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Substance related disorders Flashcards

1
Q

What is substance use, abuse, phsyical dependence?

A
  • sporadic consumption of alcohol/drugs w/ no adverse consequences
  • abuse: frequency of alcohol/drug use may vary, there are adverse consequences experienced by the user
  • physical dependence: state of adpatation that is manifested by a drug class-specific withdrawal syndrome
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2
Q

What is psychological dependence, addiction?

A
  • psychological dependence: a subjective need for a specific psychoactive substance, either for its positive effect or to avoid negative effects of its abstinence
  • addiction: primary, chronic, neurobiologic disease, with genetic, psychosocial, and enviro factors influencing its development and manifestations:
    characterized by behaviors that include impaired control over drug use, compulsive use, cont use despite harm and craving, and continuing use despite adverse consequences in the abusers life
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3
Q

Epidemiology of substance abuse?

A
  • 10% of general pop has problems due to substance abuse
  • genetic differences
  • age differences: prevalence is reduced as age increases
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4
Q

Special populations affected by substance abuse?

A
  • adolescents
  • anyone with psych comorbidity
  • those who smoke or abuse alcohol
  • elderly - alcohol
  • health care workers: rx drugs
  • pregnant women may fear admitting to drug abuse
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5
Q

How do you recognize the drug abuser?

A

you won’t know unless you ask:

  • quantity
  • amt of money spent daily/weekly/monthly
  • frequency of use and time of last use
  • route of admin
  • if hx of use is disclosed ask about prior detox or addiction tx and abstinence periods
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6
Q

Physical changes due to substance abuse?

A
  • drug use is leading cause of impotence in US
  • wt loss and sleep disturbance
  • evidence of localized or systemic infections
  • on abdominal exam may palpate enlarged or shrunken liver
  • respiratory or nasal problems (cocaine, smoking - tobacco, marijuana)
  • need marks: tracks
  • STIs in pts who are trading sex for drugs
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7
Q

CAGE questionnaire? Best in what pop?

A
  • commonly used in medical setting and has been validated as a sensitive and specific tool for detectin problem drinking (esp in men)
  • 2 or more positive answers indicate a likely dx of alcohol dependence
    1. Have you ever felt the need to Cut down on your drinking?
    1. have you ever felt Annoyed by criticism of your drinking?
    1. have you ever had Guilty feelings about your drinking?
    1. do you ever take a morning Eye-opener (steady your nerves or get rid of hangover)
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8
Q

Why does an individual take a substance to start with?

A
  • have to get to the bottom of this with your pts
  • is it solely for the high?
  • what about over time when there is no longer euphoria? Is it maintain an equilibrium?
  • is it to counter something else going on? - does the person have anxiety, depression, are they escaping something?
  • *you must always seek to determine what fxn a substance is serving for a pt
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9
Q

What is considered risky or hazardous drinking? What is unhealthy alcohol use?

A
  • in men younger than 65 - it is more than 14 drinks a week and in women that are younger than 65 - more than 7 drinks a week
  • unhealthy alcohol use: uses that can result in health consequences
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10
Q

Alcohol abuse definition?

A

assoc with one or more of the following, occurring in a 12 month period:

  • failure to fulfill work, school or social obligations
  • recurrent substance use in physically hazardous situations
  • recurrent legal probs related to substance use
  • cont use despite alcohol related social or intrapersonal problems
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11
Q

What is alcohol dependence (alcoholism)?

A

a maladaptive patterns of use assoc w/ 3 or more of the following, occurrence at any time in the same 12 month period:

  • tolerance
  • withdrawal
  • substance taken in larger quantity than intended
  • persistent desire to cut down or control use
  • time is spent obtaining, using or recovering from the substance
  • social, occupational or recreational tasks are sacrificed
  • use continues despite physical and psychosocial problems
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12
Q

epidemiology of alcohol?

A
  • over 50% of people 12 and older reported drinking regularly
  • over 23% reported binge drinking in last 30 days, 6.9% reported heavy drinking
  • 40% of all traffic fatalities are alcohol related
  • alcohol related health problems 3rd leading cause of preventable death in the US
  • leads all other substances in substance related deaths!!
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13
Q

Medical morbidity of alcohol?

