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Behavioral Health > Substance Related Disorders and Treatment of Substance Abuse > Flashcards

Substance Related Disorders and Treatment of Substance Abuse Flashcards

1
Q

Define the following:

  1. Substance use?
  2. Abuse?
  3. Physical dependance?
  4. Psychological dependence?
  5. Addiction?
A
  1. Substance use: sporadic consumption of alcohol/drugs w/ no adverse consequences
  2. Abuse: frequency of alcohol/drug use may vary, there are adverse consequences experienced by the user
  3. Physical dependence: state of adaptation that is manifested by a drug class-specific withdrawal syndrome
  4. Psychological dependence: a subjective need for a specific psychoactive substance, either for its positive effect or to avoid negative effects of its abstinence
  5. Addiction: primary, chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations
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2
Q

Addiction is characterized by what kind of behaviors?

4

A

Characterized by behaviors that include

  1. impaired control over drug use,
  2. compulsive use,
  3. continued use despite harm and craving
  4. Continuing use despite adverse consequences in the abusers life
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3
Q

Special Populations at risk for addiction

6

A
  1. Adolescents
  2. Anyone with a psychiatric comorbidity
  3. Those who smoke or who abuse alcohol (polysubstance abuse is the norm)
  4. Elderly
  5. Health care workers
  6. Pregnant women may fear admitting to drug use
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4
Q

Recognizing the Drug Abuser: For each substance what do you need to ask?
5

A
  1. Quantity
  2. Amount of money spent daily/weekly/monthly
  3. Frequency of use and time of last use
  4. Route of administration
  5. If history of use is disclosed ask about prior detox or addiction treatment and abstinence periods
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5
Q

Physical Changes
in addicts
7

A
  1. Drug use is the leading cause of impotence in the U.S.
  2. Weight loss and sleep disturbance
  3. Evidence of localized or systemic infections
  4. On abdominal exam may palpate enlarged or shrunken liver
  5. Respiratory or nasal problems
  6. Needle marks: “tracks”
  7. STIs in patients who are trading sex for drugs
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6
Q

What indicates a likely diagnosis of alcohol dependence on the CAGE questionaire?

A

Two or more positive answers

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7
Q

CAGE Questionnaire

A
  1. Have you ever felt the need to Cut down on your drinking?
  2. Have you ever felt Annoyed by criticism of your drinking?
  3. Have you ever had Guilty feelings about your drinking?
  4. Do you ever take a morning Eye-opener? (a drink first thing in the morning to steady your nerves or get rid of a hangover)
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8
Q
  1. Risky or hazardous drinking: men less than 65YO?

2. women less than 65YO?

A
  1. > 14 drinks a week

2. > 7 drinks a week

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9
Q

Alcohol abuse: associated w/ one or more of the following, occurring in a 12-month period.
4

A
  1. Failure to fulfill work, school or social obligations
  2. Recurrent substance use in physically hazardous situations
  3. Recurrent legal problems related to substance use
  4. Continued use despite alcohol-related social or interpersonal problems
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10
Q 
Alcohol dependence (“alcoholism”) is defined as?
7
A

a maladaptive patterns of use associated with 3 or more of the following, occurring at any time in the same 12-month period:

  1. Tolerance
  2. Withdrawal
  3. Substance taken in larger quantity than intended
  4. Persistent desire to cut down or control use
  5. Time is spent obtaining, using, or recovering from the substance
  6. Social, occupational or recreational tasks are sacrificed
  7. Use continues despite physical and psychosocial problems
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11
Q

Alcohol abuse associated with greater risk of:

5

A
  1. HTN, cardiomyopathy
  2. Hepatitis, cirrhosis (½ the cases in U.S. Secondary to alcohol), pancreatitis
  3. TB, Pneumonia
  4. Psych problems: anxiety, depression and eating disorders
  5. Cancers of the stomach, mouth, larynx, breast and esophagus
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12
Q

Other screening tools for alcohol abuse?

