- ______ serotonin receptors
- ______ glutamate receptors
- activates GABA receptors
- activates serotonin receptors
- inhibits glutamate receptors
How is alcohol metabolized?
- Alcohol –> acetaldehyde
- via alcohol dehydrogenase
- Acetaldehyde –> acetic acid
- via aldehyde dehydrogenase
- Upregulation of enzymes in heavy drinkers
- Asian people have less aldehyde DH
How do you screen for alcohol abuse?
CAGE questionnaire - 2 or more “yes” are positive; 1 “yes” should arouse suspicion of abuse
- Have you ever wanted to cut down on your drinking?
- Have you ever felt annoyed by criticism of your drinking?
- Have you ever felt guilty about drinking?
- Have you ever taken a drink as an “eye opener” (to prevent shakes)?
The absorption & elimination rates of alcohol depend on what factors?
- Age
- Sex
- Body weight
- Speed of consumption
- Presence of food in the stomach
- Chronic alcoholism
- Presence of advanced cirrhosis
- State of nutrition
In most states, the legal limit for alcohol intoxication is _____ mg/dL.
More than 50% of adults with BAL > ____ mg/dL show obvious signs of intoxication.
80-100 mg/dL
150 mg/dL
What is the novice drinker’s BAL for each of these clinical presentations?
- Decreased fine motor control
- Impaired judgment & coordination
- Ataxic gait & poor balance
- Lethargy; difficulty sitting upright
- Coma in the novice drinker
- Respiratory depression
- Decreased fine motor control
- 20-50 mg/dL
- Impaired judgment & coordination
- 50-100 mg/dL
- Ataxic gait & poor balance
- 100-150 mg/dL
- Lethargy; difficulty sitting upright
- 150-250 mg/dL
- Coma in the novice drinker
- 300 mg/dL
- Respiratory depression
- 400 mg/dL
What is the differential diagnosis for alcohol intoxication?
- Hypoglycemia
- Hypoxia
- Mixed EtOH-drug overdose
- Ethylene glycol or methanol poisoning
- Hepatic encephalopathy
- Psychosis
- Psychomotor seizures
What is the diagnostic evaluation for alcohol intoxication?
- Serum EtOH level
- Expired air breathalyzer
- CT scan of the head
- Rule out subdural hematoma or other brain injury
How is acute alcohol intoxication treated?
- Ensure adequate airway, breathing, circulation; monitor electrolytes & acid-base status
- Obtain finger-stick glucose level to exclude hypoglycemia
- Thiamine (prevent/treat Wernicke’s encephalopathy), naloxone (reverse opioid effects if ingested), folate administered
- GI evacuation (gastric lavage, charcoal) no role in treatment of EtOH overdose (mixed drug-EtOH)
How is long-term alcohol dependence treated?
- Alcoholics Anonymous - self-help group
- Disulfiram (Antabuse) - aversive therapy; inhibits aldehyde dehydrogenase, causing violent retching when person drinks
- Psychotherapy & SSRIs
- Naltrexone - opioid antagonist; reduces cravings for EtOH
The earliest symptoms of EtOH withdrawal being btwn ___ & ___ hrs after the pts last drink and depend on the _______ & _______ of EtOH consumption.
6-24 hrs
duration, quantity
Clinical presentation: mild vs. severe alcohol withdrawal
- Mild
- Irritability, insomnia
- Severe
- Fever, disorientation, seizures, hallucinations, delirium
What are the signs/symptoms of alcohol withdrawal syndrome?
- Insomnia
- Anxiety
- Tremor
- Irritability
- Anorexia
- Tachycardia
- Hyperreflexia
- Hypertension
- Fever
- Seizures
- Hallucinations
- Delirium
What is delirium tremens?
How many pts experience it?
What are the symptoms?
- Most serious form of EtOH withdrawal
- Begins w/i 72 hrs of cessation of drinking
- Only 5% of pts hospitalized for EtOH withdrawal
- 15-20% mortality rate if untreated
-
Symptoms
- Delirium
- Visual/tactile hallucinations
- Gross tremor
- Autonomic instability
- Fluctuating levels of psychomotor activity
How is alcohol withdrawal diagnostically evaluated?