A

assoc with greater risk of:

  • HTN, cardiomyopathy
  • hepatitis, cirrhosis (1/2 cases in US secondaray to ETOH), pancreatitis
  • TB, pneumonia
  • psych probs: anxiety, depression, and eating disorders
  • cancers of the stomach, mouth, larynx, breast, and esophagus
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14
Q

Screening tools for alcohol use? Who should be screened?

A
  • single item screening
  • alcohol use disorders identification test (audit)
  • CAGE questions (not as reliable for caucasian women)
  • screen all adult pts: intervention most likely to succeed in pts who are in risky drinking or hazardous drinking categories
  • a large # of pts need to be screened to achieve benefit
  • screening essential pts with + family hx, who smoke, have frequent ER visits, or who are on meds that interact with ETOH
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15
Q

CRAFFT screening for adolescents and college students?

A
  • Have you ever ridden in a Car driven by someone (including yourself) who was high or had been using alcohol or drugs?
  • do you ever use alcohol or drugs to Relax, feel better about yourself, or fit in?
  • do you ever use alcohol or drugs while you are Alone?
  • Do you ever use alcohol or drugs while you are Alone?
  • do you ever Forget things you did while drinking or doing drugs?
  • Do your family or Friends ever tell you that you should cut down on your drinking or drug use?
  • have you ever gotten into Trouble while you were using alcohol or drugs
  • 2 or more positive answers indicate problem use, abuse or dependence
  • performs better then CAGE for this age group
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16
Q

What is considered moderate drinking?

A
  • men: 2 drinks or less a day

- women: 1 drink or less a day

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17
Q

What is considered heavy drinking?

A
  • men: drink more than 14 drinks per week, or 4 drinks per occasion
  • women: drink more than 7 drinks a week or 3 drinks per occasion
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18
Q

What is considered binge drinking?

A
  • men: 5 or more drinks in a row

- women: 4 or more drinks in a row

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19
Q

Drink equivalents?

A

1 mixed drink with 1.5 fl oz of 80 proof liquor = 5 oz of wine = 12 oz of beer or wine cooler

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20
Q

Etiology of alcohol related disorders?

A
  • multifaceted including psychosocial, genetic and or behavioral factors
  • genetics:
    3-4x higher for severe alcohol problems in first degree relatives with alcohol problems
  • rate of alcohol problems increases with the number of alcoholic relatives and severity of illness
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21
Q

Absorption of alcohol?

A
  • 10% consumed alcohol is absorbed in the stomach, remainder from the small intestines
  • when concentration of alcohol in stomach becomes too high - mucus secretion and pyloric valve closure results in slowed absorption
  • pylorospasm results in vomit - rookie drinkers
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22
Q

metabolism of alcohol?

A
  • 90% metabolized in liver through oxidation
  • metabolized by 2 enzymes:
    ADH catalyzes conversion of alcohol into acetaldehyde, which is toxic
  • ALDH catalyzes conversion of acetaldehyde into acetate
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23
Q

Effects of alcohol on the brain? Diff levels and effects?

A
  • CNS depression (like benzodiazepines)
  • relatively mild levels: thought, judgement, and restraint are loosened
  • increasing levels: voluntary muscle dysfxn and entire motor area of the brain depressed
  • yet increasing levels: confusion, stupor, coma, and finally primitive centers that control breathing and HR are affected and can result in death either secondary to direct respiratory depression or aspiration of vomitus
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24
Q

Effects of alcohol on the liver?

A
  • metabolism of alcohol leads to chemical attack on liver (it is unknown if damage is caused by acetaldehyde or other metabolites)
  • even after all alcohol intake has stopped and all alcohol has been metabolized, the processes that damage liver cells may continue for weeks to months
  • clinical and chemical effects often become worse before disease resolves
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25
Q

3 patterns of hepatocellular injury by alcohol?

A
  • fatty liver
  • alcoholic hepatitis
  • cirrhosis (rate is 10-15% of all alcoholics)
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26
Q

What is wenicke-korsakoff syndrome?