3

A
  1. Single item screening
  2. Alcohol Use Disorders Identification Test (AUDIT)
  3. CAGE questions (not as reliable for Caucasian women)
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13
Q
  1. Intervention most likely to succeed in patients who are in what categories?
  2. Who needs to be screened to achieve benefit?
  3. Screening essential patients such as?
    4
A
  1. “risky drinking” or “hazardous drinking”
  2. A large number of patients (everyone)
    • w/ + family hx,
    • who smoke,
    • have frequent ER visits, or
    • who are on meds that interact w/ alcohol
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14
Q

For Adolescents and College Students: Questions to ask to assess for high risk alcoholic behavior?

CRAFFT

A
  1. Have you ever ridden in a Car driven by someone (including yourself) who was “high” or had been using alcohol or drugs”
  2. Do you ever use alcohol or drugs to Relax, feel better about yourself, or fit in?
  3. Do you ever use alcohol or drugs while you are Alone?
  4. Do you ever Forget things you did while using alcohol or drugs?
  5. Do you family or Friends ever tell you that you should cut down on your drinking or drug use?
  6. Have you ever gotten into Trouble while you were using alcohol or drugs?
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15
Q

CRAFFT: What indicates a problem of abuse or dependance?

A

Two or more positive answers indicate problem use, abuse or dependence

Performs better then the CAGE for this age group

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16
Q

Define the following for men and women:

  1. Moderate drinking?
  2. Heavy drinking?
  3. Binge drinking?
A
  1. Moderate drinking:
    Men: 2 drinks or less a day
    Women: 1 drink or less a day
  2. Heavy drinking:
    Men: > 14 drinks per week, or 4 drinks per occasion
    Women: > 7 drinks per week or 3 drinks per occasion
  3. Binge drinking:
    Men: 5 or more drinks in a row
    Women: 4 or more drinks in a row
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17
Q

Ethyl alcohol or ethanol

  1. Absorption: 10% consumed alcohol absorbed in the what?
  2. remainder from the where?
A
  1. stomach

2. small intestines

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18
Q

When concentration of alcohol in stomach becomes too high—what results in slowed absorption? 2

Pylorospasm results in?

A
  1. mucus secretion
  2. pyloric valve closure

Emesis

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19
Q

Metabolism:

  1. 90% metabolized in ____through oxidation
  2. Metabolized by two enzymes what are they?
A
  1. liver
    • Alcohol dehydrogenase (ADH) catalyzes conversion of alcohol into acetaldehyde, which is toxic

-Aldehyde dehydrogenase(ALDH) catalyzes conversion of acetaldehyde into acetate

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20
Q

Effects of Alcohol on the Brain
1. CNS depression much like what?

  1. Relatively mild levels: How is behavior changed?
  2. Increasing levels: how is behavior changed?
  3. Yet increasing levels— Behavior?
    - What can this result in??
A
  1. benzodiazepines
  2. thought, judgment and restraint are loosened
  3. voluntary muscle dysfunction and entire motor area of the brain depressed
  4. confusion, stupor, coma and finally primitive centers that control breathing and heart rate are affected and can result in

–death either secondary to direct respiratory depression or aspiration of vomitus

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21
Q

Effects of Alcohol on the Liver
1. Metabolism of alcohol leads to _______attack on the liver (it is unknown if damage is caused by acetaldehyde or other metabolites)

  1. Even after all alcohol intake has stopped and all alcohol has been metabolized, the processes that damage liver cells may continue for how long?
  2. Clinical and chemical effects often become what before you get better?
A
  1. chemical
  2. weeks to months
  3. worse before disease resolves
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22
Q

Three patterns of hepatocellular injury:

A
  1. Fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis (rate is 10-15% of all alcoholics)
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23
Q

Wenicke-Korsakoff Syndrome

is what?

A

Occurs in persons who have been drinking heavily for many years—rare to see in persons younger then 35YO: Caused by thiamine deficiency due to poor nutrition/malabsorption

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24
Q
  1. Wernicke’s encephalopathy: acute symptoms are? 4
  2. THese are completely reversible with what?
  3. Why before the IV glucose?
A
  1. Characterized by
    - gait ataxia,
    - vestibular dysfunction,
    - confusion and
    - ocular abnormalities
  2. treated w/ high dose thiamine:
  3. MIght cause encephalopathy
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25
Q

Alcoholic hepetitis Labs? 2

A

Tranaminines will be in the hundreds not thousands and Alk phos will be mildly elevated