- Accurate & frequent assessment of vitals
- Autonomic instability may occur
- Careful attention to level of consciousness
- Possibility of trauma should be investigated
- Signs of hepatic failure may be present
- Ascites, jaundice, caput medusae, coagulopathy
What is the differential diagnosis of alcohol withdrawal?
- Alcohol-induced hypoglycemia
- Acute schizophrenia
- Drug-induced psychosis
- Encephalitis
- Thyrotoxicosis
- Anticholinergic poisoning
- Withdrawal from other sedative-hypnotic type drugs
How is alcohol withdrawal treated?
- Tapering doses of benzodiazepines
- chlordiazepoxide, lorazepam
- Thiamine, folic acid, multivitamin to treat nutritional deficiencies
- Mg sulfate for postwithdrawal seizures
Wernicke-Korsakoff syndrome is caused by….
- Thiamine (vitamin B1) deficiency
- Poor diet of alcoholics
What is Wernicke’s encephalopathy?
- Acute & reversed by thiamine therapy
- Triad
- Ataxia
- Confusion
- Ocular abnormalities (nystagmus, gaze palsies)
- May progress to Korsakoff’s syndrome if left untreated
What is Korsakoff’s syndrome?
- Progression from Wernicke’s encephalopathy
- Chronic, often irreversible
- Triad
- Impaired recent memory
- Anterograde amnesia
- +/- confabulation
What is confabulation?
making up answers when memory has failed
What is the mechanism of cocaine?
- Blocks dopamine reuptake from the synaptic cleft
- Stimulant effect
- Dopamine plays a role in behavioral reinforcement (“reward” system of the brain)
What is the clinical presentation of cocaine intoxication?
“flight or fight” response
- Euphoria
- Increased/decreased BP
- Tachycardia/bradycardia
- Nausea
- Dilated pupils
- Weight loss
- Psychomotor agitation & depression
- Chills
- Sweating
- Respiratory depression
- Seizures
- Arrhythmias
- Hallucinations (tactile)
Cocaine’s vasoconstrictive effect may result in _____ or _____.
Myocardial infarction
Cerebrovascular accident
What is the differential diagnosis of cocaine intoxication?
- Amphetamine or PCP intoxication
- Sedative withdrawal
What is the diagnostic evaluation for cocaine intoxication?
- Urine drug screen
- Positive for 3 days, longer in heavy users
How is cocaine intoxication treated?
- Mild-to-moderate agitation: benzodiazepines
- For severe agitation or psychosis: haloperidol
- Symptomatic support
- Control HTN, arrhythmias, etc.
How is cocaine dependence treated?
- Psychotherapy, group therapy
- TCAs
- Dopamine agonists (amantadine, bromocriptine)
How does cocaine withdrawal present clinically?
How is it treated?
- Abrupt abstinence is not life threatening but produces a dysphoric “crash”
- Malaise, fatigue, depression, hunger, constricted pupils, vivid dreams, psychomotor agitation or retardation
- Treatment usually supportive; let pt sleep off crash
What are the 3 classic amphetamines?
- Dextroamphetamine (Dexedrine)
- Methylphenidate (Ritalin)
- Methamphetamine (Desoxyn, ice, speed, “crystal meth”, “crack”)
What are the 2 substituted “designer” amphetamines?
- MDMA (ecstasy)
- MDEA (eve)
What is the mechanism of classic amphetamines?
- Release dopamine from nerve endings
- Stimulant effect
- Used medically in treatment of narcolepsy, ADHD & depressive disorders
What is the mechanism of designer amphetamines?
- Release dopamine & serotonin from nerve endings
- Have both stimulant & hallucinogenic properties
Amphetamine intoxication causes symptoms similar to those of ______.
cocaine
What is the differential diagnosis of amphetamine intoxication?
