Kk&s Ch.12 Substance Related Ds

Front 1

What happened during US Alcohol prohibition?

Back 1

Use went down, but crime went up

Front 2

define intoxication

Back 2

The term intoxication is used for a reversible nondependent experience with a substance that produces impairment

Front 3

What are some of the brain reward areas involved in addiction

Back 3

These various addictions may have similar effects on the activities of specific reward areas of the brain,

such as the ventral tegmental area,

the locus ceruleus, and the

nucleus accumbens.

Front 4

Explain psychological dependence

Back 4

Psychological dependence, also referred to as habituation, is characterized by a continuous or intermittent craving for the substance to avoid a dysphoric state

Front 5

Describe codependence?

Back 5

The terms coaddiction, coalcoholism, and, more commonly, codependency or codependence are used to designate the behavioral patterns of family members who have been significantly affected by another family member's substance use or addiction.

Front 6

Describe enabling

Back 6

Sometimes, family members feel that they have little or no control over the enabling acts.

unwillingness to accept the notion of addiction as a disease. The family members continue to behave as if the substance-using behavior were voluntary and willful (if not actually spiteful) and the user cares more for alcohol and drugs than for family members

This results in feelings of anger, rejection, and failure.

Front 7

Describe denial, including reasons

Back 7

Family members, as with the substance users themselves, often behave as if the substance use that is causing obvious problems were not really a problem; that is, they engage in denial.

Sometimes denial is self-protecting, in that the family members believe that if a drug or alcohol problem exists, then they are responsible.

When additional efforts at control fail, they often attribute the failure to themselves rather than to the addict or the disease process, and along with failure come feelings of anger, lowered self-esteem, and depression.

Front 8

Describe course modifiers for substance dependence

Back 8

Early full remission. This specifier is used if, for at least 1 month, but for less than 12 months, no criteria for dependence or abuse have been met

Early partial remission. This specifier is used if, for at least 1 month, but less than 12 months, one or more criteria for dependence or abuse have been met (but the full criteria for dependence have not been met)

Sustained full remission. This specifier is used if none of the criteria for dependence or abuse has been met at any time during a period of 12 months or longer.

Sustained partial remission. This specifier is used if full criteria for dependence have not been met for a period of 12 months or longer; however, one or more criteria for dependence or abuse have been met

Front 9

What % of total US populatoin suffers from substance related disorder?

Back 9

22.5 million = 10%

Front 10

Rank US drug (not alcohol) use among users in 2004

Back 10

1. Heroin 67.8%
2. Cocaine 27.8%
3. MJ 17.6%
4. Pain Relievers: 12.3%

Front 11

Does starting drug use at earlier age increases chances of addiction? At what age is considered earlier?

Back 11

Before age 14, yes, especially for acohol

Front 12

Among adults aged 18 or older who first tried alcohol at age 14 or younger, XX percent were classified as alcoholics compared with only YY percent who first used alcohol at age 18 or older.

Back 12

XX = 18%
YY = 4%

Front 13

What age is highest rate for dependence or abuse?

Back 13

Age 21:

The rate for dependence or abuse was 1.3 percent at age 12, and rates generally increased until the highest rate (25.4 percent) at age 21. After age 21, a general decline occurred with age.

Front 14

By age 65, only about XX percent of persons have used an illicit substance within the past year, which lends credence to the clinical observation that addicts tend to “burn out” as they age

Back 14

1%

Front 15

Define Misuse

Back 15

Similar to abuse, but usually applies to drugs prescribed by physicians that are not used properly.

Front 16

List demographic details of illegal drug use: 5

Back 16

1. More men use drugs that do women;

2. the highest lifetime rate is among American Indian or Alaska Natives;

3. whites are more affected than blacks or African Americans;

4. those with some college education use more substances than those with less education;

5. and the unemployed have higher rates that those with either part-time or full-time employment.

Front 17

Compare drug rates of large city, city versus rural

Back 17

> in large city and lowest in rural

Front 18

Rates of drug use among people on parole or on unsupervised jail release?

Back 18

41% vs
9%

Front 19

Is driving under the influence of drugs or alcohol increasing or decreasing over 2000 to 2004?

Back 19

increasing
alcohol 10 to 13.5
drugs 3.1 to 6

Front 20

Describe interaction of drug factors

Back 20

Environment, Drug, Person

Thus, drug availability, social acceptability, and peer pressures may be the major determinants of initial experimentation with a drug,

but other factors, such as personality and individual biology, probably are more important in how the effects of a given drug are perceived and the degree to which repeated drug use produces changes in the central nervous system (CNS)

Front 21

Psychodynamic factors in substance abuse:

Back 21

According to classic theories, substance abuse is a masturbatory equivalent (some heroin users describe the initial “rush” as similar to a prolonged sexual orgasm),

a defense against anxious impulses,

or a manifestation of oral regression (i.e., dependency).

Front 22

Match the drug to what it might self-medicate:
alcohol
opiods
amphetamines

Back 22

As a form of self-medication,
alcohol may be used to control panic,

opioids to diminish anger, and

amphetamines to alleviate depression

Front 23

How do substances create positive reinforcement?

Back 23

Each use of the drug evokes rapid positive reinforcement, either as a result of the rush (the drug-induced euphoria), alleviation of disturbed affects, alleviation of withdrawal symptoms, or any combination of these effects

Front 24

What are secondary reinforcers?

Back 24

Eventually, the paraphernalia (needles, bottles, cigarette packs) and behaviors associated with substance use can become secondary reinforcers, as well as cues signaling availability of the substance, and in their presence, craving or a desire to experience the effects increases.

Front 25

Drug users respond to the drug-related stimuli with increased activity in which brain regions?

Back 25

Drug users respond to the drug-related stimuli with increased activity in limbic regions, including the amygdala and the anterior cingulate

Front 26

Which drugs are known to activate limbic areas?

Back 26

cocaine,
opiods,
cigarettes (nicotine)

Front 27

Which area activates brain region associated with sexual stimuli?

Back 27

Interestingly, the same regions activated by cocaine-related stimuli in cocaine users are activated by sexual stimuli in both normal controls and cocaine user

Front 28

For a long time after withdrawal (from DRUGS?l), the addict exposed to environmental stimuli previously linked with substance use or withdrawal may experience conditioned withdrawal, conditioned craving, or both

Back 28

OPIODS
NICOTINE
ALCOHOL

Front 29

What elicits the most intense cravings?

Back 29

The most intense craving is elicited by conditions associated with the availability or use of the substance, such as watching someone else use heroin or light a cigarette or being offered some drug by a friend.

Front 30

What is evidence for genetic component to alcohol and other drug abuse?

Back 30

Strong evidence from studies of twins, adoptees, and siblings brought up separately indicates that the cause of alcohol abuse has a genetic component. Many less conclusive data show that other types of substance abuse or substance dependence have a genetic pattern in their development

Front 31

Regarding endogenous opioid activity (high, low, normal), which group at risk of opiod dependence?

Back 31

A person with too little endogenous opioid activity (e.g., low concentrations of endorphins) or with too much activity of an endogenous opioid antagonist may be at risk for developing opioid dependence

Front 32

Explain tolerance at neuroreceptor level.

Back 32

Even in a person with completely normal endogenous receptor function and neurotransmitter concentration, the long-term use
P.387

of a particular substance of abuse may eventually modulate receptor systems in the brain so that the presence of the exogenous substance is needed to maintain homeostasis. Such a receptor-level process may be the mechanism for developing tolerance within the CNS.

Front 33

Which are key NT's involved in dependence/abuse?

Back 33

he major neurotransmitters possibly involved in developing substance abuse and substance dependence are the
opioid,
catecholamine (particularly dopamine), and

γ-aminobutyric acid (GABA) systems

Front 34

List structures involved in brain-reward circuitry

Back 34

The dopaminergic neurons in the

ventral tegmental area are particularly important. These neurons project to the cortical and

limbic regions, especially the

nucleus accumbens. This pathway is probably involved in the sensation of reward and may be the major mediator of the effects of such substances as amphetamine and cocaine. The

locus ceruleus, the largest group of adrenergic neurons, probably mediates the effects of the opiates and the opioids. These pathways have collectively been called the brain-reward circuitry.

Front 35

What is comorbidity rate in those with addiction

Back 35

50%

Front 36

Are you more or less likely to seek tx if have current psych problem?

Back 36

more likely

Front 37

Which Pers Ds associated with substance abuse/dependence (SU)?

Back 37

Antisocial PD
35 to 60% also meet criteria for Antisocial PD

Front 38

Patients with substance abuse or substance dependence diagnoses who have antisocial personality disorder are likely to

Back 38

use more illegal substances;
to have more psychopathology;
to be less satisfied with their lives;

and to be more impulsive,
isolated, and

depressed than patients with antisocial personality disorders alone.

Front 39

Which 2 substances do you think of when you think depressive sx?

Back 39

opiods and
alcohol

Front 40

About XX of all those with opioid abuse or opioid dependence and about YY percent of those with alcohol abuse or alcohol dependence meet the criteria for major depressive disorder sometime during their lives

Back 40

XX up to 50%-33%
YY: 40%

Front 41

Persons who abuse substances are about XX times more likely to die by suicide than the general population

Back 41

20X

Front 42

About XX percent of persons with alcohol abuse or alcohol dependence have been reported to commit suicide.

Back 42

15%

Front 43

Which disorders are most associated with suicide?

Back 43

This frequency (15% of alcohol abusers or dependents) of suicide is second only to the frequency in patients with major depressive disorder.

Front 44

Describe groups broadly?

Back 44

programs that aim to control withdrawal and consequences (detox)
programs that focus on long-term change
programs that use Rx
Degree of psychotherapy

Front 45

Government agencies recently categorized publicly funded treatment programs for drug dependence as

Back 45

(1) methadone maintenance (mostly outpatient),
(2) outpatient drug-free programs,
(3) therapeutic communities, or
(4) short-term inpatient programs

Front 46

Describe stages of change:

Back 46

pre
contemplation
preparation
action
maintenance

Front 47

Which area has more, less studies regarding tx?

Back 47

few controlled studies of brief interventions for areas other than alcohol or smoking

Front 48

To have substantial reduction in illicit drug use, antisocial behaviors, and psychiatric distress among patients dependent on COCAINE or HEROIN are more likely to follow treatment lasting at least?

Back 48

3 months

Front 49

Outcomes often considered in programs dealing with illegal drug use?

Back 49

The outcomes usually considered in programs dealing with illicit drugs have typically included measures of

social functioning,
employment, and
criminal activity, as well as decreased drug-using behavior.

Front 50

What is best in treating psych ds and addiction: parallel, serial tx, both at same time

Back 50

both

Front 51

Social Benefits of treating addiction?

Back 51

Decrease antisocial behavior
Reduce rates of HIV seroconversion
In prison, decrease post-release re-arrests
Problem: seen as moral failing rather than medical disorder

Front 52

The average alcohol-dependent person decreases his or her life span by

Back 52

10 to 15 years, and alcohol contributes to 22,000 deaths and 2 million nonfatal injuries each year

Front 53

Sx assoc with alcohol intox:

Back 53

irritability,
violent behavior,
feelings of depression, and, in rare instances, hallucinations and delusions

Front 54

List three features of alcohol withdrawal?

Back 54

insomnia
hyperactivity of autonomic nervous system
feelings of anxiety

Front 55

Alcohol and gender relation?
Highest prevalence in terms of age for drinking?

Back 55

1.3 to 1.0 (male: female)
middle teens to mid twenties

Front 56

Low or HIGH SES associated with alcohol USE?

Back 56

higher

Front 57

Higher or lower education alcohol use ?

Back 57

higher education greater proportion

Front 58

Religion and alcohol

Back 58

Jews greatest number consuming but lowest with depedence

Conservative Protestants and Catholics are less likely to use alcohol than liberal Protestants and Catholics. Other groups, such as the Irish, have higher rates of severe alcohol problems, but they also have significantly higher rates of abstention.A

Front 59

Average alcohol used for people over 14 in gallons per year?

Back 59

2.2
most was 5 during american revolution

Front 60

About XX percent of all US residents have had an alcohol-containing drink at least once in their lives, and about YY percent of all US adults are current users of alcohol.

Back 60

50
91

Front 61

Where does alcohol rank in terms of health problems in US today?

Back 61

1. heart disease
2. cancer
3. alcohol related ds

Front 62

beer accounts for about XX of all alcohol consumption, liquor for about YY, and wine for about ZZ

Back 62

X: 50%
Y: 33%
Z: 1/6

Front 63

About XX percent of all adults in the United States have had at least one transient episode of an alcohol-related problem, usually an alcohol-induced amnestic episode (e.g., a blackout)

Back 63

30 to 45%

Front 64

About WA percent of women and MA percent of men have met the diagnostic criteria for alcohol abuse during their lifetimes, and WD percent of women and MD percent of men have met the diagnostic criteria for the more serious diagnosis of alcohol dependence during their lifetimes.

Back 64

About 10 percent of women and 20 percent of men have met the diagnostic criteria for alcohol abuse during their lifetimes, and 3 to 5 percent of women and 10 percent of men have met the diagnostic criteria for the more serious diagnosis of alcohol dependence during their lifetimes.

Front 65

Annual deaths DIRECTLY related to alcohol?

Back 65

200, 000

Front 66

List 4 causes of death due to EtOH

Back 66

suicide
cancer
heart ds
liver ds

Front 67

drunken drivers are involved in about XX percent of all automotive fatalities, and this percentage increases to about YY percent when only accidents occurring in the late evening are considered

Back 67

50%
75%

Front 68

Alcohol use and alcohol-related disorders are also associated with about XX percent of all homicides and YY percent of all suicides

Back 68

50%
25%

Front 69

Which substance leads in substance realated deaths?

Back 69

alcohol

Front 70

Alcohol abuse reduces life expectancy by ?

Back 70

10 years

Front 71

The psychiatric diagnoses most commonly associated with the alcohol-related disorders are?

Back 71

other substance-related disorders,

antisocial personality disorder,
mood disorders, and
anxiety disorders

Front 72

About XX percent of persons with an alcohol-related disorder meet the diagnostic criteria for major depressive disorder sometime during their lifetimes.

Back 72

30 to 40%

Front 73

Several studies reported that depression is likely to occur in patients with alcohol-related disorders who have:

Back 73

a high daily consumption of alcohol and a family history of alcohol abuse

Front 74

Some studies have shown that persons with both alcohol-related disorder and depressive disorder diagnoses have concentrations of ???? in their cerebrospinal fluid (CSF)

Back 74

dopamine metabolites (homovanillic acid) and
γ-aminobutyric acid (GABA)

Front 75

perhaps XX percent of all persons with alcohol-related disorders also meet the diagnostic criteria for an anxiety disorder

Back 75

25 to 50%

Front 76

Which anx ds espec comorb with etoh SU?

Back 76

Phobias and Panic Disorder

Front 77

alcohol-related disorder is likely to (come after or precede) the development of panic disorder or generalized anxiety disorder

Back 77

precede

Front 78

Most estimates of the prevalence of suicide among persons with alcohol-related disorders range from XX percent, although alcohol use itself may be involved in a much higher percentage of suicide

Back 78

10 to 15%

Front 79

Factors that have been associated with suicide among persons with alcohol-related disorders include: list 4

Back 79

1. a major depressive episode,
2. weak psychosocial support systems,
3. a serious coexisting medical condition,
4. unemployment, and
5. living alone

Front 80

It is likely that a series of genetic influences combine to explain approximately XX percent of the proportion of risk for alcoholism

Back 80

60%

Front 81

A variety of psychological theories relate to the use of alcohol: list 3

Back 81

to reduce tension,

increase feelings of power, and

decrease the effects of psychological pain.

Front 82

Psychodynamic theory of alcohol use?

Back 82

to reduce unconscious stress
to reduce harsh super-ego
fixated at oral-stage

Front 83

What are socio-cultural theories of alcoholism?

Back 83

Some other groups, such as Irish men or some American Indian tribes with high rates of abstention but a tradition of drinking to the point of drunkenness among drinkers, are believed to have high rates of alcoholism. These theories, however, often depend on stereotypes that tend to be erroneous, and prominent exceptions to these rules exist. For example, some theories based on observations of the Irish and the French have incorrectly predicted high rates of alcoholism among the Italians

Front 84

In experimental studies, children at high risk for alcohol-related disorders have been found?

Back 84

possess, on average, a range of deficits on neurocognitive testing,

low amplitude of the P300 wave on evoked potential testing, and a variety of abnormalities on

electroencephalogram (EEG) recordings.

Front 85

A childhood history of (WHAT)? increases a child's risk for an alcohol-related disorder as an adult

Back 85

A childhood history of
attention-deficit/hyperactivity
disorder,
conduct disorder, or
both, increases a child's risk for an alcohol-related disorder as an adult
Personality disorders, especially
antisocial personality disorder, as noted above, also predispose a person to an alcohol-related disorder

Front 86

List Four lines of evidence support the conclusion that alcoholism is genetically influence:

Back 86

First, a three- to fourfold increased risk for severe alcohol problems is seen in close relatives of alcoholic people. The rate of alcohol problems increases with the number of alcoholic relatives, the severity of their illness, and the closeness of their genetic relationship to the person under study.

twin studies, takes the data a step further. The rate of similarity, or concordance, for severe alcohol-related problems is significantly higher in identical twins of alcoholic individuals than in fraternal twins in most investigations, which estimate that genes explain 60 percent of the variance, with the remainder relating to nonshared, probably adult environmental influences.

Third, the adoption-type studies have all revealed a significantly enhanced risk for alcoholism in the offspring of alcoholic parents, even when the children had been separated from their biological parents close to birth and raised without any knowledge of the problems within the biological family. The risk for severe alcohol-related difficulties is not further enhanced by being raised by an alcoholic adoptive family.

Finally, studies in animals support the importance of a variety of yet-to-be-identified genes in the free-choice use of alcohol, subsequent levels of intoxication, and some consequences

Front 87

? increased risk for severe alcohol problems is seen in close relatives of alcoholic people

Back 87

3 to 4 fold

Front 88

The rate of alcohol problems increases with:

Back 88

the number of alcoholic relatives,
the severity of their illness, and
the closeness of their genetic relationship to the person under study

Front 89

Alcohol and twin conconcordance?

Back 89

60% variance explained by genes

Front 90

The risk for severe alcohol-related difficulties is (decreased, =, increased by being raised by an alcoholic adoptive family

Back 90

Not further enhanced
not worse

Front 91

What is considered single drink of EtOH?

Back 91

A single drink is usually considered to contain about 12 g of ethanol, which is the content of 12 ounces of beer (7.2 proof, 3.6 percent ethanol in the United States),

one 4-ounce glass of nonfortified wine, or

1 to 1.5 ounces of an 80-proof (40 percent ethanol) liquor (e.g., whiskey or gin)

Front 92

clinicians can estimate that a single drink increases the blood alcohol level of a 150-pound man by XX 0 mg/dL.

Back 92

15 to 20mg

Front 93

XX is the concentration of alcohol that an average person can metabolize in 1 hour.