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26
Q
  1. Korsakoff’s Syndrome: chronic condition characterized by what?
  2. Treatment?
A
  1. impaired recent memory and anterograde amnesia

2. condition where only 20% of patients recover—can be treated w/ po thiamine

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27
Q

Treating Alcohol Dependence
1. Short Term Goals? 3

  1. Long term goals? 2
A
  1. Short term goals:
    - ID and initiate treatment fro patients at risk for withdrawal (determine stage)
    - Promote attendance at AA or other support groups
    - EARLY INTERVENTION**
  2. Long term goals:
    - Extended management over time
    - Determining efficacy of treatment
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28
Q

Alcohol withdrawal—Mild Symptoms

7

A
  1. Insomnia
  2. Tremulousness
  3. Mild anxiety
  4. GI upset/anorexia
  5. Headache
  6. Diaphoresis
  7. Palpitations
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29
Q

Withdrawal Symptoms
1. Mild symptoms begin within ___hrs. of cessation of drinking

  1. They resolve within ____ hrs.

Withdrawal seizures:
3. Occur within ___ hrs. after last drink
4. What kind of seizures?
Occur in 3% of chronic alcoholics

  1. Treat w/ what?
A
  1. 6
  2. 24-48
  3. 48
  4. Tonic-clonic
  5. benzodiazepines
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30
Q

Alcoholic Hallucinosis
1. Develops within ____ hrs. of last drink
2. Resolves with _____ hrs.
NOT delirium tremens

  1. Usually what kind of hallucination?
A
  1. 12-24
  2. 24-48
  3. visual; but can be auditory or tactile
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31
Q

Agents that Should NOT be used Routinely
-With alcohol
6

A
  1. Ehthanol
  2. Antipsychotics
  3. Anticonvulsants
  4. Central acting alpha-2 agonists
  5. Beta-blockers
  6. Baclofen
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32
Q

What are the symtpoms and signs of Delirium Tremens?

7

A
  1. Hallucinations
  2. Disorientation
  3. Tachycardia
  4. Hypertension
  5. Low grade fever
  6. Agitation
  7. Diaphoresis
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33
Q

Delirium Tremens

  1. Begins when after last drink?
  2. Can last how long?
  3. Risk factors? 4
A
  1. Begin 48-96 hrs. after last drink
  2. Can last 1-5 days
  3. Risk factors:
    - History of sustained drinking
    - History of previous DTs
    - Age > 30
    - Presence of concurrent illness
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34
Q
  1. Alcohol Withdrawal Diagnosis?

2. Differential DX? 6

A
  1. Dx of exclusion
  2. Differential:
    - Infection
    - Trauma/Head
    - Metabolic derangements
    - Drug overdose
    - Hepatic failure
    - GI bleed
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35
Q

General Measures for alcohol withdrawl

4

A
  1. Place patient in quiet, protective environment
  2. May need mechanical restraint
  3. Most patients tend to be dehydrated w/ hypokalemia—replace with IV fluids and KCL
  4. Thiamine 100mg IV or IM or BEFORE glucose—prevent Wernecke’s encephalopathy
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36
Q

Treamtent for Alcohol Withdrawl:

  1. Minimal? 1
  2. Mild? 2
  3. Moderate to severe? 3
A

Minimal: (no disorientation or hallucinations)
1. Thiamin and supportive care

Mild:

  1. Thiamin & supportive care
  2. Medications to reduce symptoms & monitoring

Moderate and Severe:

  1. Thiamin & Supportive care
  2. Hourly monitoring, especially respiratory rate
  3. Medication—benzodiazepines
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37
Q

Benzodiazepine use:

  1. Which two drugs?
  2. Can give how? 2
A
    • Diazepam (Valium),
    • Chlordiazepoxide (Librium) and lorazepam are used
  2. Can give orally or IV
    Scheduled vs. Symptom targeted**
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38
Q
  1. If the patient has refractory DT how should we treat? 2
  2. What can we not use??
  3. For seizures if status epilepticus?
    - do not use what?
A

Refractory DTs—
1. Add phenobarbitol or propofol

  1. Antipsychotics lower seizure threshold—DO NOT USE

Seizures:

  1. If status epilepticus use phenobarbitol
    - DO NOT USE carbemazepine
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39
Q

