Download McKim Chapter 9 - FIT ABA Materials: Eb Blakely

Chapter 5 Study Guides
1. What is the disease model? Is there an advantage to this model? What about the
disadvantages? What was the explanation of drug taking prior to the advent of the
disease model?
2. What is the physical dependence model? What was the concept of the autotoxin?
3. What is the advantage and disadvantage of the physical dependence model?
4. What is “psychological dependence”? Explain how this concept involves circular
reasoning, but physical dependence does not.
5. What is flavor toxicosis learning?
6. Look at the bottom of page 80. Why would an animal not learn to escape w/d
syndrome? How might this be solved?
7. What was the technical breakthrough that allowed demonstration of the positive
reinforcing effects of a drug?
8. Note that in the positive reinforcement model, the behavioral processes that explain
so-called “normal” behavior are applied to drug taking behavior. It makes the disease
model somewhat irrelevant.
9. Read over the study by Thompson and Pickens. What kind of design is it?
10. What are some drugs that function as positive reinforcers? Negative reinforcers?
11. Read over the discussion on page 85. The author refers to the conflict between
immediate positive reinforcers and delayed punishers. Note which one often wins.
This fact is well-documented in the literature, and should not be taken as a “problem”
with the model. Instead, it merely underscores the power of immediate
consequences.
12. Read over the circularity argument. Be able to explain this. Also, what would be
your rejoinder?
13. What system is involved in the positive reinforcement process? What is the
difference between effects of drugs and those of the “natural” reinforcers?
14. Is the concept of “pleasure” needed in the positive reinforcement model?
15. See Figure 5-3. What is demonstrated therein?
16. Don’t be concerned with the concept of “incentive value”. Stick with reinforcing
value, and know that reinforcing value can be empirically assessed in a variety of
ways.
17. Explain how rate of response, PR schedules, and choice might be used to assess
reinforcer value.
18. What is stress, in behavioral terms?
19. Know how the following impact drug taking:
a. Stress
b. Unrelated MO
c. Previous exposure to other drugs or to the same drug
d. Physical dependence
e. Priming
20. Explain place conditioning.
21. How do 2nd order schedules work? Note that in these schedules, the contingencies are
represented in the following way. First, the schedule with the conditioned reinforcer
looks like this: FR 10: S. This means that under an FR 10 schedule, a brief stimulus
is presented. Then: FR 20 (FR 10: S). This means that when the organism
completes 20 FR 10 schedules, then another reinforcer is delivered.
22. Don’t be concerned about the entire incentive sensitization explanations and
concepts. But it is important that the reinforcing effects of a drug may increase over
time. The author finds that the activation of the mesolimbic dopamine system
accounts for this. However, this may be a cause, or it might merely be an effect of
other processes.
23. Be able to explain the matching law. The equation can be found in the Poling
objectives. Be able to give this equation upon request. What are the 2 ways that a
behavior may be increased, based on the matching law implications?
24. Finally, check out the behavioral economics, as well as the graph in Fig 5-4. Be able
to interpret the graphs. Also, what is elastic and inelastic demand? What was the
effect of having an alternative response option on demand (e.g., drug intake)?
Chapter 6
1.
2.
3.
4.
What are the 3 kinds of alcohol?
What is fermentation? Distillation?
Where did “proof” come from? In the US, what does it mean?
Note that cultures have used alcohol for thousands of years. So explain what
happened to Caligula. If you don’t know the guy, look him up. He is mentioned
on episodes of “Seinfeld.”
5. Explain what happened with the 18th and 21st Amendments. Can this be related to
the ongoing controversy about legalizing marijuana?
6. Interpret Fig 6-1.
7. How is BAL measured (in metric)
8. Know the following:
a. Typical route of administration
b. Location of absorption –
c. 1st pass metabolism –
d. Why antacids increase BAL –
e. Gender differences in alcohol metabolism –
f. Time to peak levels –
9. Where is alcohol distributed?
10. Explain the 2 step metabolic process. Where does it occur?
11. Small amounts of alcohol are excreted in the …
12. Explain the MEOS and why cross tolerance occurs.
13. Note that after all of this metabolism, the final products are CO2 and water, which
are easily excreted.
14. What is the effect on neuropharmacology?
15. Note the discussion about RO 15-4513. We studied this drug in Poling’s lab, and
this was the drug that did not block the lethal effects of alcohol, but may block
some of its effects. What kinds of substances might also block the effects of
alcohol?
16. Discuss some effects of alcohol on:
a. The body –
b. Sleep
c. Subjective effects –
d. Perception –
e. Performance –
f. Shape of curve relating BAL and probability of a traffic accident. –
17. What is “disinhibition?” What is alcohol’s effects on it? What about In vino
veritas ?
18. Are there dose dependent effects? Are the effects discriminable?
19. What 2 kinds of tolerance are observed?
20. What are the 2 stages of withdrawal? How are they treated in serious cases?
21. What is the pattern of consumption in nonhumans?
22. Note that consumption will be influenced by cultural contingencies, gender,
availability and age. There is some interesting discussion on “behavioral
economics”. This field looks at reinforcers earned as a function of work
requirements and other variables. As work requirement increases (or cost), what
happens to consumption?
