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Psych > Sweatman/Rosenthal - Drug and Substance Abuse > Flashcards

Sweatman/Rosenthal - Drug and Substance Abuse Flashcards

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1
Q

What are some of the primary problem drugs that present in the ED?

A
  • Marijuana
  • Cocaine
  • Street opioids
  • Prescription opioids
  • Methamphetamine
  • Sedatives, sleeping pills, and hallucinogens
  • NOTE: younger pts and males were more likely to use alcohol, tobacco, and other drugs -> their use was also significantly associated with using other substances and severity of other substance use
    1. It is not uncommon for pts seen in the ED to be suffering from intoxication from multiple drug sources
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2
Q

Which commonly abused drugs are dose-dependent depressants of the central respiratory drive?

A
  • Antihistamines
  • BARBITURATES
  • Clonidine and other sympatholytic agents
  • ETHANOL AND ALCOHOLS
  • Gamma-hydroxybutyrate (GHB)
  • OPIOIDS
  • Phenothiazines and antipsychotic drugs
  • SEDATIVE-HYPNOTICS
  • TCA’s
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3
Q

What is the first thing you need to do for a pt coming in with depressed respiration?

A
  • ABC’s

- Ensure CV function and airway potency are maintained

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4
Q

What can you do to help pts coming in with drug intoxication?

A
  • NO pharmacologic antidote can be admin’d for the vast majority of illicit intoxications
  • Medical intervention focuses on SUPPORTIVE TX until pt eliminates intoxicant from circulation
    1. This involves pharmacologically counteracting AE’s occurring primarily with CV, respiratory, renal, and CNS
  • EXCEPTIONS: opiates (Naloxone) and BNZ’s (Flumazenil)
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5
Q

How can pupil diameter help aid in your diagnosis?

A
  • MIOSIS: sympatholytic agents, opioids, nicotine (most common rxn miosis, but occasionally mydriasis w/nicotine)
  • MYDRIASIS: sympathomimetic agents, amphetamines and derivatives, cocaine, LSD (lysergic acid diethylamide)
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6
Q

How can nystagmus help guide your diagnosis?

A
  • HORIZONTAL-GAZE: common w/variety of drugs and toxins, incl. BARBITURATES, ETHANOL, Carbamazepine, Phenytoin, and scorpion envenomation
  • PHENCYCLODINE (PCP) may cause horizontal, vertical, or even rotary nystagmus (has hallucinogenic, analgesic, stimulant effects)
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7
Q

What are some of the effects of alcohol?

A
  • CV and respiratory depressant
  • Relaxes vascular smooth muscle:
    1. Vasodilation
    2. Possible hypothermia
    3. INC gastric bloodflow
  • Relaxes uterine smooth muscle
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8
Q

How might you approach an alcohol intoxicated pt in the ED?

A
  • Monitor vital signs and airway patency
  • Thiamine: protects against Wernicke-Korsakoff
  • Dextrose: compensate for hypoglycemia
  • Correct electrolyte issues
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9
Q

How might a pt withdrawing from alcohol present in the ED? How would you approach this pt’s mgmt?

A
  • PRESENTATION: insomnia, tremor, anxiety, rarely seizures and delirium tremens (DT: tremors, agitation, hallucinations, stupor)
    1. N/V, diarrhea, arrhythmias
  • TX: BNZ sedative -> long-acting Diazepam, or where there are concerns about impaired hepatic function, Lorazepam preferred bc only processed by glucuronidation (phase II) and therefore less susceptible to prolongation in half-life
    1. Thiamine
    2. Correct electrolyte issues
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10
Q

What are the potential pharmacokinetic and pharmacodynamic drug interactions of alcohol?

A
  • KINETIC: INC teratogenicity through metabolism changes
    1. INC absorption of either component
  • DYNAMIC: additive CNS depressive actions with drugs
    1. INC toxicity of acetaminophen
    2. INC risk of bleeding with NSAID’s and anticoagulants
    3. INC risk of hypoglycemia in diabetics on meds
    4. Disulfiram-like effects (INC acetaldehyde in someone who consumes alcohol while taking these): Sulfonylureas, Cefotetan (Cephalosporin), Ketoconazole, Procarbazine (anti-cancer)
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11
Q

How might intoxication with nicotine occur?

