Principles Of Addiction Medicine Section 1 Basic Science

Front 1

Where are the changes in the brain associated with addiction?

Back 1

Addiction causes changes in the orbital frontal lobes that are permanent in addicts

Front 2

Where are the changes in the brain associated with addiction

Back 2

There are changes in the orbital frontal lobes that are permanentinaddicts

Front 3

What is the main reinforcer of addiction?

Back 3

Dopamine is the main reinforcer of addiction.
There are increased concentrations in the limbic system.
It does not in itself cause addiction

Front 4

What is the main reinforcer of addiction?

Back 4

Dopamine is the main reinforcer of addiction.
There are increased concentrations in the limbic system.
Dopamine does not in itself cause addiction

Front 5

How does dopamine cause addiction?

Back 5

Addictive drugs either cause reuptake inhibition of dopamine or increased sensitivity to dopamine.
Can produce 5-10 times greater effect

Front 6

How does dopamine cause addiction?

Back 6

Addictive drugs either cause reuptake inhibition of dopamine or increased sensitivity to dopamine.
Can produce 5-10 times greater effect

Front 7

Is addiction genetic?

Back 7

40-60% of the vulnerability to addiction is genetic.

Front 8

Risk factors for addiction.

Back 8

Stress.
Low income status.
Drug availability.
Mental illness

Front 9

Is addiction genetic?

Back 9

40-60% of the vulnerability to addiction is genetic.

Front 10

Risk factors for addiction.

Back 10

Stress.
Low income status.
Drug availability.
Mental illness

Front 11

Define
PREVALENCE

Back 11

Prevalence = number cases/number in total population

Front 12

Define
INCIDENCE

Back 12

Incidence = number of new cases/number in total population

Front 13

Define
RELATIVE RISK

Back 13

Relative risk = number of people with disease plus special condition/number number with disease without special condition

Front 14

Prevalence of alcoholism

Back 14

Prevalence of alcoholism 1980 was
13% lifetime
3% in a month

Front 15

Relationship of age to alcoholism

Back 15

One third of adolescent drinkers will develop dependence.
Alcoholism generally declines with age

Front 16

Prevalence of drug use

Back 16

Lifetime prevalence equals 0.2%.
Males 2 times more likely than females.
Half of adolescent users develop dependence

Front 17

Risk factors for drug use.

Back 17

Risk factors for drug use.

Cohabitation.
Nontraditional jobs.
Childhood sexual abuse.

Front 18

Highest Hazzard age for drug and alcohol abuse

Back 18

19 years old

Front 19

Alcoholism by race

Back 19

Whites began heavy drinking younger than blacks.
Blacks have lower drinking rates Than Whites But are more likely to be chronic drinkers.
Heavy drinking among Whites is declining.
Blacks have more problem with alcohol than Whites.
Hispanic alcohol use is lower than Whites.
Hispanic alcohol use increases with acculturation.
Hispanic cirrhosis rate is higher than Whites

Front 20

What parts of the brain are involved in addiction and what is their function

Back 20

Limbic system is involved in addiction.
----Subcallosal area.
----Cingulate.
----Parahippocampal gyri

These areas deal with emotions, identity and fight or flight

Front 21

Name opiate receptors

Back 21

There are 3 opiate receptors.
---mu.
---kappa
---Delta

there are opiate receptors throughout the brain, especially limbic system

Front 22

Effects of mu agonists

Back 22

Selective MU agonist (e.g. heroin morphine)

Produces :
analgesia and euphoria.
respiratory depression
emesis
antidiuretic action

Front 23

Effect of opioid Kappa Agonist

Back 23

Kappa Agonists produce.
Dysphoria.
Diuresis.
Analgesia.
NO respiratory depression

Front 24

cannabinoid receptors

Back 24

There are 2 cannabinoid receptors.
CB1, CB 2.
They are acted upon by endogenous and/or exogenous cannabinoids.
CB 1 is found in much of brain.
CB 2 is found in the lower levels of brain

Front 25

What is physical dependence?

Back 25

Physical dependence causes individual to become physically sick and drug administration ceases.
Physical dependence is neither necessary nor sufficient to cause addiction.