Outpatient Therapy of Alcoholism

  1. What class of drug?
  2. Used for what?
  3. SE? 5
  4. Contraindicated?
A
  1. Synthetic derivative of Homotaurine—analog of GABA
    Mechanism of action not clearly understood
  2. Used for relapse prevention with counseling!
  3. SE:
    - diarrhea,
    - low pulse,
    - high or low BP,
    - headaches,
    - impotence
  4. Contraindication: kidney disease
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40
Q

Disulfiram (Antabuse):

  1. MOA?
  2. WHat does this lead to? 6
  3. SE? 2
  4. Need to monitor what? 2
  5. Increases drug levels of what? 3
A
  1. Inhibits the activity of acetaldehyde dehydrenase (ALDH) which results in 5-10 fold increase in acetaldehyde levels after alcohol ingestion
  2. Leads to
    - flushing, dyspnea,
    - N & V,
    - HA ,
    - blurred vision,
    - vertigo, and
    - anxiety
  3. SE:
    - Hepatotoxic,
    - can cause depression, psychosis
  4. need to monitor- LFT and depression and suicide
  5. Increases drug levels of
    - phenytoin,
    - isoniazid and
    - anticoagulants
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41
Q
  1. 2nd to cannabis most widely abused drug in the world
    5% of the U.S. population have used it?
  2. Highest prevalence unemployed men in their 20s w/ only a high school education in urban areas
    Use is highly associated with use of other legal and illegal substances?
A
  1. Methamphetamine

2. Cocaine

42
Q

Methamphetamine

  1. MOA? 2
  2. What does this result in?
A
    • Displaces epinephrine, norepinephrine, dopamine & serotonin into the synaptic cleft
    • Also inactivates neurotransmitter reuptake systems
  2. Results in surge of adrenergic stimulation
43
Q

Methamphetamine Intoxication
1. Describe their general appearance? 3

  1. VS changes? 3
  2. Other symptoms? 4
A
  1. General appearance:
    - Malnourished, agitated, disheveled
    - Severe intoxication can exhibit abrupt changes in behavior and become very violent
    - “Meth Mouth”, other stigmata of trauma, diaphoresis
  2. VS:
    - Tachycardic
    - hypertensive
    - hyperthermic
  3. Other:
    - N/V,
    - seizures,
    - delirium,
    - psychosis
44
Q

Meth Intoxication

  1. Sympathomimetic toxidrome is what?
  2. DDx?
    - Toxicologic 3
    - Nontoxicologic 3
A
  1. adrenergic excess
2. 
Other toxicologic conditions:
-Cocaine & PCP 
-Theophylline and aspirin overdoses
-MAOI, serotonin syndrome, anticholinergic poisoning

Nontoxicologic

  • Heat stroke
  • Thyrotoxicosis
  • Pheochromocytoma
45
Q

Meth Intoxication Treatment
3

Biggest risk is cardiovascular collapse. How should we treat for this? 3

A
  1. Sedation for agitation
  2. Protect airway
  3. Control blood pressure and temp
  4. Vasoactive amines
  5. Correct metabolic acidosis
  6. Fluid resuscitation
46
Q

Cocaine

1. MOA? 2

A
  1. Blocks presynaptic reuptake pumps for dopamine, norepinephrine and serotonin
  2. Also blocks voltage-gated membrane sodium ion channels
47
Q

Cocaine Intoxication:

  1. Intended effects? 5
  2. Adverse effects? 5
  3. Physiological effects? 4
A
  1. Intended effects:
    - increased energy,
    - alertness, sociability;
    - elation or euphoria;
    - decreased fatigue, need for sleep and appetite;
    - “total body orgasm”
  2. Adverse effects:
    - anxiety, irritability,
    - panic attacks, paranoia,
    - gradiosity,
    - impairment in judgment,
    - psychotic symptoms
  3. Physiological effects:
    - tachycardia,
    - pupil dilation,
    - diaphoresis,
    - nausea
48
Q

Cocaine Acute Intoxicaiton

  1. CV effects? 3
  2. CNS effects? 5
  3. Lung effects? 2
A
  1. CV:
    - arterial vasoconstriction and
    - enhanced thrombus formation,
    - causes tachycardia and HTN
  2. CNS:
    - agitation,
    - seizures,
    - HA,
    - coma,
    - intracranial hemorrhage