23. The author does a nice job of explaining the circular reasoning of the term
“alcoholism.” Be able to do that.
24. There are 3 models of alcoholism. Briefly explain each.
25. Are there clear cut differences between FHP and FHN people?
26. What is “loss of control” in behavioral terms? Does this theory have any basis in
fact?
27. What is the difference between problem drinkers and “gamma alcoholics”?
28. We use priming in our work with people with disabilities. This procedure also
has an effect on alcohol consumption. Please explain. Included in your
explanation why priming might work.
29. What is the TI? What is the essence of a hangover?
30. What are some chronic effects on:
a. Liver
b. Nervous system
c. Cancer
d. Offspring
e. Heart
f. Immune system
31. Are there benefits?
32. What are some treatment strategies?
Please be aware that the author does not mention any kind of functional assessment
procedures for treatment. Be able to identify possible functions of alcohol use, and some
related treatments.
Chapter 7 McKim
1. What is the difference between anxiolytics and sedative-hypnotics? What are
their respective uses and duration of actions
2. Trace the historical development of the modern day drugs in this class. How was
Librium discovered?
3. What is Rohypnol?
4. Know the following:
a. Routes of administration
b. Distribution and Excretion
c. Metabolism
d. Effect of consuming alcohol
e. Effect on NTs
5. What is the effect on the body?
6. What are the effects on behavior and performance
7. What are the effects on the behavior of nonhumans?
8. What do the discriminative properties generalize to?
9. Is there tolerance?
10. What is the W/D syndrome?
11. What do the self administration data show?
12. What are some harmful effects?
13. Profile the drug GHB using the following issues
a. History (what was it originally used for)
b. Kinetics
c. NTs
d. Effects on humans
e. Sleep
f. Self administration in non-humans
g. Does tolerance develop
GHB (Gama Hydroxybutyric Acid) is a synthetic depressant produced in clandestine labs. While
available as a prescription for sleep disorders in some other countries GHB was banned (in the U.S.)
by the FDA in 1990 because of the dangers associated with its use. However, on July 17th, 2002,
GHB was approved for treatment of a rare form of narcolepsy. Most of the GHB used in the U.S. is
illegally manufactured within its borders. Like Rohypnol, GHB and its analogs are considered "date
rape" drugs because they can be mixed with liquids (even water) and a victim wouldn't notice by
smelling or looking at it. GHB, by itself, has a soapy or salty taste--but when mixed in a drink it
may be difficult to detect.
Other products such as GBL and 1,4 butanediol (BD) are appearing in the illegal market as GHB
substitutes. These analogs are just as dangerous and have similar effects on the body.
GHB can be made from ingredients such as GBL (gamma-butyrolactone), a solvent commonly used
as a paint stripper, or butanediol (1,4-butanediol), a chemical used in the production of plastics and
adhesives. Both GBL and butanediol are metabolized into GHB in the body. GHB, GBL, and
butanediol (BD) are difficult to trace because they quickly leave the body and may be difficult to
detect in emergency rooms and other treatment facilities. The FDA has issued warnings for both
GBL and 1,4-butanediol, stating that the drugs have a potential for abuse and are a public health
danger.
GHB and it's analogs are known as "G," "liquid x","caps," "scoop," "goop," "georgia home boy," and
"grievous bodily harm."
GHB is a clear odorless liquid (usually mixed with alcohol) or a white powder (usually made into
tablets or capsules.) GHB is snorted, smoked, or mixed into drinks. The most commonly abused
form is the liquid.
On the street, it is usually sold as a liquid by the dose (a capful from a bottle or drops). In some
cities, GHB is put into water guns, and users buy it by the squirt. In other instances, candy, such as
a lollipop, is dipped in GHB and sold.
Source: SAMHSA/CSAT, "GHB: A Club Drug to Watch," Substance Abuse Treatment Advisory, Nov. 2002
EFFECTS OF USE:
The effects of GHB vary each time a person uses it and it affects each person differently. Initial
effects include euphoria and relaxation. Within 15 minutes nausea, dizziness, drowsiness, visual
disturbances, respiratory distress, amnesia, seizures, and coma are possible. It is difficult to predict
a person's reaction to GHB-- because GHB is produced in clandestine labs, the purity and strength
of doses vary. Coma, poisoning and death resulting from ingestion of GHB have been well
documented. As of November 2000, DEA documented 71 GHB-related deaths.
Coma and seizures can occur following abuse of GHB and, when combined with methamphetamine,
there appears to be an increased risk of seizure. Combining use with other drugs such as alcohol
can result in nausea and difficulty breathing. GHB may also produce withdrawal effects, including
insomnia, anxiety, tremors, and sweating. Because of concern about Rohypnol, GHB, and other
similarly abused sedative-hypnotics, Congress passed the "Drug-Induced Rape Prevention and
Punishment Act of 1996" in October 1996. This legislation increased Federal penalties for use of any
controlled substance to aid in sexual assault.
Source: "Rohypnol and GHB," NIDA InfoFacts, #13556
Background information
Rohypnol is the trade name for the drug flunitrazepam, a benzodiazepine (central nervous system
depressant) like Valium, yet 10 times more potent. Outside the United States, Rohypnol is legally
manufactured by Hoffman-LaRoche, Inc., and is available by prescription for the short-term
treatment of severe sleep disorders. It is widely available in Europe, Mexico, and Colombia, but is
neither manufactured nor approved for sale in the United States.