Back 93

15 to 20 mg/dL, which is about the concentration of alcohol that an average person can metabolize in 1 hour

Front 94

The majority of alcohol is absorbed by the ?organ? what about the rest?

Back 94

About 10 percent of consumed alcohol is absorbed from the stomach, the remainder from the small intestine

Front 95

When do you get peak blood concentration of Alcohol? what effects it?

Back 95

in 30 to 90 minutes
- amount of food in stomach (slows absorption)
- speed of drinking (reduces time to peak)
- when % alcohol = 15 to 30% (30 to 60 proof)

Front 96

Hos does the body protect against alcohol overuse?

Back 96

if stomach concentration too high, pyloric valve closes, slowing absorption ... and possibly leading to pylorospasm ... N/Vom

Front 97

Once EtOH in blood stream, how distributed?

Back 97

to all body tissues, uniformly in body water

Front 98

Are intoxicating effects of alcohol greatest when concentration increasing or decreasing?

Back 98

increasing

Front 99

HOw is alcohol metabolized?

Back 99

About 90 percent of absorbed alcohol is metabolized through oxidation in the liver; the remaining 10 percent is excreted unchanged by the kidneys and lungs

Front 100

How much can the body metab of EtOH per hour?

Back 100

The body can metabolize about 15 mg/dL per hour, with a range of 10 to 34 mg/dL per hour. That is, the average person oxidizes three fourths of an ounce of 40 percent (80 proof) alcohol in an hour.

In persons with a history of excessive alcohol consumption, upregulation of the necessary enzymes results in rapid alcohol metabolism.

Front 101

Which enzymes involved in metab of EtOH? and fxn

Back 101

Alcohol is metabolized by two enzymes: alcohol dehydrogenase (ADH) and aldehyde dehydrogenase. ADH catalyzes the conversion of alcohol into acetaldehyde, which is a toxic compound; aldehyde dehydrogenase catalyzes the conversion of acetaldehyde into acetic acid

Front 102

Disulfram target?

Back 102

Aldehyde dehydrogenase is inhibited by disulfiram (Antabuse), often used in the treatment of alcohol-related disorders.

Front 103

Some studies have shown that women have a lower ? blood content than men

Back 103

aldehyde dehydrogenase

Front 104

What is receptor target of alcohol?

Back 104

no single target has been identified.

Front 105

What is theory of how alcohol interacts with cells?

Back 105

FLUIDITY OF MEMBRANES

Data support the hypothesis that alcohol produces its effects by intercalating itself into membranes and, thus, increasing fluidity of the membranes with short-term use.

With long-term use, however, the theory hypothesizes that the membranes become rigid or stiff. The fluidity of the membranes is critical to normal functioning of receptors, ion channels, and other membrane-bound functional proteins.

Front 106

Which receptor activity is enhanced by EtOH? Which receptor activity is inhibited by EtOH?

Back 106

Activates:
nicotinic acetylcholine,
serotonin 5-hydroxytryptamine3 (5-HT3,) and

GABA type A (GABAA) receptors are enhanced by alcohol, whereas ion channel activities associated with

glutamate receptors and
voltage-gated calcium channels are inhibited

Front 107

EtoH level?
thought, judgment, and restraint are loosened and sometimes disrupted

Back 107

0.05

Front 108

voluntary motor actions usually become perceptibly clumsy
EtoH level

Back 108

0.10

Front 109

EtoH level
function of the entire motor area of the brain is measurably depressed, and the parts of the brain that control emotional behavior are also affected

Back 109

0.20

Front 110

EtoH level
a person is commonly confused or may become stuporous

Back 110

0.30

Front 111

EtoH level
the person falls into a coma

Back 111

0.40 to 0.50

Front 112

Respiratory depression
Aspiration of vomit

Back 112

>0.50

Front 113

how does tolerance affect signs of intoxication at different alcohol levels?

Back 113

tolerance = less visible effects

Front 114

EtoH relationship to sleep?

Back 114

Decreased Sleep Latency = ease of falling asleep
Worsen Sleep architecture:
- Decreased REM
- Decreased Deep Sleep (Stage 4)
- More sleep fragmentation, with more and longer episodes of awakening

Front 115

alcohol impact on liver?

Back 115

hepatitis
cirrhosis
and fatty liver

Front 116

etoh impact on gi system?

Back 116

esophagitis & varices
gastritis,
achlorhydria, and
gastric ulcers.
pancreatitis, pancreatic cancer
Vitamin B defiencies

Front 117

Other body systems impact of etoh?

Back 117

HTN
Cholestrol/Trig abn
Increased MI, Cerebrovasc Ds
increased cancer
hypoglycemia
increased female estradiol

Front 118

Which lab tests may be abn in etoh use? and how often abn?

Back 118

all abnormally increased:

GGT - 80%
MCV 60% (esp in women)
Uric acid,
Trig
AST
ALT

Front 119

Describe drug intx with Etoh

Back 119

Enzyme induction ... which increases tolerance to some rx
When intox, compete for elimination so get more toxic levels

Certain substances, such as alcohol and phenobarbital (Luminal), are metabolized by the liver, and their prolonged use can lead to acceleration of their metabolism. When persons with alcohol-related disorders are sober, this accelerated metabolism makes them unusually tolerant to many drugs such as sedatives and hypnotics; when they are intoxicated, however, these drugs compete with the alcohol for the same detoxification mechanisms, and potentially toxic concentrations of all involved substances can accumulate in the blood.

Front 120

Which drugs to be especially cautious with?

Back 120

Any CNS depressants such as :
sedatives, hypnotics, histaminic (pain, motion sickness, head cold, allergy rx)

Front 121

According to DSM-IV-TR, the current rate of alcohol dependence is X percent

Back 121

5%

Front 122

Discuss subtype of EtOH dependence:

Back 122

type A alcohol dependence is characterized by
late onset,
few childhood risk factors,
relatively mild dependence,
few alcohol-related problems, and
little psychopathology.

B alcohol dependence is characterized by
many childhood risk factors,
severe dependence,
an early onset of alcohol-related problems,
much psychopathology,
a strong family history of alcohol abuse,
frequent polysubstance abuse,
a long history of alcohol treatment, and a lot of
severe life stresses

Front 123

What type of therapies will type A, B respond to best?

Back 123

Some researchers have found that type A persons who are alcohol dependent may respond to

interactional psychotherapies, whereas type B persons who are alcohol dependent may respond to training in

coping skills

Front 124

Describe the following:
early stage problem drinkers
affiliative drinkers
schizoid-isolated

Back 124

early-stage problem drinkers, who do not yet have complete alcohol dependence syndromes; affiliative drinkers, who tend to drink daily in moderate amounts in social settings; and schizoid-isolated drinkers, who have severe dependence and tend to drink in binges and often alone

Front 125

What is gamma alcohol dependence

Back 125

represents the alcohol dependence seen in those who are active in Alcoholics Anonymous (AA). This variant concerns control problems in which persons are unable to stop drinking once they start. When drinking is terminated as a result of ill health or lack of money, these persons can abstain for varying periods.

Front 126

What is delta alcohol dependence

Back 126

perhaps more common in Europe than in the United States, persons who are alcohol dependent must drink a certain amount each day but are unaware of a lack of control. The alcohol use disorder may not be discovered until a person who must stop drinking for some reason exhibits withdrawal sympto

Front 127

Compare Type I and II, male-limited etoh dependence

Back 127

Type I
alcohol dependence, characterized by
late onset, more evidence of
psychological than of physical dependence, and the presence of
guilt feelings

Type II
onset at an early age,
spontaneous seeking of alcohol for consumption, and a
socially disruptive set of behaviors when intoxicated

Front 128

Another model describes
List 4 types

Back 128

1. Antisocial Alcoholism
2. Developmentally cumulative alcoholism
3. Negative affect alcoholism
4. Developmentally limited alcoholism

Front 129

Antisocial alcoholism character?

Back 129

predominance in men,
a poor prognosis,
early onset of alcohol-related problems, and
a close association with antisocial personality disorder

Front 130

developmentally cumulative alcoholism,

Back 130

with a primary tendency for alcohol abuse that is exacerbated with time as cultural expectations foster increased opportunities to drink

Front 131

negative-affect alcoholism

Back 131

more common in women than in men;
according to this hypothesis, women are likely to use alcohol for mood regulation and
to help ease social relationships.

Front 132

developmentally limited alcoholism

Back 132

frequent bouts of consuming large amounts of alcohol;
the bouts become less frequent as persons age and respond to the increased expectations of society about their jobs and families

Front 133

As a conservative approach to identifying blood levels that are likely to have major effects on driving abilities, the legal definition of intoxication in most states in the United States requires a blood concentration of XX mg ethanol per deciliter of blood (mg/dL), which is the same as YY g/dL.

Back 133

80 to 100 mg /dl
0.08 to 0.10 g/dl

Front 134

Anyone who does not show significant levels of impairment in motor and mental performance at approximately (X) probably has significant pharmacodynamic tolerance What would most people experience at that range?

Back 134

150mg/dl
0.15 g/dl

severe N and vomitting

Front 135

What type of memory problem with alcohol? what dose level?

Back 135

ANTERO-grade
200 to 300mg/dl
0.2 to 0.2 g/dl

Front 136

Conditions that may predispose to, or aggravate, etoh withdrawal symptoms include (4)?

Back 136

Conditions that may predispose to, or aggravate, withdrawal symptoms include fatigue, malnutrition, physical illness, and depression.

Front 137

One recent positron emission tomographic (PET) study of blood flow during alcohol withdrawal in otherwise healthy persons with alcohol dependence reported a ?

Back 137

globally low rate of metabolic activity
although, with further inspection of the data, the authors concluded that activity was especially low in the

left parietal and
right frontal areas

Front 138

Classic sign of Etoh withdrawal? When does it usually develop?

Back 138

Tremulousness (commonly called the “shakes” or the “jitters”) develops 6 to 8 hours after the cessation of drinking,

Front 139

When do you get psychotic and perceputal sx in etoh withdrawal?

Back 139

the psychotic and perceptual symptoms begin in 8 to 12 hours

Front 140

When get withdrawal from etoh seizures

Back 140

seizures in 12 to 24 hours,

Front 141

When get DT's?

Back 141

during 72 hours and watch for 1st week

Front 142

Describe tremor of etoh withdrawal (i.e., Hz)

Back 142

The tremor of alcohol withdrawal can be similar to either physiological tremor, with a
continuous tremor of great amplitude and of more than
8 Hz, or
familial tremor, with bursts of tremor activity slower than 8 Hz

Front 143

Withdrawal sx grouping?

Back 143

Psych: general irritabiliy, confusion, psychosis, etc.
GI Sx: N/Vomitting
Sympathetic Autonomic hyperactivity: anxiety, arousal, sweating, facial flushing, mydriasis, tachycardia, mild hypertension
may startle easily

Front 144

Describe etoh withdrawal seizure

Back 144

Seizures associated with alcohol withdrawal are

-stereotyped,
generalized, and
tonic-clonic in character.

Patients often have more than one

seizure 3 to 6 hours after the first seizure.

Status epilepticus is relatively rare and occurs in less than 3 percent of patients.

Front 145

DDX for seizures?

Back 145

head injuries,
CNS infections,
CNS neoplasms, and other
cerebrovascular diseases
hypoglycemia,
hyponatremia, and
hypomagnesaemia

Front 146

These drug (s), should be given intramuscularly (IM) because of their erratic absorption by this route

Back 146

Valium
Librium

Front 147

In tx withdrawal, titrate benzo so that patients are?

Back 147

calm and sedated but not so sedated that they cannot be aroused

Front 148

Which others than benzo drugs has evidence in tx withdrawal?

Back 148

carbamazepine (Tegretol) in daily doses of 800 mg is as effective as benzodiazepines and has the added benefit of minimal abuse liability.

Front 149

How is clonidine used?

Back 149

The β-adrenergic receptor antagonists and clonidine (Catapres) have also been used to block the symptoms of sympathetic hyperactivity, but neither drug is an effective treatment for seizures or delirium

Front 150

Untreated, DTs has a mortality rate of XX percent, usually as a result of an intercurrent medical illness such as :?

Back 150

Untreated, DTs has a mortality rate of 20 percent, usually as a result of an intercurrent medical illness such as pneumonia, renal disease, hepatic insufficiency, or heart failure.

Front 151

What is key feature of etoh induced delirium?

Back 151

The essential feature of the syndrome is delirium occurring within 1 week after a person stops drinking or reduces the intake of alcohol.

Front 152

DT Sx

Back 152

autonomic hyperactivity such as tachycardia, diaphoresis, fever, anxiety, insomnia, and hypertension;

perceptual distortions, most frequently visual or tactile hallucinations;

and fluctuating levels of psychomotor activity, ranging from hyperexcitability to lethargy

Front 153

About X percent of persons with alcohol-related disorders who are hospitalized have DTs.

Back 153

5

Front 154

What day does DT usually appear in hosp patient?

Back 154

3rd day

Front 155

Episodes of DTs usually begin in a patient's AGE after TIME years of heavy drinking, typically of the binge type

Back 155

30s to 40s
5 to 15 years

Front 156

What illness predisposes to DTs?

Back 156

Physical illness

Front 157

Best tx for DTs?

Back 157

PREVENTION

Front 158

How tx withdrawal from etoh? dosage compared for DTs?

Back 158

Benzo, e.g. chlordiazepoxide 25 to 50mg ... or
Ativan every 2 to 4 hours until out of danger
60 to 100mg every 4 hours or IV Ativan

Front 159

Which kinds of meds to avoid in DTs?

Back 159

anything that can lower seizure thresh-hold ... i..e., antipsychotics

Front 160

Supportive Tx for Dts?

Back 160

high-calorie, high carb diet with MV's

Front 161

What are signs to watch out for in DTs?

Back 161

focal neurological sx
lateralizing seizures
increased ICP sx
Evidence of skull fracture
other signs of CNS pathology

Front 162

several studies have found (brain change) in persons with dementia and a history of alcohol dependence

Back 162

enlarged ventricles and cortical atrophy

Front 163

The essential feature of alcohol-induced persisting amnestic disorder is

Back 163

a disturbance in short-term memory caused by prolonged heavy use of alcohol.

Front 164

Which is more acute/chronic?

Back 164

Wernicke's encephalopathy is acute
Korsakoff's is Kronic

Front 165

Which percent of people with Korsakoff's recover?

Back 165

20% only

Front 166

Wernicke's/korsakoff's is caused by?

Back 166

THIAMINE Defiency

Front 167

Where do you see thiamine related lesions of axons?

Back 167

The neuropathological lesions are symmetrical and paraventricular,

involving the mammillary bodies,
the thalamus, the
hypothalamus, the
midbrain, the
pons, the medulla, the
fornix, and the
cerebellum

Front 168

Describe sx of Wernicke's?

Back 168

Wernicke's encephalopathy, also called alcoholic encephalopathy, is an acute neurological disorder characterized by
ataxia (affecting primarily the gait), vestibular dysfunction,

confusion, and a

variety of ocular motility abnormalities, including horizontal nystagmus, lateral orbital palsy, and gaze palsy

These eye signs are usually bilateral but not necessarily symmetrical. Other eye signs may include a sluggish reaction to light and anisocoria. Wernicke's encephalopathy may clear spontaneously in a few days or weeks or may progress into Korsakoff's syndrome

Front 169

Tx of wernicke's?

Back 169

In the early stages, Wernicke's encephalopathy responds rapidly to large doses of parenteral thiamine, which is believed to be effective in preventing the progression into Korsakoff's syndrome.

The dosage of thiamine is usually initiated at 100 mg by mouth two to three times daily and is continued for 1 to 2 weeks.

In patients with alcohol-related disorders who are receiving IV administration of glucose solution, it is good practice to include 100 mg of thiamine in each liter of the glucose solution

Front 170

The cardinal features of Korsakoff's syndrome are:

Back 170

impaired mental syndrome (especially recent memory) and anterograde amnesia in an alert and responsive patient.

The patient may or may not have the symptom of confabulation

Front 171

Tx of Korsakoff's?

Back 171

Treatment of Korsakoff's syndrome is also thiamine given 100 mg by mouth two to three times daily; the treatment regimen should continue for 3 to 12 months.

Front 172

Blackouts are similar to episodes of ?

Back 172

Blackouts are similar to episodes of transient global amnesia in that they are discrete episodes of anterograde amnesia that occur in association with alcohol intoxication

Front 173

What kind of memory impairment with etoh blackouts?

Back 173

During a blackout, persons have relatively intact remote memory but experience a specific short-term memory deficit in which they are unable to recall events that happened in the previous 5 or 10 minutes.

Because their other intellectual faculties are well preserved, they can perform complicated tasks and appear normal to casual observers.

Front 174

What is neurobiology of blackouts?

Back 174

alcohol blocks the consolidation of new memories into old memories, a process that is thought to involve the hippocampus and related temporal lobe structures.

Front 175

Etoh-Induced Psychotic Disorder: describe hallucinations/delusions?

Back 175

The most common hallucinations are auditory, usually voices, but they are often unstructured.

The voices are characteristically maligning, reproachful, or threatening, although some patients report that the voices are pleasant and nondisruptive.

The hallucinations usually last less than a week, but during that week impaired reality testing is common.

After the episode, most patients realize the hallucinatory nature of the symptoms.

Front 176

How contrasts alcohol withdrawal hallucinations from sz?

Back 176

Alcohol withdrawal-related hallucinations are differentiated from the hallucinations of schizophrenia by the temporal association with alcohol withdrawal,
the absence of classic hx of sz
usually short lived duration

Front 177

How compare etoh withdrawal halluc from DTs halluc?

Back 177

clear sensorium in withdrawal pts

Front 178

Tx of alcohol withdrawal related hallucinations?

Back 178

benzo's
sometimes antipsychotics

Front 179

What are options for alcohol and moods?

Back 179

alcohol-induced mood disorder with manic, depressive, or mixed features
and also for the specification of onset during either intoxication or withdrawal.

Front 180

alcohol intoxication (is or is not) generally accepted as a reason for judging persons not responsible for their activities

Back 180

IS NOT

Front 181

(X), however, can be used in a person's defense if a defense lawyer can argue successfully that the defendant has an unexpected, idiosyncratic, pathological reaction to a minimal amount of alcohol

Back 181

Idiosyncratic alcohol intoxication

Front 182

DX is one diagnosis of potential interest to psychiatrists presented with a patient who appears to be afflicted with Wernicke-Korsakoff syndrome but does not respond to thiamine treatment.

Back 182

Alcoholic pellagra encephalopathy

Front 183

symptoms of alcoholic pellagra encephalopathy include:

Back 183

onfusion, clouding of consciousness, myoclonus, oppositional hypertonias, fatigue, apathy, irritability, anorexia, insomnia, and sometimes delirium

Front 184

alcoholic pellagra encephalopathy: cause and treatment?

Back 184

Patients suffer from a deficiency of niacin (nicotinic acid), and the specific treatment is 50 mg of niacin by mouth four times daily or 25 mg parenterally two to three times daily.

Front 185

What is the leading cause of MR in the US?

