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ADDICITION > Ruiz. THE SUBSTANCE HANDBOOK > Flashcards

Ruiz. THE SUBSTANCE HANDBOOK Flashcards

1
Q

ODDS RATIO OF CHILDREN OF ALCOHOLICS TO BE ALCOHOLIC

A

4–5 times

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2
Q

role of aldehyde dehydrogenase in alcoholism

A

ALDH2*2 causes facial flushing, tachycardia, headache, hypotension with alcohol consumption and is therefore protective against alcoholism

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3
Q

which neurotransmitters are involved in alcoholism

A

D2 dopamine receptor(DR D2) and GABA are associated with alcoholism.

Serotonin transporter linked polymorphic region can also be involved receptors play central role in the reward process

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4
Q

percentage of genetic contribution to smoking initiation and persistence

A

50% initiation is genetically influenced. 70% of smoking continuation is genetically influenced

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5
Q

prevalence of allele of A1 RDD2

A

found in current smokers. Found in progressively increasing amounts in nonsmokers, past smokers, current smokers

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6
Q

mechanism of cocaine

A

cocaine causes blockade of dopamine reuptake and other monoamines resulting in accumulation of extracellular dopamine in the synaptic cleft

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7
Q

sounds likea cow

Mechanism of action of opioids

A

primarily act at mu opioid receptor

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8
Q

familial abuse of cannabis

A

mild heritability.

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9
Q

list limbic nuclei

A

amygdala

Hippocampus

Medial prefrontal cortex system

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10
Q

affinity of psychostimulants

A

–psychostimulants bind to all biologic amine transporters.

–Reenforcing potential is linked to dopamine but not serotonin or norepinephrine sites

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11
Q

what causes reinforcing effects of morphinelike opiates?

A

stimulation of mu opioid receptors is the main cause.

They’re widely distributed throughout the central nervous system

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12
Q

effects of ethanol on dopamine

A

–ethanol increases extracellular dopamine levels in the nucleus accumbens.

–Also affects calcium channel and potassium transport

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13
Q

effective opioid receptor antagonist on alcohol consumption

A

opioid receptor agonists increased ethanol self administration at low doses,

but decrease alcohol consumption at higher doses.

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14
Q

personality symptoms of potential addicts

A

sensation seeking

Delay discounting

Impulsivity

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15
Q

affective disorders and SUD

A

one third of comorbid individuals report that SUD preceded bipolar disorder

Major depressive disorder doubles odds of having SUD

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16
Q

schizophrenia and SUD

A

47% of schizophrenics meet lifetime diagnosis of substance abuse disorder

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17
Q

anxiety, PTSD and SUD

A

SUD much more common with anxiety and/or PTSD

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18
Q

attention deficit hyperactivity and SUD

A

20% of adults with SUD has ADHD.

Treatment of childhood ADHD with psychostimulant does not increased rates of SUD is adults

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19
Q

childhood adversity factors IN SUD

A

parental substance-abuse

Family violence Physical

Sexual abuse

Poverty

Multiple factors common! 4 family attachment

Poor school attachment

Involvement with drug using friends

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20
Q

adult alcoholism and stressful life events

A

Adults tend to use alcohol and drugs to mitigate pain in stressful life events,

but rarely are severe life stressors and independent major contributor

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21
Q

incidence of drug abuse in incarcerated people

A

in 2004 53% of state and 45% on the Federal inmates met DSM criteria for abuse or dependence

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22
Q

incidence of drug abuse at time of arrest

A

one quarter–one third of inmates were using illicit drugs at the time of their crime

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23
Q

incarcerated substance abusers by race

A

19% of white prisoners

21% Hispanic prisoners

23% a black prisoners

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24
Q

employment among substance abusers

A

17% unemployed

8% employed

Physicians and medical workers have historically higher rates of substance abuse

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25
Q

common comorbidities with substance abuse

A

depression

Antisocial personality disorder

General anxiety disorder

Mood disorders

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26
Q

HIV and substance use disorder

A

gay men traditionally had highest rate of HIV = 56%

IV drug users 11% of HIV

Recent years has seen declining in HIV in both groups

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27
Q

hepatitis C and substance abuse

A

peak incidence of hepatitis C was in the late 1990s

IVDA was most common cause

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28
Q

alcohol use by race

A

55% of all adults Americans her current alcohol user’s

21% report binge drinking

5% report heavy drinking

22% of whites report bbinge drinking

6% report heavy use

20% of Blacks report binge drinking

6% report heavy drinking

Native Americans report 23% binge drinking

12-1/2% heavy drinkers

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29
Q

percentage of Americans who have tried marijuana at least once

A

41% Americans have tried marijuana

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30
Q

rates of tobacco use

A

between 2002–20011 smoking declined from 26% to 22%

Smoking typically begins during adolescence

67% of eighth graders have tried smoking

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31
Q

rates of heroin and opioid use

A
  1. 1% of Americans have tried heroin
  2. 5% of 12 graders have used
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32
Q