A
  • Usually via abuse of multiple nicotine patches

- More recently, abuse of smokeless cigarettes, esp. amongst juvenile population

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12
Q

What are the symptoms of acute intoxication with nicotine?

A
  • Abdominal cramps
  • Agitation, restlessness, excitement
  • Muscular twitching
  • Breathing - rapid, or stops
  • Burning sensation in mouth
  • Coma, confusion, convulsions
  • Depression, difficulty breathing
  • Drooling (INC salivation)
  • Fainting, headache
  • Heartbeat - pounding and rapid, then slow HR
  • High BP, which then drops
  • Vomiting, weakness
  • NOTE: nicotine stimulates nicotinic receptors on autonomic ganglia and in CNS, leading to myriad of SYM and PARA effects
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13
Q

What is the treatment for significant nicotine intoxication?

A
  • Drugs to control symptoms, incl. agitation, rapid HR, seizures, and nausea
  • Gastric lavage
  • Activated charcoal
  • MECAMYLAMINE: specific antagonist of nicotine actions (ganglionic blocker that can be used to reverse ganglionic stimulation), but available ONLY in tablets, a form not suitable for pt who is vomiting, convulsing, or hypotensive
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14
Q

What are some commonly abused street and prescription narcotics?

A
  • Heroin
  • Opium
  • PRESCRIPTION:
    1. Hydrocodone
    2. Oxycodone
    3. Fentanyl
    4. Methadone, Codeine
  • NOTE: abuse is rampant and on the INC, most esp. in the eastern US
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15
Q

What drugs might serve as gateway drugs for heroine use?

A
  • Prescription opioids like Oxycontin and Vicodin
  • Can have effects similar to heroin when taken in doses or in ways other than prescribed
  • Nearly half of people who inject heroin surveyed in 3 recent studies reported abusing prescription opioids before taking up heroin bc it is cheaper/easier to get
  • Many also reported crushing prescription opioids to snort or inject the powder
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16
Q

What is the role of processing in the manufacturing of heroin?

A
  • INC the potency
  • Complex process beginning with harvesting sap from poppy seed, through simple alkaline precipitation, to more sophisticated organic extraction procedures
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17
Q

How can heroine and opium be taken?

A
  • HEROIN: most often IV, but also sniffing, snorting, or smoking to avoid shared needles -> misconception that snorting or smoking is less addictive
  • OPIUM: typically a black or brown block of tar-like powder, and can be smoked, injected VI, or taken as a pill
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18
Q

What are the effects of heroin upon injection?

A
  • Rush, then “on the nod”
  • Surge of euphoria with dry out, warm flushing of skin, heaviness of extremities, and clouded mental function (this is the effect lost when users take drug by means other than injection)
  • Followed by alternately wakeful and drowsy state
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19
Q

What are the commonly abused prescription narcotics? How are they typically taken?

A
  • OXYCODONE: oral liquid, tablet or extended release tablet -> crushed into fine powder and snorted, chewed, or crushed and dissolved in water for injection (may mix with alcohol to achieve even greater high)
  • HYDROCODONE: capsule, ER tablet
  • FENTANYL: IV solution, various tablets, patch
  • METHADONE: IV solution, tablet, dispersible tablet
  • CODEINE: oral liquid, tablet (many co-formulated products, incl. ASA, acetaminophen, chlorpheniramine, butalbital)
  • Most commonly injected in a solution of tablet drug, negating any time-release characteristics of original product
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20
Q

How can co-formulation with Naloxone prevent opioid abuse?

A
  • Some products contain Naloxone as anti-abuse component
  • If take correctly (orally), Naloxone not absorbed from GI tract, but opioid agonist is
  • If crushed and injected, Naloxone will antagonize euphoric effects of opiate agonist
  • REMEMBER: Naloxone is SHORT-ACTING (case in class where you do not want to let pt go after giving Naloxone to relieve profound respiratory depression)
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21
Q

How do the opiates vary in their potency and duration of action? Why is this important?