Back 185

Fetal Alcohol syndrome

Front 186

How does alcohol intefer with fetus?

Back 186

inhibits growth and development

Front 187

FAS features?

Back 187

MICROcephaly,
Craniofacial malform
Limb and Heart Defects
Short Stature

Front 188

Women with alcohol-related disorders have a XX percent risk of having a child with defects.

Back 188

35%

Front 189

What are positive prognostic factors to treatment?

Back 189

1. First is the absence of preexisting antisocial personality disorder or a diagnosis of other substance abuse or dependence.

2.Second, evidence of general life stability with a job, continuing close family contacts, and the absence of severe legal problems also bodes well for the patient.

3. Third, if the patient stays for the full course of the initial rehabilitation (perhaps 2 to 4 weeks), the chances of maintaining abstinence are good. The combination of these three attributes predicts at least a 60 percent chance for 1 or more years of abstinence

Front 190

Alcoholic persons with severe drug problems
(especially IV drug use or cocaine or amphetamine dependence) and those who are

homeless may have only a XX percent or so chance of achieving 1 year of abstinence

Back 190

10 to 15%

Front 191

Electrolyte probs with EtoH

Back 191

Electrolyte imbalances leading to acute confusional states and, rarely, local neurological signs and symptoms
Hypoglycemia
Hyperglycemia
Hyponatremia
Hypercalcemia
Hypomagnesemia
Hypophosphatemi

Front 192

Three general steps are involved in treating the alcoholic person after the disorder has been diagnosed:

Back 192

intervention, detoxification, and rehabilitation

Front 193

Describe confrontation:

Back 193

break through feelings of denial and help the patient recognize the adverse consequences likely to occur if the disorder is not treated. Intervention is a process aimed at maximizing the motivation for treatment and continued abstinence.
This step often involves convincing patients that they are responsible for their own actions while reminding them of how alcohol has created significant life impairments.

Front 194

What can family do to help?

Back 194

not protect patient from problems caused by EtOH
Suggest AA

Front 195

Steps in Detox?

Back 195

The essential first step in detoxification is a thorough physical examination. In the absence of a serious medical disorder or combined drug abuse, severe alcohol withdrawal is unlikely. The second step is to offer rest, adequate nutrition, and multiple vitamins, especially those containing thiamine.

Front 196

How tx mild or moderate withdrawal from etoh?

Back 196

Giving enough of benzo or barbiturate in first day, ofter 5 days of support

Front 197

General Mild/Mod EtoH Withdrawal plans in terms of dosing?

Back 197

Start at required dose to calm, mild sedate and then decrease by 20% per day

Front 198

What is drawback in using B-adrenergic antagonist or alpha adrenergic receptor agonist?

Back 198

does not protect against seizurs

Front 199

For the approximately XX percent of alcoholic patients with extreme autonomic dysfunction, agitation, and confusion—that is, those with alcoholic withdrawal delirium, or DTs— what is optimal tx?

Back 199

1 to 3%

no optimal tx yet

Front 200

Steps to tx severe withdrawal/DT's?

Back 200

The first step is to ask why such a severe and relatively uncommon withdrawal syndrome has occurred; the answer often relates to a severe

concomitant medical problem that needs immediate treatment. The withdrawal symptoms can then be minimized through the use of either

benzodiazepines (in which case high doses are sometimes required) or

antipsychotic agents, such as haloperidol. Once again, on the first or second day doses are used to control behavior, and the patient can be weaned off the medication by about the fifth day.

Front 201

Do patients withdrawing from alcohol having grand mal seizure benefit from anticonvulsant?

Back 201

not necessarily

Front 202

Key steps to Etoh Rehab?

Back 202

1) continued efforts to increase and maintain high levels of motivation for abstinence;
(2) work to help the patient readjust to a lifestyle free of alcohol; and
(3) relapse prevention.

Front 203

Research, data from records, and resource persons usually reveal that (alcohol vs mood ds, accidident life stres) contributed to the (alcohol ds vs mood disorder, accident, or life stress, not vice versa.

Back 203

Research, data from records, and resource persons usually reveal that alcohol contributed to the mood disorder, accident, or life stress, not vice versa.

Front 204

What type of counselling helps in etoh abstinence?

Back 204

Counseling efforts in the first several months should focus on day-to-day life issues to help patients maintain a high level of motivation for abstinence and to enhance their functioning. Psychotherapy techniques that provoke anxiety or that require deep insights have not been shown to be of benefit during the early months of recovery and, at least theoretically, may actually impair efforts at maintaining abstinence. Thus, this discussion focuses on the efforts likely to characterize the first 3 to 6 months of care.

The technique used is not likely to matter greatly and usually boils down to simple day-to-day counseling or almost any behavioral or psychotherapeutic approach focusing on the here and now. To optimize motivation, treatment sessions should explore the consequences of drinking, the likely future course of alcohol-related life problems, and the marked improvement that can be expected with abstinence

Front 205

Which approach best in etoh - individual or group therapy?

Back 205

no data say one is superior

Front 206

What type of timing is best for tx?

Back 206

Whether in an inpatient or an outpatient setting, individual or group counseling is usually offered a minimum of three times a week for the first 2 to 4 weeks, followed by less intense efforts, perhaps once a week, for the subsequent 3 to 6 months

Front 207

What is major focus in counselling?

Back 207

Much time in counseling deals with how to build a lifestyle free of alcohol. Discussions cover the need for a sober peer group, a plan for social and recreational events without drinking, and approaches for reestablishing communication with family members and friends.

Front 208

Relapse Prevention focus?

Back 208

identify high risk situations/triggers

Front 209

How does counsellor talk about "slips"

Back 209

recovery is a process of trial and error; patients use slips that occur to identify high-risk situations and to develop more appropriate coping techniques

Front 210

If detoxification has been completed and the patient is not one of the (XX) percent of alcoholic persons who have an independent mood disorder, schizophrenia, or anxiety disorder, (there is little, moderate, good) evidence favoring prescribing psychotropic medications for the treatment of alcoholism.

Back 210

10 to 15%

little

Front 211

Controlled clinical trials, indicate (no, little, some, much) benefit in prescribing antidepressant medications or lithium to treat the average alcoholic person who has no independent or long-lasting psychiatric disorder.

Back 211

No

Front 212

List contraindications to: Disulfram

Back 212

Preparations with alcohol also being used
Metronidazole
Coronary Artery Disease
Severe Heart Ds

Front 213

List contraindications to: Naltrexone

Back 213

Currently using opiods
In opioid withdrawal
expect need for opiod pain meds
acute hepatitis or liver failure

Front 214

List contraindications to: Acamprosate

Back 214

Severe RENAL impairment
i.e., CrCl < 30mL/min

Front 215

Mechanism of Action for: Disulfram

Back 215

causes building up acetaldyhde becaues inhibits acetaldyhde dehydrogenase resulting in toxic levels of that acid = flushing, sweating, nausea, and tachycardia if drink

Front 216

Mechanism of Action for: Naltrexone

Back 216

reduces craviing because blocks opioid receptor

Front 217

Mechanism of Action for: Acamprosate?

Back 217

Affects glutamate and GABA

Front 218

Dosing for Disulfram and monitoring

Back 218

Oral dose: 250 mg daily (range 125–500 mg)

Before prescribing: (1) warn that the patient should not take disulfiram for at least 12 hours after drinking and that a disulfiram-alcohol reaction can occur up to 2 weeks after the last dose; and
(2) warn about alcohol in the diet (e.g., sauces and vinegars) and in medications and toiletries

Follow up: Monitor liver function tests periodically

Front 219

Dosing for Naltexone and monitoring

Back 219

Oral dose: 50 mg daily

Before prescribing: Evaluate for possible current opioid use; consider a urine toxicology screen for opioids, including synthetic opioids. Obtain liver function tests


Follow up: Monitor liver function tests periodically

Front 220

Dosing for Acamprosate and monitoring?

Back 220

Oral dose: 666 mg (two 333-mg tablets) three times daily or, for patients with moderate renal impairment (CrCl* 30–50 mL/min), reduce to 333 mg (one tablet) three times daily

Before prescribing: Establish
abstinence

Front 221

What has use of disulfram gone down?

Back 221

dangers associated with the drug itself: mood swings, rare instances of psychosis, the possibility of increased peripheral neuropathies, the relatively rare occurrence of other significant neuropathies, and potentially fatal hepatitis

patients with preexisting heart disease, cerebral thrombosis, diabetes, and a number of other conditions cannot be given disulfiram because an alcohol reaction to the disulfiram could be fatal

Front 222

What is evidence of agents other than disulfram, acamprosate, and naltrexone in tx alcoholism?

Back 222

Another medication with potential promise in the treatment of alcoholism is the nonbenzodiazepine antianxiety drug buspirone (BuSpar), although the effect of this drug on alcohol rehabilitation is inconsistent between studies. No evidence exists that antidepressant medications, such as the selective serotonin reuptake inhibitors (SSRIs), lithium, or antipsychotic medications, are significantly effective in the treatment of alcoholism.

Front 223

Describe key features of AA:

Back 223

Members of AA have help available 24 hours a day,
associate with a sober peer group,

learn that it is possible to participate in social functions without drinking,

and are given a model of recovery by observing the accomplishments of sober members of the group.

Front 224

Amphetamine ranks where in terms of illicit substances?

Back 224

2nd only to cannabis

Front 225

What are FDA approved uses of amphetamaines?

Back 225

NARCOLEPSY &
ADHD

Front 226

What conditions are aphetamines often used in?

Back 226

treatment of obesity,
depression,
dysthymia,
chronic fatigue syndrome,
acquired immune deficiency syndrome (AIDS), dementia, and
neurasthenia

Front 227

List 4 prescription amphetamines

Back 227

dextroamphetamine (Dexedrine),
methamphetamine (Desoxyn), a

mixed dextroamphetamine-amphetamine salt (Adderall), and

the amphetamine-like compound methylphenidate (Ritalin)

Front 228

What is more addictive: cocacine or amphetamines?

Back 228

cocaine

Front 229

What are some other amphetamine like substances?

Back 229

Other amphetamine-like substances are
ephedrine,
pseudoephedrine, and
phenylpropanolamine

Front 230

phenylpropanolamine can do what (PPA?)

Back 230

can dangerously exacerbate hypertension (narrow maragine of safety with 4 Xdose = lifethreating HTN), precipitate a toxic psychosis, cause intestinal infarction, or result in death

Front 231

phendimetrazine is what?

Back 231

an amphetamine like drug with abuse potential

Front 232

diethylpropion is what?

Back 232

an amphetamine like drug with abuse potential

Front 233

benzphetamine is what?

Back 233

an amphetamine like drug with abuse potential

Front 234

phentermine is what?

Back 234

abuse potential amphetamines

Front 235

what is MOdafinil?

Back 235

stimulant but toxicity unknown

Front 236

What is methamphetamine?

Back 236

Methamphetamine is a potent form of amphetamine that abusers of the substance inhale, smoke, or inject intravenously (IV). Its psychological effects last for hours and are described as particularly powerful. Unlike cocaine (see Section 12.6), which must be imported, methamphetamine is a synthetic drug that can be manufactured domestically in illicit laboratories

Front 237

The National Household Survey on Drug Abuse (NHSDA) conducted in 2001 found that XX percent of persons (12 years of age and older) reported lifetime nonmedical use of stimulants

Back 237

7.1

Front 238

Highest rates of stimulant use by age?

Back 238

18 to 25 year olds

Front 239

According to the text revision of the 4th edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), the lifetime prevalence of amphetamine dependence and abuse is XX percent, and the male to female ratio is YY

Back 239

1.5% lifetime
1 male to female ratio

Front 240

The classic amphetamines (i.e., dextroamphetamine, methamphetamine, and methylphenidate) produce their primary effects by (mechanism)

Back 240

causing the release of catecholamines, particularly dopamine, from presynaptic terminals

Front 241

Amphetamine especially act on ?

Back 241

The effects are particularly potent for the dopaminergic neurons projecting from the ventral tegmental area to the cerebral cortex and the limbic areas. This pathway has been termed the reward circuit pathway, and its activation is probably the major addicting mechanism for the amphetamines.

Front 242

How do designed amphetamines mech of action?

Back 242

The designer amphetamines cause the release of catecholamines (dopamine and norepinephrine) and of serotonin, the neurotransmitter implicated as the major neurochemical pathway for hallucinogens. Therefore, the clinical effects of designer amphetamines are a blend of the effects of classic amphetamines and those of hallucinogens.

Front 243

The intoxication syndromes of (cocaine or amphetamines) which blocks dopamine reuptake and (cocaine or amphetamines) which cause the release of dopamine are similar

Back 243

The intoxication syndromes of cocaine (which blocks dopamine reuptake) and amphetamines (which cause the release of dopamine) are similar.

Front 244

DSM criteria for cocaine and amphetamine intoxication or similar or different?

Back 244

similar

Front 245

When does amphetamine intox resolve?

Back 245

mostly by 24 hours
completely by 48hours

Front 246

Describe amphetamine withdrawal including timing

Back 246

After amphetamine intoxication, a crash occurs with symptoms of

anxiety,
tremulousness,
dysphoric mood,
lethargy, fatigue,
nightmares (accompanied by rebound rapid eye movement [REM] sleep),
headache,
profuse sweating,
muscle cramps,
stomach cramps, and
insatiable hunger.

The withdrawal symptoms generally peak in 2 to 4 days and are resolved in 1 week

Front 247

What is most serious withdrawal symptom of amphetamine withdrawal?

Back 247

depression,
can be associated with SI

Front 248

The hallmark of amphetamine-induced psychotic disorder is the presence of

Back 248

paranoia.

Front 249

Amphetamine-induced psychotic disorder can be distinguished from paranoid schizophrenia by:

Back 249

predominance of visual hallucinations,
generally appropriate affects,

hyperactivity,
hypersexuality,
confusion and incoherence, and

little evidence of disordered thinking (e.g., looseness of associations)

amphetamine-induced psychotic disorder generally
lacks the affective flattening and
alogia of schizophrenia

Front 250

Amphetamine and relation to mood ds?

Back 250

In general, intoxication is associated with manic or mixed mood features, whereas withdrawal is associated with depressive mood features

Front 251

Amphetamine, as with cocaine, can induce symptoms similar to those seen in which anx ds?

Back 251

obsessive-compulsive disorder, panic disorder, and phobic disorders, in particular

Front 252

assoc of amphetamine with sexual fxn?

Back 252

Amphetamines may be prescribed as an antidote to the sexual side effects of serotonergic agents such as fluoxetine (Prozac), but they are often misused by persons to enhance sexual experiences. High doses and long-term use are associated with erectile disorder and other sexual dysfunctions. These dysfunctions are classified in DSM-IV-TR as amphetamine-induced sexual dysfunction with onset during intoxication

Front 253

Amphetamine intoxication and withdrawal?

Back 253

Amphetamine intoxication can produce insomnia and sleep deprivation, whereas persons undergoing amphetamine withdrawal can experience hypersomnolence and nightmares

Front 254

List effects of small dose of amphetamine

Back 254

In persons who have not previously used amphetamines, a single 5-mg dose increases the
sense of well-being and induces elation,
euphoria, and
friendliness. Small doses generally improve
attention and
increase performance on written, oral, and performance tasks.

An associated decrease in fatigue, induction of anorexia, and heightening of the pain threshold are also seen.

Undesirable effects result from the use of high doses for long periods.

Front 255

List life-threatening adverse affects of amphetamine

Back 255

cerebrovascular, cardiac, and gastrointestinal effects.

Among the specific life-threatening conditions are myocardial infarction, severe hypertension, cerebrovascular disease, and ischemic colitis.

A continuum of neurological symptoms, from twitching to tetany to seizures to coma and death, is associated with increasingly high amphetamine doses.

Intravenous use of amphetamines can transmit human immunodeficiency virus (HIV) and hepatitis and further the development of lung abscesses, endocarditis, and necrotizing angiitis.

Several studies have shown that abusers of amphetamines knew little—or did not care—about safe-sex practices and the use of condoms

Front 256

Non life threatening adverse effects of amphetamine?

Back 256

The non–life-threatening adverse effects of amphetamine abuse include flushing, pallor, cyanosis, fever,
headache, tachycardia, palpitations, nausea, vomiting,

bruxism (teeth grinding),
shortness of breath,
tremor, and
ataxia.

Front 257

Pregnant women who use amphetamines often have babies with

Back 257

low birthweight,
small head circumference,
early gestational age, and
growth retardation

Front 258

Adverse psychiatric affects of amphetamines

Back 258

The adverse psychological effects associated with amphetamine use include restlessness, dysphoria, insomnia, irritability, hostility, and confusion. Amphetamine use can also induce symptoms of anxiety disorders, such as generalized anxiety disorder and panic disorder, as well as ideas of reference, paranoid delusions, and hallucinations.

Front 259

Give eg. of SUBSTITUTED Amphetamines

Back 259

MDMA (3,4-methylene-dioxymethamphetamine) is one of a series of substituted amphetamines that also includes MDEA, MDA (3,4-methylene-dioxyamphetamine), DOB (2,5-dimethoxy-4-bromoamphetamine), PMA (paramethoxyamphetamine), and others.

Front 260

Substituted amphetamines give effects similar to?

Back 260

These drugs produce subjective effects resembling those of amphetamine and LSD (lysergic acid diethylamide), and in that sense, MDMA and similar analogues may represent a distinct category of drugs.

Front 261

MDMA mechanism of action?

Back 261

he unusual properties of the drugs may be a consequence of the different actions of the optical isomers:

the R(-) isomers produce LSD-like effects and the

amphetamine-like properties are linked to S(+) isomers.

The LSD-like actions, in turn, may be linked to the capacity to release

serotonin. The various derivatives may exhibit significant differences in subjective effects and toxicity. Animals in laboratory experiments will self-administer the drugs, suggesting prominent amphetamine-like effects.

Front 262

MDMA Subjective experience?

Back 262

After taking usual doses (100 to 150 mg), MDMA users experience elevated mood and, according to various reports, increased self-confidence and sensory sensitivity; peaceful feelings coupled with insight, empathy, and closeness to persons; and decreased appetite

Difficulty concentrating and an increased capacity to focus have both been reported.

Dysphoric reactions, psychotomimetic effects, and psychosis have also been reported. Higher doses seem more likely to produce psychotomimetic effects

Front 263

MDMA physical effect?

Back 263

Sympathomimetic effects of tachycardia, palpitation, increased blood pressure, sweating, and bruxism are common.

Front 264

Duratoin of MDMA action usually?

Back 264

4 to 8 hours

Front 265

Which is more toxic: MDA or MDMA?

Back 265

MDA

Front 266

MDMA toxicity?

Back 266

Users of MDMA show differences in neuroendocrine responses to serotonergic probes, and studies of former MDMA users show global and regional decreases in serotonin transporter binding, as measured by positron emission tomography.

Front 267

What is Khat?

Back 267

The fresh leaves of Catha edulis, a bush native to East Africa, have been used as a stimulant in the Middle East, Africa, and the Arabian Peninsula for at least 1,000 years.