Lungs:
When smoked can cause
-angioedema and
-pharyngeal burns

Passive cocaine exposure: those in close proximity to users of inhalational cocaine can present w/ toxicity

49
Q

Stimulant Intoxication Management

  1. Initial Labs? 4
  2. Specific management? 2
A

Initial labs:

  • Fingerstick glucose
  • Acetaminophen and salicylate levels
  • EKG
  • Pregnancy test in women of childbearing age

Specific management:

  • Toward patient’s condition
  • Toward symptomatic problems
50
Q

Cannibis (Marijuana)

  1. What is the psychoactove componenet?
  2. Plant processed into three drug products. What are they?
A
  1. Psychoactive component:
    delta-9-tetrahydrocannabinol (THC)
  2. Plant processed into three drug products:
    - Dry leaves and flowers (herbal cannabis)
    - Pressed, dry resin or secretion (hashish)
    - Oil (hash oil)
51
Q

Pharmacology of Cannabis?

3

A
  1. THC reaches the brain, crosses the BBB and binds to endogenous cannabinoid receptors (CB1)
  2. THC activates CB1 receptors in the mesolimbic dopamine system,
  3. which is hypothesized to modulate the positive reinforcing and rewarding effects of most drugs of abuse
52
Q

Cannabis Effects
Mood, perception, thought content?
4

A
  1. Usually causes euphoria, decreases anxiety, and tension
  2. Time perception is distorted, time is perceived faster
  3. Increased self consciousness and transient grandiosity can occur
  4. as well as paranoia and even psychosis
53
Q

Cognition, 3

psychomotor function 2

affected by Cannabis how?

A

Decreases

  1. reaction time &
  2. impairs attention,concentration, short term memory, and
  3. risk assessment
  4. Impairs motor coordination and
  5. the ability to do complex tasks (lasts 12-24 hours past initial euphoria)
54
Q

Cannabis Physiologic Signs

6

A
  1. Tachycardia
  2. Increased BP
  3. Increased RR
  4. Conjunctival injection
  5. Dry mouth
  6. Increased appetite
55
Q

Treatment for Marijuana Addiction

4

A
  1. Buspirone (Buspar) has shown to be helpful for treating withdrawal symptoms
  2. Inpatient treatment advised
    - -Changing the setting where the patient is habitually using marijuana
  3. At times oral THC in reducing doses
  4. Treating underlying comorbid psychiatric disease appropriately and carefully
56
Q

Hallucinogens describes substances whose primary effects include what?

A

the alteration of sensory perception, mood & thought pattern

57
Q

“Trip”–effects experienced from acute intoxication

-Describe a “Bad trip”

A

“Bad trip”–acute intoxication w/ dysphoria, fear, agitation or other unwanted effects predominate

58
Q

What is a flashback?

A

Flashback”–recurrence of symptoms associated w/ hallucinogen after the effects of the acute intoxication have worn off, may occur months or years after the last use of the drug

59
Q

Pharmacology of Hallucinogens:
1. Which neurotransmitters are involved? 3

  1. MOA?
  2. May cause what syndrome?
  3. Effects of the drug?
A
  1. Involves the interaction of numerous neurotransmitters
    - Serotonin,
    - dopamine and
    - glutamate
  2. Exact mechanism unknown, but one property common to the drugs is their ability to bind 5-HT2A receptors
  3. This serotonergic activity may cause serotonin syndrome
  4. synesthesia (blending of senses)
60
Q

LSD (lysergic acid diethylamide):
1. What symptoms?
2

A
  • Neuropsychiatric symptoms,

- person remains oriented and aware their experience is drug-induced

61
Q
  1. What is Dextromethorphan (DXM)?
  2. What is it found in?
  3. What is the recreational dose and what can it cause?
  4. what kind of toxicity can occur? 2
A
  1. Codeine analog
  2. OTC in cold and cough preparations
  3. Recreational dose—100-200mg–can produce hallucinations and coma
    • Anticholinergic delirium
    • acetaminophen toxicity have occurred
62
Q

Mescaline

  1. Active ingrediant in what?
  2. What often precedes the onset of psychadelic effects?
A
  1. (active ingredient in peyote cactus)