- Cocaine or PCP intoxication
- Chronic use in high doses may cause a psychotic state similar to schizophrenia
What is the diagnostic evaluation for amphetamine intoxication?
- UDA (positive for 1-2 days)
- Negative routine drug screen doesn’t rule it out
- Most assays not of adequate sensitivity
- Negative drug screen can NEVER completely rule out substance abuse or dependence
Treatmentof amphetamine intoxication/withdrawal of amphetamines is similar to ____.
cocaine
What is the mechanism of PCP?
- “angel dust”
- Hallucinogen that antagonizes N-methyl-D-aspartate (NMDA) glutamate receptors & activate dopaminergic neurons
- Ketamine similar to PCP (anesthetic agents)
__________ is pathognomonic for PCP intoxication.
More than with other drugs, intoxication w/ PCP results in _______.
Rotary nystagmus
violence
How does PCP intoxication present?
Overdose?
- Intoxication
- Recklessness
- Impulsiveness
- Impaired judgment
- Assaultiveness
- Rotatory nystagmus
- Ataxia
- HTN
- Tachycardia
- Muscle rigidity
- High tolerance or pain
- Overdose
- Seizures, coma
How is PCP intoxication treated?
- Monitor BP, temp, electrolytes
- Acidify urine w/ ammonium chloride & ascorbic acid
- Benzodiazepines or dopamine antagonists to control agitation & anxiety
- Diazepam for muscle spasms & seizures
- Haloperidol to control severe agitation or psychotic symptoms
What is the differential diagnosis for PCP intoxication?
- Acute psychotic states
- Schizophrenia
What is the diagnostic evaluation for PCP intoxication?
- Urine drug screen (positive for >1 wk)
- Creatine phosphokinase (CPK) & aspartate aminotransferase (AST) are often elevated
How does PCP withdrawal clinically present?
- No withdrawal syndrome
- “Flashbacks” may occur
What types of sedatives/hypnotics are typically abused?
-
Benzodiazepines
- Used to treat anxiety disorders
- Obtained via prescription
- Potentiates GABA by increasing frequency of chloride channel opening
-
Barbiturates
- Used to treat epilepsy; anesthetic
- Potentiates GABA by increasing duration of chloride channel opening
- High doses: act as direct GABA agonists; lower margin of safety compared to BDZs
- Benzos & Barbs are synergistic in their complementary effect on GABA channel opening
- Respiratory depression can be a complication
What is Gamma-hydroxybutyrate (GHB)?
“Grievous Bodily Harm”
- Dose-specific CNS depressant that produces memory loss, respiratory distress, coma
- Commonly used as a date-rape drug
What is the clinical presentation of sedative-hypnotic intoxication?
Symptoms are augmented when combined with ____.
- Drowsiness
- Slurred speech
- Incoordination
- Ataxia
- Mood lability
- Impaired judgment
- Nystagmus
- Respiratory depression
- Coma/death in overdose (esp barbs)
- Symptoms augmented w/ EtOH
- Long-term sedative use causes dependence
What is the differential diagnosis for sedative-hypnotic intoxication?
- Alcohol intoxication
- Generalized cerebral dysfunction (ex: delirium)
What is the diagnostic evaluation for sedative-hypnotic intoxication?
- Urine or serum drug screen (positive for 1 wk)
- Electrolytes
- ECG
How is sedative-hypnotic intoxication treated?
- Maintain airway, breathing, circulation
- Activated charcoal to prevent further GI absorption
- For barbiturates only
- Alkalinize urine w/ sodium bicarbonate to promote renal excretion
- For benzos only
- Flumazenil in overdose
- Supportive care
- Improve respiratory status, control hypotension
What is Flumazenil?
- Very short-acting BDZ antagonist
- Use w/ caution when treating overdose, as it may precipitate seizures
What is the clinical presentation of sedative-hypnotic withdrawal?