Illicit use of Rohypnol began in the 1970s in Europe and appeared in the United States in the
early 1990s. Much of the concern surrounding Rohypnol is its abuse as a "date rape" drug.
Rohypnol is a tasteless and odorless drug and, until recent manufacturer efforts, dissolved clear
in liquid, which masked its presence. Rohypnol comes in pill form and is usually sold in the
manufacturer’s bubble packaging, which can mislead users in the United States into believing the
drug is safe and legal. Since February 1999, reformulated Rohypnol tablets, which turn blue in a
drink to increase visibility, have been approved and marketed in 20 countries. The old noncolored
tablets are still available, however. In response to the reformulated blue tablets, people who
intend to commit a sexual assault facilitated by Rohypnol are now serving blue tropical drinks and
punches in which the blue dye can be disguised.
Effects
Rohypnol can be ingested orally, snorted, or injected. It is often combined with alcohol or used as
a remedy for the depression that follows a stimulant high. The effects of Rohypnol begin within 15
to 20 minutes of administration and, depending on the amount ingested, may persist for more
than 12 hours. The drug’s metabolic properties are detectable in urine for up to 72 hours after
ingestion.
Under Rohypnol, individuals may experience a slowing of psychomotor performance, muscle
relaxation, decreased blood pressure, sleepiness, and/or amnesia. Some of the adverse side
effects associated with the drug’s use are drowsiness, headaches, memory impairment,
dizziness, nightmares, confusion, and tremors. Although classified as a depressant, Rohypnol
can induce aggression and/or excitability.
Drug-Facilitated Rape
Drug-facilitated rape can be defined as sexual assault made easier by the offender’s use of an
"anesthesia" type drug that can render the victim physically incapacitated or helpless and unable
to give consent to sexual activity. Whether the victim is unwittingly administered the drug or
willingly ingests it for recreational use is irrelevant. The person is victimized because of an
inability to consciously consent to sexual acts.
Rohypnol is one of the drugs most commonly implicated in drug-facilitated rape. It can mentally
and physically paralyze an individual. Effects of the drug are of particular concern in combination
with alcohol and can lead to anterograde amnesia, where events that occurred during the time
the drug was in effect are forgotten.
During 2000, some 261,000 rapes/sexual assaults occurred, but it is unknown how many were
drug facilitated. Many factors contribute to this lack of data, including the short period of time that
the drug can be detected in the victim’s system. Also, victims may not seek help until days after
the assault, partly because the drug impairs their memory and partly because of their inability to
recognize signs of sexual assault. As with any sexual assault, survivors need help regaining a
sense of control and security. Many victims rely on a support system to help them deal with the
flood of emotions in the aftermath of the assault.
McKim Chapter 9
Tobacco and Nicotine
1. Note that tobacco is the only natural source of nicotine, and that there are many
strains of it.
2. Where did the word “nicotine” come from?
3. Note the average # of cigarettes/day smoked in the 80s-90s. Why has it not
decreased as the demand in developed countries has decreased?
4. What is the current legal status of tobacco (i.e., can the FDA regulate it, and what
did the courts say has to happen to allow regulation)?
5. Comment on the results of the following activities:
a. Chewing tobacco
b. Swallowing tobacco juice
c. Snuff
d. Smoking a cigarette
6. What is a nicotine bolus? Note that you get one when nicotine is absorbed
through the lungs, but not from the mouth or nose.
7. McKim discusses 3 methods of nicotine replacements: what are they? What is
the effect of each?
8. Note the blood levels as a function of route of administration in Fig 9-2. What is
the fastest?
9. Distribution and excretion
a. Where does nicotine go?
b. Where is it excreted
c. What is the genetic defect?
10. What is the major receptor site affected? Note that it also affects NE, which will
increase motor activity.
a. ACH
b. What is the biphasic effect?
11. Note some of nicotine’s effects on:
a. PNS
b. CNS
c. Reward center
d. Vomiting center
e. Serotonin- note also what happens to those who try and quit
12. Explain Nebitt’s Paradox
13. There is a long discussion on the effects on performance. Briefly state some of
the effects. Note, however, that other studies show no effect, or even a
detrimental effects.
14. Explain how nicotine initially decreases SMA then increases it.
15. Note the rate dependent effect in the “Conditioned Behavior” section. We will
talk this over in class.
16. Note also the drug discrimination procedure. I will talk about this in class. In
general, are the effects discriminable?
17. What is the withdrawal syndrome?
18. Read over the self administration section. What is the overall conclusion about
this topic?
19. Read over the theories about self administration in humans. Be able to respond to
the following:
a. Constant blood level theory
b. Nicotine
c. Psychological tool
d. Do we need all 3 to explain smoking?
20. Note that genetics may be involved in smoking. Think of a reason why that might
be the case.
21. Know 2 important facts regarding heart disease:
a. Nicotine decreases available oxygen, and this requires the heart to work
harder – consider the effects on a developing fetus, which depends on
oxygen from the mother!
b. Nicotine is correlated with atherosclerosis
22. What is the mechanism by which smoking can increase the risk of lung diseases?
23. Note that the link to cancer is more correlational than causation, and that mothers
who smoke tend to have lighter babies, and the children have lower achievement
scores/more hyperactivity. There is also a correlation with SIDs.