Khat is still widely used in Ethiopia, Kenya, Somalia, and Yemen

only since the 1970s has
P.412

cathinone

been identified as the substance responsible.

Cathinone is a precursor moiety that is normally enzymatically converted in the plant to the less-active entities norephedrine and cathine (norpseudoephedrine), which explains why only the fresh leaves of the plant are valued for their stimulant effects

Because it is typically absorbed buccally after chewing the leaf and because the alkaloid is metabolized relatively rapidly, high toxic blood levels are rarely reached

Front 268

Main concern around dhat?

Back 268

Concern about khat use is linked to its dependence-producing properties rather than to its acute toxicity

Front 269

What is north american Khat called?

Back 269

In the 1990s, several clandestine laboratories began synthesizing methcathinone, a drug with actions similar to those of cathinone. Known by a number of street names (e.g., “CAT,” “goob,” and “crank”), its popularity is primarily owing to its ease of synthesis from ephedrine or pseudoephedrine,

Front 270

Which drugs are associated with date rape?

Back 270

GHB
ketamine
and Rohypnol

Front 271

Tx of amphetamine related ds?

Back 271

in patient
multimodal therapy
rx: antipsychotic, anxiolytics
valium used to tx agitation and hyperactivity
tx underlying psych: depression, personality disorder

Front 272

Which Rx to consider in amphetamine abuse with depression?

Back 272

Bupropion (Wellbutrin) may be of use after patients have withdrawn from amphetamine.

It has the effect of producing feelings of well-being as these patients cope with the dysphoria that may accompany abstinence

Front 273

Which is the most widely consumed psychoactive substance in the world?

Back 273

caffeine

Front 274

Which caffeine disorders are not part of dsm?

Back 274

caffeine withdrawal and
caffeine dependence

Front 275

An adult in the United States consumes about XXX mg of caffeine per day on average, although 20 to 30 percent of all adults consume more than YYYY mg per day

Back 275

200mg
500mg

Front 276

How much does a cup of coffee contain in caffeine? tea?

Back 276

100 to 150mg of caffeine
tea = 1/3 of coffee

Front 277

In kids, what amount of food related caffeine would cause sx of caffeine intoxication?

Back 277

1 candy bar
1 12 ounce cola drink

Front 278

Which Rx has most caffeine? 2nd most?

Back 278

caffin-td, caffedrine ... 250mg
vivarin, ver .. 200mg
Quick-pep 140-150mg
cafergot, migralam ... 100mg
pain rx and cold preparations .. 60mg

Front 279

According to DSM-IV-TR, the actual prevalence of caffeine-related disorders is YY, but up to XX percent of adults consume caffeine in any given year.

Back 279

YY = unknown
85%

Front 280

What is comorbidity of caffeine ds?

Back 280

have additional SU; ie.e.,
2/3's use sedative and hypnotics

Front 281

caffeine half life, peak conc

Back 281

3 to 10hours
peak 30 to 60minutes

Front 282

does caffeine cross BB barrier?

Back 282

yes

Front 283

Caffeine mech?

Back 283

Adenosine receptors activate an inhibitory G protein (Gi) and, thus, inhibit the formation of the second-messenger cyclic adenosine monophosphate (cAMP). Caffeine intake, therefore, results in an increase in intraneuronal cAMP concentrations in neurons with adenosine receptors. Three cups of coffee are estimated to deliver so much caffeine to the brain that about 50 percent of the adenosine receptors are occupied by caffeine

Specifically, dopamine activity may be enhanced by caffeine, a

Activation of noradrenergic neurons has been hypothesized to be involved in the mediation of some symptoms of caffeine withdrawal

Front 284

Doses of caffeine in the range of XXX mg (the equivalent of several cups of brewed coffee ingested at once) produce effects that are often rated as being unpleasant, such as anxiety and nervousness

Back 284

300 to 800mg

Front 285

Investigations comparing coffee or caffeine use in monozygotic and dizygotic twins have shown higher concordance rates for monozygotic twins for total caffeine consumption, heavy use, caffeine tolerance, caffeine withdrawal, and caffeine intoxication, with heritabilities ranging between XX percen

Back 285

35 to 77%

Front 286

caffeine relation to smoking?

Back 286

Cigarette smokers consume more caffeine than nonsmokers. This observation may reflect a common genetic vulnerability to caffeine use and cigarette smoking. It may also be related to increased rates of caffeine elimination in cigarette smokers. Preclinical and clinical studies indicate that regular caffeine use can potentiate the reinforcing effects of nicotine

Front 287

caffeine and alcohol relation?

Back 287

Heavy use and clinical dependence on alcohol is associated with heavy use and clinical dependence on caffeine as well.

Front 288

Individuals with anxiety disorders tend to report (lower or higher) levels of caffeine use,

one study showed that a (lesser or greater) proportion of heavy caffeine consumers also use benzodiazepines

Back 288

lower in anx
higher in benzo's

Front 289

Most studies have found that caffeine results in global cerebral vasodilation or vasoconstriction,

with a resultant increase/decrease in cerebral blood flow (CBF)

Back 289

Most studies have found that caffeine results in global cerebral vasoconstriction, with a resultant decrease in cerebral blood flow (CBF), although this effect may not occur in persons over 65 years of age

CBF shows a rebound increase after withdrawal from caffeine.

Front 290

Do you develop tolerance to cerebral vasoconstriction with caffeine?

Back 290

no

Front 291

DDX for caffeine ds?

Back 291

generalized anxiety disorder, panic disorder with or without agoraphobia, bipolar II disorder, attention-deficit/hyperactivity disorder, and sleep disorders.

The differential diagnosis should include the abuse of caffeine-containing over-the-counter medications, anabolic steroids, and other stimulants, such as amphetamines and cocaine. A urine sample may be needed to screen for these substances.

The differential diagnosis should also include hyperthyroidism and pheochromocytoma.

Front 292

Where does caffeine withdrawal fit?

Back 292

caffeine related ds nos

Front 293

What amount of caffeine usually assoc with intox in adults?

Back 293

250mg ormore

Front 294

sx of caffeine intox?

Back 294

anxiety, psychomotor agitation, restlessness, irritability, and

psychophysiological complaints such as muscle twitching, flushed face, nausea, diuresis, gastrointestinal distress, excessive perspiration, tingling in the fingers and toes
insomnia

Front 295

how does >1g of caffeine look?

Back 295

rambling speech, confused thinking, cardiac arrhythmias, inexhaustibleness, marked agitation, tinnitus, and mild visual hallucinations (light flashes)

Front 296

>10grams of caffeine?
10, 000 mg/50mg = 200 cans of pop

Back 296

generalized tonic-clonic seizures, respiratory failure, and death

Front 297

caffeine withdrawal --- such thing?

Back 297

Despite that the DSM-IV-TR does not include a diagnosis of caffeine withdrawal, several well-controlled studies indicate that caffeine withdrawal is a real phenomenon, and DSM-IV-TR gives research criteria for caffeine withdrawal

Front 298

sx of caffeine withdrawal?

Back 298

most common symptoms are headache and fatigue;

anxiety, irritability, mild depressive symptoms, impaired psychomotor performance, nausea, vomiting, craving for caffeine, and muscle pain and stiffness.

onset 12 to 24 hours
peak sx 24 to 48 hours

Front 299

over what amount of time should caffeine be reduced?

Back 299

7 to 14 days

Front 300

which anxiety ds looks like caffeine use?

Back 300

GAD

Patients with the disorder may be perceived as “wired,” overly talkative, and irritable; they may complain of not sleeping well and of having energy to burn. Caffeine can induce and exacerbate panic attacks in persons with a panic disorder and although a causative association between caffeine and a panic disorder has not yet been demonstrated, patients with panic disorder should avoid caffeine.

Front 301

caffeine and relation to sleep?

Back 301

Caffeine-induced sleep disorder, which can occur during caffeine intoxication, is a DSM-IV-TR diagnosis (see Table 24.2-21). Caffeine is associated with

delay in falling asleep,

inability to remain asleep, and

early morning awakening

Front 302

does caffeine dependence exist?

Back 302

A diagnosis of Substance Dependence can be
applied to every class of substance except caffeine

Front 303

After the ingestion of 50 to 100 mg of caffeine, common symptoms include

Back 303

increased alertness, a mild sense of well-being, and a sense of improved verbal and motor performance. Caffeine ingestion is also associated with diuresis, cardiac muscle stimulation, increased intestinal peristalsis, increased gastric acid secretion, and (usually mildly) increased blood pressure

Front 304

caffeine use is often considered to be contraindicated for various conditions, including

Back 304

generalized anxiety disorder,
panic disorder,
primary insomnia,
gastroesophageal reflux, and pregnancy

Front 305

Caffeine and relation to pregnancy

Back 305

there may be a mild association between higher daily caffeine use in women and delayed conception and slightly lower birth weight. Studies, however, have not found such associations, and effects, when found, are usually with relatively high daily dosages of caffeine (e.g., the equivalent of five cups of brewed coffee per day).

Front 306

Tx of caffeine withdrawal?

Back 306

analegesics to control headache
benzo's very rarely
1. track caffeine intake
2. decrease by 10% every 2 days

Front 307

Most commonly used illegal drug?

Back 307

cannabis

Front 308

THC =?

Back 308

-)-Δ9-tetrahydrocannabinol (Δ9-THC

Front 309

The potency of marijuana preparations has increased in recent years because of improved agricultural techniques used in cultivation so that plants may contain up to XX percent THC

Back 309

15 to 20%

Front 310

Based on the 2003 National Surveys on Drug Use and Health (NSDUH), an estimated XXXXXX million adults (YYY percent) aged 18 years or older had used marijuana at least once in their lifetime

Back 310

43%
91 million

Front 311

Among this group, about A percent used the drug before age 12, about B percent between 12 and 17 and about C percent after age 18

Back 311

2% before 12
53% teens to 17
45% after age 18

Front 312

According to the text revision of the fourth edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), there is a Xpercent lifetime rate of cannabis abuse or dependence.

Back 312

5%
but considered too low according to NSDUH survey

Front 313

where is cannabinoid receptuer binding densest?

Back 313

dense in the hippocampus (Hipp),

the globus pallidus (GP),

the entopeduncular nucleus (EP),

the substantia nigra pars reticulata (SNr), and the

cerebellum (Cer

Binding is moderate in the cerebral cortex (Cx) and the caudate putamen (CP) and

sparse in the brainstem (Br St) and spinal cord.

Front 314

Cannabis and gender?

Back 314

males 2x females over age 26 ... no difference 12 to 17

Front 315

cannabis plants has how many compounds?
main one active in humans?

Back 315

> 400

In humans, Δ9-THC is rapidly converted into 11-hydroxy-Δ9-THC, the metabolite that is active in the central nervous system (CNS).

Front 316

The cannabinoid receptor is found in highest concentrations in the

Back 316

the basal ganglia, the hippocampus, and the cerebellum, with lower concentrations in the cerebral cortex

Front 317

cannabis receptors not found in ?

Back 317

It is not found in the brainstem, a fact consistent with cannabis's minimal effects on respiratory and cardiac functions.

Front 318

cannabis evidence for tolerance? dependence?

Back 318

Tolerance to cannabis does develop, however, and psychological dependence has been found, although the evidence for physiological dependence is not strong.

Front 319

cannabis withdrawal sx?

Back 319

Withdrawal symptoms in humans are limited to modest increases in irritability, restlessness, insomnia, and anorexia and mild nausea

Front 320

cannabis euphoria? duration?

Back 320

When cannabis is smoked, the euphoric effects appear within minutes, peak in about 30 minutes, and last 2 to 4 hours. Some motor and cognitive effects last 5 to 12 hours. Cannabis can also be taken orally when it is prepared in food, such as brownies and cakes. About two to three times as much cannabis must be taken orally to be as potent as cannabis taken by inhaling its smoke.

Front 321

The most common physical effects of cannabis are :

Back 321

The most common physical effects of cannabis are dilation of the conjunctival blood vessels (red eye) and mild tachycardia

Front 322

most serious side effect cannabis?

Back 322

The most serious potential adverse effects of cannabis use are those caused by inhaling the same carcinogenic hydrocarbons present in conventional tobacco, and some data indicate that heavy cannabis users are at risk for chronic respiratory disease and lung cancer.

Front 323

dsm coding for cannabis intoxication?

Back 323

The DSM-IV-TR formalizes the diagnostic criteria for cannabis intoxication (Table 12.5-2). These criteria state that the diagnosis can be augmented with the phrase “with perceptual disturbances.” If intact reality testing is not present, the diagnosis is cannabis-induced psychotic disorder

Front 324

cannabis intoxication effects?

Back 324

Cannabis intoxication commonly heightens users' sensitivities to external stimuli, reveals new details, makes colors seem brighter and richer than in the past, and subjectively slows the appreciation of time. In high doses, users may experience depersonalization and derealization.

Motor skills are impaired by cannabis use, and the impairment in motor skills remains after the subjective, euphoriant effects have resolved.

For 8 to 12 hours after using cannabis, users' impaired motor skills interfere with the operation of motor vehicles and other heavy machinery.

Moreover, these effects are additive to those of alcohol, which is commonly used in combination with cannabis

Front 325

cannabis impact on cog fxn?

Back 325

The delirium associated with cannabis intoxication is characterized by marked impairment on cognition and performance tasks. Even modest doses of cannabis impair memory, reaction time, perception, motor coordination, and attention

Front 326

Cannabis-induced psychotic disorder is RARE, COMMON?

Back 326

rare
; transient paranoid ideation is more common.

Front 327

describe cannabis induced sleep ds? sexual dysfxn?

Back 327

The DSM-IV-TR also does not formally recognize cannabis-induced sleep disorders or cannabis-induced sexual dysfunction; therefore, both are classified as cannabis-related disorders not otherwise specified. When either sleep disorder or sexual dysfunction symptoms are related to cannabis use, they almost always resolve within days or a week after cessation of cannabis use.

Front 328

Describe amotivational syndrome

Back 328

A controversial cannabis-related syndrome is amotivational syndrome. Whether the syndrome is related to cannabis use or reflects characterological traits in a subgroup of persons regardless of cannabis use is under debate. Traditionally, the amotivational syndrome has been associated with long-term heavy use and has been characterized by a person's unwillingness to persist in a task—be it at school, at work, or in any setting that requires prolonged attention or tenacity. Persons are described as becoming apathetic and anergic, usually gaining weight, and appearing slothfu

Front 329

Tx of cannabis abuse?

Back 329

abstinence
support

Front 330

how long does urine stay +

Back 330

up to 4 weeks after use

Front 331

Medical uses of MJ?

Back 331

nausea secondary to chemotherapy,

multiple sclerosis (MS) chronic pain,

acquired immune deficiency syndrome (AIDS),

epilepsy, and
glaucoma

Front 332

Synthetic THC?

Back 332

Dronabinol (oral)
Sativex (oral spray)

Front 333

Cocaine highest use age group?
gender?
lowest use ethnicity?

Back 333

18 to 25,
6.7%
males 2X females
asians lowest rate of cocaine use

Front 334

Comorbidity and cocaine?

Back 334

The development of
mood disorders and alcohol-related disorders usually
follows the onset of cocaine-related disorders, whereas

anxiety disorders,
antisocial personality disorder, and

attention-deficit/hyperactivity disorder (ADHD) are thought to precede the development of cocaine-related disorders

Front 335

Cocaine comorbidity?

Back 335

major depressive disorder,
bipolar II disorder,
cyclothymic disorder,
anxiety disorders, and
antisocial personality disorder are the most commonly associated psychiatric ds (excluding other sub)

Front 336

Genetic role in cocaine?

Back 336

Monozygotic twins have higher concordance rates for stimulant dependence (cocaine, amphetamines, and amphetamine-like drugs) than dizygotic twins. The analyses indicate that genetic factors and unique (unshared) environmental factors contribute about equally to the development of stimulant dependence.

Front 337

Increased metabolic activity in the (list brain regions) correlates with reports of craving for cocaine, but the degree of ? does not.

Back 337

limbic-related regions, such as the amygdala, parahippocampal gyrus, and dorsolateral prefrontal cortex, reportedly

EEG arousal does not

Front 338

Describe cocaine Mech of action

Back 338

Cocaine's primary pharmacodynamic action related to its behavioral effects is competitive blockade of dopamine reuptake by the dopamine transporter. This blockade increases the concentration of dopamine in the synaptic cleft and results in increased activation of both dopamine type 1 (D1) and type 2 (D2) receptors. The effects of cocaine on the activity mediated by D3, D4, and D5 receptors are not yet well understood, but at least one preclinical study has implicated the D3 receptor

Although the behavioral effects are attributed primarily to the blockade of dopamine reuptake, cocaine also blocks the reuptake of norepinephrine and serotonin.

Front 339

cocaine relation to cerebral blood flow and brain glucose use?

Back 339

cocaine is associated with

decreased cerebral blood flow and possibly with the development of

patchy areas of decreased glucose use.

Front 340

cocaine onset?

Back 340

The behavioral effects of cocaine are felt almost immediately and last for a relatively brief time (30 to 60 minutes); thus, users require repeated doses of the drug to maintain the feelings of intoxication.

Front 341

how long can you find cocaine metabolites in blood and urine?

Back 341

Despite the short-lived behavioral effects, metabolites of cocaine can be present in the blood and urine for up to 10 days.

Front 342

Can you become dependent after one use of cocaine?

Back 342

Because of its potency as a positive reinforcer of behavior, psychological dependence on cocaine can develop after a single use

Front 343

Which is worse in terms of withdrawal ... cocaine or opiods?

Back 343

Physiological dependence on cocaine does occur, although cocaine withdrawal is mild compared with withdrawal from opiates and opioids.

Front 344

what does PET show in cocaine addict?

Back 344

Researchers recently reported that positron emission tomography (PET) scans of the brains of patients being treated for cocaine addiction show high activation in the

mesolimbic dopamine system when addicts profoundly crave a drug.

Researchers exposed patients to cues that had previously caused them to crave cocaine, and patients described feelings of intense cravings for the drug while PET scans showed activation in areas from the amygdala and the anterior cingulate to the tip of both temporal lobes

Front 345

which receptor associated with craving?

Back 345

The D2 receptors in the mesolimbic dopamine system have been held responsible for the heightened activity during periods of craving.

Front 346

Long term affect of cocaine on neurochem as shown by PET?

Back 346

PET scans of patients recovering from cocaine addiction are reported to show a drop in neuronal activity consistent with a lessened ability to receive dopamine, and the reduction in this ability, although it decreases over time, is apparent as long as a year and a half after withdrawal.

Front 347

When is cocaine relapse risk at highest after stopping?

Back 347

The pattern of reduced brain activity reflects the course of the craving; between the third and fourth weeks of withdrawal, the activity is at its lowest level, and the risk of patient relapse is highest

Front 348

When would most say brain of cocaine addict back to normal after stopping use?

Back 348

After about 1 year,
the brains of former addicts are almost back to normal, although whether the dopamine cells ever return to a completely normal state is debatable.

Front 349

What is cocaine often cut with?