- Autonomic hyperactivity (tachycardia, sweating)
- Insomnia
- Anxiety
- Tremor
- Nausea/vomiting
- Delirium
- Hallucinations
- Seizures may occur (can be life-threatening)
In general, withdrawal from drugs that are ________ is life threatening, while withdrawal from ______ & _______ is not.
sedating
stimulants, hallucinogens
How is sedative-hypnotic withdrawal treated?
- Admin of long-acting benzodiazepine (chlorodiazepoxide, diazepam) w/ tapering of the dose
- Tegretol or valproic acid may be used for seizure control
____________ is a common ingredient in cough syrup.
dextromethorphan
Opiates
- Examples
- Mechanism of action
- Endogenous vs. exogenous
- Heroin, codeine, dextromethorphan, morphine, methadone, meperidine (Demerol)
- Stimulate opiate receptors (mu, kappa, delta) which are stimulated by endogenous opiates
- Analgesia, sedation, dependence
- Mediates addictive & rewarding properties through effects on the dopaminergic system
- Endogenous opiates: endorphins, enkephalins
What is the clinical presentation of opiate intoxication?
- Drowsiness
- Nausea/vomiting
- Constipation
- Slurred speech
- Constricted pupils
- Seizures
- Respiratory depression
- Coma/death in overdose
What is serotonin syndrome?
How is it caused?
- Caused by combination of meperidine & monoamine oxidase inhibitors
- Hyperthermia, confusion, hyper/hypo-tension & muscular rigidity
What is the differential diagnosis for opiate intoxication?
- Sedative-hypnotic intoxication
- Severe EtOH intoxication
What is the diagnostic evaluation for opiate intoxication?
- Rapid recovery of consciousness following the admin of IV naloxone (opiate antagonist)
- Urine & blood tests remain positive for 12-36 hrs
How is opiate intoxication treated?
Ensure adequate airway, breathing, circulation
How is opiate overdose treated?
Admin of naloxone or naltrexone (opiate antagonists)
- Will improve respiratory depression
- May cause severe withdrawal in an opiate-dependent patient; ventilatory support may be required
How is opiate dependence treated?
- Oral methadone once daily, tapered over months to years
- Psychotherapy, support groups (Narcotics Anonymous, etc)
_________ is the exception to opioids producing miosis.
Meperidine
“Demerol dilates pupils)
What is the classic triad of opioid overdose?
“Rebels Admire Morphine”
- Respiratory depression
- Altered mental status
- Miosis
What is the clinical presentation for opiate withdrawal?
- Not life threatening
- Dysphoria
- Insominia
- Lacrimation
- Rhinorrhea
- Yawning
- Weakness
- Sweating
- Piloerection
- Nausea/vomiting
- Fever
- Dilated pupils
- Muscle ache
How is opiate withdrawal treated?
- Moderate symptoms
- Clonidine and/or buprenorphine
- Severe symptoms
- Detox w/ methadone tapered over 7 days
What are some examples of hallucinogens?
What effects do they have?
- Psilocybin (mushrooms), mescaline, lysergic acid diethylamide (LSD)
- Pharmacological effects vary
- LSD known to act on serotonergic system
- Tolerance to hallucinogens develops quickly but reverses rapidly after cessation
- Don’t cause physical dependence or withdrawal
What is the clinical presentation and treatment of hallucinogen intoxication?
- Perceptual changes, papillary dilation, tachycardia, tremors, incoordination, sweating, palpitations
- Guidance & reassurance (“talking down” the patient) are usually enough
- Severe cases: antipsychotics or benzos
Describe hallucinogen withdrawal
- No withdrawal syndrome is produced
- Patients may experience “flashbacks” later in life (recurrence of symptoms due to reaborption from lipid stores)
What do methyl pemolines produce?
- 92C-B, U4EUH, Nexus
- Classic psychedelic distortion of senses
- Feeling of harmony, anxiety, paranoia, panic
What can Ketamine produce symptomatically?
“special K”
- Tachycardia, tachypnea w/ hallucinations at higher doses
- Amnesia & numbed confusion
What is the main component of marijuana?
What is the mechanism of action?
How is it used?