A
  • occurs in persons who have been drinking heavily for many years - rare to see in persons younger than 35, caused by thiamine deficiency due to poor nutrition/malabsorption
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27
Q

What is wernicke’s encephalopathy?

A
  • acute sxs which are completely reversible when tx w/ high dose thiamine: characterized by gait ataxia, vestibular dysfxn, confusion and ocular abnormalities
    (remember to give thiamine b/f glucose to prevent encephalopathy)
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28
Q

What is korsakoff’s syndrome?

A
  • chronic condition where only 20% of pts recover - can be tx with po thiamine
  • characterized by impaired recent memory and anterograde amnesia
  • this isn’t as well tx with thiamine as wernickes
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29
Q

How is drinking good for the heart?

A
  • several studies have shown that drinking in moderation may have health benefits particularly in regard to CAD and the risk of MI
  • meta-analysis of 34 studies found that 1-2 drinks a day in women and 2-4 drinks in men, are inversely related with total mortality while GREATER intake INCreased mortality
  • pts will bring this up all the time, pts ofte fail to consider their comorbidities
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30
Q

Goals for tx alcohol dependence?

A

short term:

  • ID and initiate tx for pts at risk for withdrawal (determine stage)
  • promote attendance at AA or other support groups
  • early intervention

long term goals:

  • extended management over time
  • determining efficacy of tx
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31
Q

Mild sxs of alcohol withdrawal?

A
  • insomnia
  • tremulousness
  • mild anxiety
  • GI upset/anorexia
  • HA
  • diaphoresis
  • palpitations
  • mild sxs begin w/in 6 hrs of cessation of drinking
  • they resolve w/in 24-48 hrs
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32
Q

WHen do withdrawal seizzures occur? Tx?

A
  • occur w/in 48 hrs after last drink
  • tonic-clonic
  • occur in 3% of chronic alcoholics
  • tx with benzodiazepines - not anticonvulsants
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33
Q

What is alcoholic hallucinosis, when does this develop?

A
  • within 12-24 hrs of last drink
  • resolves with 24-48 hrs
  • not delirium tremens
  • usually visual: but can be auditory or tactile
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34
Q

What agents shouldn’t be used for tx of alcohol dependence?

A
  • ethanol
  • antipsychotics
  • anticonvulsants
  • central actiing alpha-2-agonists
  • B-blockers
  • baclofen (muscle relaxant)
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35
Q

What is delirium tremens, how common? When does it begin, last? RFs? Why is it so impt to dx this?

A
  • 5% of pts who withdraw from alcohol will develop this
  • sxs and signs:
    hallucinations
    disorientation
    tachycardia
    HTN
    low grade fever
    agitation
    diaphoresis
  • begins 48-96 hrs after last drink, can last 1-5 days
  • RFs:
    hx of sustained drinking
    hx of previous DTs
    over 30
    presence of concurrent illness
  • mortality rate of 5%
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36
Q

DDx of alcohol withdrawal?

A
  • dx of exclusion
  • differential:
    infection
    trauma/head
    metabolic derangements
    drug overdose
    hepatic failure
    GI bleed
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37
Q

General tx measures for alcohol dependence?

A
  • place pt in quiet, protective enviro, may need mechanical restraint, most pts tend to be dehydrated with hypokalemia - replace with IV fluids and KCl
  • thimaine - 100 mg IV or IM b/f glucose
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38
Q

Tx for minimal sxs of alcohol withdrawal syndrome?

A
  • no disorientation or hallucinations

- thiamin and supportive care

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39
Q

Tx for mild sxs of alcohol withdrawal syndrome?

A
  • thiamin and supportive care

- meds to reduce sxs and monitoring

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40
Q

Tx for moderate and severe alcohol withdrawal syndrome?

A
  • thiamin and supportive care
  • hourly monitoring, especially respiratory rate
  • meds: benzos
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41
Q

What benzos are used in tx of alcohol withdrawal syndrome?