Back 349

amphetamine

Front 350

Describe crack cocaine

Back 350

Crack, a freebase form of cocaine, is extremely potent. It is sold in small, ready-to-smoke amounts, often called “rocks.” Crack cocaine is highly addictive; even one or two experiences with the drug can cause intense craving for more. Users have been known to resort to extremes of behavior to obtain the money to buy more crack. Reports from urban emergency rooms have also associated extremes of violence with crack abuse.

Front 351

Who to suspect as cocaine users?

Back 351

Clinically and practically, cocaine dependence or cocaine abuse can be suspected in patients who evidence unexplained changes in personality

Front 352

Sx assoc with cocaine use?

Back 352

Common changes associated with cocaine use are irritability, impaired ability to concentrate, compulsive behavior, severe insomnia, and weight loss.

The patient may show new evidence of increased debt or inability to pay bills on time because of the large sums used to buy cocaine.

Front 353

Subtle signs of cocaine addiction?

Back 353

social situation exclusion every 30 to 60 minutes

Because of the vasoconstricting effects of cocaine, users almost always develop nasal congestion, which they may attempt to self-medicate with decongestant sprays.

Front 354

Physical sx of cocaine intoxication?

Back 354

The major associated physical symptoms are tachycardia, hypertension, and mydriasis

Front 355

Sx of cocaine intoxication?

Back 355

With high doses, however, the symptoms of intoxication include agitation, irritability, impaired judgment, impulsive and potentially dangerous sexual behavior, aggression, a generalized increase in psychomotor activity, and, potentially, symptoms of mania

Front 356

Sx of cocaine withdrawal for mild to mod use vs heavy use?

Back 356

symptoms of dysphoria, anhedonia, anxiety, irritability, fatigue, hypersomnolence, and sometimes agitation.

With mild to moderate cocaine use, these withdrawal symptoms end within 18 hours.

With heavy use, as in cocaine dependence, withdrawal symptoms can last up to a week, but usually peak in 2 to 4 days.

can have SI

Front 357

How do people experiencing cocaine withdrawal self-medicate?

Back 357

Persons experiencing cocaine withdrawal often attempt to self-medicate with alcohol,

sedatives,
hypnotics, or
antianxiety agents such as diazepam (Valium).

Front 358

Paranoid delusions and hallucinations can occur in up to XX percent of all persons who use cocaine

Back 358

50%

Front 359

Cocaine-induced psychotic disorders are most common with what type of cocaine users?

Back 359

IV and crack users

Front 360

most frequent psychotic sx in cocaine users?

Back 360

Paranoid delusions are the most frequent psychotic symptoms.

Auditory hallucinations are also common, but visual and tactile hallucinations may be
less common than paranoid delusions.

The sensation of bugs crawling just beneath the skin (formication) has been reported to be associated with cocaine use.

Front 361

cocaine relation to mood ds?

Back 361

Classically, the mood disorder symptoms associated with intoxication are hypomanic or manic; the mood disorder symptoms associated with withdrawal are characteristic of depression.

Front 362

cocaine relation to anx ds?

Back 362

Common anxiety disorder symptoms associated with cocaine intoxication or withdrawal are those of obsessive–compulsive disorder, panic disorders, and phobias.

Front 363

cocaine and sexul fxn?

Back 363

The DSM-IV-TR allows for the diagnosis of cocaine-induced sexual dysfunction (see Table 21.2-17), which can begin when a person is intoxicated with cocaine. Although cocaine is used as an aphrodisiac and as a way to delay orgasm, its repeated use can result in impotence.

Front 364

cocaine and sleep relation?

Back 364

Cocaine intoxication is associated with the inability to sleep; cocaine withdrawal is associated with disrupted sleep or hypersomnolence.

Front 365

Cocaine and adverse physical effects? including major complications?

Back 365

A common adverse effect associated with cocaine use is nasal congestion; serious inflammation, swelling, bleeding, and ulceration of the nasal mucosa can also occur. Long-term use of cocaine can also lead to perforation of the nasal septa.

Freebasing and smoking crack can damage the bronchial passages and the lungs.

The IV use of cocaine can result in infection, embolisms, and the transmission of human immunodeficiency virus (HIV).

Minor neurological complications with cocaine use include the development of acute dystonia, tics, and migraine-like headaches.

The major complications of cocaine use, however, are cerebrovascular, epileptic, and cardiac. About two thirds of these acute toxic effects occur within 1 hour of intoxication, about one fifth occur in 1 to 3 hours, and the remainder occurs up to several days later.

Front 366

The most common cerebrovascular diseases associated with cocaine use are

Back 366

nonhemorrhagic cerebral infarctions

When hemorrhagic infarctions do occur, they can include subarachnoid, intraparenchymal, and intraventricular hemorrhages. Transient ischemic attacks have also been associated with cocaine use. Although these vascular disorders usually affect the brain, spinal cord hemorrhages have also been reported. The obvious pathophysiological mechanism for these vascular disorders is vasoconstriction, but other pathophysiological mechanisms have also been proposed

Front 367

WHich is the substance of abuse most commonly associated with seizures

Back 367

cocaine?

Front 368

SUBSTANCE1 is the substance of abuse most commonly associated with seizures; the second most common substance is 2?

Back 368

Cocaine
2. Amphetamine

Front 369

a patient who seems to have cocaine-induced psychotic disorder with an unusually fluctuating cours ... think of what dx?

Back 369

A rare and easily misdiagnosed complication of cocaine use is partial complex status epilepticus, which should be considered as a diagnosis in a patient who seems to have cocaine-induced psychotic disorder with an unusually fluctuating course

Front 370

The risk of having cocaine-induced seizures is highest in patients

Back 370

with a history of epilepsy who use high doses of cocaine as well as crack.

Front 371

What are perhaps the most common cocaine-induced cardiac abnormalities

Back 371

Myocardial infarctions and arrhythmia

Cardiomyopathies can develop with long-term use of cocaine, and cardioembolic cerebral infarctions can be a further complication of cocaine-induced myocardial dysfunction.

Front 372

What can cause death with cocaine?

Back 372

High doses of cocaine are associated with seizures, respiratory depression, cerebrovascular diseases, and myocardial infarctions—all of which can lead to death in persons who use cocaine

Front 373

What is a speedball?

Back 373

Deaths have also been reported with the ingestion of “speedballs,” which are combinations of opioids and cocaine.

Front 374

What is unique about cocaine withdrawal treatment?

Back 374

The cocaine withdrawal syndrome is distinct from that of opioids, alcohol, or sedative-hypnotic agents, because no physiological disturbances necessitate inpatient or residential drug withdrawal. Thus, it is generally possible to engage in a therapeutic trial of outpatient withdrawal before deciding whether a more intensive or controlled setting is required for patients unable to stop without help in limiting their access to cocaine.

Front 375

Sx of cocaine withdrawal?

Back 375

Patients withdrawing from cocaine typically experience fatigue, dysphoria, disturbed sleep, and some craving; some may experience depression.

Front 376

Which Rx reduces coc w/d

Back 376

No pharmacological agents reliably reduce the intensity of withdrawal, but recovery over a week or two is generally uneventful.

Front 377

How often do cocaine users seek tx?

Back 377

Most cocaine users do not come to treatment voluntarily. Their experience with the substance is too positive, and the negative effects are perceived as too minimal, to warrant seeking treatment.

Front 378

Describe people NOT seeking Tx?

Back 378

Those who do not seek treatment often have
polysubstance-related disorder,

fewer negative consequences associated with cocaine use,

fewer work- or family-related obligations, and

increased contact with the legal system and with illegal activities.

Front 379

The major hurdle to overcome in the treatment of cocaine-related disorders is

Back 379

is the user's intense craving for the drug.

Front 380

What do animal studies with cocaine show regarding reinforcement?

Back 380

animals limit their use of cocaine when negative reinforcers are experimentally linked to the cocaine intake. In humans, negative reinforcers may take the form of work and family-related problems brought on by cocaine use

Front 381

cocaine Tx strategies?

Back 381

Attaining abstinence from cocaine in patients may require complete or partial hospitalization to remove them from the usual social settings in which they had obtained or used cocaine. Frequent, unscheduled urine testing is almost always necessary to monitor patients' continued abstinence, especially in the first weeks and months of treatment. Relapse prevention therapy (RPT) relies on cognitive and behavioral techniques in addition to hospitalization and outpatient therapy to achieve the goal of abstinence.

Front 382

3 goals of individual cocaine counselling

Back 382

therapists should focus on the

1. dynamics leading to cocaine use,

2. the perceived positive effects of the cocaine, and

3. other ways to achieve these effects.

Front 383

cocaine and family tx focus?

Back 383

Common issues discussed in family therapy are the ways the

patient's past behavior has harmed the family and the

responses of family members to these behaviors.

Therapy should also focus, however, on the future and on changes in the family's activities that may help the patient stay off the drug and direct energies in different directions.

Front 384

what is network therapy?

Back 384

Network therapy uses both psychodynamic and cognitive-behavioral approaches to individual therapy while engaging the patient in a group support network.

The group, composed of the patient's family and peers, is used as a therapeutic network joining the patient and therapist at intervals in therapy sessions.

The approach promotes group cohesiveness as a vehicle for engaging patients in this treatment. This network is managed by the therapist to provide cohesiveness and support and to promote compliance with treatment.

Front 385

which drug helps decrease cocaine use?

Back 385

none(unlike opiod addictions)

Front 386

which comorbid ds might you tx with rx?

Back 386

Cocaine users presumed to have preexisting ADHD or mood disorders have been treated with methylphenidate (Ritalin) and lithium (Eskalith), respectively. Those drugs are of little or no benefit in patients without the disorders, and clinicians should adhere strictly to maximal diagnostic criteria before using either of them in the treatment of cocaine dependence. In patients with ADHD, slow-release forms of methylphenidate may be less likely to trigger cocaine craving, but the impact of such pharmacotherapy on cocaine use remains to be demonstrated.

Front 387

Which classes of drug have some effect in mild use but not so much severe?

Back 387

Also tried but not confirmed effective in controlled studies are other antidepressants, such as bupropion, monoamine oxidase inhibitors (MAOIs), selective serotonin reuptake inhibitors (SSRIs), antipsychotics, lithium, several different calcium channel inhibitors, and anticonvulsants. One study found that 300 mg a day of phenytoin (Dilantin) reduced cocaine use; this study requires further replication.

Front 388

list 4 naturally occuring hallucinogens

Back 388

naturally occurring hallucinogens are psilocybin (from some mushrooms) and mescaline (from peyote cactus); others are harmine, harmaline, ibogaine, and dimethyltryptamine (DMT)

Front 389

According to the text revision of the fourth edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), XX percent of persons in the United States had used a hallucinogen at least once

Back 389

10

Front 390

Hallucinogen use is most common among?

Back 390

young (15 to 35 years of age) white men

Front 391

Hallucinogen use is most common among age group?

Back 391

Persons 26 to 34 years of age show the highest use of hallucinogens, with 15.5 percent having used a hallucinogen at least once. Persons 18 to 25 years of age have the highest recent use of a hallucinogen

Front 392

How dangerous are hallucinogens?

Back 392

Hallucinogen use is associated with less morbidity and less mortality than that of some other substances. For example, one study found that only 1 percent of substance-related emergency room visits were related to hallucinogens, compared with 40 percent for cocaine-related problems.

Front 393

LSD mech?

Back 393

Data at this time suggest that LSD acts as a partial agonist at postsynaptic serotonin receptor

The pharmacodynamic effect of LSD remains controversial, although it is generally agreed that the drug acts on the serotonergic system, either as an antagonist or as an agonist

Front 394

describe tolerance assoc with lsd

Back 394

Tolerance for LSD and other hallucinogens develops rapidly and is virtually complete after 3 or 4 days of continuous use.

Tolerance also reverses quickly, usually in 4 to 7 days.

Front 395

describe lsd/hallucinogen dependence

Back 395

Neither physical dependence nor withdrawal symptoms occur with hallucinogens, but a user can develop a psychological dependence on the insight-inducing experiences of episodes of hallucinogen use.

Front 396

DDx for hallucinogen intoxication?

Back 396

The differential diagnosis for hallucinogen intoxication includes anticholinergic and amphetamine intoxication and alcohol withdrawal.

Front 397

The preferred treatment for hallucinogen intoxication

Back 397

is talking down the patient; during this process, guides can reassure patients that the symptoms are drug induced, that they are not going crazy, and that the symptoms will resolve shortly.

Front 398

Tx for halluc intox? how about in severe cases?

Back 398

The preferred treatment for hallucinogen intoxication is talking down the patient; during this process, guides can reassure patients that the symptoms are drug induced, that they are not going crazy, and that the symptoms will resolve shortly.
In the most severe cases, dopaminergic antagonists—for example, haloperidol (Haldol)—or benzodiazepines—for example, diazepam (Valium)—can be used for a limited time.

Front 399

hallucinogen persisting perception disorder =?

Back 399

Long after ingesting a hallucinogen, a person can experience a flashback of hallucinogenic symptoms. This syndrome is diagnosed as hallucinogen persisting perception disorder (Table 12.7-4) in DSM-IV-TR. According to studies, from 15 to 80 percent of users of hallucinogens report having experienced flashbacks.

Front 400

The differential diagnosis for flashbacks includes ?

Back 400

halluc
migraine,
seizures, visual
system abnormalities, and
posttraumatic stress disorder.

Front 401

what can trigger a flashback?

Back 401

emotional stress;
sensory deprivation, such as monotonous driving;
or use of another psychoactive substance, such as alcohol or marijuana

Front 402

describe flashbacks ...
how long do they last
do people have insight while having them

Back 402

Flashbacks are spontaneous, transitory recurrences of the substance-induced experience.

Most flashbacks are episodes of visual distortion, geometric hallucinations, hallucinations of sounds or voices, false perceptions of movement in peripheral fields, flashes of color, trails of images from moving objects, positive afterimages and halos, macropsia, micropsia, time expansion, physical symptoms, or relived intense emotion.

The episodes usually last a few seconds to a few minutes, but sometimes last longer.

Most often, even in the presence of distinct perceptual disturbances, the person has insight into the pathological nature of the disturbance.

Suicidal behavior, major depressive disorder, and panic disorders are potential complications.

Front 403

What is a "bad trip"

Back 403

The most common adverse effect of LSD and related substances is a “bad trip,” an experience resembling the acute panic reaction to cannabis but sometimes more severe; a bad trip can occasionally produce true psychotic symptoms. The bad trip generally ends when the immediate effects of the hallucinogen wear off, but its course is variable. Occasionally, a protracted psychotic episode is difficult to distinguish from a nonorganic psychotic disorder.

Front 404

compare hallucinogen induced mood ds to cocaine/amphetamine

Back 404

Unlike cocaine-induced mood disorder and amphetamine-induced mood disorder, in which the symptoms are somewhat predictable, mood disorder symptoms accompanying hallucinogen abuse can vary

Abusers may experience manic-like symptoms with grandiose delusions or depression-like feelings and ideas or mixed symptoms. As with the hallucinogen-induced psychotic disorder symptoms, the symptoms of hallucinogen-induced mood disorder usually resolve once the drug has been eliminated from the person's body.

Front 405

assoc of anxiety ds with hallucinogen?

Back 405

Anecdotally, emergency room physicians who treat patients with hallucinogen-related disorders frequently report panic disorder with agoraphobia

Front 406

Physiological symptoms from LSD

Back 406

typically few and relatively mild

Dilated pupils, increased deep tendon motor reflexes and muscle tension, and mild motor incoordination and ataxia are common. Increased heart rate, respiration, and blood pressure are modest in degree and variable, as are nausea, decreased appetite, and salivation.

Front 407

give sequence of LSD effects

Back 407

The usual sequence of changes follows a pattern of somatic symptoms appearing first, then mood and perceptual changes, and, finally, psychological changes, although effects overlap and, depending on the particular hallucinogen, the time of onset and offset varies

Front 408

Which is most potent:
LSD
mescaline
psilocybin?

Back 408

The major difference among LSD, psilocybin, and mescaline is potency. A 1.5 µg/kg dose of LSD is roughly equivalent to 225 µg/kg of psilocybin, which is equivalent to 5 mg/kg of mescaline. With mescaline, onset of symptoms is slower and more nausea and vomiting occurs, but in general, the perceptual effects are more similar than different.

Front 409

X days free of LSD is necessary to lose significant tolerance.

Back 409

4 to 6

Front 410

LSD timing
onset, peak, duration?

Back 410

The onset of action of LSD occurs within an hour,
peaks in 2 to 4 hours, and lasts
The sympathomimetic effects of LSD include tremors, tachycardia, hypertension, hyperthermia, sweating, blurring of vision, and mydriasis.8 to 12 hours

Front 411

LSD physical effects?

Back 411

The sympathomimetic effects of LSD include tremors, tachycardia, hypertension, hyperthermia, sweating, blurring of vision, and mydriasis

Front 412

LSD danger?

Back 412

Death caused by cardiac or cerebrovascular pathology related to hypertension or hyperthermia can occur with hallucinogenic use. A syndrome similar to neuroleptic malignant syndrome has reportedly been associated with LSD. Death can also be caused by a physical injury when LSD use impairs judgment about traffic or a person's ability to fly, for example

Front 413

describe perception with hallucinogens ...

Back 413

With hallucinogen use, perceptions become unusually brilliant and intense. Colors and textures seem to be richer than in the past, contours sharpened, music more emotionally profound, and smells and tastes heightened. Synesthesia is common; colors may be heard or sounds seen. Changes in body image and alterations of time and space perception also occur. Hallucinations are usually visual, often of geometric forms and figures, but auditory and tactile hallucinations are sometimes experienced.

Front 414

LSD and emotional change?

Back 414

Emotions become unusually intense and may change abruptly and often; two seemingly incompatible feelings may be experienced at the same time. Suggestibility is greatly heightened, and sensitivity or detachment from other persons may arise.

Front 415

LSD and sense of self?

Back 415

The sense of self is greatly changed, sometimes to the point of depersonalization, merging with the external world, separation of self from body, or total dissolution of the ego in mystical ecstasy

Front 416

LSD ongoing use and relation to personality?

Back 416

No clear evidence indicates a drastic personality change or chronic psychosis produced by long-term LSD use by moderate users not otherwise predisposed to these conditions. Some heavy users of hallucinogens, however, may experience chronic anxiety or depression and may benefit from a psychological or pharmacological approach that addresses the underlying problem.

Front 417

What are peyote “buttons,” picked from the small blue-green cacti Lophophora williamsii and Lophophora diffusa.

Back 417

Mescaline
hallucinogen
The buttons are the dried, round, fleshy cacti tops. Mescaline is the active hallucinogenic alkaloid in the buttons. Use of peyote is legal for the Native American Church members in some states. Adverse reactions to peyote are rare during structured religious use. Peyote usually is not consumed casually because of its bitter taste and sometimes severe nausea and vomiting preceding the hallucinogenic effects.

Front 418

active ingredient in mushrooms?

Back 418

Psilocybin is usually ingested as mushrooms.