2. N/V often precede the onset of psychedelic effects

63
Q

Phencyclidine (PCP)

  1. What is it?
  2. Commonly found in what?
A
  1. Dissociative anesthetic similar to ketamine

2. Commonly added to cigarettes, marijuana, or other herbs for smoking

64
Q

Distinguishing features of PCP intoxication:

3

A
  1. Bizarre violent behavior
  2. Nystagmus
  3. Catatonic stupor and coma can occur at higher doses
65
Q

Treating patients on Hallucinogens

3

A
  1. Quiet, calm environment
  2. Supportive care
  3. Careful, mild sedation if agitated with monitoring
66
Q

Inhalants:
1. Wide variety of chemical structures mainly of what? 3

  1. Highly volatile, _____ soluble and absorbed from where?
  2. They act as what—initial euphoria is followed by lethargy
  3. Nitrites cause intense __________ producing a sensation of what? 2
A
    • hydrocarbons,
    • nitrites or
    • nitrous oxide
  2. lipid, pulmonary system
  3. CNS depressants
  4. vasodilation, heat and warmth, prolong penile erection
67
Q

Inhalant effects:

  1. CNS? (immediate 7 and Long term 3)
  2. GI? 4
  3. Hematologic? 2
  4. Sudden sniffing death due to?
A
  1. CNS:
  2. Immediate:
    - slurred speech,
    - ataxia,
    - disorientation,
    - HA,
    - hallucinations,
    - violent behavior,
    - seizures

Long-term:

  • neurocognitive impairment,
  • cerebellar dysfunction and
  • peripheral neuropathy
  1. GI:
    - N/V,
    - anorexia and
    - weight loss,
    - some solvents are hepatotoxic
  2. Hematologic: Use of benzene can cause
    - aplastic anemia and
    - malignancy
  3. “Sudden sniffing death” due to cardiovascular collapse
68
Q

Inhalant Intoxicaiton

  1. Presentation? 3
  2. Labs? 6
  3. May smell like what?
  4. Treatment?
A
  1. Presentation:
    - Extreme behavior problems
    - Neuropsychiatric problems
    - Altered mental status
  2. Labs:
    - CBC,
    - CMP,
    - UA
    - ABGs,
    - pulse oximetry
    - EKG, monitor
  3. May smell sweet solvent odor of halogenated hydrocarbons
  4. Treatment: supportive
69
Q

Nicotine
Highly addictive
Etiology of:
3

Second-hand smoke 3

A

Etiology of:

  1. Lung cancer
  2. COPD
  3. Cardiovascular disease

Second-hand smoke:

  1. Lung cancer in adults
  2. URI,
  3. SIDS in infants and children
70
Q
  1. Nicotine MOA?
  2. Reaches that brain how quickly?
  3. half life?
  4. Activates what?
  5. Increases circulation of what?
  6. Compare its addiction to opioids?
A
  1. Agonist at nicotinic subtype of acetylcholine receptors:
  2. Reaches the brain in 15 seconds!
  3. ½ life of 2 hours
  4. Activates the dopamine reward system
  5. Increases circulation of norepinephrine and epinephrine

MORE addictive than opioids

71
Q

Nicotine:
1. Mean onset age __YO

  1. Few people start smoking after age ___YO
A
  1. 16

2. 20

72
Q

Nicotine Abuse: Mortality includes what?

4

A
  1. atherosclerotic CVD,
  2. lung
  3. CA, and
  4. COPD
73
Q

Nicotine Withdrawal Symptoms

8

A
  1. Loss of euphoric effects
  2. Dysphoric or depressed mood
  3. Insomnia
  4. Irritability, frustration, anger, anxiety***
  5. Difficulty concentrating
  6. Restlessness
  7. Decreased heart rate
  8. Increased appetite/weight gain*
74
Q

Behavioral Approaches
Clinician counseling CAN increase quit rates

3

A
  1. Ask
  2. Urge to quit
  3. Assess stage of change:
75
Q

Assess stage of change: What are the stages of quitting? 5

A
  1. Precontemplation
  2. Contemplation
  3. Determination
    4, Action
  4. Maintenance
76
Q

Three successful smoking cessation treatment strategies:

A
  1. Social support
  2. Pharmacological therapy
  3. Skills training or problem solving techniques
77
Q

Smoking: What is considered 1st line agent?