A
  • diazepam (valium), chlordiazepoxide (librium), lorazepam
  • can give orally or IV
  • scheduled vs sx targeted
    sx targeted - preferred - pt will be more alert
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42
Q

Other meds used in alcohol withdrawal syndrome?

A
  • for refractory DTs - add phenobarbitol and propofol (monitor respirations)
  • antipsychotics lower seizure threshold - DONT USE
  • seizures: if status epilepticus use phenobarbitol
  • DONT use carbemazepine
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43
Q

Outpt therapy of alcoholism - acomprosate (campral)? SEs, CI?

A
  • synthetic derivative of homotaurine - analog of GABA
  • MOA not clearly understood (take it b/f drinking - take a drink - get super sick)
  • used for relapse prevention with counseling
  • SE: diarrhea, low pulse, high or low BP, HAs, impotence
  • CI: kidney disease
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44
Q

Outpt therapy of disulfiram (antabuse)? SEs, drug interactions?

A
  • inhibits the activity of acetaldehyde dehydrenase (ALDH) which results in 5-10 fold increase in acetaldehyde levels after alcohol ingestion
  • leads to flushing, dyspnea, N&V, HA, blurred vision, vertigo, and anxiety
  • SE: hepatotoxic, can cause depression, psychosis - need to monitor psych sxs
  • increases drug levels of phenytoin, isoniazide and anticoagulants
  • pt has to be motivated to follow through with this - if liver already harmed - don’t use
  • works better than acomprosate
45
Q

Stimulants epidemiology?

A
  • methamphetamine:
    2nd to cannabis most widely abused drug in the world, 5% of US pop have used it
  • cocaine: highest prevalence unemployed men in their 20s w/ only a high school educationin urban areas, use is highly assoc with use of other legal and illegal substances
46
Q

Pharm of metahmphetamine?

A
  • displaces epi, NE, dopamine, and serotonin into synaptic cleft
  • also activates NT reuptake systems
  • this results in surge of adrenergic stimulation
  • sxs and signs produced: high energy, increased HR, pupil dilation, Increased BP, agitated, psychosis)
  • readily absorbed via oral, pulm, nasal, IM, IV, rectal, and vaginal routes, body stuffing has been reported
47
Q

General appearance of a pt with meth intoxication? VS?

A

general appearance:

  • malnourished, agitated, disheveled
  • severe intoxication can exhibit abrupt changes in behavior and become very violent
  • “meth mouth”, other stigmata of trauma, diaphoresis
  • VS: tachy, HTN, hyperthermic
  • other: N/V, seizures, delirium, psychosis
  • may have sympathomimetic toxidrome: adrenergic excess
48
Q

DDx of meth intoxication?

A

Other toxicologic conditions:

  • cocaine and PCP
  • theophylline and ASA overdose
  • MAOI, serotonin syndrome, antcholinergic poisoning

nontoxicologic:
heat stroke
thyrotoxicosis
pheochromocytoma

49
Q

Meth intoxication tx?

A
  • sedation for agitation
  • protect airway
  • control BP and temp
50
Q

Biggest risk is what in meth intoxication? Tx?

A
  • cardiovascular collapse
  • tx:
    vasoactive amines
    correct metabolic acidosis
    fluid resuscitation
51
Q

MOA of cocaine?

Pharmokinetics?

A
  • blocks presynaptic reuptake pumps for dopamine, NE and serotonin
  • also blocks voltage gated membrane Na channes

pharmacokinetics: cocaine base - can be smoked
- cocaine salt is readily injected or snorted
- when used with alcohol forms cocethylene - longer acting

52
Q

Cocaine intoxication - intended effects, adverse effects, and physiological effects?

A
  • intended effects: increased energy, alertness, sociability, elation or euphoria, decreased fatigue, need for sleep and appetite, “total body orgasm”
  • adverse effects:
    anxiety, irritability, panic attacks, paranoia, gradiosity, impairment in judgement, psychotic sxs
  • physiological effects: tachycardia, pupil dilation, diaphoresis, nausea
53
Q

Effects of cocaine acute intoxication on CV, CNS, lungs?