- THC (tetrahydrocannabinol)
- Cannabinoid receptors in the brain inhibit adenylate cyclase
- Effects increased when used w/ EtOH
- Marijuana shown to successfully treat nausea in cancer patients & increase appetite in AIDS patients
- No dependence or withdrawal syndrome has been shown
What are the clinical symptoms of marijuana intoxication?
- Euphoria
- Impaired coordination
- Mild tachycardia
- Conjunctival injection
- Dry mouth
- Increased appetite
What is the treatment & diagnostic evaluation for marijuana intoxication?
- Supportive & symptomatic
- Urine drug screen is positive for up to 4 wks in heavy users (released from adipose stores)
What is the clinical presentation & treatment of marijuana withdrawal?
- No withdrawal syndrome
- Mild irritability, insomnia, nausea, decreased appetite in heavy users
- Treatment: supportive & symptomatic
What are some examples of inhalants?
- Solvents, glue, paint thinners, fuels, isobutyl nitreates (“rush”, “locker room”, “bolt”)
- Inhalants generally act as CNS depressants
- User is typically an adolescent male
What is the clinical presentation of inhalent intoxication?
- Impaired judgment, belligerence, impulsivity, perceptual disturbances, lethargy, dizziness, nystagmus, tremor, muscle weakness, hyporeflexia, ataxia, slurred speech, euphoria, stupor, coma
- Overdose may be fatal
- Respiratory depression
- Arrhythmias
- Long-term use may cause permanent damage
- CNS, PNS, liver, kidney, muscle
What is the diagnostic evaluation & treatment for inhalent intoxication?
- Serum drug screen (positive for 4-10 hrs)
- Treatment
- Monitor airway, breathing, circulation
- Symptomatic treatment as needed
- Psychotherapy & counseling for dependent patients
What is the clinical presentation of inhalent withdrawal?
- Withdrawal syndrome does not usually occur
- Symptoms may include
- Irritability
- Nausea/vomiting
- Tachycardia
- Occasional hallucinations
What is the mechanism of caffeine?
- Most commonly used psychoactive substance in the US (coffee, tea)
- Adenosine antagonist
- Increases cAMP
- Stimulates dopaminergic system
How much caffeine is in one cup of coffee? tea?
- One cup of coffee: 100-150 mg
- One cup of tea: 40-60 mg
What is the clinical presentation of caffeine intoxication?
How is it treated?
-
>250 mg caffeine
- Anxiety, insomnia, twitching, rambling speech, flushed face, diuresis, GI disturbance, restlessness
-
>1 g caffeine
- Tinnitus, severe agitation, cardiac arrhythmias
-
>10 g caffeine
- Death secondary to seizures & respiratory failure
- Treatment: supportive & symptomatic
What is the clinical presentation & treatment of caffeine withdrawal?
- Withdrawal symptoms resolve w/i 1 wk
- Headache, nausea/vomiting, drowsiness, anxiety, depression
- Treatment
- Taper consumption of caffeine-containing products
- Use analgesics to treat headaches
- Short course of benzos for anxiety (rare)
What is the mechanism of action of nicotine?
- Derived from the tobacco plant
- Stimulates nicotinic receptors in autonomic ganglia of the sympathetic & parasympathetic nervous systems
- Cigarette smoking poses many health risks
- Nicotine rapidly addictive through effects on dopaminergic systems
Cigarette smoking during pregnancy is associated with…..
low birth weight
persistent pulmonary HTN of newborn
What is the clinical presentation & treatment of nicotine intoxication?
- CNS stimulant
- Restlessness, insomnia, anxiety, increased GI motility
- Improved attention, improved mood, decreased tension
- Treatment: cessation
What is the clinical presentation & treatment of nicotine withdrawal?
- Intense craving, dysphoria, anxiety, increased appetite, irritability, insomnia
- Treatment: smoking cessation with…
- Behavioral counseling
- Nicotine replacement therapy (gum, transdermal patch)
- Zyban: antidepressant that helps reduce cravings
- Clonidine
- Relapse after abstinence is common
