Exam 2 Flashcards
History of Cocaine
- Incas in Peru, chew on coca plant for strength/energy
- Cocaine = active drug in coca, extracted by lime
- Inca religious ceremonies, settler currency
- European interest in last half of 1800s
- 3 individuals
- Mariani - coca wine, other coca products
- Halsted - local anesthesia
- Freud - psychiatric uses, withdrawal - 1887-1914: 46 states had cocaine regulation laws, bc associated with undesirables “cocaine fiend”
- 1960s concern bc amphetamines harder to obtain, so use grew
- seemed to have few side effects–bulk amounts expensive–restricted access masked negative consequences
- associated with elite until 1985, wealth and fame (60-85)
- mid/late 80s dealers started selling crack–$5-10
- Len Bias 1986, thought died of crack, fr used powder
- Don Rogers
- Oct 1986: Reagan’s Crack Cocaine Awareness Month
- Congress passed Anti-Drug Abuse Act of 1986: 100:1 ratio
- 2010: Obama –> 18:1
Cocaine Forms
- Coca leaves mixed with organic solvent, such as kerosine or gasoline —> soaked and filtered to form coca paste
- absorbed slowly through mucous membranes, slow onset of effects, lower blood levels
- In SA, paste mixed with tobacco and smoked - Paste can be made into cocaine hydrochloride, a salt that mixes easily in water and is stable enough that heating can’t produce vapors for inhalation
- Either snort or shoot up- Snorting = most common route
- cocaine hydrochloride powder up nose to nasal mucosa; absorbed rapidly and reaches brain quickly
- Snorting = most common route
- Freebase: smokable cocaine/heroin
- Done by extracting it into volatile organic solvent, like ether
- Dangerous: combination of fire + fumes = explosive
- freebase declined in 80s, when crack discovered by mixing with household chems like baking soda+H2O - Cocaine can be taken by mouth, insufflation (blow/snort), injection, or inhalation
- intravenous > inhalation > oral > intranasal
Adulterated
- make something poorer in quality by adding another substance
- bc crack cocaine is very adulterated, actually more expensive than powder
Anti-Drug Abuse Act
1986
Reagan
100:1 ratio
add details
2010: Obama 18:1
US Sentencing Commission Study
(1) Penalties most impacted blacks (85% of convicted)
(2) Exaggerated relative harmfulness of crack
(3) Penalties sweep too broadly and most often applied to low-level offenders
(4) Quantity-based penalties overstated seriousness of crack offenses and failed to provide proportionality
Cocaine Chemical Structure
- Blocks the reuptake of DA, NE, and Serotonin…causing prolonged effect of these neurotransmitters in synapse
- Focus used to be on DA (blockage/destruction of DA neurons lessened animal self-admin rates of cocaine)
Cocaine Metabolism
- Metabolized by enzymes in the blood and liver
- Rapidly removed, with half-life of one hour
- Major metabolites: 8 hrs
- 3 days for complete elimination
Cocaine Beneficial Uses
Local anesthesia
- Still used in nasal, laryngeal, and esophageal surgeries bc absorbed so well into mucous membranes
Other claims
- overcome fatigue (celebs, athletes)
Cocaine Causes for Concern
- Acute toxicity
- Acute cocaine poisoning leads to profound CNS stimulation, progressing into convulsions, which can lead to respiratory and cardiac arrest
- Toxicity dependent on dosage size, adulteration
- Cocaethylene: (c+alc) more toxic than cocaine in mice, less potent in humans - Chronic toxicity
- In a binge (taken repeatedly and at increasingly high dosages) produces irritability, restlessness, paranoia
- Extreme cases: paranoid psychosis—lose touch with reality, auditory hallucinations
- Most recover after drug leaves system - Dependence Potential
- Majority do not become addicted
- Powerfully reinforcing drug (lab and animals will perform tasks to receive, big % of drug rehab causes)
- Withdrawal: anxiety, depression, craving, etc. - Reproductive Effects
- Increased risk of miscarriage and torn placenta
Chronic v. Acute Toxicity
- Acute: effects of single exposure or few in short period of time (24 hrs)
- Chronic: effects of repeated, long-term exposure