A
  • CV: arterial vasoconstriction and enhanced thrombus formation, causes tachycardia, and HTN
  • CNS: agitation, seizures, HA, coma, intracranial hemorrhage
  • lungs: when smoked can cause angioedema and pharyngeal burns
    passive cocaine exposures: those in close proximity to users of inhalational cocaine can present with toxicity
54
Q

Initial labs of stimulant intoxication management?

Specific management?

A
  • fingerstick glucose
  • acetaminophen and salicylate levels
  • EKG
  • pregnancy test in women of childbearing age
  • others as indicated
  • management:
    towards pt’s condition
    toward sx problems
55
Q

Components of cannibis?

A
  • psychoactive component: delta-9-tetrahydrocannabinol (THC)
  • THC: has increased from 1-5% in 60s to 10-15% currently
  • plant is processed into 3 drug products:
    dry leaves and flowers (herbal cannabis)
    pressed, dry resin or secretion (hashish)
    oil (hash oil)
56
Q

Epidemiology of cannabis?

A
  • most commonly used illegal substance worldwide
  • more commonly used in US
  • men 2x as much as women
  • blacks use it greater than whites and hispanics
  • lifetime cannabis use is greater in those who are separated or divorced compared to those married
  • use assoc with other substance use - alcohol and other ilict drugs
  • cannabis used at early age is assoc with use of other substances at later age
  • use occurs more frequently in those with mental illness
57
Q

Pharmacology of cannabis?

A
  • THC reaches brain, crosses BBB and bidns to endogenous cannabinoid receptors (CB1)
  • THC activates CB1 receptors in mesolimbic dopamine system, which is hypothesized to modulate the positive reinforcing and rewarding effects of most drugs of abuse
  • abstinence of drug cuases withdrawal sxs
  • repeated chronic use leads to down regulation of the receptor - tolerance which leads to having to have increased amt to have same effect
58
Q

Comorbid mental illnesses assoc with cannabis use?

A
  • occur frequently in pts with cannabis disorders
  • mood disorders: 61% of those with cannabis dependence, 36% of those with cannabis abuse
  • anxiety disorders: 46% in those with cannabis dependence, and 25% in those with cannabis abuse
59
Q

Genetics of cannabis use?

A
  • there is substantial degree of heritability of cannabis dependence (60% genetic)
60
Q

Psychosocial aspect of cannabis use?

A
  • used to relieve tension and cope with stress
  • many young adults believe it is relatively harmless
  • actually it can lead to school dropout, using other illict drugs, interpersonal problems, crime and unemployment
61
Q

Cannabis effects - mood, perception, thought content?

A
  • usually causes euphoria, decreases anxiety, and tension
  • time perception is distorted, time is perceived faster
  • increased self consciousness and transient grandiosity can occur as well as paranoia and even psychosis
62
Q

Cannabis effects - cognition, and psychomotor fxn?

A
  • decreases rxn time and impairs attention, concentration, short term memory, and risk assessmnet
  • impairs motor coordination, and ability to do complex tasks - lasts 12-24 hrs past initial euphoria
63
Q

Physiologic signs of cannabis use?

A
  • tachycardia
  • increased BP
  • increased RR
  • conjunctival injection
  • dry mouth
  • increased appetite
64
Q

Marijuana withdrawal sxs?

A
  • craving for marijuana
  • irritability
  • restlessness
  • depression
  • anxiety
  • decreased quantity and quality of sleep
  • vivid or strange dreams
  • decreased food intake, with assoc wt loss
  • increased aggression
  • physical tension
  • sweating
  • runny nose
  • stomach pain
  • nausea
65
Q

Tx for marijuana addiction?

A
  • difficult
  • buspirone (buspar) has shown to be helpful for tx withdrawal sxs
  • inpt tx advised
  • changing setting where the pt is habitually using marijuana
  • at times oral THC in reducing doses
  • tx underlying comorbid psychiatric disease appropriately and carefully
66
Q

What are hallucinogens?