Front 26

kappa agonists produce

Back 26

kappa Agonists produce
dysphoria
Diuresis
Analgesia.
No respiratory depression

Front 27

List impulse control disorders

Back 27

impulse control disorders

Explosive disorder.
Kleptomania.
Pathologic gambling.
Pyromania.
Trichotillomania

DSM 5 will include.
Excessive intranet use.
Excessive shopping.
Sex addition.
Skin picking.
Nailbiting

Front 28

Criteria for pathologic gambling

Back 28

PATHOLOGIC GAMBLING HAS 5 OR MORE THE FOLLOWING.
Gambling with greater amounts of money to achieve same experience.
Unsuccessful attempt to reduce or quit gambling.
Restless or irritable while trying to stop gambling (withdrawal).
Gambling to escape dysphoric state.
Gambling to regain gambling losses.
Lies in significant relationships about gambling.
Engages in illegal activity to fund gambling.
Has risked or lost the job or significant other because of gambling.
Relies on others to fund gambling

Front 29

Paraphilia sexual behavior versus
non-paraphilia sexual behavior

Back 29

PARAPHILIA SEXUAL BEHAVIOR = uses abnormal selection e.g. animal, unwilling person, and an object.

NON-PARAPHILIA SEXUAL BEHAVIOR engages in socially normative behavior and excessive, obsessive or compulsive manner without a disturbance of object twice

Front 30

Examples of non-paraphilia sexual behavior

Back 30

Compulsive cruising and multiple partners.
Compulsive multiple love relationships.
Compulsive sexuality in a relationship.
Compulsive autoeroticism.
Compulsive use of Internet.
Compulsive fixation on unobtainable partner.
Repetitive sexual fantasies causing distress or associated with loss of control.
Repeated sexual urges causing distress or associated with loss of control.
Repetitive engagement in sexual behavior causing distress or associated with loss of control

Front 31

Neurotransmitters that contribute to sexual behavior

Back 31

Neurotransmitters that contribute to sexual behavior

Dopamine.
Serotonin.
Norepinephrine.
Opioid system

Front 32

Described problematic intranet use

Back 32

PROBLEMATIC INTERNET USE
Reduced face-to-face social activity.
Withdrawal, tolerance.
Pre-occupational with Internet.
Longer than intended time on the Internet.
Risks significant other relationships or employment.
Lying about Internet use.
Repeat unsuccessful attempts to stop Internet use.
Associated with decreased social involvement and increased loneliness and depression

Front 33

Describe
INTERMITTENT EXPLOSIVE DISORDER

Back 33

INTERMITTENT EXPLOSIVE DISORDER.

Failure to in inhibit aggressive impulses that out of proportion to any precipitating stressor resulting in destruction of property or physical assault.
Stressors may be internal/external.
7% on Americans meet lifetime criteria.
4% of Americans meet 12 months criteria

Front 34

Define
PHARMACOKINETICS

Back 34

PHARMACOKINETICS = movement of the drug within the body.
What the body does to the drug

Front 35

Define
PHARMACODYNAMICS

Back 35

PHARMACODYNAMICS = biochemical and physiologic effects of the drug mechanism of action.

What the drug does to the body

Front 36

First-pass metabolism

Back 36

First-pass metabolism = Metabolism before the drug reaches systemic circulation.
Particularly important in oral and rectal routes.
Usually occurs in the liver.
Not significant in intervenous, sublingual, transdermal, injected routes

Front 37

Define
VOLUME OF DISTRIBUTION

Back 37

VOLUME OF DISTRIBUTION =
amount of serum, plasma, blood required for culture of all the drug of the body if uniformly dispersed.

Drugs with a small VD are confined to the intravascular space of approximately 5 L.
Drugs with large VD (up to 50,000 L) are tightly bound to tissue sites or are lipophilic

Front 38

Define
FIRST-ORDER ELIMINATION KINETICS

Back 38

FIRST-ORDER ELIMINATION KINETICS =
exponential decay caused by eliminating fixed percentage of the drug

Front 39

Define
ZERO ORDER ELIMINATION KINETICS

Back 39

Zero Order Elimination Kinetics =
linear decay of concentration.
Fixed amount of drug as eliminated per unit of time.