Supplies of Cocaine
- Price and purity by DEA indicators of supply
- Columbia, Bolivia, Peru
Cocaine Trends
1880s: first appeared, positive, benign substance
1890s: more use–>dangers became well known
1990s: society against it, laws to control it
Cocaine - Amphetamines
As cocaine use declines, amphetamine use increases
History of Amphetamines
- Chinese medicinal tea from herbs
- Active ingredient: ephedrine, used to dilate bronchial passages in asthma patients
- does so by stimulating sympathetic branch of autonomic nervous system
- also raises blood pressure
- in 1920s synthesized similar chemical: amphetamine, patented in 1932
- First use: ASTHMA replacement for ephedrine (potent dilator for nasal and bronchial passages, efficiently delivered through inhalation)
- Stay awake and study longer: students and truck drivers; Adderall
- Narcolepsy
- Appetite suppression
- Hyperactivity in children
Wartime: WWII used to improve soldier efficiency (Germans first)
Misuse in 60s: became widespread after WWII, legally manufactured oral preparation, realized that you could get similar cocaine effect if injected heroin + amph “speed”; widely available and cheap to use with heroin or alone. Not hard to get prescription
Most desired: methamphetamine (liquid or ampules for injection; used to be used to stimulate breathing in sleeping pill OD patients, sometimes injected to treat obesity
Use grew in 60s, by 70s restrictions were in place, associated with drug-abusing hippies
REACTIONS
- Rise in cocaine use
- Rise in illicit meth labs (meth called “cranks”)
- relative ease, synthesis difficult, so crank often very impure, many chemicals more toxic
1990s “smoking” crystal meth
- meth in more rural areas – Honolulu, midwest
- cocaine in cities
Adderall
mixture of amphetamine salts used to treat ADHD
Amphetamines Chemical Structure
- similar structure to catecholamine neurotransmitters, produces its effects bc recognized as catecholamine in CNS and PNS
- the methyl group allows to BBB more readily, increasing CNS potency
- increase activity of monoamine neurotransmitters by stimulating release
- DOPAMINE, norepinephrine, serotonin
- more potent releaser of norepinephrine (NE most likely causes euphoria)
Amphetamines Forms
intravenous, smoked, intranasal, oral
intravenous and smoked: 5-10 mins
intranasal: 5-20 mins
oral: 1.5 hrs
Amphetamines Metabolism
Half life: 5-12 hrs
Complete elimination: 2-3 days
Effect of high amphetamine dosage
Tachyphylaxis
- (rapid tolerance)
- produce effects by displacing/releasing neurotransmitters from their storage sites, monoamines may be depleted with large doses, resulting in reduced effect
Amphetamine Beneficial Uses
- Depression
- in 1950s were TOC for depression and fatigue; stigmatized in 60s, use decreased
- used for depression only in adjunctive therapy (used to assist primary treatment)
- ADV: antidepressant effects within 1-2 days
- potential for abuse, although little evidence in controlled trials - Weight Control
- 60s most common use was weight control
- reduce appetite and food intake (few weeks, short term) - Narcolepsy
- ADHD (Ritalin –> increases catecholamine activity in response to deficit)
- suppresses height and weight gain - Reduces shift-related disruptions
- reduce performance effects
- fatigue and sleep deprivation
Adjunctive Therapy
- Treatment used to assist primary treatment
- Amphetamines
Amphetamine Addiction
- Was not thought to produce “withdrawal” therefore soft
- Oral by prescription «_space;intravenous to get high
- Addiction depends on dose, route, and reason for use
Table 6.1
- Federal cocaine offenders
- powder:
- crack:
while % were roughly comparable in powder situations (usually mostly hispanic) there was HUGEly disproportionately high for black crack situations (always 80s/90s)
Cocaine Individuals
- Mariani - coca wine, other coca products
- Halsted - local anesthesia
- Freud - psychiatric uses, withdrawal
ADHD
- inattention, hyperactivity, impulsivity
Treatments:
amphets: Ridalin increases catecholamine activity in response to deficit
Adderal: keep awake