24. What are the 2 sources of 2nd hand smoke?
25. Freud had a bad time of it. Provide a behavioral explanation of a “compulsion to
smoke.”
26. Check out the nicotine replacement procedures.
a. Which provides more constant blood levels
b. What about the combination of 2 procedures?
c. What about the 3rd procedure that relates to the reinforcing effects of
nicotine?
d. What is the mechanism that is involved in the immunization?
Chapter 10
Xanthines
1.
2.
3.
4.
5.
6.
What are the 3 types of methylxanthines?
What are some sources
How many mg of caffeine in the average cup of coffee?
What are the 2 stimulants in chocolate?
What is the original source of coffee, tea, and cocoa?
Know the basic facts regarding:
a. Typical route of administration
b. Absorption
c. Time for peak levels
d. Distribution
e. Excretion
f. T ½
g. Metabolism in newborns
7. What neurotransmitters are affected?
Caffeine and Adenosine
Why do so many people consume so much caffeine? Why does caffeine wake you up? By
understanding the drug's actions inside the body you can see why people use it so much.
In the HowStuffWorks article How Sleep Works, the action of adenosine is discussed. As
adenosine is created in the brain, it binds to adenosine receptors. The binding of adenosine
causes drowsiness by slowing down nerve cell activity. In the brain, adenosine binding also
causes blood vessels to dilate (presumably to let more oxygen in during sleep).
To a nerve cell, caffeine looks like adenosine. Caffeine therefore binds to the adenosine
receptor. However, it doesn't slow down the cell's activity like adenosine would. So the cell
cannot "see" adenosine anymore because caffeine is taking up all the receptors adenosine
binds to. So instead of slowing down because of the adenosine level, the cells speed up.
You can see that caffeine also causes the brain's blood vessels to constrict, because it
blocks adenosine's ability to open them up. This effect is why some headache medicines like
Anacin contain caffeine -- if you have a vascular headache, the caffeine will close down the
blood vessels and relieve it.
8. What are the effects on the following:
a. Body
b. Blood vessels
c. Breathing mechanisms Performance
d. Sports
e. Sleep
9. Discuss some effects on:
a. Unconditioned behavior
b. Respondent behavior (note the effect on “negative” stimuli)
c. Operant behavior
10. Can caffeine be discriminated? What do the effects generalize to?
11. What are turkey drugs? Note how a study determined that such a substance had
similar effects to cocaine. See the description of PPA below.
See PPA description below:
Description
Phenylpropanolamine ( fen-ill-proe-pa-NOLE-a-meen) , commonly known as PPA, is used as a
nasal decongestant or as an appetite suppressant. It acts on many different parts of the body.
PPA produces effects that may be helpful or harmful. This depends on a patient's individual
condition and response and the amount of medicine taken.
Phenylpropanolamine clears nasal congestion (stuffy nose) by narrowing or constricting the blood
vessels. However, this same action may cause an increase in blood pressure in patients who
have hypertension (high blood pressure).
Phenylpropanolamine also decreases appetite. However, the way PPA and similar medicines do
this is unclear. Stimulation of the central nervous system (CNS) may be a major reason.
Phenylpropanolamine in combination with dieting, exercise, and changes in eating habits can
help obese patients lose weight. However, this appetite-reducing effect is only temporary, and is
useful only for the first few weeks of dieting until new eating habits are established.
Phenylpropanolamine has caused serious side effects (even death) when too much was taken.
12. What are the subjective effects? Note that they are dose dependent.
13. How does tolerance develop? See below. Poling has some discussion about upregulation and down-regulation.
Caffeine and other methylxanthines competitively inhibit the binding of adenosine
receptor ligands in brain tissue (Snyder 81). This action has been proposed as the
mechanism of well documented behavioral stimulant effects of caffeine 81, 84 .
Chronic daily administration of caffeine leads to the development of tolerance to
many effects of drug on the behavior 82,83,88. It has also been associated with an
increase in the number of adenosine binding sites in the brain 83,85,86,88,
suggesting that upregulation of adenosine receptors is the cellular basis of
caffeine tolerance (Marangos 85; Snyder 85).
14. What is the withdrawal syndrome? Can you have a w/d with just a single cup of
coffee/day? What is the time course?
15. Be able to interpret Fig 10-1.
16. Will caffeine be self administered by nonhumans?
17. What about in humans?
18. What does it mean to be caffeine “dependent?” Below, see the DSM-IV criteria
for substance dependence. To be diagnosed, you must have at least 3 of the
characteristics.
1. Tolerance
– Do you need more of the substance to get high or achieve the effect it used to? (I.e. more
alcohol is needed to get drunk)
2. Withdrawal
- Do you suffer from characteristic withdrawal symptoms?
(i.e. Shakes / Sweats)
- Do you use the same substance (or one closely related to it) to avoid or relieve withdrawal
symptoms?
(i.e. "Hair of the dog")
3. Have you drank / used the substance in larger amounts or over a longer period than you
intended to?