cocaine use rates

A

approximately 1% hhave tried cocaine

Crack use is approximately 0.1%

blacks and White’s use approximately equal

Majority of cocaine hospitalizations were for chronic smoker’s

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33
Q

list most common club drugs

A

MDMA

GHB

Ketamine

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34
Q

methamphetamine rates

A

less than 1%

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35
Q

Rates of pharmacological stimulants

A

approximately 5% for nonmedical use of psychostimulants in K–12

7% of college students use them

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36
Q

rates of substance-abuse treatment

A

40% of treatment admissions for SUDwere not in labor force

30% of admissions were unemployed people

Majority of admissions were between 25 and 44 years old

70% men,

60% white,

25% black

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37
Q

What substances cause admission to treatment centers?

A

Alcohol 40%

Opiates, especially heroin 19%

Marijuana/hashish 16%

Cocaine 13%

Stimulants, especially methamphetamine 8%

40% at both alcohol and illicit drug

51% of opioids were self admits

14% were in criminal justice system

56% of marijuana users came to criminal justice

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38
Q

list dimensions of ASAM placement criteria

A

–Acute alcohol or drug intoxication or withdrawal potential.

–Vital medical considerations and complications

–Emotional behavioral or cognitive conditions

–Readiness to change

–Relapse continued use and continued problem potential

–Recovery environment

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39
Q

list levels of care based on dimensions of ASAM planning dimensions

A

level 0.5 early intervention

Level I outpatient treatment

Level II intensive outpatient treatment/partial hospitalization

Level III residential/intensive inpatient treatment

Level IV medically managed intensive inpatient treatment

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40
Q

Federal 5 drug tests– SAMHSA panel 1

A

amphetamine

Cannabinoids

Cocaine

Opioids

PCP

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41
Q

SAMHSA panel 2

A

barbiturates

Benzodiazepines

Methadone

Oxycodone

methylene dioxy methamphetamine (MDMA )

MDA

Alcohol

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42
Q

SAMHSA panel 3

A

LSD

Psilocybin

Ketamine

Other Club drugs

Other designer drugs

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43
Q

percent alcohol in various drinks

A

beer 3.2%–4.5%

wine 7 – 14%

Distilled beverages 40–75%

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44
Q

amount of alcohol needed to be legally drunk

A

4 drinks in an hour we will produce 0.08 g per 100 mL blood alcohol

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45
Q

biomarkers of alcohol use

A

gamma GT

ALT

AST

Carbohyydrate deficient transferrin

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46
Q

direct biomarkers for alcohol

A

ethyl glucuronide

Ethyl sulfate

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47
Q

in DSM 5, how many of how many criteria need to be met for diagnosis?

A

must meet 2 of the 11 criteria to diagnose SUD

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48
Q

changes from DSM-IV to DSM-V

A

–eliminating legal problems as criteria

–Adding cravings as a criteria

–Eliminated distinction between abuse and dependence

–Has separate criteria for each abusable substances

–Added caffeine withdrawal and can have his withdrawal

–Nicotine dependence is now nicotine use disorder

–Cocaine and amphetamines lumped in single stimulant use category

–Added severity codes mild, moderate, severe

–Added gambling disorder

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49
Q

how many criteria are needed in the severity codes in DSM-V

A

–mild equals 2–3 criteria

–Moderate = 4–5 criteria

–Severe = 6+ criteria

–early remission = >3 months

–Sustained remission = > 12 months

–Also’s for some diagnosis includes maintenance therapy or if patient is in a contained environment

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50
Q

ICD–10 dependence course modifiers

A

currently abstinent

Currently abstinent, in protected environment

Control dependence (methadone, nicotine gum etc.)

Currently abstinent, receiving adversive or blocking drugs e.g. naloxone disulfiram

Currently using actively

Continue issues Episodic use = dipsomania

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51
Q

number of people worldwide who consume alcoholic beverage

A

2 billion = one half of world population consume alcohol

–55% men

–34% women

30% of drinkers consumes 75% of all alcohol

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52
Q

highest and lowest countries for alcoholism

A

Hong Kong equals 4.5% alcoholism

Korea equals 22% alcoholic

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53
Q

statistics and US alcoholism

A

–87% of US adults have drank alcohol in their life

– 14% of adolescence male and female consume alcohol

–Highest drinking rate are young men 18–25 years old

Highest drinking rates

–Non-Hispanic whites

–Native Americans and Hispanics

–Non-Hispanic Caucasian

–College education usually doubles drinking rates

–5% of Americans meet criteria for alcohol abuse

–4% meet criteria for alcohol dependence

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54
Q

number of criteria needed for diagnosis of alcoholism under DSM-V

A

2 criteria are needed for diagnosis of substance use disorder under DSM-V

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55
Q

progression of alcohol behavior to the ages

A

early and mid 20s = daily heavy drinking frequent binge drinking.