Front 40

Define
pharmacokinetic tolerance

Back 40

Pharmacokinetic tolerance =
increase metabolism resulting from repeated exposure

Front 41

Defined
LEARNED TOLERANCE

Back 41

Learned tolerance =
reduction of effects of drugs because of compensatory mechanism that are learned.
EG roofers can walk a straight line despite alcohol intoxication

Front 42

Define the class alcohol

Back 42

Alcohol is a chemical name for a group of related compounds to contain a hydroxyl group bound to a carbon atom

Front 43

List standard drinks
Absolute alcohol
Beer
Wine
distilled spirits

Back 43

Standard alcoholic drink =
0.6 fluid ounces of absolute alcohol.
12 ounces of beer.
5 ounces of wine.
1.5 ounces of distilled spirits

Front 44

Percentage of 21-25-year-old using alcohol

Back 44

70% of 21-25-year-old use alcohol

Front 45

Economic costs of alcoholism

Back 45

Loss of productivity and healthcare from alcohol usage is estimated 185 billion-dollars annually

Front 46

Volume distribution of alcohol is

Back 46

Volume distribution of alcohol is all tissues

Front 47

Metabolism of alcohol
where.
Excretion
enzymes affecting alcohol.
Zero order or first-order elimination kinetics

Back 47

Most alcohol is metabolized rather than excreted.
Alcohol metabolized by alcohol dehydrogenase primarily.
Zero order kinetics means alcohol is metabolized as a constant rate

Front 48

How long does it take to metabolize alcohol?

Back 48

Adults can metabolize 1 ounce of absolute alcohol per 3 hours

Front 49

Early Effects of rising alcohol level

Back 49

Early Effects of Rising Alcohol Levels =.
Relief of anxiety.
Increase talkativeness.
Feelings of confidence and euphoria
Increase assertiveness

Front 50

Effects of rising blood alcohol at moderate levels

Back 50

Moderate levels of alcohol =
impaired judgment.
Impaired reaction time.
Increases emotional outbursts.
Ataxia

Front 51

Alcohol at higher levels produce

Back 51

Higher levels of alcohol...

Acts as a sedative and hypnotic.
Reduce quality of sleep.
Increases frequency and severity of apenic episodes in OSA.
Potentiates other sedative hypnotic products
May provoke violent behavior

Front 52

Define
Wernicke's psychosis

Back 52

Wernicke psychosis =
encephalopathy
ophthalmoplegia
ataxia
caused by vitamin B-1 deficiency

Front 53

Define
Korsakoff's psychosis

Back 53

Korsakoff psychosis =
Extension of Wernicke psychosis.
Anterograde amnesia.
Retrograde amnesia.
Confabulation.
Meager content in conversation.
Lack of insight.
Apathy

Front 54

Mechanism of action of all addicting drugs

Back 54

Mechanism of addiction of all addicting drugs is to affect reward pathways by enhancing releases of dopamine from midbrain dopaminergic projections that regulate expiratory glutamatertic neurotransmission within the knee is Olympic and meso cortical areas of the forebrain

Front 55

What is on compulsive buying disorder?

Back 55

Compulsive buying disorder = oniomania

Front 56

Discuss kleptomania

Back 56

Diminished ability to inhibit impulses steel.
Has increased tension prior to theft.
Has subjective pleasure or relief associated with this.
Generally begins in adolescence or early adulthood.
Incidence equals 1%.
More common in women

Front 57

What disorders are associated with kleptomania?

Back 57

Kleptomania is associated with.
Mood disorders.
Obsessive compulsive disorder.
Panic disorder.
Separation anxiety disorder.
Body dysmorphic disorder other impulse control disorders

Front 58

Drug Treatment of kleptomania

Back 58

Fluoxetine 80 mg per day.
Naltrexone.
Topiramate.
Nonwork 100%

Front 59

Discuss trichotillomania

Back 59

Trichotillomania = pulling out of hair
Trichophagia = eating hair.
Onset usually in adolescence. Often associated with other impulse control disorders or substance abuse disorders especially OCD

Front 60

Drug treatment of trichotillomania

Back 60

Naltrexone we'll treat trichotillomania

Front 61

Discuss skin picking

Back 61

Skin taking.
Classified as a stereotypic movement disorder.
25% of institutionalized retarded people have stereotypic behaviors. Using done in isolation.
Often comorbid with suicide ideation.
More common in females. Occurs and 4% of college students.
2% of dermatology patient's meet criteria for skin taking

Front 62

Drug treatment of skin picking

Back 62

The treatment for skin picking is SSRIs

Front 63

Define intermittent explosive disorder

Back 63

Intermittent explosive disorder = failure to in inhibit aggressive impulses that out of proportion to any precipitating stressor resulting in destruction of property or physical assault

Front 64

Define
Bioavailability

Back 64

Bioavailability = fraction of unchanged drug reaches systemic circulation

Front 65

Which routes of drug administration are subject to first-pass metabolism?