A
  • Codeine (metabolized to active form, morphine): 60 dose, 2-4hr 1/2-life, 4-6hr durability of analgesia
  • FENTANYL: 0.2 dose, 1-5hr 1/2-life, 0.5-2hr durability
  • Heroin: 4 dose, rapidly hydrolyzed to 6-acetylmorphine and morphine, 3-4hr durability
  • HYDROCODONE: 5 dose, 3-4hr 1/2 life, 4-8hr durability
  • Morphine: 10 dose, 2-4hr 1/2 life, 3-6 hr durability
  • Oxycodone: 4.5 dose, 2-5hr 1/2 life, 4-6hr durability
  • NOTE: important implications in regards to ONSET of opiate WITHDRAWAL, and rate of recovery from toxicity
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22
Q

What are the typical symptoms of opiate toxicity? How is it dx’d?

A
  • Shallow, slow respirations, pupillary miosis, bradycardia, hypothermia, stupor or coma
    1. Mydriasis when significant brain anoxia supervenes
    2. Death from respiratory and CV collapse -> toxic dose varies widely, depending on agent, route of admin, and pre-existing pt tolerance
  • Seizures usually associated with mixed intoxication, e.g., with Meperidine (opioid with anticholinergic effects) or Tramadol (opioid that also INH reuptake of 5-HT and NE)
  • QT prolongation with METHADONE
  • DX generally relies on clinical signs and symptoms, NOT blood/urine toxicology
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23
Q

How is opiate toxicity managed in the ED? What is the goal?

A
  • Support of CV FUNCTIONS: cardiac monitoring to detect QT prolongation
  • NALOXONE given at 0.4-2mg IV or IM: expect response w/in 1-2min -> higher dose needed for Buprenorphine because it is a STRONGER BINDER
  • GOAL to reverse respiratory depression, NOT precipitate acute withdrawal
  • May need to repeat Naloxone dose owing to relatively short 1/2-life compared to opiate agonists
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24
Q

What do you do if you are treating opiate toxicity in the ED, and Naloxone response is inadequate?

A
  • Failure to completely reverse respiratory depression with Naloxone usually signifies presence of other intoxicants, most commonly BNZ’s
    1. Admin Flumazenil at 0.2mg/min (max 3g/h)
    2. May precipitate seizures and INC intracranial pressure
    3. May need to supplement owing to relatively short 1/2-life
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25
Q

Are BNZ’s or barbiturates safer? Why?

A
  • BNZ’s, because they produce only an allosteric effect, for which a max magnitude cannot be surpassed -> BUT, they can be fatal if consumed with large quantities of alcohol
  • Barbiturates, on the other hand, can function as GABA itself in high doses
  • NOTE: alcohols, BNZ’s, and barbiturates are all classified as sedative-hypnotics, BUT only BNZ’s are reversed by Flumazenil
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26
Q

What BNZ’s are typically abused?

A
  • Ultra short-acting: Midazolam, Triazolam
  • Short-acting: Alprazolam, Lorazepam
  • Long-acting: Chlordiazepoxide, Diazepam
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27
Q

What are the major risks with sedative-hypnotic intoxication?

A
  • Aspiration
  • Respiratory depression or failure
  • Hypoxia
  • Hypotension
  • Cardiac arrhythmias
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28
Q

How would you manage intoxication with a long-acting barbiturate?

A
  • Alkaline diuresis

- NOTE: can do this with combined lactated ringer solution and sodium bicarb IV

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29
Q

How do you tx BNZ intoxication? Considerations?

A
  • FLUMAZENIL: use is controversial, unless only BNZ ingestion
  • Slow admin (titrated) because can precipitate agitation and withdrawal
    1. Serious RISK OF SEIZURES
  • CONTRA with INC ICP or closed head injury, history of epilepsy, or ingested TCA’s
30
Q

What are the symptoms of marijuana intoxication?

A
  • Cognitive dysfunction, changes in perception, and reaction time impairment
  • Panic, paranoia, or acute psychosis are uncommon, except in NEW USERS or with pre-existing psych disease
  • Conjunctival reddening (injection) may be observed: role for cannabinoid receptors in loco-regional arterial dilation
  • Rarely life-threatening
  • NOTE: marijuana 10% THC, hashish paste 40%
31
Q

What are the symptoms of TCA OD?

A
  • Mental status changes
  • Hypotension
  • Arrhythmias
  • Anticholinergic effects
32
Q

What do the cannabinoids do at a molecular level? Effects?