–Produces euphoria and inhalation following first drinks

Early 30s = alcohol related psychosocial problems began to emerge, work absences, family conflicts, legal problems, accidents Frank loss of control over drinking worsening social and work problems, medical complications, often cognitive deficits

Early 40s = liver cirrhosis, chronic pancreatitis, emergency room visits, DVTs and trying to withdraw

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56
Q

absorption of alcohol

A

an empty stomach, 80% of alcohol is absorbed in duodenum and jejunum,

20% of alcohol is absorbed in stomach If consumable food because gastric emptying slowed

–stomach is main site of absorption

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57
Q

distribution of alcohol in the body

A

–poor solubility in fat

–Crosses all biologic membranes

–Women and elderly get drunk faster because of lower total body water, i.e. they reach a greater peak BAL with an equivalent dose of alcohol

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58
Q

alcohol dehydrogenase

A

ADH found in gastric mucosa

First-pass metabolism greatly determines alcohol toxicity is a determines bioavailability

First-pass metabolism is reduced and women and alcoholics due to decreased ADH activity

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59
Q

drugs that affect first-pass metabolism of alcohol

A

cimetidine, ranitidine, aspirin decrease gastric first-pass metabolism by inhibiting gastric ALDH aldehyde dehydrogenase in mitochondria

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60
Q

pharmacology of alcohol elimination

A

–90% eliminated as water and carbon dioxide

–1% transformed to ethyl gluconeride and eliminated in urine

–4% excreted unchanged in breath urine and sweat

–Averages about 1 drink per hour

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61
Q

effects of alcohol on neurotransmission–dopamine

A

alcohol enhances dopamine release by directly increasing fired rate of dopamine cells.

–Chronic alcohol exposure and withdrawal produced changes in dopaminergic transmission that are the opposite of acute effects of alcohol

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62
Q

effects of alcohol on neurotransmission–GABA

A

acts similar to benzodiazepine or barbiturates

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63
Q

effects of alcohol and neurotransmission –endorphins

A

alcohol administration stimulates hypothalamic symphysis and release of endogenous opioids

–such as beta endorphin and enkephalin

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64
Q

effects of alcohol on neurotransmission–serotonin

A

alcohol administration increases brain concentrations of serotonin (5-HT)

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65
Q

genetics of alcohol dependence

A

sevenfold increase in alcohol dependence in first-degree relatives of alcohol dependence persons

–However majority of alcohol dependence people do not have alcohol dependent first-degree relatives

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66
Q

chromosomal site of alcohol dependence

A

long arm of chromosome #4, where the ADH Gene cluster occurs.

Among African-Americans, significant linkage noted between alcohol dependence and chromosome 10

–Multiple other genes involved and they all interconnect with environment

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67
Q

evaluation questions for alcoholism

A

take complete drinking history

–Typical quantity and frequency of alcohol consumption

–Maximum number of drinks per drinking occasion

–Frequency of heavy drinking episodes

–History of alcohol-related problems

–Psychiatric symptoms–precipitation or exacerbation –History of medical complications

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68
Q

cage questions

A

cut down on drinking

Annoyed by people criticizing her drinking

Guilty about drinking

Eye-opener

–2 or greater suggests alcoholism

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69
Q

laboratory markers of alcoholism

A

carbohydrate deficient transferrin (CDT)

–Increase and despite heavy drinking

–Very specific

–Return to normal 1–2 weeks of abstinence

–Good indicator of relapse to alcohol

–Is only laboratory test approved by FDA for detection of heavy alcohol consumption Gamma glutamyl transpeptidase

–induced by alcohol consumption

–Falls by 50% within 2 weeks a sensation

–Normalization inhibited I alcoholic liver disease

–Also elevated in many nonalcoholic liver diseases

–Present in three fourths of alcoholics before evidence of liver disease

–More specific for alcoholic liver disease than CBT

LFTs

–SGPT/SGOT

–Nonspecific

–Ratio greater than 1.5 suggests alcohol damage

MCV

–Caused by folate deficiency

Alcohol breath test and blood alcohol level

–But alcohol greater than 1 50 mg/dL in patient showing no signs of intoxication is generally physiologic tolerance

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70
Q

treatment of alcohol withdrawal

A

social detoxification

–frequent reassurance

–Monitoring

–Generally outpatient Medical detoxification

–Use of agents acting on GABAergic transmitter

––Benzodiazepines our first choice

–––Diazepam and chlordiazepoxide are bests preventing seizures and DTs

––––Because they are long-acting

–administer thiamine 50–100 milligrams to prevent Wernicke-Korsakoff syndrome

71
Q

medications used to treat alcoholism

A

–disulfiram

–Naltrexone

–Acamprosate

–Topiramate being studied

–Ondansetron being studied

72
Q

treatment of anxiety and depression and alcoholism

A

buspirone his drug of choice for anxiety after detoxification.