Back 65

Oral and rectal routes are subject to first pass metabolism

Front 66

Effects of concurrent cocaine and alcohol

Back 66

Concurrent cocaine and alcohol. Enhances effects of cocaine and inhibits metabolism of cocaine

Front 67

Define
Potency

Back 67

Potency = amount of drug to induce a given effect

Front 68

Define
Tolerance

Back 68

Tolerance = reduction in response to a drug after repeated use

Front 69

Define
Sensitization

Back 69

Sensitization = increase in drug response after repeated administration

Front 70

Define
Cross tolerance

Back 70

Cross tolerance = tolerance to one drug generalized by other drugs in the same category

Front 71

At what rate will blood alcohol drop?

Back 71

Blood alcohol level will drop about 20 mg/dL per hour

Front 72

Define
Sedative

Back 72

Sedatives are diverse group a chemical agents that suppress CNS activity.
Includes
anxiolytics.
Hypnotics.
Anticonvulsants.
Muscle relaxants.
Anesthesia induction agents

Front 73

What are the classes of sedatives?

Back 73

Classes a sedatives.

Benzodiazepines.
Non-benzodiazepine hypnotics (zopiclone, eszopiclone, zaleplon, zolpidem).
Barbiturates.
Miscellaneous compounds

Front 74

What drug use used to treat sedative withdrawal.?

Back 74

Phenobarbital is used to treat sedative withdrawal

Front 75

Which benzodiazepines are most commonly abused?

Back 75

Zolpidem (Ambien) is the most commonly abused benzodiazepine

Front 76

How many Americans use benzodiazepines

in one month

In one year

Back 76

7-17% of Americans use benzodiazepines for up to one month

1% of Americans use benzodiazepines for greater than one year

Front 77

What are some long-term users of benzodiazepines?

Back 77

Long-term users of benzodiazepines:

Older woman.
High anxiety persons.
Persons with chronic health problems.
Alcoholics 20%.
Methadone users 70-90%

Front 78

Benzodiazepines and suicide

Back 78

Benzodiazepines are involved in a great number of suicide.

Abuse to benzodiazepines as a solitary drug is rare

Front 79

How are benzodiazepines metabolized?

Back 79

Benzodiazepines I metabolized by CT wife for 50 enzyme and liver

Front 80

What drug characteristics affect euphoria?

Back 80

Euphoria is affected by.
Drug.
Lipid solubility.
Protein binding.
Rate of entry into brain

Front 81

What neurotransmitter is affected by benzodiazepines?

Back 81

Benzodiazepines mediate GABA, which is the main inhibitory neurotransmitter of the brain

Front 82

What drug gives the most serious sedation when taken with benzodiazepines?

Back 82

Alcohol gives the most serious sedation when combined with benzodiazepines

Front 83

Benzodiazepines are inhibited by?

Back 83

Benzodiazepines are inhibited by.
ketoconazole
Itraconazole.
Macrolide antibiotics.
Fluoxetine.
Nefazodone

Front 84

What drugs may enhance benzodiazepine effect?

Back 84

Birth control pills may enhance benzodiazepine effect

Front 85

Barbiturates will decrease the activity of what drugs?

Back 85

Barbiturates will decrease the effect of.
Anticoagulants.
Birth control pills.
Steroids.
And others

Front 86

benzodiazepines and hedonic effects?

Back 86

Benzodiazepines alone are rarely used for hedonic effects.
Usually mixed with methadone

Front 87

Discuss
tolerance to benzodiazepines

Back 87

Tolerance to benzodiazepines.
Causes escalation of the dose to get same effect.
Is rapidly developed for sedative effect.

Tolerance does not occur to anxiolytic effects therefore patient likely to reduce the dose

Front 88

Benzodiazepines with the least risk of addiction

Back 88

Benzodiazepines with the least risk of addiction.
Clonazepam.
Chlordiazepoxide.
Oxazepam

Front 89

Benzodiazepines with the highest risk of addiction?