4. Have you wanted to cut down or stop for long time now or tried to do so unsuccessfully several
times?
5. Time Commitment
- Do you spend a lot of your time using the substance (drinking) or recovering from its effects?
- Do you spend a lot of time in activities trying to obtain the substance?
6. Have you given up or reduced important social, occupational or recreational activities because
of your drinking / substance use?
7. Have you continued to use the substance, despite knowing that you have a persistent or
recurrent physical or psychological problem that is likely to have been caused or made worse by
your alcohol or substance use?
19. What are some effects on the reproductive process?
20. What are the effects of pregnancy on blood levels?
21. What are the effects on the heart?
22. Note the effect on bone density in women.
23. What is caffeinism?
24. Explain the issue with the benzodiazepines? Antipsychotics?
25. Explain the ILSI issue. See the members of a special committee below. Yikes!
The ILSI North America Technical Committee on Caffeine currently has the following members:
BASF Corporation
The Coca-Cola Company
Kraft Foods, Inc.
The Procter & Gamble Company
The Pepsi-Cola Company
From:
http://www.ilsi.org/file/Caffeine.pdf
Chapter 11
Stimulants
1. What neurotransmitters are affected by stimulants?
2. There are synthetic and natural stimulants. Name a couple.
3. Know the sources of the following:
a. Cocaine
b. Ephedrine
c. Amphetamine (for what was this drug used)
4. What are the most common routes of administration? What gives the best high?
5. What is free basing? What is crack?
6. Where do these drugs go?
7. How are they excreted?
8. Compare the T1/2 of amphetamines vs cocaine.
9. What is the difference between the effects on the CNS vs PNS
10. How does Cocaine work in local anesthesia?
11. Name some of the effects on the body? What about subjective effects?
12. What is “punding?”
13. Explain amphetamine psychosis:
a. What NT is involved
b. What is the link with schizophrenia?
14. What are the effects on performance?
15. What is the clock test?
16. What are the MO effects of stimulants?
17. What is the “automutilation” effect?
18. Describe the rate dependent effects.
19. Explain the drug discrimination procedure w/respect to amphetamine.
20. What is acute tolerance? What is the toxic problem?
21. What about chronic tolerance?
22. What about sensitization?
23. What is the withdrawal syndrome?
24. Briefly discuss the self administration of cocaine and amphetamine.
25. What is the run-abstinence pattern of self administration?
26. Suffice it to say the animals (both human and nonhuman) will self administer
stimulants, may do so until death occurs.
27. Note the effects on the following functions:
a. Liver
b. Nasal passages
c. Behavior
d. Heart and BP
e. Blood vessels
f. Lifestyle issues
g. Effects on offspring
28. What is the interesting problem with different sensitivity to the reinforcing vs
lethal effects that might explain cocaine “sudden death” syndrome?
29. Discuss some treatment options for cocaine addiction.
Chapter 12: Opiates
1. What is the natural source of opiates? What about the derivatives?
2. What are some synthetics?
3. Explain the following:
a. Route of administration –
b. Absorption
c. Distribution
d. Excretion
e. T ½
f. Why methadone is used in maintenance therapy
g. Mechanism of action
h. Site of action
i. The 3 receptors
4. Explain the fact that some opiates have different affinities for, and effects on, the
opiate receptors.
5. What is a mixed antagonist/agonist?
6. What are some effects on the body and physiology?
7. Effects on performance?
8. Explain the rate dependent effects.
9. Discuss the w/d syndrome
10. Are opiates discriminable? What about generalization?
11. Explain the tolerance process, and whether all effects diminish with chronic use.
12. Are there risks with the opiates?
13. Explain the British System
14. Talk about methadone maintenance, and how it works
15. What is LAAM
16. How are antagonists drugs used
17. What is dextromethorphan? Dextrophan? How does it work?
Possible Effects of PCP
PCP or Phencyclidine, is a single drug that forms a distinct category of its own, because the
effects it produces are unlike those of any category. In some respects, PCP acts like an
hallucinogen; and, it is frequently classed as an hallucinogen in medical texts and scientific /
research reports. In other respects, it acts like a stimulant, and still in other respects it is similar to
a depressant.
The formal chemical name for this drug is Phenyl Cyclohexyl Piperidine, from which the initials
PCP are derived. "Phencyclidine" is simply a contracted form of the actual chemical name.
PCP was first developed as an anesthetic for humans in 1959. Its use was discontinued a few
years later due to its extreme side effects which included delirium and confusion. In the early
1960's PCP was brought back to medical use as a veterinary anesthetic under the trade name
Sernylan.
Among PCP's least desirable side effects are delirium, visual disturbances and hallucinations
and, occasionally, violence. Some evidence of long term memory disorders and psychological
disturbances resembling schizophrenia has also been linked to PCP.
Many PCP users ingest their drugs by smoking. PCP can be applied in either liquid or powder
form to a variety of vegetable or leafy substances, such as mint leaves, parsley, oregano,
tobacco, or marijuana. When applied to marijuana the street name for this mixture is "Killer
Weed" or "Super Weed". The substances then can be smoked in a pipe or cigarette. Because
PCP smoke is very hot and can irritate the mouth and tongue, many users prefer to use mint
leaves and similar material to cool the smoke. For the same reason PCP smokers who adulterate
commercial cigarettes prefer to use mentholated brands.