A

Varenicline (Chantex)

78
Q

Varenicline (Chantex)

  1. MOA? 3
  2. SE? 4
  3. Monitor what?
A
  1. MOA:
    - Partial agonist of nicotinic acetylcholine receptors:
    - Reduces withdrawal symptoms
    - Blocks nicotine from tobacco thereby reducing the reward aspect of smoking
  2. SE:
    - nausea,
    - insomnia,
    - abnormal dreams,
    - depression and suicidality**
  3. USE: NOTE: Monitor for neuropsychiatric symptoms
79
Q

Buproprion (Zyban)

  1. MOA?
  2. SE? 5
  3. contraindications? 2

Careful with insurance coverage

A
  1. MOA: enhances CNS noradrenergic and dopaminergic function
  2. SE:
    - dry mouth,
    - insomnia,
    - HA,
    - seizures,
    - monitor for neuropsychiatric symptoms

CI: seizure disorders and pregnancy

Careful with insurance coverage

80
Q

Treatment for Nicotine Cessation
Nicotine polacrilex:
Types of this? 2

A
  1. Gum (Nicorette) or
  2. lozenge

Withdrawal symptoms not totally prevented

81
Q

Transdermal Nicotine patches

  1. How does it affect withdrawal symtpoms?
  2. Delivery of nicotine how?
  3. How does this benefit some pts?
A
  1. Reduces intensity of withdrawal symptoms
  2. Delivery of nicotine at night can cause sleep disturbance and vivid dreams
  3. Increased am nicotine levels benefit some patients
82
Q

Opioids

3

A
  1. Heroin—diacetylmorphine (dope, horse, smack, tar)
  2. Opium (more prevalent outside the U.S.)
  3. Prescription opiates:
83
Q

Prescription Opiate Drugs

3

A
  1. Fentanyl—patch
  2. Percocet (oxycodone/acetominophen)
  3. Vicodin (hydrocodone/acetominophen)
84
Q

Opiod Mechanism of action:

4

A
  1. Opioids activate specific transmembrane neurotransmitter receptors (mu, kappa, delta) that couple G proteins
  2. The G proteins are intermediaries that initiate the intracellular communication process
  3. Activation of CNS mu receptors results in euphoria, respiratory depression, analgesia and miosis
  4. Stimulation of peripheral mu receptors causes cough suppression and constipation
85
Q

Opioid Toxicity classic signs

5

A
  1. Depressed mental status
  2. Decreased respiratory rate*
  3. Decreased tidal volume
  4. Miotic pupils
  5. With meperidine and propoxyphene or the presence of coingestants—such as sympahtomimetics or anticholinergics—pupils may be normal or large
86
Q

Opioid Toxicity

  1. VS changes? 3
  2. Secondary survey: What do we need to look for? 3
A

VS changes:

  • Low heart rate
  • Mild hypotension
  • Hypothermia (can occur even at room temperature)

Secondary survey:

  • Look for signs of trauma especially to the head
  • Check for medication patches that need to be removed
  • May need to do rectal/pelvic exams for hidden drugs
87
Q

Opioid Toxicity: DDx?

6

A
  1. Ethanol—no miosis or change in bowel sounds
  2. Clonidine—bradycardia and hypotension more prominent
  3. Sedative-hypnotics—less respiratory depression
  4. CVA
  5. Electrolyte abnormality
  6. Sepsis
88
Q

Opioid Toxicity treatment?

3

A
  1. Mainstay of treatment ABC’s particularly airway management
  2. Use of naloxone (opioid antagonist) to increase respirations to 12 or greater NOT to attain a normal level of consciousness
  3. Several opioids possess uncommon toxicities requiring specific management
89
Q

Withdrawal Symptoms to Opioids

  1. 3-4 hrs. last dose: 2
  2. 8-14 hrs. last dose: 5
  3. 1-3 days last dose: 5
A
  1. 3-4 hrs. last dose:
    - Drug craving and anxiety
    - Fear of withdrawal
  2. 8-14 hrs. last dose:
    - Anxiety, restlessness, insomnia and yawning
    - Rhinorrhea, lacrimation
    - diaphoresis
    - Stomach cramps
    - mydriasis
    • Tremor, muscle spasm
    • Vomiting and diarrhea
    • HTN and Tachycardia
    • Fever, chills
    • piloerection
90
Q