- due to catecholamine deficits
General Behavioral Effects of Depressants
- decreased CNS activity
- induce sleep
- relaxation, exhilaration, inebriation, drowsiness, stuporous/uncoordinated
- entered market to keep people calm and relaxed
Types of Depressants
Sedatives (anxiety reduction, low-dose prescription)
Hypnotics (sleeping pills)
Sedatives
Low doses of prescription depressants used to reduce anxiety
- Xanax, Ativan (both benzodiazapenes)
Hypontics
Depressants used as sleeping pills
Inhalants
Ex: glue, paint, solvents
Effects can also be similar to depressant drugs
History of Depressants
- Chloral Hydrate
- Early 1900s bartender Mickey Finn would slip chloral hydrate into drinks and rob; slipping someone a “mickey”
- Richardson introduced into GB in 1869
//rapidly metabolized by hypnotic agent=rapid onset <hr> unintentional and intentional CODs (respiratory depression) - Meprobamate
- patented in 1952, thought to be new CNS depressant
- FDA approved in 1955 –> wide use
- also produced same dependence - Methaqualone
- wide search of better hypnotic (sleeping pill)
- synthesized in India for sedative properties
- Germany introduced it in 1962, changed status when 10-20% of people misusing and ODing
- marketed in US in 1965, “ludes” “supors” qualades, by 1985 no longer available for prescription, now sched 1 - Benzodiazepine
- Librium marketed in 1960s as a more selective “antianxiety” that produced less drowsiness and OD
- no dependency/OD, much safer than barbiturates
- Replaced with Valium in 1970s
- important difference in DOSE AND TIME COURSE OF DRUG TAKING (not chem class)
Dependence Potential
Duration of action
- Reinforcement –> Psych Dependence
- Short-acting drugs more likely to - Withdrawal –> Physical Dependence
- drugs leaving body quickly more likely to
Short acting = more dependency!
Benzodiazepine “Date Rape” Drug
Rohypnol (GHP) - a benzodiazepine “date rape” drug
- other drugs include!!!!!!!!!!!!!!!!!!!!
- 1990s, illegal in US, put in drinks, Rohypnol+alc = profound intoxication (suggestibility and can’t remember what happened); now changes color of drink
- similar to benzo + alc effects in general
- 1995 Drug-Induced Rape Prevention and Punishment Act (20 yrs in prison and give drug without person’s knowledge, with intent of violent crime)
Benzodiazepine Mechanism of Action
- Benzodiazepines have high affinity for receptors near GABA
- enhance inhibitory effects of GABA on its receptors
Barbiturates Mechanism of Action
- Barbiturates act at a separate binding site nearby
- Creates a GABA-receptor COMPLEX, which includes barbiturate binding site + benzo receptor
Inhalants
- gaseous anesthetics (nitrous oxide “laughing gas”)
- nitrites (amyl nitrite “increase sexual pleasure)
- volatile substances (“glue sniffing,” paint, white-out)
GHP
- similar structure to GABA
- CNS depressant
- similar behavioral effects as alcohol
- increasing use made FDA ban it as supplement
- date rape –> Schedule 1
- exception: Xyrem, narcolepsy drug = schedule 3
Life Saver Box
- don’t combine depressants with alc or opioids
Myth Busters Box
- such strong /blind faith in drugs
- drugs reduce, at best, not eliminate, symptoms
- long-term effects may be more detrimental
- not a panacea or “cure”
Unintended Consequences Box
New drugs developed and tested by companies that profit from their approval
A new drug may be approved and widely prescribed even when it produces only small effects, is less helpful than other drugs on the market, and produces more unwanted side effects than is implied in the published research
Conditions Antidepressants Used to Treat
- most work by increasing NE or SO in synapse
- symptoms
Drugs being Investigated for Antidepressants
- Antidepressant treat moderate to severe depression on hamilton scale
Issues with Mental Disorders Model
Model: patient appears to have set of symptoms, disease diagnosis is made, cause and cure determined once disease is known
Is a mental disorder really a disease with a biological cause and cure? Or does a mental disorder merely describe a set of behaviors?