PCP produces impairments and other observable effects on the human mind and body that are a
combination of effects produced by depressants, stimulants, and hallucinogens. Blank stare
Disorientation Loss of memory Muscle rigidity Non-communicative Sensory distortions Slow,
slurred speech Agitation - Excitement Auditory hallucinations Increased pain threshold Loss of a
sense of personal identity A feeling of extreme heat, profuse perspiration Passivity - but many
users may abruptly turn violent if confronted with a threatening situation
DXM Summary
Licit Uses
Dextromethorphan hydrobromide (DXM HBr) is a cough suppressant found in more than 120
over-the-counter cold medications either alone or in combination with other drugs such as
acetaminophen, antihistamines (e.g. chlorpheniramine) and/or expectorants (e.g. guaifenesin).
These preparations are formulated as cough syrups, tablets, gel capsules and lozenges. The
average dose of DXM HBr is 15 or 30 mg. taken three to four times daily. The anticoughing
effects of DXM HBr persist for 5 to 6 hours after administration. When taken in therapeutic doses,
side-effects are rarely observed.
Chemistry/Pharmacology
Dextromethorphan (d-3-methoxy-N-methyl-morphinan) is the dextro isomer of levomethorphan. It
has for some time been used as a cough suppressant and may be useful for pain treatment and
protection against nerve cell damage. The drug acts centrally, in a manner independent of that of
opioids (e.g. codeine), to elevate the threshold for coughing by an, as yet, ill-defined mechanism.
DXM, as well as its metabolite, methorphan, have been shown to be antagonists at the N-methyld-aspartate (NMDA) receptor which is linked to other amino acid neurotransmitters, glutamate
and glycine. Clinical trials are underway to examine the efficacy of DXM in combination with
morphine for the treatment of chronic pain. DXM moderately enhances the analgesic effects of
morphine without significant changes in its subjective or pharmacokinetic effects. Because of its
antagonist activity at the NMDA receptors in the brain, ongoing research is investigating the
usefulness of DXM as a neuroprotective drug in the treatment of strokes, and in the treatment of
severe bacterial meningitis in children. There have been recent reports from these clinical trials
that DXM induced insulin-dependent (type I) diabetes mellitus.
Illicit Uses
The abuse of DXM by teenagers and young adults seems related to its over-the-counter
availability and more recently to the sale of the powdered form over the Internet. Most popular
products for abuse are CoricidinHBP gel capsules and Robitussin cough syrup.
DXM abusers report a heightened sense of perceptual awareness, altered time perception, and
visual hallucinations. The behaviorally-active metabolite of DXM, dextrorphan, is related to a
family of drugs containing PCP and ketamine and may contribute to its abuse potential. The
typical clinical presentation of DXM intoxication involves hyperexcitability, lethargy, ataxia, slurred
speech, sweating, hypertension, and/or nystagmus. Depending upon the brand of DXMcontaining product abused, there may also be signs of antihistamine or bromide toxicity.
The approximate minimum ingested dose of DXM for producing some mind-altering effects is 100
mg. DXM is commonly abused at doses of 240 mg to 360 mg, but doses can be higher. Abusers
have been reported to ingest from 8 to 30 or more Coricidin tablets at one time. Four ounces of
Robitussin contains either 240 or 360 mg of DXM, depending on the formulation, and either
quantity is sufficient to cause intoxication. Case reports identify abuse patterns from 4 ozs (1/2
bottle) up to 3 to 4 bottles a day. Internet sites inform the young users to drink the syrup
expeditiously in order to absorb enough DXM from the drink prior to the impending incidence of
vomiting which will occur as a result of the ingestion of the large volume of syrup required for
intoxication.
Chapter 13
Antipsychotics
1.
2.
3.
4.
5.
6.
7.
8.
What are the 3 names of this class of drugs?
From where does the term “neuroleptic” derive?
2 kinds of psychosis?
Why is “major tranquilizer” inappropriate?
How are the effects different for typical vs atypical drugs?
What are some characteristics of schizophrenia?
How was Thorazine discovered?
Know the following:
a. Routes of administration
b. Absorption
c. Distribution
d. Metabolism
e. Excretion
f. T ½:
9. Explain the neurophysiology of the antipsychotics, including:
a. The 2 systems involved
b. What each system appears to be involved in
c. Relation to Parkinson’s disease
d. EPS – see below
e. Neuroleptic Malignant Syndrome – see below.
f. Which drugs affect D2, and which affect D3 and D4.
g. Why larger doses are needed for some typical antipsychotics
h. The role of blocking serotonin on the appearance of EPS
10. What are some of the effects on the body?
11. Are there effects on sleep and lethality? What is the TI
12. What are the subjective effects?
13. What are the effects on SMA?
14. Note the effects on avoidance behavior, while leaving escape unaffected.
15. Is the drug easily discriminated? Is there state-dependent learning? What are the
implications of this issue?
16. Know the following:
a. Tolerance
b. W/D
c. Self administration potential
d. Effects on reproduction
e. Uses in other problems
Side effects of antipsychotics
Antipsychotic medication can produce a wide range of side-effects ranging from mildly unpleasant to severe and potentially debilitating.