–Treated with antidepressants as needed

73
Q

concurrent use of substances with alcohol

A

13% of alcoholicS use substances

50% of SUD use alcohol

74
Q

signs and symptoms of alcohol withdrawal–mild

A

signs and symptoms of autonomic hyperactivity

–Tachycardia

–Diaphoresis

–Tremor

–Nausea vomiting

–Insomnia –Anxiety Began 4-12 hours after last drink

–cheeks in 48 hours

–Subsided 4-5 days of sobriety

–Less severe symptoms last for a few weeks or up to 6 months

75
Q

signs and symptoms of alcohol withdrawal–severe alcoholism

A

10% of withdrawals are severe

–Delirium, and/or grand mal seizures

–Delirium tremens occur 5% of the time

––Severe signs of autonomic hyperactivity

––Fluctuating level of consciousness and disorientation

–––(2-3 days after last drink

–Vivid hallucinations of auditory visual or tactile nature even and clear sensorium

–Seizures occur 5% of the time within 48 hours of sobriety

Predictors of complicated alcohol withdrawal

–Old age –Poor nutritional status

– Occurring medical or surgical conditions

–History of high tolerance alcohol

–History of previous DTs

76
Q

alcohol-induced cognitive disorders

A

chronic alcohol drinking can result in severe folate and thiamine deficiency leading to severe neurocognitive problems

–Wernicke encephalopathy

––Confusion, disorientation ataxia, nystagmus and cane palsies

–Response to thiamine repletion. Repeated episodes of Wernicke encephalopathy can lead to persistent alcohol-induced amnestic disorder known is Korsakoff psychosis

–Confabulation caused by deficits and antegrade and retrograde memory

–Patient’s are unaware of their condition

77
Q

4 known opioid receptors

A

–mu

–Sigma

–kappa

–SQ peptide

78
Q

effects of mu receptors

A

mu receptors are preferentially activated by beta endorphin

–Responsible for classic morphinelike actions

––Analgesia

––Euphoria

––Cough suppression

––Respiratory suppression

––Pupillary constriction

––Constipation

79
Q

effects of Sigma receptors

A

–anxiolytic

–Antidepressant like

–Pro convulsant effects

80
Q

effects of kappa receptors

A

–analgesia

–Pro-depression

–Dysphoric effects

81
Q

criteria under DSM-V for SUD

A

–neither tolerance nor withdrawal is necessary nor sufficient for the diagnosis of an opioid use disorder

–DSM-V merges diagnosis abuse and dependence

–criteria for opioid SUD is a fulfill 2 of 11 criteria

–More criteria means more severity

82
Q

relatives speed of action of opioids by route of use

A

slowest

Oral Intranasal

Intramuscular

Subcutaneous

Intravenous

Inhalation (smoking)

Fastest

83
Q

country with the largest licit production of opioids

A

India is a largest producer of licit opioids, and the highest use of illicit opium

84
Q

demographics of cocaine use in USA

A

about 1% of Americans use cocaine

About 25% of these use crack cocaine

Total about 800,000 people with cocaine abuse or dependence

75% of cocaine users entering treatment are crack cocaine users

Higher usage with less education

Young smokers have 15 times higher cocaine use of than nonsmokers

85
Q

chemical name for cocaine

A

benzoyl methyl ecgonine

86
Q

drugs also in cocaine family

A

tropane family includes

–cocaine,

–atropine,

–scopolamine

87
Q

primary neuro-pharmacologic effect of cocaine

A

blocks uptake of monoamines released into synapses of CNS

Page 59

88
Q

pharmacology of cocaine

A

–lipophilic molecule

–Readily absorbent by mucous membranes and alveoli lining

–one third of oral or nasal dose absorbed

–95% of inhaled dose of freebase or crack bioavailable

–Readily penetrates blood-brain barrier

–Volume distribution is low

89
Q

benzoylecgonine

A

metabolite of cocaine –Cardiotoxic

90
Q

street cocaine

A

–rarely pure on street

–Adulterated with mannitol, lactose or glucose to add weight

–Adulterated with caffeine, lidocaine, amphetamines, quinine, heroin to add taste and additional CNS stimulation

–Usual street cocaine = 10%–50% pure

91
Q

smoked cocaine effects

A

–any form of smoke cocaine is the most addictive, most rapid onset and most intense effect

–Can be 10 seconds to feel high

–High from smoking is faster than IV

–Often smoked with alcohol opioid to blunt undesirable effects and prolong high

–Coca ethylene = cardio toxic metabolite increases mortality

92
Q

why is smoked crack cocaine so addictive?