Antidepressants
- Monoamine Oxidase Inhibitors
- originated with TB drugs
- MAO = enzyme that breaks down DA, SO, and NE
- inhibition of MAO increases NT at synapse
- LIMITATIONS: toxicity and side effects have limited their use; alter normal metabolism of dietary AA, tyramine, high blood pressure will result, death/stroke can arise; also should avoid sympathomimetic drugs - Tricyclic Antidepressants
- originated with anti-psychotic drugs
- interfere with reuptake of DA, SO, and NE - Selective Serotonin Reuptake Inhibitors
- Prozac (SSRI)
- less likely to OD compared to tricyclic
- more selective (less action) compared to tricyclics
- now developed for SO and NE - Selective SO-NE Reuptake Inhibitors
- more selective (less action) compared to tricyclics
DSM-5 Anxiety Disorders
- phobia (unreasonable fear), social anxiety, panic disorder (recurrent panic attacks), agoraphobia (public transport, open spaces, shops/theatres, lines, outside, home alone), generalized anxiety disorder (excessive worry)
DSM-5 Mood Disorders
- bipolar: irritable mood, inflated self-esteem, decreased sleep, more talkative, flight of ideas, distractibility, increased activity, excessive pleasurable activity //> marked impairment in functioning
- major depressive: for 2 weeks, 5+
- depressed mood nearly every day, diminished interest/pleasure, changes in body weight, insomnia, psychomotor agitation or retardation (incr/decr activity), fatigue, worthlessness/guilt, can’t concentrate, thoughts of suicide
//> significant impairment, not due to medical condition or loss of loved one
DSM-5 Schizophrenia
- delusions (irrational belief), hallucinations (voices), disorganized speech or behavior, negative symptoms (no emotion)
- interferences in function, duration 6+ months
ECT Therapy
Electroconvulsive shock therapy
- single most effective treatment for depression
- 7/8 studies more effective than placebos
- more rapid effect (sometimes immediate)
History and Importance of Phenothiazine
- used to treat psychosis
- French surgeon with anesthesia, made them not worried about operation –> reduces emotionality
History and Importance of Antipsychotics
- introduction of antipsychotics in 1950s started mental health revolution and increased interest in pharmacology
- reduce symptoms of schizophrenia, but often produce movement disorders
- less people in mental hospitals now
Mechanism of Antidepressant Action
- most increase SO or NE in synapse
- MAO inhibitors, tricyclics, and SSRIs have a “lag period”
- 2 week wait even though drugs act in minutes
- other drugs like Wellbutrin are effective through different mechanisms
- the fact that drugs with a wide variety of biochemical effects have a relatively equal effect means it is possible that there does not exist a single biochemical mechanism to explain the effects of these drugs
Alcohol Prohibition
In Effect:
- 1851 Maine
- 1851-1855: 13 states
- by 1868, 9 had repealed
- Nat’l Prohibition Party and Women’s Christian Temperance Union (1874) started second wave in 1880s
- 1880-1889: 7 states
- by 1896, 4 repealed
- 1907-1919: 34 states, only 2 repealed
- Jan 1918: Mississippi first state to ratify 18th amendment. in 1919 Nebraska became 36th state
- Jan 1920: yr after 36th state ratified it, making it official
Repealed:
- Association Against Prohibition (small # of America’s wealthiest men)
- concern: income taxes (prior gov relied on alcohol sales)
- irreverence to law created sense of “lawlessness” revolt
- repealed by 21st amendment in 1933
Effects:
- alcohol demonized, blamed for human problems
- organized crime became more organized and profitable
- it did reduce overall alcohol intake, but the rates of dependence and alcohol-related deaths rose during the period, but still remained lower than before
- did not reduce availability, use, or related problems