Psilocybin sold as pills or capsules usually contains phencyclidine (PCP) or LSD instead.

Front 419

Class of Rx? Ibogaine

Back 419

Ibogaine is a complex alkaloid found in the African shrub Tabernanthe iboga. Ibogaine is a hallucinogen at the 400-mg dose range. The plant originates in Africa and traditionally is used in sacramental initiation ceremonies.

Front 420

What is Ayahuasca?

Back 420

Ayahuasca, much discussed on Internet hallucinogen

The substance contains the alkaloids harmaline and harmine. Both of those β-carboline alkaloids have hallucinogenic properties, but the resulting visual sensory alterations are accompanied by considerable nausea

Front 421

Salvia Divinorum

Back 421

Salvia divinorum as a medicine and as a sacred sacrament, which is now widely discussed, advertised, and sold on the Internet. When the plant is chewed or dried leaves smoked, it produces hallucinogen effects. Salvinorin-A, an active component in the plant, is parenterally potent, active at 250-µg doses when smoked, and of scientific and potential medical interest because it binds to the opioid κ-receptor.

Front 422

Tx of hallucinogen intox?

Back 422

Persons have historically been treated for hallucinogen intoxication by psychological support for the remainder of the trip, so-called “talking down.” This is a time-consuming and potentially hazardous undertaking, given the lability of a patient with hallucinogen-related delusions. Accordingly, treatment of hallucinogen intoxication is the oral administration of 20 mg of diazepam. This medication brings the LSD experience and any associated panic to a halt within 20 minutes and should be considered superior to “talking down” the patient over a period of hours or to administering antipsychotic agents.

Front 423

Tx of hallucinogen persisting perception disorder

Back 423

Treatment for hallucinogen persisting perception disorder is palliative. The first step in the process is correct identification of the disorder; it is not uncommon for the patient to consult a number of specialists before the diagnosis is made. Pharmacological approaches include long-lasting benzodiazepines, such as clonazepam (Klonopin) and, to a lesser extent, anticonvulsants including valproic acid (Depakene) and carbamazepine (Tegretol). Currently, no drug is completely effective in ablating symptoms.

Antipsychotic agents should only be used in the treatment of hallucinogen-induced psychoses, because they may have a paradoxical effect and exacerbate symptoms.

A second dimension of treatment is behavioral. The patient must be instructed to avoid gratuitous stimulation in the form of over-the-counter drugs, caffeine, and alcohol, and avoidable physical and emotional stressors. Marijuana smoke is a particularly strong intensifier of the disorder, even when passively inhaled.

Finally, three comorbid conditions are associated with hallucinogen persisting perception disorder: panic disorder, major depression, and alcohol dependence

Front 424

Tx of hallucinogen induced psychosis?

Back 424

Treatment of hallucinogen-induced psychosis does not differ from conventional treatment for other psychoses. In addition to antipsychotic medications, a number of agents are reportedly effective, including lithium carbonate, carbamazepine, and electroconvulsive therapy. Antidepressant drugs, benzodiazepines, and anticonvulsant agents may each have a role in treatment as well. One hallmark of this disorder is that, as opposed to schizophrenia, in which negative symptoms and poor interpersonal relatedness may commonly be found, patients with hallucinogen-induced psychosis exhibit the positive symptoms of hallucinations and delusions while retaining the ability to relate to the psychiatrist.

Front 425

Goals of hallucinogen tx?

Back 425

The goals of treatment are the control of symptoms, a minimal use of hospitals,
daily work,
the development and preservation of social relationships,
and the management of comorbid illnesses such as alcohol dependence.

Front 426

toluene, n-hexane, methyl butyl ketone, trichloroethylene, trichloroethane, dichloromethane, gasoline, and butane are examples of ?

Back 426

INHALANTS

Front 427

Why people use inhalants?

Back 427

Inhalant substances are easily available, legal, and inexpensive. These three factors contribute to the high use of inhalants among poor persons and young persons

Front 428

Inhalant use accounts for X percent of all substance-related deaths and less than Y percent of all substance-related emergency room visits.

Back 428

1%
0.5%

Front 429

Inhalant use among adolescents is also associated with an increased likelihood of: psych ds?

Back 429

conduct disorder or
antisocial personality disorder

Front 430

Inhalants most used by American adolescents are (in descending order) gasoline

Back 430

gasoline, glue (which usually contains toluene), spray paint, solvents, cleaning fluids, and assorted other aerosol

Front 431

Inhalants effect?
onset?

Back 431

Inhalants generally act as a central nervous system (CNS) depressant. Tolerance for inhalants can develop, although withdrawal symptoms are usually fairly mild and are not classified as a disorder in DSM-IV-TR

The effects appear within 5 minutes and can last for 30 minutes to several hours, depending on the inhalant substance and the dose.

Front 432

Inhalants are detectable in the blood for ? after use

Back 432

4 to 10 hours

Front 433

inhalant tox sx?

Back 433

The intoxicated state is often characterized by apathy, diminished social and occupational functioning, impaired judgment, and impulsive or aggressive behavior, and it can be accompanied by nausea, anorexia, nystagmus, depressed reflexes, and diplopia.

Front 434

high dose inhalant sx and signs?

Back 434

With high doses and long exposures, a user's neurological status can progress to stupor and unconsciousness, and a person may later be amnestic for the period of intoxication.

Front 435

how can you identify recent inhalant use?

Back 435

by rashes around the patient's nose and mouth; unusual breath odors; the residue of the inhalant substances on the patient's face, hands, or clothing; and irritation of the patient's eyes, throat, lungs, and nose

Front 436

How tx inhalant intoxication delirium?

Back 436

If the delirium results in severe behavioral disturbances, short-term treatment with a dopamine receptor antagonist, such as haloperidol (Haldol), may be necessary.

Benzodiazepines should be avoided because of the possibility of increasing the patient's respiratory depression.

Front 437

Long term danger of inhalant use?

Back 437

Inhalant-induced persisting dementia (see Table 10.3-8), as with delirium, may result from the neurotoxic effects of the inhalants themselves; the neurotoxic effects of the metals (e.g., lead) commonly used in inhalants; or the effects of frequent and prolonged periods of hypoxia. The dementia caused by inhalants is likely to be irreversible in all but the mildest cases

Front 438

Psychotic SX? probably the most common psychotic syndromes during inhalant intoxication.

Back 438

Paranoid states

are probably the most common psychotic syndromes during inhalant intoxication.

Front 439

most common mood and anxiety ds

Back 439

Depressive disorders are the most common mood disorders associated with inhalant use, and panic disorders and generalized anxiety disorder are the most common anxiety disorders.

Front 440

Low doses of inhalants associated with?

Back 440

In small initial doses, inhalants can be disinhibiting and produce feelings of euphoria and excitement and pleasant floating sensations, the effects for which persons presumably use the drugs.

Front 441

High doses of inhalants can cause?

Back 441

High doses of inhalants can cause psychological symptoms of fearfulness, sensory illusions, auditory and visual hallucinations, and distortions of body size.

The neurological symptoms can include slurred speech, decreased speed of talking, and ataxia

Front 442

Long-term use of inhalants?

Back 442

Long-term use can be associated with irritability, emotional lability, and impaired memory

Front 443

Inhalants and tolerance/withdrawal?

Back 443

Tolerance for the inhalants does develop; although not recognized by DSM-IV-TR, a withdrawal syndrome can accompany the cessation of inhalant use.

The withdrawal syndrome does not occur frequently; when it does, it can be characterized by sleep disturbances, irritability, jitteriness, sweating, nausea, vomiting, tachycardia, and (sometimes) delusions and hallucinations.

Front 444

The most serious of these is death, which can result from

Back 444

respiratory depression, cardiac arrhythmias, asphyxiation, aspiration of vomitus, or accident or injury (e.g., driving while intoxicated with inhalants).

Front 445

CT findings of chronic inhalant use?

Back 445

Computed tomography (CT) and magnetic resonance imaging (MRI) reveal diffuse cerebral, cerebellar, and brainstem atrophy with white matter disease, a leukoencephalopathy.

Front 446

Several studies of house painters and factory workers who have been exposed to solvents for long periods also have found evidence of ? on CT?

Back 446

of brain atrophy on CT scans, with decreased cerebral blood flow.

Front 447

Neuro sx and signs of inhalant use?

Back 447

Neurological and behavioral signs and symptoms can include hearing loss, peripheral neuropathy, headache, paresthesias, cerebellar signs, persisting motor impairment, parkinsonism, apathy, poor concentration, memory loss, visual-spatial dysfunction, impaired processing of linguistic material, and lead encephalopathy. White matter changes, or pontine atrophy on MRI, have been associated with worse intelligence quotient (IQ) test

Front 448

The combination of organic solvents with high concentrations of copper, zinc, and heavy metals has been associated with the development of what brain findings?

Back 448

brain atrophy, temporal lobe epilepsy, decreased IQ, and a variety of electroencephalographic (EEG) changes

Front 449

inhalant and other organ damage?

Back 449

Other serious adverse effects associated with long-term inhalant use include irreversible

hepatic disease or

renal damage (tubular acidosis) and

permanent muscle damage associated with rhabdomyolysis.

Additional adverse effects include
cardiovascular and

pulmonary symptoms (e.g., chest pain and bronchospasm) as well as

gastrointestinal (GI) symptoms (e.g., pain, nausea, vomiting, and hematemesis).

Front 450

Inhalants and fetal effects?

Back 450

There are several clinical reports of toluene embryopathy, with signs such as those of fetal alcohol syndrome. These include low birth weight, microcephaly, shortened palpebral fissures, small face, low-set ears, and other dysmorphic signs. These babies reportedly develop slowly, show hyperactivity, and have cerebellar dysfunction. No convincing evidence indicates, however, that toluene, the best-studied inhalant, produces genetic damage in somatic cells

Front 451

Which drugs contraindicated in inhalant intox?

Back 451

Sedative drugs, including benzodiazepines, are contraindicated because they worsen inhalant intoxication.

Front 452

General approach to inhalant intox?

Back 452

Supportive tx

Front 453

How long duse inhalant-induced psychotic disorder last?

Back 453

The disorder is brief, lasting a few hours to (at most) a very few weeks beyond the intoxication.

Front 454

Inhalant comorbidity?

Back 454

conduct disorder or, in other instances, may be attention-deficit/hyperactivity disorder (ADHD), major depressive disorder, dysthymic disorder, and posttraumatic stress disorder (PTSD.

Attention is also directed to experiences of abuse or neglect, which is very common in these patients)

Front 455

% of americans who continue to smoke? what % of direct health care costs in the US go to tx tobacco related illness?

Back 455

30%

60%

Front 456

The World Health Organization (WHO) estimates there are X billion smokers worldwide, and they smoke Y trillion cigarettes a year. The WHO also estimates that tobacco kills more than Z million persons each year

Back 456

1 billion

6 trillion

3 million/year

Front 457

Developing country rates increasing or decreasing? How about developed?

Back 457

Developing increasing
Developed decreasing

Front 458

Smoking onset?

Back 458

The mean age of onset of smoking is 16 years, and few persons start smoking after 2

Front 459

about XX percent of the population develops nicotine dependence

Back 459

20%

Front 460

According to the text revision of the fourth edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), approximately XX percent of current daily smokers are nicotine dependent. Nicotine withdrawal occurs in about YY percent of smokers who try to quit

Back 460

85%
50%

Front 461

What's more assoc with smoking: higher or lower education?

Back 461

lower

Front 462

Approximately A percent of all psychiatric outpatients, B percent of outpatients with bipolar I disorder, almost C percent of outpatients with schizophrenia, and D percent of substance use disorder patients smoke

Back 462

Approximately 50 percent of all psychiatric outpatients, 70 percent of outpatients with bipolar I disorder, almost 90 percent of outpatients with schizophrenia, and 70 percent of substance use disorder patients smoke

Front 463

Smoking assoc with Sz?

Back 463

The high percentage of patients with schizophrenia who smoke has been attributed to nicotine's ability to

reduce their extraordinary sensitivity to outside sensory stimuli and to

increase their concentration. In that sense, such patients are self-monitoring to relieve distress

Front 464

Researchers have found that X percent of cancer deaths in the United States are caused by tobacco smoke, the single most lethal carcinogen in the United States

Back 464

30%

Front 465

How does nicotine work?

Back 465

nicotine, which affects the central nervous system (CNS) by acting as an agonist at the

nicotinic subtype of
acetylcholine receptors.

Front 466

nicotine half life?

Back 466

2 hours

Front 467

Nicotine is believed to produce its positive reinforcing and addictive properties by

Back 467

activating the dopaminergic pathway projecting from the ventral tegmental area to the cerebral cortex and the limbic system.

In addition to activating this dopamine reward system, nicotine causes an increase in the concentrations of circulating

norepinephrine and epinephrine and an increase in the release of

vasopressin,
β-endorphin,
adrenocorticotropic hormone (ACTH), and
cortisol

Front 468

DSM nicotine diagnoses?

Back 468

The DSM-IV-TR lists three nicotine-related disorders (Table 12.9-1), but contains specific diagnostic criteria for only nicotine withdrawal

i.e., NO nicotine abuse
No intoxication

Front 469

Nicotine Withdrawal Sx?

Back 469

Abrupt cessation of nicotine use, or reduction in the amount of nicotine used, followed within 24 hours by

four (or more) of the following signs:

1. dysphoric or depressed mood
2. insomnia
3. irritability, frustration, or anger
4. anxiety
5. difficulty concentrating
6. restlessness
7. decreased heart rate
8. increased ap

Front 470

What do you use Nicotine Related Ds NOS for?

Back 470

anything but dependence or withdrawal
include nicotine intoxication, nicotine abuse, and mood disorders and anxiety disorders associated with nicotine use.

Front 471

Smoking Brain effects? Muscle effects?

Back 471

Results of studies of the effects of nicotine on cerebral blood flow (CBF) suggest that short-term nicotine exposure increases CBF without changing cerebral oxygen metabolism, but long-term nicotine exposure decreases CBF. In contrast to its stimulatory CNS effects, nicotine acts as a skeletal muscle relaxant.

Front 472

Nicotine relation to REM?

Back 472

decrease in amount of REM sleep

Front 473

Tobacco and pregancy relation?

Back 473

Tobacco use during pregnancy has been associated with an increased incidence of low birth weight babies and an increased incidence of newborns with persistent pulmonary hypertension

Front 474

Smoking cessation benefits?

Back 474

Former smokers live longer than those who continue to smoke.

Smoking cessation decreases the risk for lung cancer and other cancers, myocardial infarction, cerebrovascular diseases, and chronic lung diseases.

Women who stop smoking before pregnancy or during the first 3 to 4 months of pregnancy reduce their risk for having low birth weight infants to that of women who never smoked.

The health benefits of smoking cessation substantially exceed any risks from the average 5-pound (2.3 kg) weight gain or any adverse psychological effects after quitting.

Front 475

Tx for nicotine dependence?

Back 475

Set a quit date

Set follow-up 2 to 3 days after aquit date

Psychosocial: reduce triggers and find alternate activities when smoking occurs.
Aversive therapy: smoke to the point of nausea

Front 476

Nicotine deplacement therapy changes cessation rate by how much?

Back 476

2X, b/c reduces withdrawal

Front 477

Describe how dose nicotine replacement

Back 477

6 to 12 weeks of maintenance then
gradual reduction over 6 to 12 weeks

Front 478

What is gum dosing?

Back 478

2mg if smoke less than 25 cigarettes a day
4mg if smoke > 25 cigarettes a day

Front 479

What decreases gum absorption?

Back 479

acidic compounds like coffee, tea, soda, and juice

Front 480

Rank quit rates for tobacco:

Back 480

Medication plus group therapy - 30%
Behavior tx alone - 30%
Meds + advice 20%
Gum - 15%
Doctor advice 10%
Self-help books 10%
Self-quit 5%

Front 481

Which replacemtn provides most nicotine?

Back 481

lozenges

Front 482

Nicotine patch varieties and how compare to smoking

Back 482

Nicotine patches, also sold OTC, are available in a 16-hour, no-taper preparation (Nicotrol) and a 24- or 16-hour tapering preparation (Nicoderm CQ). Patches are administered each morning and produce blood concentrations about half those of smoking

Front 483

Side fx of patch?

Back 483

Compliance is high, and the only major adverse effects are rashes and, with 24-hour wear, insomnia. Using gum and patches in high-risk situations increases quit rates by another 5 to 10 percent.

Front 484

When d/c nicotine patch?

Back 484

After 6 to 12 weeks, the patch is discontinued because it is not for long-term use

Front 485

Nicotine spray?

Back 485

Nicotine nasal spray (Nicotrol), available only by prescription, produces nicotine concentrations in the blood that are more similar to those from smoking a cigarette, and it appears to be especially helpful for heavily dependent smokers. The spray, however, causes rhinitis, watering eyes, and coughing in more than 70 percent of patients. Although initial data suggested abuse liability, further trials have not found this.

Front 486

Nicotine inhaler?

Back 486

The nicotine inhaler, a prescription product, was designed to deliver nicotine to the lungs, but the nicotine is actually absorbed in the upper throat. It delivers 4 mg per cartridge and resultant nicotine levels are low. The major asset of the inhaler is that it provides a behavioral substitute for smoking. The inhaler doubles quit rates. These devices require frequent puffing—about 20 minutes to extract 4 mg of nicotine—and have minor adverse effects.

Front 487

Bupropion dosing, duration of tx, and minimum amount needed to decrease smoking?

Back 487

Bupropion is started at 150 mg per day for 3 days and increased to 150 mg twice a day for 6 to 12 weeks. Daily dosages of 300 mg doubles quit rates in smokers with and without a history of depression

Front 488

Side fx bupropion?
Use with other drug?

Back 488

Adverse effects include insomnia and nausea, but these are rarely significant

In one study, combined bupropion and nicotine patch had higher quit rates than either alone

Front 489

Other drug to help with smoking cessation?

Back 489

nortriptyline (Pamelor) appears to be effective for smoking cessation and is recommended as a second-line drug.

Clonidine (Catapres) decreases sympathetic activity from the locus ceruleus and, thus, is thought to abate withdrawal symptoms.
Whether given as a patch or orally, 0.2 to 0.4 mg a day of clonidine appears to double quit rates

Front 490

Among children, secondhand smoke is implicated in

Back 490

sudden infant death syndrome,
low birth weight,
chronic middle ear infections, and

respiratory illnesses (e.g., asthma, bronchitis, and pneumonia)

Front 491

Most abused opiod?

Back 491

HEROIN

Front 492

Which receptor do opiods usually work on?

Back 492

Mu agonist

Front 493

Levorphanol is what kind of drug?

Back 493

opiod

Front 494

Meperidine is what kind of drug

Back 494

opiod

Front 495

Drocode is what kind of drug

Back 495

opiod

Front 496

Propoxyphene is what kind of drug?

Back 496

opiod

Front 497

Pentazocine is what kind of drug?

Back 497

Opiod

Front 498

Nalbuphine is what kind of drug?

Back 498

Opiod

Front 499

Butorphanol?