A

–high lasts only 5–10 minutes

–High is followed by extremely anxious and depressed sensation in users immediately crave the euphoria they just felt

93
Q

neurobiology of cocaine

A

–sometimes called disease of brains pleasure centers

–Affects dopamine

–acts on basal forebrain, including nucleus accumbens, and entire limbic system

–Impairs dopamine uptake, but also serotonin and norepinephrine

94
Q

effects of cocaine on dominant and submissive animals

A

seem to have greater high in dominant animals and less effect on submissive animals

95
Q

initial evaluation and management of cocaine intoxication

A

–withdrawal may not be prominent

–largely psychologic withdrawal

–Dysphoria, intense cravings

96
Q

patterns of cocaine use

A

–severity withdrawal symptoms can be estimated from pattern use

–Chronicity of abuse tends to reflect disarray in the patient’s life

–Rarely find a “functioning cocaine user”

–With continued use, often less pleasure due to tolerance, and increased dysphoric effects and accumulation of adverse consequences

97
Q

inpatient versus outpatient cocaine rehabilitation

A

usually outpatient

–No severe withdrawals

–Goal is return to normal life

–more convenient, especially for women with children

–inpatient therapy when there are multiple relapses or other Complications

98
Q

pharmacologic management of cocaine use

A

–immunotherapies are being developed

––Include inactivated cholera B toxin

––may diminish euphoria

99
Q

cocaine agonist therapy

A

modafinil has had some success but has abuse potential

100
Q

relapse prevention of cocaine

A

disulfiram may be helpful in preventing cocaine relapse

N acetylcysteine may be useful

Antidepressants and anticonvulsants have not shown value

101
Q

cocaine associated psychiatric disorders

A

–75% of cocaine users may have other psychiatric illness

–However cocaine symptoms may mimic other diseases

–Depression and anxiety disorders may drive reinforcing effects of cocaine and increased risk of relapse

–depression, dysthymia, anxiety, bipolar disorder are most common

–Up to 30% of cocaine user’s have residual ADHD and can give paradoxical relaxation similar to the stimulants

–Methylphenidate has been used for maintenance equivalent to methadone maintenance

––Most effects occur in patients with residual ADHD

–Acute, subacute, and chronic paranoia are common with cocaine use

–Cocaine delirium with or without psychosis features resolved in 3-5 days

–co–occurring alcoholism occurs in about 90% of cocaine abusers

102
Q

medical complications of cocaine use

A

sudden cardiac death,

fatal intracranial hemorrhage,

malignant hyperthermia,

rhabdomyolysis,

renal failure have been documented with first-time use or chronic use

103
Q

cardiovascular syndromes with cocaine use

A

cocaine affects release and uptake of epinephrine and norepinephrine causing a shift in the blood supply from the skin and the viscera into the skeletal musculature

increases oxygen levels and blood sugar levels

–Produces tachycardia with increased cardiac contractility and hypertension –Myocardial oxygen demand may outstrip supply

–Increases atherosclerotic coronary artery and renal artery disease

104
Q

EKG changes with cocaine

A

atrial-ventricular nodal conduction block

–QT interval

–widening PVCs,

–ventricular tachycardia and asystole are common causes of death

105
Q

presentation of cocaine users in the emergency room

A

–effects of violence

–Atypical, even bizarre chest pain

–Multiple other pathologies may develop

–Consider cocaine toxicity in young adult with chest pains or signs of congestive heart failure with or without other risk factors

106
Q

pulmonary changes with cocaine–

A

–shortness of breath is second-most common cocaine related medical systems in ER

––Often related to cocaine inhalation

––Exacerbates asthma

–Can cause telltale disruption of the nasal septum, nasal cartilage, and hard or soft palate

107
Q

crack lung syndrome

A

crack lung syndrome

–pneumonia type symptoms

–Shortness of breath

–Atypical chest pain

–High-temperature

–Negative or nonspecific abnormal chest x-ray

–May be related to talcum talcum or baking soda used to cut cocaine

108
Q

neuropathology of cocaine

A

–global cerebral hypoxia

–Ischemia secondary to cardiopulmonary failure

–Hypertensive encephalopathy

–Intractable seizures

–Thromboembolic stroke

–Lobar hemorrhages

–Subarachnoid hemorrhages

109
Q

–treatment of cocaine-induced seizures

A

benzodiazepines preferred

–Neuroleptics should be avoided due to seizure threshold lowering

110
Q

neurologic effects of chronic cocaine abuse

A

chronic cocaine use can

–can cause dopamine disinhibition phenomena

–Increase release a prolactin (most common endocrine abnormality with cocaine)

–Extrapyramidal dysfunction including

––akathisia

––dystonias

––Choreiform movements

––bruxism

––severe typical movements and disordered gait (=crack dancing)

111
Q

effects of cocaine on appetite

A

increase glucocorticoid response

–Inactivation of feeding center resulting in loss of primary drive to eat

–Severe loss of appetite and body weight

–Muscle wasting

112
Q

effects of cocaine and sexuality

A

–something it may be an aphrodisiac

–Can produce spontaneous organism

–Chronic use results and loss of interest in sex (possibly due to hyperprolactinemia)

–Derangements in menstrual cycle Galactorrhea, amenorrhea, infertility

–Crack smoking isn’t independent predictor of HIV seropositivity

113
Q

cocaine and pregnancy

A

crack babies are partially affected by poor nutrition, hygiene and neglect

–High rate a spontaneous abortion, higher than heroin because she hadn’t to be pain