- increased organized crime and expensive law enforcement
Alcohol Absorption
- some absorbed in stomach, most through small intestine
- rate depends on concentration of alcohol
- alc taken with/after a meal is absorbed more slowly bc protein in food retains the alc in stomach
- water slows absorption and carbonated drinks speed up
Fetal Alcohol Syndrome (FAS)
- facial and developmental abnormalities due to alc use during pregnancy
- growth retardation
- abnormal features
- CNS abnormality (neural retardation)
0.2-1.5 per 1000 births of drinking mothers
23-29 per births of problematic drinkers
Consequence of overstating %
- guilt, stress on baby
- abortion
Wernicke-Korskakoff Syndrome
- chronic mental impairments produced by heavy alcohol use over long period of time
- loss of brain tissue, global decline in intellect,
Alcohol Hangover Syndrome
- Hangovers compare to symptoms of withdrawal from a short- or long-term dependence on alcohol.
–> Only known cure is analgesic for headache, and rest/time.
Cellular dehydration, alcohol causes fluid inside cells to move outside. Basis of an increased thirst during hangover.
Alcohol is a gas irritant, irritates local mucosa lining the stomach. This is the cause of nausea and upset stomach, as well as the accumulation of acetaldehyde (toxic).
drink in moderation
Alcohol Withdrawal
-
Blackouts v. Unconciousness
- Blackout- when person becomes intoxicated and doesn’t remember certain parts of the night, or party etc
- Unconsciousness- the brain shuts itself down making the person not aware of their surroundings or activity going on around them. Inability to function normally.
Family History Role in Alcohol Use Disorder
- Children of alcoholics are more likely to have alcohol problems
Not entirely determined by family history
Most children of alcoholics do not develop alcohol problems
Twin studies
Monozygotic (identical)
Dizygotic ( fraternal)
Almost all studies higher concordant rates for monozygotic twins range 20-50%
Adoption studies
Adopted son of alcoholics have a greater chance of being diagnosed with alcoholism evidence- 18% vs 5%
Biological markers
Males of alcoholic parents have a reduced response to alcohol
Concerns with this data
90% was white males
Small effects only
Female data differ
Alcohol Metabolism
- mostly metabolized in liver (small amount <2% excreted in breath, sweat, urine)
- MAIN FACTOR: alc dehydrogenase
- Alcohol dehydrogenase converts alcohol to acetaldehyde
- Aldehyde dehydrogenase converts it to citric acid
- metabolic rate is constant (.25-.3) regardless of BAC
Why is alcohol no longer used as anesthesia?
- Metabolizes slowly (long duration of action that cannot be controlled)
- Dose effective of surgical anesthesia not much lower than OD levels
Alcohol Mechanisms of Action
-
Aspirin v. Acetaminophen v. Ibuprofen
Similarities:
Differences:
- acetaminophine safer than aspirin (analgesic, antiparetic)
Aspirin (Acetylsalicylic acid): Used in place of/More potent than Salicylic acid because Aspirin irritates the stomach lining less, thus is absorbed more rapidly. Serves as an analgesic that effectively blocks mild-moderate somatic pain, antipyretic meaning it reduces fever, and an anti-inflammatory to reduce swelling in an injured area (arthritis). However, it does increase bleeding time by inhibiting blood platelet aggregation, induced gastrointestinal bleeding in ~70% of normal subjects, Reye’s syndrome if used to treat à common cold.
Acetaminophen (Tylenol and Datril): Advertised as having the most of the good points of “other pain relievers” and many fewer disadvantages. If ONLY fever reduction and analgesia are desired, acetaminophen might be safer than aspirin if dosage is carefully observed. Overuse can cause serious liver disorders, surpassed aspirin for drug-related ER visits and deaths.