A
  • Cannabinoid component of marijuana binds to presynaptic CB1 cannabinoid receptors and prevents entry of Ca ions and vesicular binding, preventing release of glutamate or GABA
  • Leads to disINH of dopaminergic neurons in ventral tegmental area (VTA), and feeling of EUPHORIA
  • EFFECTS: euphoria and relaxation, well-being, altered perception of passage of time
    1. Dose-dependent perceptual changes, drowsiness, diminished coordination, and memory impairment may also occur
33
Q

What is the role of endogenous cannabinoids?

A
  • Endocannabinoids (anandamide, AEA; 2-arachidonoylglyceral, 2-AG) responsible for maintaining homeostasis of variety of physiological processes, incl. sleep, appetite, analgesia, and spasticity by binding CB1 or CB2 receptors
  • Regulate release of various NT’s like glutamate and GABA
  • Called retrograde messengers
34
Q

How can marijuana be “modified?” Consequences? Tx?

A
  • Often cut with hallucinogens and other drugs, leading to:
    1. Sudden high BP and headache
    2. Chest pain and arrhythmia
    3. Extreme hyperactivity and physical violence
    4. Heart attack - seizures - stroke - cardiac arrest
  • Prevent injury and reassure those with panic reactions
  • Diazepam or Lorazepam
  • Beta-blockers to control sinus tachycardia
35
Q

Which drugs carry the risk of rhabdomyolysis? Tx?

A
  • Intoxicants known to cause excessive muscular hyperactivity, rigidity, or seizures:
    1. Amphetamines and derivatives
    2. Clozapine and Olanzapine
    3. Cocaine
    4. Lithium
    5. MAOI’s
    6. PCP (phencyclidine)
  • Vigorous hydration to avoid renal damage bc release of myoglobin from damaged mm can lead to renal failure
  • Alkalinize urine with sodium bicarbonate: acidic urine may promote deposition of myoglobin in tubules
36
Q

How are the mechanisms of cocaine and amphetamines the same/different?

A
  • COCAINE: INH presynaptic DAT, DEC DA clearance from synaptic cleft, and causing INC in EC DA concentration
  • AMPHETAMINE: substrate of DAT that competitively INH DA transport; once in cell, amphetamine interferes w/vesicular monoamine transporter (VMAT) in the presynaptic terminal bc it is a weak base and reverses the proton pump, impeding filling of synaptic vesicles -> vesicles depleted and cytoplasmic DA INC, leading to reversal of DAT direction, and strongly INC nonvascular release of CA, further INC EC DA concentrations
37
Q

What classic set of symptoms do cocaine/amphetamines produce? Tx?

A
  • Classic sympathomimetic sings: dose-dependent INC HR and BP, INC arousal, vigilance, alertness; sense of self-confidence and well-being (euphoria in high doses), dilated pupils
  • Diazepam or Lorazepam for seizures and anxiety
  • Nitroglycerin (vasodilator) or Phentolamine (alpha-1 blocker) for HTN: do NOT give pure beta-blocker -> unopposed alpha-effects (use Labetalol: alpha-1 and beta-1/2 antagonist)
  • Adenosine (SVTach) or Lidocaine (ventricular arrhythmia)
  • Pay close attention to pt’s temp, applying external cooling measures when necessary
38
Q

What does amphetamine/cocaine withdrawal look like?

A
  • Generally mild, and usually requires no intervention

- Dysphoria, depression, sleepiness, fatigue, craving, bradycardia

39
Q

How accurate is the rapid amphetamine test?

A
  • Apparently, not very

- Many drugs give false (+) on rapid amphetamine test

40
Q

What are the club drugs? Presenting symptoms? Clinical mgmt?

A
  • Amphetamine derivatives and related drugs: meth, MDMA, ephedrine, methcathinone and derivatives (bath salts)
  • Presenting symptoms similar to cocaine/amphetamines:
    1. Anxiety, tremulousness, tachycardia, HTN, diaphoresis, dilated pupils, agitation, muscular hyperactivity, psychosis
    2. Muscle hyperactivity may lead to metabolic acidosis and rhabdomyolysis
    3. Hyponatremia has been reported after MDMA use; mech unknown, but may involve excessive H2O intake, SIADH, or both
  • Clinical MGMT as for cocaine and amphetamines (BNZ, vasodilators, anti-arrhythmics)
  • NOTE: amphetamine-like rxns have also been reported after use of synthetic cannabinoids
41
Q

How do PCP and Ketamine work? Effects?