It is beyond the scope of this article to list every single possible side-effect, but here are a few of the more common ones.
Extrapyramidal side-effects, or EPS, are the most common side-effects of typical antipsychotic medication and occur when these
drugs affect transmission of the neurotransmitter, dopamine which has a key role in the brain in controlling movement. Figures for the
incidence of EPS vary widely (from 5-50%) but some people are more at risk of certain side-effects than others. Schizophrenia itself may
be a risk factor for developing EPS because altered dopamine transmission is an inherent feature of the disease. (Atypical
antipsychotics are generally associated with few or no EPS.)
Some EPS (such as parkinson-like symptoms) appear within days of beginning treatment and decrease as the brain adjusts to the drug.
Others, e.g. tardive dyskinesia may not appear at first but can develop during the course of treatment.
The types of EPS are listed below.
Parkinson-like symptoms
Characterised by muscle rigidity, tremor, people with symptoms of drug-induced Parkinsonism may appear to have fixed facial
expressions and speak slow manner with a monotonous tone.
Parkinsonism affects up to 4 out of 10 people on typical neuroleptic medication and older people are more susceptible to the
symptoms at lower does of medication. Symptoms appear within days of starting medication but usually improves
spontaneously within 3 months of treatment.
Dystonia
Sustained muscle contraction, contorting and twisting movements are all signs of dystonia. Spasms are often painful and
distressing and can be frightening. In extreme cases, dystonic movements can cause injuries such as dislocated jaw.
The prevalence of dystonia is rare but is more common in younger people and children. Acute dystonia can appear within one or
two days of beginning treatment and is usually transient. 1.5-2% of people are affected by persistent or tardive dystonia.
Akathisia
Characterised by jittery and restless movements, akathisia literally means 'can't sit down'. It is one of the more common EPS
side-effects (it affects about a quarter of people on neuroleptic treatment) and can be extremely distressing.
Tardive dyskinesia
Abnormal facial movements; smacking lips, chewing, sucking, twisting the tongue can all be signs of tardive dyskinesia (TD).
Jerky, often purposeless limb movements are also characteristic signs.
Approximately 1 person in 5 on antipsychotic medication will experience TD, although the incidence increases with prolonged
exposure to neuroleptic medication.
Neuroleptic malignant syndrome
Neuromalignant syndrome (NMS) is a very rare, yet potentially fatal side-effect of neuroleptic medication. Symptoms include
movement disorders typical of EPS and an extremely high temperature and it is important to detect the symptoms early in order
to treat this condition.
Sedation is a common side-effect of neuroleptic treatment. Patients may feel tired, lethargic or weak when they are taking
antipsychotics such as chlorpromazine.
Anticholinergic effects - a dry mouth, feelings of dizziness or light headedness, constipation and blurred vision while taking
antipsychotics are due to the action of these drugs on cholinergic receptors in the brain and in the rest of the body. Anticholinergic
effects may also get worse if patients are also prescribed anticholinergic medication such as procyclidine.
Convulsions - some antipsychotics can increase the risk of convulsions, a factor that is possibly related to their anticholinergic action.
Weight gain is a relatively common side-effect of antipsychotics and often causes a great deal of distress. It is also associated with
health risks such as high blood pressure, diabetes and respiratory problems.
The mechanism for antipsychotic-related weight gain unknown - they may stimulate the appetite or lead to an altered food preference for
foods rich in fats and carbohydrates. Alternatively, they may alter the body's metabolic rates. Monitoring diet and instigating a program of
exercise may help to keep weight gain to a minimum.
Information to follow on: increased prolactin levels, sexual dysfunction, cardiac effects, hypotension, agranulocytosis and skin, eye,
kidney, gastrointestinal, respiratory, liver disorders and drug interactions associated with antipsychotic use.
What is Neuroleptic Malignant Syndrome?
Neuroleptic malignant syndrome is a life-threatening, neurological disorder most often caused by an adverse reaction to
neuroleptic or antipsychotic drugs. Symptoms include high fever, sweating, unstable blood pressure, stupor, muscular rigidity, and
autonomic dysfunction. In most cases, the disorder develops within the first 2 weeks of treatment with the drug; however, the
disorder may develop any time during the therapy period. The syndrome can also occur in people taking anti-Parkinsonism drugs
known as dopaminergics if those drugs are discontinued abruptly.
Huntington’s Chorea
The disease was Huntington's Chorea, which is an inherited, degenerative disorder of
the Central Nervous System, caused by a dominant gene. This means that everyone
who inherits the gene from one of his/her parents WILL develop the disease, and the
likelihood of doing so is therefore 50%.
The symptoms of the disease are caused by a significant reduction (volume and
activity) of two principal neurotransmitters (naturally occurring chemicals in the
brain) - namely Acetylcholine and GABA, in turn affecting the activity of the
neurotransmitter Dopamine, which becomes hyperactive. Huntington's Chorea is
therefore the 'flip side of the coin' to another movement disorder - Parkinson's
Disease where there is dopamine under activity.
Huntington's Chorea is principally characterized by hyperkinesias - abnormal,
purposeless, involuntary motor movements that can occur spontaneously or only
when the patient is trying to do something. These movements may be repetitive or
non-repetitive.