Ibuprofen: works similar to aspirin by inhibiting the two COX enzymes, more potent analgesic and anti-inflammatory (arthritis). Gastrointestinal side effects like nausea, cramping, and stomach pain. Fatal liver damage reported with overdose. Nonsteroidal anti-inflammatory drugs (NSAIDs).
Ingredients found in over-the-counter analgesics, cold/flu medications, sleep aids, and stimulants
- OTC analgesics: Aspirin, Acetaminophen, Ibuprofen, Naproxen, Caffeine
OTC cold/flu meds: Chlorpheniramine maleate, Phenylephrine, Acetaminophen
OTC sleep aids: Diphenhydramine
OTC stimulants: Caffeine
Belmont Report
Three elements:
- Respect for persons
Allowing for informed consent and treating people with courtesy and respect - Beneficence
Maximize benefits of research and minimize risk to subjects “do no harm” motto - Justice
Reasonable and non-exploitative procedures administered to subjects, cost and benefits distributed fairly
FDA Role in Dietary Supplement Industry
- needs to be pure and safe, but doesn’t need to prove effective beneficial
- % active ingredient doesn’t need to be listed
- if they can demonstrate significant/damaging risk, then can remove
ex: St. John’s wort, seen as natural remedy for depression
SA: Negative Reinforcement and Punishment
- The difference between Negative reinforcement and punishment is that in negative reinforcement you are increasing a behavior while a punishment you are decreasing a behavior.
Ex neg reinforcement : Bob does the dishes (behavior) to avoid his mothers nagging(aversive stimulus)
Ex: punishment: Bobs mom takes away video games because he is being a brat.
SA: Contingencies of Reinforcement
Fixed v. variable
Ratio (#) v. interval (time)
- variable ratio more likely to produce a lot of behavior (operant conditioning)
- Antecedents (events that set occasion)
Behavior
Consequence
Ex. rat sees a light (antecedent), so it pulls a lever (behavior), and it is administered cocaine (consequence)
SA: Evidence that Drug Effects are not Determined Solely by Pharmacology
- Ex. Alcohol Studies (peers + environment + expectations of effects)
Antidepressants (Placebo effect)
SA: Examples of Racism Influencing Cocaine Laws
- Crack was steeped in a narrative of race and pathology. Problems related to crack were described as being prevalent in “poor”, “urban”, or “troubled neighborhoods”, “inner cities” and “ghettos” were codes for Blacks and other undesired people. In 1986, Congress passed the infamous Anti-Drug Abuse Act, setting penalties that were 100 times harsher for crack than for powder cocaine convictions. 85% of those sentenced for crack cocaine offenses were Black, even though the majority of users of the drug were, and are, White.
SA: Please explain the actions of amphetamine on monoamine neurotransmitters. In other words, what does
amphetamine do monoamine transmission and through what mechanism(s) is this accomplished?
- Amphetamines increase the activity of monoamine neurotransmitters (dopamine, norepinephrine, and serotonin) by augmenting the activity of these neurotransmitters by stimulating release rather than by inhibiting reuptake like cocaine.
SA: Evaluate the claim that methamphetamine causes “meth mouth.”
- It has been reported that one effect of methamphetamine is the restriction of salivary flow, which could lead to dryness of the mouth. Dryness of the mouth can increase tooth decay and plaque formation. However, dryness of the mouth is a common side effect of many medications and no dental study has been performed directly linking methamphetamine use to dental problems. Thus the myth of “meth mouth” has less to do with the direct pharmacological effects of methamphetamine and more to do with the non pharmacological factors, ranging from poor dental hygiene to media sensationalism.
SA: Compare and contrast the efficacy of aspirin, acetaminophen, and ibuprofen in terms of analgesic,
antipyretic, and anti-inflammatory effects.