A
  • PCP (angel dust) and Ketamine bind different receptors in the CNS w/varying degrees of affinity (lack discrimination)
  • INC concentration necessary to achieve various clinical effects
  • At lower doses, glutamate signaling INH at NMDA (initial action): analgesia, anesthesia, cognitive deficits, psychosis
  • CV effects via INC SYM activity following INH of MAO degradation of endogenous catecholamines: HTN, tachycardia, bronchodilation, agitation
42
Q

What will you see with mild and severe PCP/Ketamine intoxication?

A
  • MILD intoxication: lethargy, euphoria, hallucinations, and occasionally bizarre or violent behavior; hyper salivation and lacrimation may occur; abrupt swings from quiet catatonia to loud or agitated behavior
  • SEVERE PCP intoxication: dx suggested by rapidly fluctuating behavior, VERTICAL NYSTAGMUS, and sympathomimetic sings; pupils sometimes paradoxically small
  • NOTE: these psychedelic agents are often part of mixed intoxications, and while their clinical effects are similar, Ketamine causes less agitation and violent behavior
43
Q

What are the clinical features, complications, and tx for LSD intoxication?

A
  • FEATURES: mydriasis, tachycardia, anxiety, mm tension
  • CXS: coma, hyperthermia, coagulopathy, persistent psychosis
  • TX: supportive care and careful observation until pt recovers naturally, BNZ may be applied to tx seizure or anxiety, Haloperidol for psychosis
44
Q

What are the clinical features, complications, and tx for Psilocybin (magic mushroom) intoxication?

A
  • FEATURES: mydriasis, tachycardia, anxiety, N/V, mm tension
  • CXS: seizures, hyperthermia (RARE)
  • TX: supportive, BNZ
45
Q

What are the clinical features, complications, and tx for Mescaline (peyote cactus) intoxication?

A
  • FEATURES: mydriasis, abdominal pain, N/V, dizziness, nystagmus, ataxia
  • CXS: RARE
  • TX: supportive, BNZ
46
Q

How do the inhaled hydrocarbons work? Presentation?

A
  • Intoxication via displacement of O2 from atmosphere
  • Sensitization of myocardium to catecholamines can cause cardiac DYSRHYTHMIAS
  • Presentation can be highly variable:
    1. Confusion, ataxia, lethargy, headache
    2. Arrhythmias, syncope, coma, respiratory arrest w/high exposure
    3. Many agents may also cause hepatic and renal injury
    4. Skin or eye contact causes local irritation, burns, or corneal injury
    5. Chronic skin exposure often causes defatting dermatitis, esp. of peri-oral region (contact irritation from bag being used to inhale)
    6. Hippuric acid commonly elevated with exposure to toluene (i.e., sniffing glue)
    7. Order an MRI if neuro deficits (bc can cause demyelination) -> may see multifocal white matter hypo-densities
47
Q

How should you manage a pt presenting with inhaled hydrocarbon intoxication?

A
  • Largely supportive, ensuring adequate O2 supply
  • ABC’s
  • Monitor arterial blood gases or oximetry, chest radiographs, and ECG, and admit symptomatic pts to intensive care setting
  • Use epinephrine and other beta-adrenergic meds with caution in pts with significant hydrocarbon intoxication -> arrhythmias may be induced
48
Q

What hormone is responsible for hallucinogenic effects of drugs?

A
  • Serotonin
49
Q

What drug is used in heroin detoxification programs?

A
  • Buprenorphine
50
Q

Girl who had never used recreational drugs joined in smoking multiple marijuana cigarettes at a party. What symptom might she experience just after smoking?

A
  • Increased HR and bloodshot eyes (red conjunctivae)

- Even experienced users will experience this

51
Q

Pt. comes in with muscle aches, nausea, and anxiety. He was a heroin addict, and smoked PCP occasionally for the past 6 months. He was sweating, shaking, kept yawning, had high BP, tachycardia, hyperventilation, and hypothermia. What drug will provide the most immediate relief?

A
  • Mu receptor agonist
52
Q

Girl experiences euphoria, uncontrollable laughter, depersonalization, and sharpened vision after smoking something with her friends. She had injection of the conjunctivae, but no change in pupil diameter. What was the drug?