A
  • substances whose primary effects include alteration of sensory perception, mood and though pattern
  • Trip: effects experienced from acute intoxication - bad trip - acute intoxication with dysphoria, fear, agitation, or other unwanted effects predominate
  • flashback: recurrence of sxs assoc with hallucinogen after the effects of the acute intoxication have worn off. May occur months or years after the last use of drug
67
Q

Pharmacology of hallucinogens? Effects?

A
  • involves the interaction of numerous NTs: serotonin, dopamine, glutamate
  • exact mecahnism unknown, but one property common to the drugs is their ability to bind 5-HT2A receptors (this serotonergic activity may cause serotonin syndrome)
  • effects: phenomenon - synesthesia (blending of senses) - feel like your whole body is alive
68
Q

What is LSD?

A
  • lysergic acid diethyl amide
    available as capsule, pill or liquid, neuropsychiatric sxs, person remains oriented and aware their experience is drug induced
69
Q

What is dextromethorphan (DXM)?

A
  • codeine analog
  • OTC in cold and cough preparations
  • recreational dose: 100-200 mg can produce hallucinations and coma
  • anticholinergic delirium and acetaminophen toxicity have occurred
70
Q

What is mescaline?

A
  • active ingredient in peyote cactus

- N/V often precede onset of psychedelic effects

71
Q

What is 4-bromo-2-5-dimethoxpheethylamine?

2CT-7 or blue mystic?

A
  • 2CB or Bromo: gentler than LSD

- 2CT-7: little is known about it, deaths have been reported

72
Q

What is PCP? intoxication features?

A
  • dissociative anesthetic similar to ketamine
  • resurgence of use in certain cities
  • commonly added to cigaretts, marijuana, or other herbs for smoking
  • distinguishing features of intoxication:
    bizarre violent behavior
    nystagmus
    catatonic stupor and coma can occur at higher doses
73
Q

main components of tx pts on hallucinogens?

A
  • quiet, calm enviro
  • supportive care
  • careful, mild sedation if agitated with monitoring
74
Q

Use of inhalants?

A
  • 13% of middle school and high school students report using inhalants in US
  • since 2002 incidence increasing
  • male=female
  • inhalant abuse is common problem in adolescents - readily accessible, inexpensive an dlegal to buy and possess, perceived risk of use is loq
75
Q

What do inhalants contain? How do they effect the body?

A
  • wide variety of chemical structures mainly hydrocarbons, nitrites or nitrous oxide
  • highly volatile, lipid soluble and absorbed from pulmonary system
  • they act as CNS depressants - inital euphoria is followed by lethargy
  • nitrites cause intence vasodilation producing a sensation of heat and warmth, prolong penile erection
76
Q

Most commonly used inhalants? Techniques?

A
  • US: glue, shoe polish, and toulene, then gas and lighter fluid, nitrous oxide (wippits), spray paints

techniques:

  • spray directly on heated surface to vaporize (sniffing)
  • saturate cloth and hold near nose or mouth (huffing)
  • put substance in a bag that is placed over nose, mouth or head (bagging)
77
Q

Inhalant effects on CNS, GI, hematologic?

A

CNS: immediate - slurred speech, ataxia, disorientation, HA, hallucinations, violent behavior, seizures
long term: neurocognitive impairment, cerebellar dysfxn, and peripheral neuropathy

GI: N/V, anorexia, and wt loss, some solvents are hepatotoxic

hematologic: use of benzene can cause aplastic anemia and malignancy
- sudden sniffing death due to CV collapse

78
Q

Presentation of inhalant intoxication? Labs? Tx?

A
  • extreme behavior probs
    neuropsychiatric probs
    altered mental status
  • labs: CBC, CMP, UA, ABGs (gas exchage), pulse ox, EKG, monitor
  • may smeel sweet solvent odor of halogenated hydrocarbons
    tx: supportive
79
Q

Smoking tobacco- results in?

A
  • highly addictive
  • etiology of:
    lung cancer
    COPD
    CVD
    second hand smoke: lung cancer in adults
    URI, SIDS in infants and kis
80
Q

What is nicotine, how does it work?