114
Q

active ingredient in cannabis

A

9 tetra hydro-cannabinol

115
Q

epidemiology of cannabis

A

most common illicit drug

–41% of US population have tried it

–10% have used in the last year

–6% in past month

–2% use cannabis daily

–Similar in European countries

–Much lower but increasing rates in Third World countries

116
Q

characteristics of cannabis users

A

male greater than female

–Most common use between 18 and 25 years old

–Highest initiation rates among 12-25-year-olds

–Self identified multiracial have highest rate of use

––Following African-Americans

––Followed by whites

––Followed by Hispanics (lowest rates)

117
Q

sinsemilla

A

unfertilized flowers of female cannabis Plant

–7–15 percent THC versus 1-5% for whole Plant

118
Q

hashish

A

–the resin of cannabis Plant, containing 10-20% THC

–hash oil is derived from concentrated resident extract–up to 60% THC

119
Q

physiologic effects of cannabis use

A

–dry mouth

–Stimulated appetite

–anti-emetics effect at low dose –

–Vomiting at higher doses

–Increased resting heart rate

–Increase orthostatic hypotension

–Redness of the eyes caused by dilatation of small vessels

120
Q

mental effects of cannabis use

A

impaired focus and divided attention

–short-term and episodic memory loss

–Decreased complex cognitive processing

–Some decrease in motor ability

–Sustained use may impair attention, memory

121
Q

cannabis withdrawal syndrome

A

–anger and aggression

–Anxiety

–Depressed mood

–Irritability and restlessness

–Sleep difficulty and strange dreams

–Decrease appetite and weight loss

–Chills, headaches physical tension

–Sweating

–Stomach pain

–General physical discomforts

–Begins within 24 hours of cessation

–Peak some the first week

–Last 1-2 weeks

122
Q

discuss cannabinoids

A

–90 different cannabinoids Known

–Excreted through Feces and Urine

–THC Is Highly Lipophilic, Therefore Stored in Fatty Tissues

––THC recruited from fatty tissues does not seem to produce intoxication

123
Q

cannabinoid receptors

A

CB 1 and CB 2

–CB 1 is the most psychoactive and causes the most reinforcement

124
Q

genetics of cannabis

A

heritable factors contributed 30%–80% of total variance in risk for cannabis use disorder

125
Q

quantity of cannabis produced yearly

A

worldwide approximately 100,000 metric tons

126
Q

comorbidities of cannabis use

A

–high rates of alcohol and nicotine dependence

–Associated with poor life satisfaction

–Higher rates of depression, anxiety, suicide attempts, conduct disorders

–Higher rates of most psychiatric disorders

127
Q

cannabis and psychotic disorders

A

some evidence the cannabis can cause psychotic disorders and symptoms.

Evidence is not definitive

128
Q

respiratory effects of cannabis

A

half of cannabis smokers also smoke tobacco

–Contains respiratory toxins similar to tobacco

–Could have more carcinogens and greater Tarr deposits in the lung than filtered cigarettes

–Cannabis smokers inhale deeply, hold the smoke longer than tobacco users

–Is a bronchodilator, which increases vulnerability to smoke

–Cannabis increases absorption of carbon monoxide

129
Q

cannabidiol and cancer

A

–while THC seems to have cancer fostering properties, cannabidiols may have some tumor reducing effects in rodents

130
Q

cannabis and pregnancy

A

up to 20% of women use cannabis during pregnancy

–Little evidence of major congenital abnormalities has been found

131
Q

cannabis and cardiovascular

A

–primary effect is tachycardia that diminishes with tolerance

––No evidence of long-term cardiovascular problems in otherwise healthy users

132
Q

brain function and cannabis

A

chronic cannabis produces changes in brain areas with higher cognitive functions

–Early initiation of cannabis produces some structural abnormalities

–Many acute effects reduced with tolerance

–Consistent effects observed on short-term memory, especially immediate memory, recall and retrieval

133
Q

most common users of amphetamines

A

Military

––Because of long hours of sleep deprivation

––Military investigating modafinil as possible alternatives

Students

––Higher levels of alcohol, cannabis and, and cocaine use with amphetamine users and school

Athletes

––Evidence for performance enhancement is equivocal

––Thought to improve mood, aggression, self-confidence

––Deaths due to overheating due to peripheral vasoconstrictionresulted in amphetamines being the first drug block for Olympics

134
Q

mechanism of action of amphetamines

A

amphetamines increased synaptic concentrations of the mono means dopamine, serotonin, and norepinephrine