Aspirin
Analgesic effects
Antipyretic effects
Anti-inflammatory effects
Acetaminophen
Analgesic effects
Antipyretic effects
Ibuprofen
Analgesic effects
Anti-inflammatory effectsSA: Beneficial Effects of Alcohol (lecture)
- Benefits of alcohol consumption Moderate alcohol consumption associated with in Lowers risk of Coronary heart disease Hearts attacks Ischemic strokes Risk for depression Better cognition Better well being Fewer depressive symptoms
SA: Relationship between alcohol, expectancies, and behavior (mention studies)
- (This from notes please add on to it)
Alcohol outcome expectancies
Double placebo studies (bold=what they were told, regular text= what they actually had)
alcohol=alcohol, alcohol=no alcohol, no alcohol=alcohol, no alcohol= no alcohol
If I drink, then I will
Positive and negative expectancies
Peer expectancies
Different from peer pressure
Expectation to act a certain way when drunk
Drink to get drunk
Overestimated the amount and frequency of peer drinking
Peer permission
Permission (lack of discouragement) for bad behavior when drunk
Allow peers to act a certain way cause they are drinking (may not be socially acceptable)
SA: Monoamine Theory of Depression
The monoamine theory of depression is based off the idea of excess or depletion of monoamines in the brain.
Antidepressants-increase activity of monoamines
Serepines- depletes activity of monoamines
Popularized
Easy way to describe behavior that we dont understand
Hope for future medical cures/ treatments
Explains inability to correct behavior
Concerns
No direct evidences of monoamines (excess or depletion) in MDD
Antidepressant treatment requires to weeks for benefits/clinical improvements of treatment to be seen
small portion of people get better from treatment (20%)
New theories like Glutemate neuroplasticity theory comes about due to uncertainty
Stressed induced brain hyper-cortisolemia is the new monoamine deficency
“Provides most promising framework”
E: Hart et al.
6 people studied (previous history of cocaine smoking)
Wanted to test whether or not different reinforcers modified self administration of cocaine
Did this by have 8 sessions where cocaine was offered as well as an alternative which was a money voucher
Results non significant
But cocaine users did self administer more with higher dosage
Huge drop in usage as well when money increased
Money vouchers are more of an reinforcer than cocaine with cocaine abusers
E: Frequently, drug policy is not determined by pharmacological evidence. Please describe the similarities and differences between crack and powder cocaine in order to give an example of this statement. In
your response, please address the drugs’ chemical structure, behavioral effects, and legal status
- Similarities: same drug molecule in the body, same behavioral effects
Differences:
Crack: doesn’t have HCl group, 100x harsher penalties under Anti-Drug Abuse act of 1986, 18x harsher penalties under Fair Sentencing Act, associated with “despised groups” throughout American history
Powder: has HCl group associated with it, less strict penalties for possession of much larger amounts than crack
E: Methamphetamine and Adderall
Relationship between them
If and why the drugs are used medically and something about their chemical structures
E: Compare and contrast the neurobiological and behavior effects produced by cocaine and
methamphetamine
- Methamphetamine & Amphetamines
Sequestered dopamine in vesicles, amphetamines trick these vesicles into packaging them and disrupt these vesicles and then leaks out
Causes release of neurotransmitters while (crack blocks reuptake)
Dopamine and norepinephrine more active on receptors
Causes reverse of transport
Comparison to cocaine
Amphetamines increases the amount of dopamine
Reverse transport and trick vesicles of sequestering dopamine
Crack blocks dopamine receptors (also increases dopamine but amphetamines does it to a larger extent)
Similar
Increase HR, BP
Increase euphoria
Increase alertness
Different
Amphetamines have longer duration’
Longer ½ life (12hrs)
Effects last longer
E: Crack baby
- Please explain what is meant by the term “crack baby,” when the phenomenon first appeared, and the evidence supporting (or against) this notion