Symptom Management for Acute Withdrawal

5

A
  1. Muscle relaxants
  2. NSAIDS
  3. Antiemetics
  4. Antidiarrheal agents
  5. Sleeping agent with low abuse potential (melatonin, benedryl)
91
Q

Managing Opioid Dependence
Long-term addiction treatment:
3

A
  1. Abstinence based treatment programs
  2. Naltrexone (opioid antagonist)
  3. Opioid agonists
92
Q

What are your opiod agonists?2

A
  1. Methadone

2. Buprenorphine

93
Q

Opioid Withdrawal

Naltrexone

  1. Administered at what time?
  2. Administered how? 2
  3. Antagonist prevents the patient from what?
  4. Most effective in highly motivated patients: How should it be managed? 2
A
  1. Administered after patient completely detoxed
  2. Oral or monthly depot preparation
  3. from experiencing any euphoric effects with subsequent opioid use
  4. Most effective in highly motivated patients:
    - Closely supervised
    - Can be mandated by legal or other authorities
94
Q

Opioid Withdrawal
Methadone
1. Long term or short term treatment?
2. How and in what setting does it need to be administered?
3. How many days for maintenance and how many for detoxification?
4. SE? 4

  1. What schedule of drug?
A
  1. Method of long term opioid treatment
  2. Administration of single daily dose in a controlled setting with counseling and social services
  3. > 180 days maintenance; less than 180 days detoxification
  4. SE:
    - Constipation, drowsiness
    - Reduced libido, excess sweating
    - Peripheral edema
    - Prolonged QT
  5. methadone Schedule II
95
Q

Opioid Withdrawal
Buprenorphine
1. What class?
2. What are the two kinds of preparations?
3. Can be prescribed by clinicians in their office. But they need to go through what?
4. What schedule of drug?

A
  1. Partial opioid agonist
    • Sublingual preparation—Subutex
    • Combined with naloxone—Suboxone
  3. —need to go through training program
  4. Schedule III drug,
96
Q

Opioid Withdrawal
Clonidine:
1. Class of drug?
2. May decrease withdrawal symptoms in who?
3. SE? 3
4. What drug can this be combined with that pts often abuse?

A
  1. Alpha-2-adrenergic receptor agonist
  2. May decrease withdrawal symptoms in patients using low doses of opioids
  3. SE:
    - Orthostatic Hypotension
    - Dry mouth
    - Constipation
  4. Some patients combine clonidine and methadone to get a euphoric effect—hence abuse these meds
97
Q

Anxiolytic-Disorders
1. Often __________ are used to treat these and they can be highly addictive

  1. It is important to take a good history because people who have abused other substances are at a higher risk to abuse _____________?

Careful monitoring of drug use and using them short-term at low doses is important

A
  1. benzodiazepines

2. benzodiazepines

98
Q

Benzodiazepine Withdrawal: Signs and symptoms?

8

A
  1. Increased body temperature
  2. Elevated blood pressure
  3. Increased pulse and respiratory rate
  4. Aroused level of conciousness/delirium
  5. Tremulousness
  6. Increased DTRs/seizures
  7. Disorientation
  8. Psychotic behavior/hallucinations
99
Q

Tx Benzodiazepine Withdrawal

  1. Mild to moderate? 2
  2. Severe withdrawal? 2
A

Mild to moderate:

  1. Most patients can be managed by a slow taper of the drug they were on over several months
  2. Objectively determining drug tolerance may be difficult

Severe withdrawal:

  1. Can be life-threatening
  2. Use long acting benzodiazepines watching for respiratory depression
100
Q

Severe/serious withdrawal:

3

A
  1. Anticonvulsants can be used:
  2. Symptom rebound may occur—insomnia and anxiety**
  3. ICU for severe withdrawal with abnormal vital signs
101
Q

Which anticonvulsants would you want to use for benzo withdrawal?

A
  1. Carbamazepine

2. Valproate

Behavioral Health (20 decks)

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