The illness may continue relentlessly for 10-20 years once it has been diagnosed,
and cause of death is commonly heart disease after a bout of illness, or due to falls,
choking or suicide before dementia sets in. New advances in medicine may provide
hope for patients suffering from this devastating disease in the future. Research and
clinical trials are currently underway.
Chapter 14
Antidepressants and Mood Stabilizers
1. What are the 1st generation and 2nd generation anti-depressants?
2. Provide some characteristics of major depression
3. What is mania?
4. What is the monoamine theory of depression?
5. What is the more current view of depression?
6. How were the MAOIs discovered?
7. What is the history of the tricyclics?
8. What is the author’s take on the relative efficacy of the 1st and 2nd generation AD?
9. Note that Prozac (fluoxetine) has been in the news lately.
10. What is the history of Lithium?
11. What are the benefits of lithium?
12. Know the following:
a. Route of administration
b. Absorption
c. Distribution
d. Metabolism
e. Excretion
f. Why some people might become toxic with TCAs
13. Know in general how the MAOIs, TCAs, and SSRIs work.
14. The author discusses the reason why anti-depressants take 2 weeks to act, despite
the fact that the effect on the MA is immediate. What are the 2 explanations?
15. Note that how lithium works in unknown, but there are many possibilities.
16. Note that carbemazepine is tegretol, and valproic acid is Depakene.
17. What are some anti-ACH symptoms of the TCAs? Other side effects?
18. Side effects of the SSRIs?
19. Side effects of the MAOs
20. Know the following:
a. Effects on sleep
b. Subjective effects
c. Performance
d. “Personality”
e. Are the effects discriminable?
f. Tolerance
g. W/D –
h. Abuse potential
21. One of the issues in treating depression is convincing people to take the drugs,
despite the side effects. That there are no known reinforcing effects of these
drugs makes this task more challenging. Design a plan to strengthen taking these
meds in a person.
22. Are there sexual side effects? Teratogenic effects?
23. Note the discussion about violence and suicide. Possible effects on violence and
suicide are hard to study, as patients are probably pre-disposed to such behavior.
Thus, those who take the drug may engage in the behavior because of: 1) lack of
a drug effect or 2) a drug-induced effect. Be able to explain this point.
24. Another possible side effect is akathesia. This also obtains with the antipsychotics.
25. Are there concerns with overdosing?
http://www.psyweb.com/Drughtm/jsp/buprop.jsp
See this link for information on Wellbutrin. Will talk about this in class.
Chapter 15
Cannabis
1.
2.
3.
4.
5.
6.
Where does pot come from? What is the active ingredient?
What is hashish? Hash oil?
Note the long history of the use of pot. Where did it start?
What is the rate of absorption with oral administration? What about inhalation?
Check out figure 15-1. Be able to interpret.
Know the following:
a. Distribution
b. T ½
c. What receptors are affected
d. Effects on body
e. Medicinal uses
f. Sleep
g. Perceptual effects
h. Memory problems
i. Attention
j. Driving
k. Aggression
l. Immune system
7. Provide a behavioral interpretation of “short term” memory.
8. What is the relation to Korsakoff’s syndrome?
9. There is some discussion of the effects on reaction time. Studies show an
increase in the average, but note the explanation. To measure central tendency,
what measure would be a better one than the mean?
10. Be able to design a within subject experiment that studies state dependent learning
with cannabis.
11. Is there tolerance of the effects of cannabis?
12. W/D syndrome
13. The author discusses a study by Kelly et al. wherein participants smoked
placebos as often as 2.3% THC. Recall the Kelly study cited by Poling. What
was the reason for this outcome? Also recall what the more sensitive procedure
was for assaying preference.
14. Compare the use of cannabis in the US with that in the Middle East countries.
15. Is there an effect on mental illness?
16. Are there effects on brain structure or “intellectual” functioning?
a. Rats
b. Monkeys
c. Humans
17. What is the amotivational syndrome?
18. Is there any evidence that it is a gateway drug?
19. One of the concerns is the capacity of produce lung cancer. What is the risk?
Chapter 16
Hallucinogens
1. What are the 3 problems with hallucinogens?
2. Know the following about LSD:
a. Hallucinogen class –
b. Source
c. T ½
d. Duration of action
e. Typical dose
f. Metabolized?
g. Effects
h. Mechanism
3. Know the following about psilocybin
a. Hallucinogen class
b. Source
c. Duration of action urs
d. Dose
e. Mechanism
4. Know the following about mescaline
a. Hallucinogen class
b. Source
c. How it is used by indigenous peoples
d. Usual dose
e. Effects –
5. Know the following about MDMA/MDA (ecstasy)
a. Hallucinogen class
b. Usual dose
c. Effects
d. Untoward effect?
e. Typical use
f. Mechanism
6. Know the following about atropine
a. Hallucinogen class
b. Source –
c. Uses
d. Mechanism
7. PCP
a. Source
b. Use
c. Effects
d. Neuropharmacology 8. Effects
9. Note that there are many other hallucinogens and they come from a variety of sources
(e.g., roots, plants, )
10. Know some of the overall effects:
a. Perception
b. Performance
c. Tolerance
d. W/D
e. Self admin
11. What are some harmful effects?