E: Based on the readings and lectures, please summarize the effectiveness of antidepressant medications
in treating depression
- Most effective at treating severe (>23 HAM-D) depression
Moderate effects on moderate-severe depression
Placebo effects - 40% effectiveness in placebo group
- 50% effectiveness in antidepressant group
- Only a 10% increase attributed to drug (moderate-severe only)
- Mild-mod: no difference
E: Dietary Supplement Health and Education Act
Please explain how the passage of the Dietary Supplement Health and Education Act has changed the
dietary supplement industry
Early 1990s: aggressive supplement marketing worried FDA, in 93 FDA approved 7 health claims for use, document of dietary supplement hazards
- concerned that supplements would become prescriptioned, pressured Congress to limit FDA
- Redefined dietary supplements to include a variety of substances such as herbs, amino acids, and extracts of herbs (before had only allowed items deemed “essential nutrients” -vitamins and minerals- to be sold)
- The safety guidelines altered. FDA could declare product adulterated only if it presents significant or unreasonable risk of illness or injury
- anything at time assumed to be fine, new must prove - Products cannot claim cure, but can claim they have beneficial effect
- don’t have to approve but do have to have supporting evidence that not misleading
- has to be CLEARLY FALSE AND MISLEADING - Products must include disclaimer
- “not approved by FDA”
- not intended to treat/cure any disease
RESULT:
- manufacturers free to market wide variety of products with little regulation
- industry boomed, expanding from $3.5B in 1992 to $24.7 billion in 2007
- ephedra (weight loss supplement), baseball player Steven Bechler died 10 yrs later, banned by FDA
- burden of proof too strong on FDA
**Change!
6. FDA now has right to establish “good manufacturing practices” that require makers to ensure products have correct ingredients and not adulterated; FDA then spot checks to make sure in place
- harder for small companies
7. Adverse events reporting - for customers to call in manufacturer
Mcain - ds safety act - report ingredients - withdrew after month
Please list an antidepressant medication from three classes of antidepressants and explain how each
drug is proposed to exert its antidepressant effect
- MAOIs: Iproniazid; prevents breakdown of monoamine neurotransmitters
Tricyclics: he didn’t give any examples; interferes with the reuptake of monoamine neurotransmitters (from google: an example is doxepin)
Tofranil (Imipramine)
SSRI: prozac; prevents reuptake of serotonin into the pre-synaptic neuron
SNRI: cymbalta; prevents reuptake of norepinephrine and serotonin into the pre-synaptic neuron
Kefauver-Harris Amendment
- required that all OTC drugs be monitored for safety and efficacy
Classes of drugs for pain
- anesthetics: reduces all sensation or blocks consciousness
local anesthetics (dentist)
general anesthetics (general) - analgesics: selectively reduce pain
opioids
OTCs (aspirin, acetaminophen, ibuprofen)
Aspirin
- Hoffman’s father had RA, needed solution for gastric issues + nausea of other meds
- aspirin is converted to salicylic acid in bloodstream in gastro track or bloodstream
- more potent bc irritates stomach less so absorbed more quickly
USES:
- Algesic: mild-moderate pain blocker
- Antipyretic: reduces fever
- Anti-inflammatory: reduces swelling, inflam, soreness
Algesic uses: does not affect pain anticipation, just ability to withstand continuing pain
- especially effective against headache
Antipyretic use: acts on temp area of hypothalamus to increase heat loss (vasodilation of periph blood vessels, + sweating)
Main use: anti-inflammatory
Adverse reactions ==> bleeding
works by inhibiting COX enzymes
Acetaminophen
Analgesic and antipyretic
- tylenol and datril popularized this in 70s
- overuse: liver disorders
Ibuprofen
Analgesic and anti-inflammatory
- developed as a more potent analgesic
- used for arthritis too
- side effect: nausea, gastric issues
Hypnotics v. Sedatives
- Hypnotics = stronger sedatives
- Hypnotics tend to use larger dose (larger dose, comes on fast, wears of quickly ~~shorter half-life), sedatives smaller (lower dose, comes on slower, wears off longer ~~longer half-life)