Back 89

Highest risk of addiction with benzodiazepines with highest risk of addiction.
Diazepam.
aprazolam
Lorazepam

Front 90

Benzodiazepine toxicity produces

Back 90

Benzodiazepine toxicity symptoms are.

Sedation.
Anterograde amnesia.
Difficulty acquiring new learning.
Difficulty concentrating.

Chronic heavy benzodiazepine users can suffer cognitive impairment which is often permanent

Front 91

What drug is associated with sleep walking?

Back 91

Zolpidem is often associated with complex nocturnal activities such as sleepwalking or sleep driving.

Front 92

Taking benzodiazepines during pregnancy may produce the following syndromes.

Back 92

Benzodiazepines taken during pregnancy.
May increase cleft palate risk.
Floppy baby syndrome

Front 93

What is
GHB?

Back 93

GHB = Gamma hydroxybutyrate.
Club drug.
Can induce absence seizures.
Can treat catalepsy and narcolepsy

Front 94

What are the effects of GHB?

Back 94

Effects of GHB.

Slurred speech.
Feelings of increase sexual intimacy.
Drowsiness.
Depression after use.
Physical dependence and addiction.
Withdrawal if used for >one week.

Front 95

Treatment for GHB intoxication?

Back 95

GHB intoxication is treated with high dose benzodiazepines followed by a taper

Front 96

List endogenous opioid peptides

Back 96

Endogenous opioid peptides are.
Beta endorphin.
Enkephalins.
Dynophins

Front 97

Decay products of heroin are

Back 97

Decay products of heroin are.
morphine.
6 mono acetyl morphine

Front 98

List synthetic Opioid agonists

Back 98

Synthetic opioids are.
Hydrocodone.
Oxycodone.
Hydromorphone.
Heroin

Front 99

Synthetic opioid antagonists

Back 99

Synthetic opioid antagonists include.
Naloxone.
Naltrexone.
Nalmefene

Front 100

Discuss
Oxycodone

Back 100

Oxycodone.
Semisynthetic compound derived from thebaine.
Structurally similar to codeine but pharmacodynamics similar to morphine

Front 101

. Discussed codeine

Back 101

Codeine = methyl morphine.
More lipophilic than morphine.
Less first-pass metabolism therefore greater bioavailability than morphine.
Less potent than morphine

Front 102

What is Talwin NX?

Back 102

Talwin NX is pentazocine plus naloxone to reduce abuse

Front 103

What is L AAM?

Back 103

LAAM = levo-alpha methanol.
Is a 48 hour congener of methadone

Front 104

What are the side effects of LAAM

Back 104

The side effects of LAAM are.
Prolonged QT intervals.
Torsades de points

Front 105

How many people have used heroin?

Back 105

Number of heroin users =.
1 million in the United States.
3.5 million worldwide.
100,000 new users annually.
15% of substance abuse treatment is for heroin

Front 106

Heroin pharmacokinetics

Back 106

Heroin pharmacokinetics.

Liposoluble and water-soluble.
More potent than morphine.
Is prodrug, no intrinsic opioid activity.

Front 107

What is the half-life of heroin in the blood

Back 107

The half-life of heroin and blood is 3 minutes!

Front 108

Why is heroin not used orally?

Back 108

Oral heroin is metabolized by first-pass metabolism to liver. Has very limited bile availability when given orally

Front 109

When do peak blood levels of heroin occur after using?

Back 109

Heroin peaks and the blood within 5 minutes of intranasal, intramuscular, or subcutaneous use

Front 110

What is the half-life of morphine?

Back 110

The half-life of morphine is 3 hours but analgesia last longer

Front 111

How is morphine eliminated from the body?

Back 111

90% of morphine as excreted in urine within 24 hours

Front 112

What is the half-life of immediate release oxycodone?

Back 112

The half-life of immediate release oxycodone is 3-4 hours

Front 113

Technical name for codeine

Back 113

Codeine is also known as methyl morphine

Front 114

Meperidine analgesia.
Begins.
Peaks were metabolized?

Back 114

Meperidine analgesia begins in 15 minutes.
Peaks in one to 2 hours.
Mostly metabolized in the liver

Front 115

Methadone pharmacokinetics

Back 115

Methadone pharmacokinetics.

Is a full mu opioid agonist.
Oral methadone is rapid absorption but delayed onset of action.
Half-life of methadone is 24 hours

Front 116

What is the half -life of methadone?

Back 116

The half life of methadone is 24 hours