A
  • addictive component in tobacco
  • agonist at nicotinc subtype of acetylcholine receptors: reaches brain in 15 seconds, 1/2 life of 2 hrs
  • activates the dopamine reward system
    increases circulation of NE and epi
  • more addictive than opioids
81
Q

Nicotine use?

A
  • mean onset: 16 yo
  • few people start smoking after 20
  • dependence develops quickly
  • 20% of pop develops nicotine dependence at some pt in their life
82
Q

outcomes of nicotine use?

A
  • death
  • 400,000 premature deaths a year
  • 30% of cancer deaths in US are caused by tobacco smoke
  • suffocation
  • chronic cough and SOB (COPD)
  • mortality: atherosclerotic CVD, lung CA, and COPD
83
Q

Nicotine withdrawal sxs?

A
  • loss of euphoric effects
  • dysphoric or depressed mood
  • insomnia
  • irritability, frustration, anger, anxiety
  • difficulty concentrating
  • restlessness
  • decreased HR
  • increased heart rate
  • increased appetite/wt gain
84
Q

Behavioral approaches that we can use to influence smoking cessation?

A
  1. ask
  2. urge to quit
  3. assess stage of change:
    precontemplation
    contemplation
    determination
    action
    maintenance
85
Q

3 successful smoking cessation tx strategies?

A
  • social support
  • pharm therapy
  • skills training or problem solving techniques
  • clinician counseling: dose-response relationship b/t intensitivity of tobacco dependence counseling and its effectiveness in smoking cessation - give positive reinforcement to pt for quiting
86
Q

1st line smoking cessation drug? MOA, SE?

A
  • Varenicline (chantex)
    MOA: partial agonist of nicotinic acetylcholine receptors - reduces withdrawal sxs, blocks nicotine from tobacco thereby reducing the reward aspect of smoking
  • SE: nausea, insomnia, abnormal dreams, depression and suicidality (BBW)
  • monitor for neuropsychiatric sxs
87
Q

Use of buproprion (zyban or welbutrin) in smoking cessation?

A
  • MOA: enhances CNS noradrenergic and dopaminergic fxn
  • SE: dry mouth, insomnia, HA, seizures, monitor for neuropsych sxs
  • CI: seizure disorders and pregnancy
  • careful with insurance coverage
  • doesn’t work as well as chantix
88
Q

Use of nicotine polacrilex in smoking cessation?

A
  • gum (nicorette) or lozenge
  • gum use - need to pack it not just chew it to get effect
  • withdrawal sxs not totally prevented
  • some people become chronic gum chewers
  • lozenge has higher rates of abstinence at one years
89
Q

Use of transdermal nicotine patches?

A
  • several dosage formulations
  • use/can do patch + other pharm
  • reduces intensity of withdrawal sxs
  • delivery of nicotine at night can cause sleep disturbance and vivid dreams
  • increased am nicotine levels benefit some pts
90
Q

Opioids include?

A
  • heroin: diacetlymorphine (dope, horse, smack, tar)
  • opium
  • Rx opiates: abuse of these increasing, used these more than cocaine, heroin, hallucinogens, ectasy and inhalants combined
91
Q

Prescription opioids?

A
  • fentanyl - patch
  • percocet (oxycodone/acetaminophen)
  • vicodin (hydrocodone/acetaminophen)
92
Q

MOA of opioids?

A
  • opioids activate specific transmembrane NT receptors (mu, kappa, delta) that couple G proteins
  • G proteins are intermediates that initiate the intracellular communication process
  • activation of CNS mu receptors results in euphoria, respiratory depression, analgesia and miosis
  • stimulation of peripheral mu receptors causes cough suppression and constipation
93
Q

Classic signs of opioid toxicity?

A
  • depressed, mental status
  • decreased respiratory rate
  • decreased tidal volume
  • miotic pupils
  • with meperidine and propoxyphene or presence of coingestants - such as sympathomimetics or anticholinergics - pupils may be normal or large
94
Q

VS changes and secondary survey findings in opioid toxicity?

A
  • VS changes:
    low HR
    mild hypotension
    hypothermia (can even occur at room temp)
  • secondary survey:
    look for signs of trauma esp to the head, check for med patches that need to be removed, may need to do rectal/pelvic exams for hidden drugs
95
Q

DDx of opioid toxicity?