135
Q

types of amphetamine stimulants

A

–amphetamine

–Methamphetamine

–Methylphenidate

136
Q

scope of amphetamine use worldwide

A

–55 million people worldwide use amphetamines regularly

––But only 21 million people use cocaine and opioids daily

–Methamphetamine is most available and most abused

–About 500 metric tons produced yearly

Page 83

137
Q

comorbidities of amphetamine use disorder

A

–increased likelihood of psychiatric symptoms

–Increased drug use psychotic syndromes

–Increased previous suicide attempts and violent behavior problems

–Difficult to distinguish amphetamine psychosis from schizophrenia

–Treat amphetamine psychosis as with any other psychosis

–Methamphetamine associated with violent criminal behavior and recidivism

138
Q

pharmacodynamic effects of amphetamines

A

–amphetamines have long duration of action

–Initial rush of euphoria––may last up to 12 hours

–Hyperalertness

–Increased energy

–Decreased appetite

–Intensified emotions

139
Q

withdrawal effects of amphetamines

A

amphetamine withdrawal

–Insomnia

Restlessness

Hyperthermia

–Seizures

–Abuse and dependence

–Agitation

–Paranoia

–Mood disturbances

–Psychosis

–Cognitive impairment

140
Q

amphetamines as drugs of abuse

A

–cognitive behavioral therapy and contingency management have value in reducing amphetamine use

–bupropion may have some value in amphetamine rehabilitation

–Modafinil may have some value, given that his stimulant like material

–no good pharmacotherapy for amphetamine use

141
Q

epidemiology of sedative hypnotics–benzodiazepines

A

–benzodiazepine rarely first drug of abuse

–low rates of abuse

–Rarely primary drug of abuse

––Usually tied to marijuana, opioids or alcohol

–Peak use of benzodiazepines was in 1973

–Mostly replaced by Z drugs

–About 1% of population uses benzodiazepines for more than a year

–Long-term use more common among elderly, women, and people with chronic health problems

–20% of alcoholics also take benzos

–30% of psychiatric patient’s are prescribed benzodiazepines

–Anxiety disorder patient’s generally do not misuse benzodiazepines

142
Q

comorbidities of sedative hypnotic drugs

A

–all are CNS depressants

–And higher doses slurred speech, ataxia, impaired gag reflex

–To therapeutic doses to adverse effects

–Side effects stronger in elderly patients

–No evidence of cleft palate when taken during pregnancy

–Benzodiazepine during pregnancy can lead to withdrawal syndrome in baby or floppy baby syndrome

–Barbiturates can produce major fetal malformations

143
Q

sedative hypnotic abuse determinants

A

–barbiturates produce to greatest pleasant mood alterations

–Rapid onset, short duration benzodiazepines have greatest risk of abuse

–Alprazolam Produces the best high

–Tolerance to benzos and Barbies is well-established

144
Q

tolerance to barbiturates and benzodiazepines

A

–temazepam and eszopiclone do not develop tolerance to hypnotic effect

––Low rebound insomnia

–Patient’s developed little or no tolerance to anti-anxiety effects of benzos and barbiturates

145
Q

primary mediator of inhibition of neurotransmission in mammalian brain

A

GABA is mediator of inhibition

146
Q

determinants of abuse in benzodiazepines and barbiturates

A

–benzodiazepines have moderate potential for abuse

––Lower the methyl Quaalude or barbiturates and older hypnotics

Most addictive

––Diazepam

––Lorazepam

––Alprazolam

––Triazolam

–Chlordiazepoxide and oxazepam are the least abuse potential

147
Q

how are benzodiazepines metabolized in the liver?

A

benzodiazepines capitalized by cytochrome P 50 enzymes

–Therefore potential for drug–drug interactions

148
Q

name some Z drugs

A

zopiclone

Eszopiclone

zolpidem

zaleplon

149
Q

differences between Z drugs and benzodiazepines and barbiturates

A

–Z drugs do not produce marked changes in sleep architecture

but produce

––amnestic effects(less than benzos)

––anticonvulsant actions

––anxiolytic activity

––motor impairing effects

––muscle relaxant effects

150
Q

half-life of Z drugs

A

half-life of Z drugs is 1–4 hours for varying drugs

Can be up to 7 hours in the elderly

151
Q

determinants of abuse of Z drugs

A

–zolpidem is often abuse in the range of 100s of milligrams (therapeutic equals 10 mg daily)

–Use for anxiolytic, you for reck, or stimulant effects

–Effects can be additive with alcohol

–low tolerance developed with therapeutic doses

–Seizures can develop after high-dose abuse of Z drugs

152
Q

discussed barbiturates

A

–uses anticonvulsants, sedative hypnotics, anesthetic agents

–Low therapeutic index, therefore frequent toxic reactions

–High risk of abuse and dependence

–Can have severe even lethal withdrawal

153
Q

adverse effects of barbiturates

A

–nonselective, cannot separate anti-anxiety effects from other depressant effects

–Reduced slow-wave and REM sleep

–Produce sedation and disruption of motor coordination

–An elderly can produce paradoxical excitement

–Occasional exfoliative dermatitis and/or allergic reactions

–Cause of death is usually respiratory depression, respiratory acidosis, cerebral hypoxia and possibly pulmonary edema and renal failure