Back 499

Opiod

Front 500

Which receptor site asocciated with pscychiatric disorders

Back 500

NOT mu
Opioid-induced psychotic disorder, opioid-induced mood disorder, and opioid-induced anxiety disorder, by contrast, are quite uncommon with µ-agonist opioids, but have been seen with certain

mixed agonist-antagonist opioids acting at other receptors.

Front 501

DRUG is the current gold standard in the treatment of opioid dependence

Back 501

Methadone

Front 502

List some opioid ANTAGonists

Back 502

Naloxone
Naltrexone
Nalorphine
Levallorphan
apo morphine

Front 503

Compounds with mixed agonist and antagonist activity at opioid receptors have been synthesized and they include

Back 503

pentazocine,
butorphanol (Stadol),
and buprenorphine (Buprenex)

Front 504

Studies have found DRUG to be an effective treatment for opioid dependence.

Back 504

Studies have found buprenorphine to be an effective treatment for opioid dependence.

Front 505

The average age of first use of OPIODS among recent initiates was X years in 2004

Back 505

24.4

Front 506

The male-to-female ratio of persons with heroin dependence is

Back 506

about 3 to 1

Front 507

How much $ spend on opiods for average user?

Back 507

A heroin habit can cost a person hundreds of dollars a day; thus, a person with opioid dependence needs to obtain money through criminal activities and prostitution.

Front 508

According to DSM-IV-TR, the lifetime prevalence for heroin use is about X percent, with Y percent having taken the drug during the prior year

Back 508

1 %
0.2%

Front 509

Which receptor?
analgesia, respiratory depression, constipation, and dependence

Back 509

MU opiod receptor

Front 510

Which receptor
analgesia, diuresis, and sedation

Back 510

K-opiod receptor

Front 511

analgesia = which opiod receptor

Back 511

δ-opioid receptors,

Front 512

what is enkephalin

Back 512

enkephalin, an endogenous pentapeptide with opioid-like actions, was identified. This discovery led to the identification of three classes of endogenous opioids within the brain, including the endorphins and the enkephalins. Endorphins are involved in neural transmission and pain suppression. They are released naturally in the body when a person is physically hurt and account, in part, for the absence of pain during acute injuries.

Front 513

Several types of data indicate that the addictive rewarding properties of opioids are mediated through (brain region?)

Back 513

activation of the ventral tegmental area dopaminergic neurons that project to the cerebral cortex and the limbic system

Front 514

Heroin, the most commonly abused opioid, is (LESS, EQUALLY, MORE) potent and lipid soluble than morphine

Back 514

MORE
. Because of those properties, heroin crosses the blood–brain barrier faster and has a more rapid onset than morphine.

Front 515

Results of at least one study using positron emission tomography (PET) have suggested that one effect of all opioids is (increased, decreased) cerebral blood flow in selected brain regions in persons with opioid dependence.

Back 515

DECREASED

Front 516

Is tolerance to opiods equal across drugs? Give eg

Back 516

No, e.g. terminally ill cancer patients may need 200 to 300 mg a day of morphine, whereas a dose of 60 mg can easily be fatal to an opioid-naïve person

Front 517

When often get opiod withdrawal?

Back 517

Abrupt cessation or ANTAGONIST given

Front 518

Long term use of opioids is associated with increased sensitivity of what types of neurons?

Back 518

dopaminergic, cholinergic, and serotonergic neurons,

Front 519

Which NT system most associated with opiod withdrawal?

Back 519

Noradrenergic

Front 520

Compare short term and long term effects of opiods on main NT system invovled in opiods

Back 520

Short-term use of opioids apparently decreases the activity of the noradrenergic neurons in the locus ceruleus; long-term use activates a compensatory homeostatic mechanism within the neurons and opioid withdrawal results in rebound hyperactivity

Front 521

How does Clonidine work and what is it's relation to opiods?

Back 521

clonidine (Catapres), an _2-adrenergic receptor agonist that decreases the release of norepinephrine, is useful in the treatment of opioid withdrawal symptoms

Front 522

About X percent of persons with opioid dependence have an additional psychiatric disorder.

Back 522

90%

Front 523

The most common opiod depedence comorbid psychiatric diagnoses are

Back 523

major depressive disorder, alcohol use disorders, antisocial personality disorder, and anxiety disorders

Front 524

About X percent of persons with opioid dependence attempt to commit suicide at least once

Back 524

15

Front 525

opiod dependence greater in lower or higher SES?

Back 525

lower

Front 526

describe family back ground of urban heroin users

Back 526

About 50 percent of urban heroin users are children of single parents or divorced parents and are from families in which at least one other member has a substance-related disorder

Front 527

Describe heroin behavior syndrome

Back 527

Teens
underlying depression, often of an agitated type and frequently accompanied by anxiety symptoms;

impulsiveness expressed by a passive-aggressive orientation;

fear of failure;

use of heroin as an antianxiety agent to mask feelings of low self-esteem, hopelessness, and aggression;

limited coping strategies and low frustration tolerance, accompanied by the need for immediate gratification;

sensitivity to drug contingencies, with a keen awareness of the relation between good feelings and the act of drug taking;

feelings of behavioral impotence counteracted by momentary control over the life situation by means of substances;

disturbances in social and interpersonal relationships with peers maintained by mutual substance experiences.

Front 528

Genetic connection to opioid dependence?

Back 528

more in monozygotic twins
may have genetically determined HYPOactivity of opiate system ... predisposes to wanting exogenous opiods

Front 529

Opioid Intoxication key criteria?

Back 529

Pupillary constriction (or pupillary dilation due to anoxia from severe overdose) and one (or more) of the following signs, developing during, or shortly after, opioid use:

1. drowsiness or coma
2. slurred speech
3. impairment in attention or memory

Front 530

Opioid Withdrawal key sx?

Back 530

Three (or more) of the following, developing within minutes to several days after Criterion A:

1. dysphoric mood
2. nausea or vomiting
3. muscle aches
4. lacrimation or rhinorrhea
5. pupillary dilation, piloerection, or sweating
6. diarrhea
7. yawning
8. fever
9. insomnia

Front 531

Describe timing of morphine and heroind withdrawal

Back 531

The morphine and heroin withdrawal syndrome
begins 6 to 8 hours after the last dose, usually after a 1- to 2-week period of continuous use or after the administration of a narcotic antagonist. The withdrawal syndrome reaches its

peak intensity during the second or third day and subsides during the next 7 to 10 days, but

some symptoms may persist for 6 months or longer.

Front 532

Meperidine withdrawal timing

Back 532

The withdrawal syndrome from meperidine begins quickly, reaches a peak in 8 to 12 hours, and ends in 4 to 5 days.

Front 533

Methadone withdrawal?

Back 533

Methadone withdrawal usually begins 1 to 3 days after the last dose and ends in 10 to 14 days.

Front 534

Describe opiod withdrawal in general

Back 534

Opioid withdrawal (Table 12.10-5) consists of severe muscle cramps and bone aches, profuse diarrhea, abdominal cramps, rhinorrhea, lacrimation, piloerection or gooseflesh (from which comes the term cold turkey for the abstinence syndrome), yawning, fever, pupillary dilation, hypertension, tachycardia, and temperature dysregulation, including hypothermia and hyperthermia.

Front 535

can you die from opiod withdrawal

Back 535

mostly no, unless severe underlying cardiac disease

Front 536

Residual sx of opiod withdrawal?

Back 536

Residual symptoms—such as insomnia, bradycardia, temperature dysregulation, and a craving for opioids—can persist for months after withdrawal. Associated features of opioid withdrawal include restlessness, irritability, depression, tremor, weakness, nausea, and vomiting.

Front 537

How does reintroducing opiod relate to withdrawal

Back 537

At any time during the abstinence syndrome, a single injection of morphine or heroin eliminates all the symptoms.

Front 538

Describe opiod-induced mood ds

Back 538

A person coming to psychiatric attention with opioid-induced mood disorder usually has mixed symptoms, combining irritability, expansiveness, and depression

Front 539

what is more associated with opiods - hypersomnia or insomnia

Back 539

Hypersomnia is likely to be more common with opioids than insomnia.

Front 540

most common sexual side effect of opiods?

Back 540

impotence

Front 541

Describe opioid initial effects ...
after initial effects
... what happens to opiod naive

Back 541

Opioids are subjectively addictive because of the euphoric high (the rush) that users experience, especially those who take the substances IV. The associated symptoms include a feeling of warmth, heaviness of the extremities, dry mouth, itchy face (especially the nose), and facial flushing

The initial euphoria is followed by a period of sedation, known in street parlance as “nodding off.”

Opioid use can induce dysphoria, nausea, and vomiting in opioid-naïve persons.

Front 542

What are physical effects of opiods?

Back 542

The physical effects of opioids include respiratory depression, pupillary constriction, smooth muscle contraction (including the ureters and the bile ducts), constipation, and changes in blood pressure, heart rate, and body temperature.

The respiratory depressant effects are mediated at the level of the brainstem

Front 543

The most common and most serious adverse effect associated with the opioid-related disorders is

Back 543

the potential transmission of hepatitis and HIV through the use of contaminated needles by more than one person

Front 544

Other Serious adverse effects of opiates?

Back 544

Persons can experience idiosyncratic allergic reactions to opioids, which result in anaphylactic shock, pulmonary edema, and death if they do not receive prompt and adequate treatment.

Front 545

Opiate Drug Intx?

Back 545

idiosyncratic drug interaction between meperidine and monoamine oxidase inhibitors (MAOIs), which can produce gross

autonomic instability, severe behavioral agitation,

coma, seizures, and death.

Opioids and MAOIs should not be given together for this reason.

Front 546

Death from an overdose of an opioid is usually attributable to

Back 546

respiratory arrest from the respiratory depressant effect of the drug

Front 547

Sx of opioid overdose?

Back 547

marked unresponsiveness, coma, slow respiration, hypothermia, hypotension, and bradycardia. When presented with the
clinical triad of
coma,
pinpoint pupils, and
respiratory depression

Front 548

What illness is associated with contaminated opiods?

Back 548

Parkinsons and MPTP

In 1976, after ingesting an opioid contaminated with methyl-phenyltetrahydropyridine (MPTP), several persons developed a syndrome of irreversible parkinsonism. The mechanism for the neurotoxic effect is as follows: MPTP is converted into 1-methyl-4-phenylpyridinium (MPP+) by the enzyme monoamine oxidase and is then taken up by dopaminergic neurons. Because MPP+ binds to melanin in substantia nigra neurons, MPP+ is concentrated in these neurons and eventually kills the cells. PET studies of persons who ingested MPTP but remained asymptomatic have shown a decreased number of dopamine-binding sites in the substantia nigra. This decrease reflects a loss in the number of dopaminergic neurons in that region.

Front 549

Tx of overdose?

Back 549

Ensure AIRWAY
Ventilate until able to give
NALOXONE (antagonist)
should see signs of improved resp, pup dilation asap

Front 550

Naloxine delivery?

Back 550

0.8mg per 70kg

Front 551

usual dose for methadone

Back 551

20 to 80mg up to 120mg

Front 552

Duration of action for methadone?

Back 552

>24 hours

Front 553

What is given during methadone detox?

Back 553

Clonidine 0.1 to 0.3mg 3 to 4 X/day

Front 554

List advantages of methadone maintenance

Back 554

First, it frees persons with opioid dependence from using injectable heroin and, thus, reduces the chance of spreading HIV through contaminated needles.

Second, methadone produces minimal euphoria and rarely causes drowsiness or depression when taken for a long time.

Third, methadone allows patients to engage in gainful employment instead of criminal activity. The major disadvantage of methadone use is that patients remain dependent on a narcotic.

Front 555

What is Levomethadyl (LAAM) and how is it used?

Back 555

LAAM is an opioid agonist that suppresses opioid withdrawal. It is no longer used, however, because some patients developed prolonged QT intervals associated with potentially fatal arrhythmias (torsades de pointes).

Front 556

What is Buprenorphine and how used?

Back 556

As with methadone and LAAM, buprenorphine is an

opioid agonist approved for opioid dependence in 2002. It can be dispensed on an outpatient basis but prescribing physicians must demonstrate that they have revived special training in its use. Buprenorphine in a daily dose of 8 to 10 mg appears to reduce heroin use. Buprenorphine also is effective in thrice-weekly dosing because of its slow dissociation from opioid receptors. After repeated administration, it attenuates or blocks the subjective effects of parenterally administered opioids such as heroin or morphine. A mild opioid withdrawal syndrome occurs if the drug is abruptly discontinued after chronic administrations

Front 557

How does naltrexone work?

Back 557

longest acting opiod ANTAGONIST at 72 hours

Front 558

+ and - of opioid antagonists in tx opioid dependence?

Back 558

The theory for using an antagonist for opioid-related disorders is that blocking opioid agonist effects, particularly euphoria, discourages persons with opioid dependence from substance-seeking behavior and, thus, deconditions this behavior.

The major weakness of the antagonist treatment model is the lack of any mechanism that compels a person to continue to take the antagonist.

Front 559

Describe opioid and relation to fetus

Back 559

Although opioid withdrawal rarely is fatal for the otherwise healthy adult, it is hazardous to the fetus and can lead to miscarriage or fetal death.

Maintaining a pregnant woman with opioid dependence on a low dose of methadone (10 to 40 mg daily) may be the least hazardous course to follow.
At this dose, neonatal withdrawal is usually mild and can be managed with low doses of paregoric. If pregnancy begins while a woman is taking high doses of methadone, the dosage should be reduced slowly (e.g., 1 mg every 3 days), and fetal movements should be monitored. If withdrawal is necessary or desired, it is least hazardous during the second trimester.

Acquired immune deficiency syndrome (AIDS) is the other major risk to the fetus of a woman with opioid dependence.

Front 560

What is angel dust?

Back 560

Phencyclidine (PCP; 1-1 [phenylcyclohexyl] piperidine), also known as angel dust, was first developed as a novel anesthetic in the late 1950s

Front 561

What is effect of PCP?

Back 561

This drug and the closely related compound ketamine were termed dissociative anesthetics, because they produced a condition in which subjects were awake but apparently insensitive to, or dissociated from, the environment

Front 562

How does PCP and ketamine exert behavioral effects?

Back 562

by blocking N-methyl-D-aspartate (NMDA)–type receptors for the excitatory neurotransmitter glutamate

Front 563

PCP and ketamine intoxication can present with :
Tx?

Back 563

a variety of symptoms, from anxiety to psychosis.
Tx Sx and Supportive

Front 564

According to DSM-IV-TR, the actual rate of PCP dependence and abuse is not known, but PCP is associated with X percent of substance abuse deaths and YY percent of substance-related emergency room visits nationally.

Back 564

3%
32%

Front 565

Is PCP use on the rise or decreasing?

Back 565

on the rise

Front 566

PCP half life vs ketamine?

Back 566

PCP = 20 hours
Ketamine = 2 hours

Front 567

How do PCP and ketamine work?
include brain areas

Back 567

The primary pharmacodynamic effect of PCP and ketamine is as an antagonist at the NMDA subtype of glutamate receptors.

PCP binds to a site within the NMDA-associated calcium channel and prevents the influx of calcium ions.

PCP also activates the dopaminergic neurons of the ventral tegmental area, which project to the cerebral cortex and the limbic system.

Activation of these neurons is usually involved in mediating the reinforcing qualities of PCP

Front 568

Describe PCP tolerance, dependence ...

Back 568

Tolerance for the effects of PCP occurs in humans,

although physical dependence generally does not occur.

Front 569

Describe PCP intoxication

Back 569

Within an hour (less when smoked, “snorted,” or used intravenously), two (or more) of the following signs:

1. vertical or horizontal nystagmus
2. hypertension or tachycardia
3. numbness or diminished responsiveness to pain
4. ataxia
5. dysarthria
6. muscle rigidity
7. seizures or coma
8. hyperacusis

Front 570

Some long-term users of PCP are said to be “crystallized,” a syndrome characterized by

Back 570

dulled thinking,
decreased reflexes,
loss of memory,
loss of impulse control,
depression,
lethargy, and
impaired concentration.

Front 571

When do patients intox on PCP show to hosp?

Back 571

2-3 days after bc friends trying to talk down

Front 572

Describe PCP intox sx

Back 572

dulled thinking, decreased reflexes, loss of memory, loss of impulse control, depression, lethargy, and impaired concentration.

Front 573

Describe PCP Delirium

Back 573

Phencyclidine intoxication delirium is included as a diagnostic category in DSM-IV-TR (see Table 10.2-6). An estimated 25 percent of all PCP-related emergency room patients may meet the criteria for the disorder, which can be characterized by agitated, violent, and bizarre behavio

Front 574

How long does PCP induced psychotic ds last?

Back 574

The psychosis can last from 1 to 30 days, with an average of 4 to 5 days.

Front 575

X is probably the most common symptom causing a PCP-intoxicated person to seek help in an emergency room.

Back 575

Anxiety

Front 576

Describe high , low amount of PCP

Back 576

Less than 5 mg of PCP is considered a low dose, and doses above 10 mg are considered high.

Front 577

Describe initial PCP efffects

Back 577

Persons who have just taken PCP are frequently uncommunicative, appear to be oblivious, and report active fantasy production.

They experience speedy feelings, euphoria, bodily warmth, tingling, peaceful floating sensations, and, occasionally, feelings of depersonalization, isolation, and estrangement. Sometimes, they have auditory and visual hallucinations. They often have striking alterations of body image, distortions of space and time perception, and delusions. They may experience intensified dependence feelings, confusion, and disorganization of thought.

Users may be sympathetic, sociable, and talkative at one moment but hostile and negative at another.

Anxiety is sometimes reported; it is often the most prominent presenting symptom during an adverse reaction.

Nystagmus, hypertension, and hyperthermia are common effects of PCP.

Head-rolling movements, stroking, grimacing, muscle rigidity on stimulation, repeated episodes of vomiting, and repetitive chanting speech are sometimes observed.

Front 578

laboratory tests show that PCP can remain in the patient's blood and urine for

Back 578

more than a week.

Front 579

The short-term effects of PCP last X hours and sometimes give way to SX?

Back 579

3 to 6 hours
a mild depression in which the user becomes irritable, somewhat paranoid, and occasionally belligerent, irrationally assaultive, suicidal, or homicidal

Front 580

DDX of PCP intox?

Back 580

Depending on a patient's status at the time of admission, the differential diagnosis may include
sedative or
narcotic overdose,
psychotic disorder as a consequence of the use of psychedelic drugs, and
brief psychotic disorder

Front 581

How tx PCP intox?

Back 581

Trapping of ionized PCP in the stomach has led to the suggestion of continuous nasogastric suction as a treatment for PCP intoxication. This strategy, however, can be needlessly intrusive and can induce electrolyte imbalances.

Administration of activated charcoal is safer, and it binds PCP and diminishes toxic effects of PCP in animals.

Because PCP disrupts sensory input, environmental stimuli can cause unpredictable, exaggerated, distorted, or violent reactions. A cornerstone of treatment, therefore, is minimization of sensory inputs to PCP-intoxicated patients

Front 582

Ketamine effects?