A
  • ethanol: no miosis or change in bowel sounds
  • clonidine - bradycardia and hypotension more prominent
  • sedative hypnotics - less respiratory depression
  • CVA
  • lyte abnormalities
  • sepsis
96
Q

Tx of opioid toxicity?

A
  • mainstay of tx: ABCs particulary airway management
  • use of naloxone (opioid antagonist) to increase respirations to 12 or greater not to attain a normal level of consciousness
  • several opioids possess uncommon toxicities requiring specific management
  • opioids are implicated in more drug related deaths than any other ilicit agent
97
Q

Withdrawal sxs to opioids: 3-4 hrs from last dose?

A
  • drug craving and anxiety

- fear of withdrawal

98
Q

Withdrawal sxs to opioids: 8-14 hrs last dose?

A
  • anxiety, restlessness, insomnia, and yawning
  • rhinorrhea, lacrimation, and diaphoresis
  • stomach cramps and mydriasis
99
Q

Withdrawal sxs to opioids - 1-3 days from last dose?

A
  • tremor, muscle spasm
  • vomiting, diarrhea
  • HTN and tachycardia
  • fever, chills, and piloerection
100
Q

Sx managment for acute withdrawal?

A
  • muscle relaxants
  • NSAIDs
  • antiemetics
  • antidiarrheal agents
  • sleeping agent with low abuse potential: melatonin, benadryl
101
Q

Long term opioid addiction tx?

A
  • abstinence based tx programs
  • naltrexone (opioid antagonist)
  • opioid agonists:
    methadone
    buprenorphine
102
Q

use of naltrexone in opioid addiction tx?

A
  • admin after pt completely detoxed
  • oral or monthly depot prep
  • antagonist prevents the pt from experiencing any euphoric effects with subsequent opioid use
  • most effective in highly motivated pts:
    closely supervised
    can be mandated by legal or other authorities
103
Q

Use of methadone in opioid addiction tx?

A
  • method of long term opioid tx
  • admin of single daily dose in controlled setting with counseling and social services
  • more than 180 days maintenace, and less than 180 days detoxification
  • SEs:
    constipation, drowsiness
    reduced libido, excess sweating, peripheral edema, prolonged QT
104
Q

Use of buprenorphine in opioid addiction tx?

A
  • partial opioid agonist
  • sublingual preparation - subutex
  • combined with naloxone (antagonist) - suboxone
  • can be prescribed by clinicians in their office - need to go through their training program
  • schedule III drug, methadone schedule II
105
Q

Use of clonidine in opioid withdrawal tx?

A
  • alpha-2-adrenergic receptor agonist
  • may decrease withdrawal sxs in pts using low doses of opioids
    -SEs:
    orthostatic hypotension
    dry mouth
    constipation
  • some pts combine clonidine and methadone to get euphoric effect - will abuse these meds
106
Q

What is used to tx anxiolytic disorders? Why is this a problem? What should you do when seeing these pts?

A
  • often benzodiazepines are used to tx these and they can be highly addictive
  • it is impt to take a good hx b/c people who have abused other substances are at higher risk to abuse benzodiazepines
  • careful monitoring of drug abuse and using them short term at low doses is impt
107
Q

What are sxs of benzodiazepine withdrawal?

A
  • increased body temp
  • elevated BP
  • increased pulse and RR
  • aroused level of consciousness/delirium
  • tremulousness
  • increased DTRs/seizures
  • disorientation
  • psychotic behavior/hallucinations
108
Q

Tx of benzo withdrawal?

A
  • mild to moderate:
    most pts can be managed by a slow taper of the drug they were on over several months, objectively determining drug tolerance may be difficult
  • severe withdrawal: can be life threatening, use long acting benzos watching for respiratory depression
  • severe/serious withdrawal: anticonvulsants can be used - carbamazepine or valproate
    sx rebound may occur - insomnia and anxiety
  • ICU for severe withdrawal with abnormal vital signs

Psych (20 decks)

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