154
Q

barbiturates induced drug tolerance of other drugs

A

–barbiturates induce cytochrome P4 50 enzymes and liver therefore may reduce plasma concentrations of the large number of drugs

page 99

155
Q

withdrawal effects of barbiturates

A

–barbiturate withdrawal can be severe even life-threatening

–Produced delirium and seizures

–Migraine patients receiving a talbutal risk developing withdrawal including seizures

156
Q

gamma hydroxybutyrate

A

–gamma hydroxybutyrate = GHB

–Approved in US for treatment of cataplexy, excessive daytime sleepy

–Used in Europe for alcohol dependence and withdrawal

–Sometimes abused in nightclub settings with other club drugs

157
Q

effects of GHB

A

–readily crosses brain blood barrier

–Produces sedation and sleep

–At higher doses produces anesthesia

–Abuse produces euphoria, disinhibition, increased libido

GHB has low therapeutic index

–Toxic doses produced, respiratory depression seizures bradycardia and death

158
Q

pharmacology of GHB

A

–half-life of GHB = 20–40 minutes

–Difficult to detect in urine because a short half-life

–

Often rapid recovery from toxic dose

159
Q

determine us of GHB abuse

A

tolerance to GHB

160
Q

list common hallucinogens,

A

LST = lysergic acid diethylamide

Psilocybin

psilocin

DMT = dimethyl tryptamine

mescaline

DOM = dimethyloxy methyl amphetamine

Cannabis

Phencyclidine = PCP

MDMA = methylene dioxy methamphetamine

161
Q

discuss LSD

A

–first synthesizing 1938

–Hoffman accidentally ingested some and had worlds first trip on bicycle ride home

–Seeds of morning glory contain lysergic acid derivatives, especially lysergic acid amide

––Commercial packed often have insecticides, fungicides etc.

–Used rarely more than once per week due to rapidly developing tolerance

–Is one of the most potent hallucinogens known

162
Q

–discuss psilocin and psilocybin

A

occur naturally in a variety of mushrooms

–Mexican magic mushroom psilocybe mexicana

–Most product is produced sympathetically

–Related to ayahuasca

163
Q

discuss mescaline

A

–present in peyote cactus lophophra

–grown in Northern Mexico and southwestern US

–Effect lasts 6-10 hours

164
Q

acute effects of hallucinogen

A

–most acute effects of hallucinogens are very similar

–Different rate of onset, duration of action, absolute intensity

–First 4 hours of LSD are called pretrip

––Include dizziness, paresthesias, weakness, tremor, altered visual and hearing changes, mood changes, altered time sent, depersonalizations

– later visual alterations intensify

–Developed synesthesia = seeing smells, hearing colors

–Rapid mood changes can be extreme

–Later still, paranoia occurs. Dissipates 10-12 hours later

–Satiation is completely after event

–Memory for the events is quite clear afterwards

165
Q

effects of chronic hallucinogen use–tolerance

A

–tolerance develops rapidly after repeated dosing and disappears rapidly with abstinence

166
Q

mechanism of actions of hallucinogens

A

LSD and hallucinogens alter serotonin neurotransmission

–Many hallucinogens, including LSD, are structurally similar to serotonin

–

167
Q

adverse reactions to hallucinogens

A

–hallucinating trip can be pleasant or unpleasant

–Individuals who value self-control do poorly

Adverse experiences during trip EEG being arrested may precipitate anxiety reactions

–Previous pleasurable traps give no immunity to adverse reaction

–Higher doses tend to give worse reactions

–Treated with benzodiazepines for anxiety reactions

–”Bad trip” is anxiety or panic reaction

–Depression and suicidal ideation can occur several days after LSD

–Differential diagnosis is between LSD psychosis and paranoid schizophrenia

––Auditory hallucinations suggest schizophrenia

–Therapeutic index of LSD is very high therefore generally safe,

168
Q

treatment of acute hallucinogen crisis

A

–Treatment drug of choice = benzodiazepine

–Severe reactions can be controlled with Haldol

169
Q

long-term adverse effects of hallucinogen usage

A

long-term use of hallucinogens

–No evidence of brain cell damage or teratogenic effects

Chronic effects

––Psychosis

––Depressive reactions

––Acting out

––paranoid states

––Flashbacks

––––Can occur even months after good or bad trip, last only a few seconds, but her frightening because of lack of control

Flashbacks can be initiated by SSRIs

–Flashbacks treated with SSRIs, psychotherapy, or benzos

170
Q

Effects of PCP intoxication

A

At low doses, PCP resembles alcohol intoxication with getting euphoria

––Can produce anxiety, paranoia, emotional outbursts

Higher doses can lead to dysarthria, ataxia, increased deep tendon reflexes, decreased pain sensation, tachycardia, hypertension, altered perception

Is one of few drugs that can cause vertical nystagmus

171
Q

Use of PCP

A

PCP is fairly cheap and is often used adulterated other substances

People often unaware that they were getting PCP

Usually smoked with marijuana

Occasionally inhaled or taken orally

172
Q
A
173
Q

Alternate Names for PCP

A

PCP is often called

–Angel dust

–Killer weed

–Ozone

–There is other names

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