Back 582

Ketamine functions by working at the NMDA receptor and, as with PCP, can cause hallucinations and a dissociated state in which the patient has an altered sense of the body and reality and little concern for the environment.

Front 583

Ketamine physical effects?

Back 583

Ketamine causes cardiovascular stimulation and no respiratory depression. On physical examination, the patient may be hypertensive and tachycardic, have increased salivation and bidirectional or rotary nystagmus, or both. The onset of action is within seconds when used intravenously, and analgesia lasting 40 minutes and dissociative effects lasting for hours have been described. Cardiovascular status should be monitored and supportive care administered. A dystonic reaction has been described, as have flashbacks, but a more common complication is related to a lack of concern for the environment or personal safety.

Front 584

Ketamine duration of action?

Back 584

Ketamine has a briefer duration of effect than PCP. Peak ketamine levels occur approximately 20 minutes after IM injection. After intranasal administration, the duration of effect is approximately 1 hour.

Front 585

Why are barbiturates not as often prescribed these days?

Back 585

high abuse potential

Front 586

What is range of safety in barbiturates?

Back 586

10X normal dose ... produces coma and death

Front 587

The most commonly abused barbiturate-like substance is

Back 587

methaqualone,

Front 588

describe methaqualone

Back 588

It is often used by young persons who believe that the substance heightens the pleasure of sexual activity.
Abusers of methaqualone commonly take one or two standard tablets (usually 300 mg per tablet) to obtain the desired effects.

The street names for methaqualone include “mandrakes” (from the United Kingdom preparation Mandrax) and “soapers” (from the brand name Sopor). “Luding out” (from the brand name Quaalude) means getting high on methaqualone, which is often combined with excessive alcohol intake

Front 589

What is chloral hydrate?

Back 589

chloral hydrate, a hypnotic which is highly toxic to the gastrointestinal (GI) system
Barbiturate

Front 590

The benzodiazepines, barbiturates, and barbiturate-like substances all have their primary effects on the ? receptor.

Back 590

γ-aminobutyric acid (GABA) type A (GABA A) receptor complex, which contains a chloride ion channel, a binding site for GABA, and a well-defined binding site for benzodiazepines

Front 591

How do benzo's, barbs effect GABa receptor complex?

Back 591

Neuron gets hyper-polarized

The effect is to increase the affinity of the receptor for its endogenous neurotransmitter, GABA, and to increase the flow of chloride ions through the channel into the neuron. The influx of negatively charged chloride ions into the neuron is inhibitory, and hyperpolarizes the neuron relative to the extracellular space.

Front 592

Describe benzo and tolerance at receptor level

Back 592

DECREASED COUPLING between GABA binding site and activation of Chloride Channel

After long-term benzodiazepine use, the receptor effects caused by the agonist are attenuated. Specifically, GABA stimulation of the GABAA receptors results in less chloride influx than was caused by GABA stimulation before the benzodiazepine administration. This downregulation of receptor response is not caused by a decrease in receptor number or by decreased affinity of the receptor for GABA. The basis for the downregulation seems to be in the coupling between the GABA binding site and the activation of the chloride ion channel. This decreased efficiency in coupling may be regulated within the GABAA receptor complex itself or by other neuronal mechanisms.

Front 593

DSM Criteria C for Sedative, Hypnotic, or Anxiolytic Intoxication

Back 593

One (or more) of the following signs, developing during, or shortly after, sedative, hypnotic, or anxiolytic use:

1. slurred speech
2. incoordination
3. unsteady gait
4. nystagmus
5. impairment in attention or memory
6. stupor or coma

Front 594

Benzo withdrawal DSm criteria C?

Back 594

Two (or more) of the following, developing within several hours to a few days after criterion A:

1. autonomic hyperactivity (e.g., sweating or pulse rate greater than 100)
2. increased hand tremor
3. insomnia
4. nausea or vomiting
5. transient visual, tactile, or auditory hallucinations or illusions
6. psychomotor agitation
7. anxiety
8. grand mal seizure

Front 595

Barbiturate intox looks like?

Back 595

alcohol intox

Front 596

Sx of barbiturate intox?

Back 596

The symptoms include sluggishness, incoordination, difficulty thinking, poor memory, slow speech and comprehension, faulty judgment, disinhibited sexual aggressive impulses, narrowed range of attention, emotional lability, and exaggerated basic personality traits. The sluggishness usually resolves after a few hours, but depending primarily on the half-life of the abused substance, impaired judgment, distorted mood, and impaired motor skills may remain for 12 to 24 hours. Other potential symptoms are hostility, argumentativeness, moroseness, and, occasionally, paranoid and suicidal ideation. The neurological effects include nystagmus, diplopia, strabismus, ataxic gait, positive Romberg's sign, hypotonia, and decreased superficial reflexes.

Front 597

When is onset of benzo abrupt cessation withdrawal usually?

Back 597

2 to 3 days ... longer half life drugs = 5 to 6 days later

Front 598

sx of withdrawal from benzo?

Back 598

The symptoms include anxiety, dysphoria, intolerance for bright lights and loud noises, nausea, sweating, muscle twitching, and sometimes seizures (generally at dosages of 50 mg a day or more of diazepam)

Front 599

Persons who have been abusing phenobarbital in the range of XXX mg a day may experience mild withdrawal symptoms; those who have been abusing the substance in the range of YYY mg a day can experience orthostatic hypotension, weakness, tremor, and severe anxiety.

Back 599

400mg

800mg

Front 600

Barbiturate (phenobarb): > XXX mg have
About 75 percent of these persons have withdrawal-related seizures and may experience anorexia, delirium, hallucinations, and repeated seizures.

Back 600

> 800mg

Front 601

When do most sx of barbiturate withdrawal occur?
seizures?
psychotic ds?

Back 601

Most symptoms appear in the first 3 days of abstinence, and seizures generally occur on the second or third day, when the symptoms are worst. If seizures do occur, they always precede the development of delirium. The symptoms rarely occur more than a week after stopping the substance.
A psychotic disorder, if it develops, starts on the third to eighth day.

Front 602

Delirium that is indistinguishable from delirium tremens associated with alcohol withdrawal is seen more commonly with DRUG1 withdrawal than with DRUG2 withdrawal

Back 602

Barbiturate > benzo withdrawal

Front 603

Which benzo especially associated with Sedative, Hypnotic, or Anxiolytic Persisting Amnestic Ds?

Back 603

Triazolam

Front 604

Which drug - barbs or benzo's more common to have psychotic sx during intox or withdrawal?

Back 604

barbs

Front 605

What is The ratio of lethal dose to effective dose is about XXX to 1 or higher with benzo's, because of the minimal degree of respiratory depression associated with the benzodiazepines.

Back 605

200

Front 606

How tx benzo overdose and what are sx?

Back 606

Even when grossly excessive amounts (more than 2 g) are taken in suicide attempts, the symptoms include only drowsiness, lethargy, ataxia, some confusion, and mild depression of the user's vital signs.

The availability of flumazenil (Romazicon), a specific benzodiazepine antagonist, has reduced the lethality of the benzodiazepines. Flumazenil can be used in emergency rooms to reverse the effects of the benzodiazepines.

Front 607

Barbiturates are (harmful, dangerous, lethal) when taken in overdose because they induce respiratory depression

Back 607

LETHAL

Front 608

Give equivalents to 2 mg of Ativan

Back 608

0.5 of Clonazepam

1mg of Alprazolam
10mg of Diazepam
10mg of Zolpidem
10mg of Zaleplon
20mg of Temazepam
30mg of Oxazepam
25 mg of Chlordiazepoxide

Front 609

For the most commonly abused barbiturates, the ratio of lethal dose to effective dose ranges between What to 1?

Back 609

3 to 1 and 30 to 1

Front 610

Several reports indicate that DRUG may be useful in the treatment of benzodiazepine withdrawal

Back 610

Several reports indicate that carbamazepine (Tegretol) may be useful in the treatment of benzodiazepine withdrawal

Front 611

Describe Tx protocol for patient on higher than therapeutic benzo dose

Back 611

1. Hosp if unstable
2. Switch longer acting benzo
3. Reduce dose by 30% on 3rd
4. Reuce by 10% daily as tolerated

Front 612

Describe Tx protocol for patient on therapeutic benzo dose

Back 612

1. Reduce dose by 10% to 25% and see response and then continue weekly
2. Consider placebo pill

Front 613

How can you tell how much of a barbital a patient is on?

Back 613

give test dose of 200mg of pentobarbital
if usually not take it, will fall asleep
if mild sedated with slurred speech probably takes 500-600mg (you would give not more than 200mg)
if only nystagmus, pt prob takes 800mg but you wuold give up to 250
if no effects, pt prob taking 1gram, you would give between 300mg and 600mg

Front 614

Barb, Benzo overdose Tx?

Back 614

involves gastric lavage,
activated charcoal, and
careful monitoring of vital signs and central nervous system (CNS) activity.

Vomiting should be induced, and activated charcoal should be administered to delay gastric absorption

Front 615

Barb benzo overdose with pt comatose, tx?

Back 615

If a patient is comatose, the clinician must establish an intravenous fluid line, monitor the patient's vital signs, insert an endotracheal tube to maintain a patent airway, and provide mechanical ventilation, if necessary. Hospitalization of a comatose patient in an intensive care unit is usually required during the early stages of recovery from such overdoses

Front 616

What is difference between anabolic steroids and corticosteroids?

Back 616

It is important not to confuse the anabolic-androgenic steroids (AAS) (testosterone-like hormones) with corticosteroids (cortisol-like hormones such as hydrocortisone and prednisone).
Corticosteroids have no muscle-building properties and, hence, little abuse potential; they are widely prescribed to treat numerous inflammatory conditions such as poison ivy or asthma.

AAS, by contrast, have only limited legitimate medical applications, such as in the treatment of hypogonadal men, the wasting syndrome associated with human immunodeficiency virus (HIV) infection, and a few specific diseases such as hereditary angioedema and Fanconi's anemia

Front 617

Across studies of high school students, it is estimated that XX percent of males and 0.5 to 2.0 percent of females have used AAS during their lifetimes.

Back 617

3 to 12

Front 618

Normal testosterone plasma concentrations for men range from ?

Back 618

Normal testosterone plasma concentrations for men range from 300 to 1,000 ng/dL

Front 619

What happens if eugonadal man takes testosterone?

Back 619

no net gain in testosterone concentrations because exogenously administered AAS shut down endogenous testosterone production via feedback inhibition of the hypothalamic-pituitary-gonadal axis. Consequently, illicit users take higher than therapeutic dosages to achieve supraphysiological effects.

Front 620

How much testosterone do abusers take?

Back 620

The dose–response curve for anabolic effects may be logarithmic, which could explain why illicit users generally take 10 to 100 times the therapeutic dosages. Doses in this range are most easily achieved by taking combinations of oral and injected AAS, which illicit AAS users often do. Transdermal testosterone, available by prescription for testosterone replacement therapy, may also be used.

Front 621

Therapeutic uses of Testosterone?

Back 621

The AAS are primarily indicated for testosterone deficiency (male hypogonadism), hereditary angioedema (a congenital skin disorder), and some uncommon forms of anemia caused by bone marrow or renal failure. In women, they are given, although not as first-choice agents, for metastatic breast cancer, osteoporosis, endometriosis, and adjunctive treatment of menopausal symptoms. In men, they have been used experimentally as a male contraceptive and for treating major depressive disorder and sexual disorders in eugonadal men. Recently, they have been used to treat wasting syndromes associated with acquired immune deficiency syndrome (AIDS). Controlled studies have also suggested that testosterone has antidepressant effects in some men infected with HIV with major depressive disorder, and is also a supplementary (augmentation) treatment in some depressed men with low endogenous testosterone levels who are refractory to conventional antidepressants.

Front 622

Anabolic S on cholesterol?

Back 622

increasing levels of low-density lipoprotein cholesterol and decreasing levels of high-density lipoprotein cholesterol

Front 623

Anabolic S and BP?

Back 623

High-dose use of AAS can also activate hemostasis and increase blood pressure. Isolated case reports of myocardial infarction, cardiomyopathy, left ventricular hypertrophy, and stroke among users of AAS, including fatalities, have appeared,

Front 624

AAS endocrine effects? Males

Back 624

Among the AAS-induced endocrine effects in men are testicular atrophy and sterility, both usually reversible after discontinuing AAS, and gynecomastia, which may persist until surgical removal

Front 625

AAS effects on Females?

Back 625

In women, shrinkage of breast tissue, irregular menses (diminution or cessation), and masculinization (clitoral hypertrophy, hirsutism, and deepened voice) can occur. Masculinizing effects in women may be irreversible

Front 626

Androgens during preg?

Back 626

can masculinize female fetus

Front 627

Derm effects of AAS?

Back 627

acne,
baldness

Front 628

AAS and bone growth

Back 628

shortened stature

Front 629

AAS physical effects of ?

Back 629

Other uncommon adverse effects include edema of the extremities caused by water retention, exacerbation of tic disorders, sleep apnea, and polycythemia

Front 630

AAS:
> in males or females
athletes or non?

Back 630

males,
athletes

Front 631

Several studies have demonstrated that X percent of anabolic steroid abusers experience hypomanic or manic episodes, and a smaller percentage may have clearly psychotic symptoms

Back 631

2 to 15%

Front 632

Difference between other substance and Anabolic Steroid Addiction?

Back 632

1. Delayed euphoria
2. > emphasis of users on fitness
3. preoccupied with self-image

Front 633

Main concern Re: anabolic steroid withdrawal?

Back 633

DEPRESSION

Front 634

Psychotic symptoms are rare in association with anabolic steroid use, but they have been described in a few cases, primarily in individuals who were using the equivalent of more than Xmg of testosterone a week.

Back 634

1000

Front 635

Anabolic steroids psychosis describe

Back 635

Usually, these symptoms have consisted of grandiose or paranoid delusions, generally occurring in the context of a manic episode, although occasionally occurring in the absence of a frank manic syndrome. In most cases reported, psychotic symptoms have disappeared promptly (within a few weeks) after the discontinuation of the offending agent, although temporary treatment with antipsychotic agents was sometimes required.

Front 636

AAS use may serve as a “gateway to the use of ?

Back 636

opioid agonist or antagonists, such as nalbuphine, or to use of frank opioid agonists, such as heroin.

Front 637

Describe DHEA: use, dose, side fx, major worries

Back 637

Dehydroepiandrosterone (DHEA), a precursor hormone for both estrogens and androgens, is available over the counter. Recent years have seen an interest in DHEA for improving cognition, depression, sex drive, and general well-being in elderly adults. Some reports suggest that DHEA in dosages of 50 to 100 mg per day increases the sense of physical and social well-being in women aged 40 to 70 years. Reports also exist of androgenic

effects, including irreversible hirsutism, hair loss, voice deepening, and other undesirable sequelae. In addition, DHEA has at least a theoretical potential of enhancing tumor growth in persons with latent, hormone-sensitive malignancies, such as prostate, cervical, and breast cancer. Despite its significant popularity, few controlled data exist on the safety or efficacy of DHEA

Front 638

What is GHB? Fxn? How work? Treats?

Back 638

Gamma hydroxybutyrate (GHB) is a naturally occurring transmitter in the brain that is related to sleep regulation.

GHB increases dopamine levels in the brain.

In general, GHB is a central nervous system (CNS) depressant with effects through the endogenous opioid system.

It is used to induce anesthesia and long-term sedation, but its unpredictable duration of action limits its use.

It has recently been studied for the treatment of alcohol and opioid withdrawal and narcolepsy

Front 639

Adverse effects of GHB

Back 639

Adverse effects include nausea, vomiting, respiratory problems, seizures, coma, and death. In some reports, GHB abuse has been linked to a syndrome similar to Wernicke-Korsakoff syndrome.

Front 640

What are poppers? effect?

Back 640

The nitrite inhalants include amyl, butyl, and isobutyl nitrites, all of which are called “poppers” in popular jargon. The intoxication syndromes seen with nitrites can differ markedly from the syndromes seen with the standard inhalant substances, such as lighter fluid and airplane glue. Nitrite inhalants are used by persons seeking the associated mild euphoria, altered sense of time, feeling of fullness in the head, and, possibly, increased sexual feelings

Front 641

nitrite inhalants or poppers advs rxn?

Back 641

Adverse reactions include a toxic syndrome characterized by nausea, vomiting, headache, hypotension, drowsiness, and irritation of the respiratory tract. Some evidence indicates that nitrite inhalants can adversely affect immune function.

Front 642

nitrite inhalant + what drug is lethal?

Back 642

Sildenafil

Front 643

Nitrous Oxide .. + effects, Negative?

Back 643

Nitrous oxide, commonly known as “laughing gas,” is a widely available anesthetic agent that is subject to abuse because of its ability to produce feelings of

lightheadedness and of floating, sometimes experienced as pleasurable or specifically as sexual.

With long-term abuse patterns, nitrous oxide use has been associated with delirium and paranoia.

Female dental assistants exposed to high levels of nitrous oxide have reportedly experienced reduced fertility.

Front 644

Nutmeg effects?

Back 644

Nutmeg can be ingested in a number of preparations. When nutmeg is taken in sufficiently high doses, it can induce depersonalization, derealization, and a feeling of heaviness in the limbs.

Front 645

Morning GLory seeds effects?

Back 645

an produce a syndrome resembling that seen with lysergic acid diethylamide (LSD), characterized by altered sensory perceptions and mild visual hallucinations.

Front 646

catnip =?

Back 646

which can produce states similar to those observed with marijuana and which in high doses is reported to result in LSD-type perceptions

Front 647

betel nut?

Back 647

betel nut, which is chewed in many cultures to produce a mild euphoria and floating sensation

Front 648

kava?

Back 648

(a substance derived from the South Pacific pepper plant), which produces sedation, incoordination, weight loss, mild forms of hepatitis, and lung abnormalities.

Front 649

What is DSM category for other abused substances?

Back 649

Other (or Unknown) Substance-Related Disorders

Front 650

What is Ephedra?

Back 650

Ephedra, a natural substance found in herbal tea, acts like epinephrine and, when abused, produces cardiac arrhythmia and fatalitie

Front 651

Substances in chocolate?

Back 651

A controversial possible substance of abuse is chocolate derived from the cacao bean.

Anandamide, an ingredient in chocolate, stimulates the same receptors as marijuana.

Other compounds in chocolate include tryptophan, the precursor of serotonin, and phenylalanine, an amphetamine-like substance, both of which improve mood.

So-called chocoholics may be self-medicating because of a depressive diathesis

Front 652

polysubstance dependence = ?

Back 652

for a period of at least 12 months, a person has repeatedly used substances from at least three categories (not including nicotine and caffeine), even if the diagnostic criteria for a substance-related disorder are not met for any single substance, as long as, during this period, the criteria for substance dependence have been met for the substances considered as a group

Front 653

Major Tx goals of treating "other" substances?

Back 653

Two major treatment goals for substance abuse have been determined:

the first is abstinence from the substance, and

the second is the physical, psychiatric, and psychosocial well-being of the patient