A
  • Cannabis
53
Q

Man suffering from delirium tremens. What physical signs and symptoms might he show?

A
  • Nightmares, agitation, global confusion, disorientation
  • Visual and auditory hallucinations, tactile hallucinations
  • Fever, high BP, heavy sweating, and other signs of autonomic hyperactivity
54
Q

If person is drinking, and they see a snowstorm in their vision, what did they drink?

A
  • Methanol
55
Q

Man found dead in his home by his roommate. He had a blood level of morphine that was substantially lower than the minimum lethal concentration of the drug. What was the other drug most likely involved in his death?

A
  • Alcohol: additive CNS depression
  • BNZ or barbiturate could also do this via the same mechanism
  • REMEMBER: morphine is an opiate
56
Q

15-y/o with “zombied out” symptoms after drinking alcohol. What might be causing these symptoms? What should you do?

A
  • BNZ
  • Give Flumazenil: be careful when administering, so you don’t cause seizures
  • Call his parents
57
Q

18-y/o does drugs with his friends, then runs toward balcony in the library because he says he is being chased by snakes. His friend saves him. What was he on? What can you do?

A
  • Peyote: N/V more common with peyote and mushrooms
  • Magic mushrooms
  • LSD
  • Supportive tx, and minimize sensory stimuli (provide some level of sedation)
  • NOTE: be careful about administering activated charcoal because it can be aspirated and kill the pt
58
Q

How is sleep affected in major depression?

A
  • Shortened REM latency
  • Early AM awakening
  • Fitful sleep
  • Hypersomnia also possible in mood disorders
59
Q

How is sleep affected in PTSD

A
  • Nightmares
60
Q

How is sleep affected by bipolar disorder?

A
  • Manic: drastically reduced need for sleep and highly irritable -> manic episode can even be precipitated by sleep deprivation (jet travel)
61
Q

How do sleep apnea manifest itself in the daytime?

A
  • Often manifests as daytime lethargy

- Can be mistaken for depression or lack of motivation

62
Q

How can schizophrenia affect sleep?

A
  • Pt is often up all night in agitated, aimless activity drive by delusional thinking
  • NOTE: restoring good sleep is a high priority in all psych pts
63
Q

How do pts with eating disorders eventually present in the clinic?

A
  • Typically, pts do not seek psychiatric help, but their medical symptoms bring them to the attention of dentists, pediatricians, and internists
  • The consequences can be life-threatening; 10% of severe cases of AN die
64
Q

How can sexual dysfunction impact medication effectiveness?

A
  • This is a side effect that can compromise pharm mgmt by causing NONCOMPLIANCE
65
Q

What are the paraphilia disorders as a group?

A
  • Intense and persistent sexual interest other than sexual interest in genital stimulation or preparatory fondling with phenotypically normal, physically mature, consenting partners
  • There is an addictive quality to these
66
Q

What are the two categories of “intense and persistent erotic interest?”

A
  • Erotic ACTIVITIES: spanking, bondage, whipping, strangulation, autoerotic asphyxiation, frottage (rubbing up against people)
  • Erotic TARGETS: children, animals, corpses, amputees, inanimate objects
67
Q

What are hypoactive desire and sexual aversion disorders?

A
  • 20% of adults have hypoactive desire
  • Reduced desire for sexual contact, or total aversion to sexual activity
  • These are sexual DESIRE disorders
68
Q

What are female sexual arousal and male erectile disorder?

A
  • These are sexual AROUSAL disorders
  • 35% of married females; 2-4% of M under 35, and 75% of those >80
  • Inability to maintain sexual arousal sufficient to initiate or complete sexual acts
69
Q

What are female orgasmic, male orgasmic, and premature ejaculation disorders?

A
  • ORGASMIC disorders
  • 5% of adult F; 4% and 30% of M, respectively
  • Excessive orgasmic delay, absence of orgasmic response, premature orgasm
70
Q

What are the sexual pain disorders?

A
  • Dyspareunia and vaginismus: pain in sexual organs during sexual activity that interferes with or prevents sexual activity
71
Q

What are the 7 paraphilias?

A
  • Exhibitionism
  • Fetishism
  • Frotteurism
  • Pedophilia
  • Masochism/sadism
  • Transvestite fetishism
  • Voyeurism

Psych (11 decks)

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