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Drugs and Behaviour > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Which is bigger, caffeine or tobacco industry?

A

Caffeine

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2
Q

Where did tea and coffee start becoming popular?

A

Coffee houses
Gentlemens clubs

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3
Q

Is caffeine derived from natural sources or synthetic?

A

Natural: coffee, tea, cocoa, maté, yaupon, guarana, cola tree nut

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4
Q

What are the risks of excessive energy drink consumption?

A

Flushing, headache, dizziness, tremors, hyperventilation, renal failure, vomiting, diarrhea, incontinence, fluctuating BP, anaphylaxis, heart palpitations, heart attack, chest pains, hemorrhage, stroke, disorientation, spontaneous abortion, depression, anxiety, aggression, blindness, deafness, hallucinations, convulsions, DEATH

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5
Q

Why are there such detrimental effects to energy drink consumption?

A
  1. Often consumed quickly
  2. Marketed to teens/young adults as cool
  3. Full quantity of caffeine not listed
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6
Q

Think about the effects of caffeine on a developing body/brain, how can you incorporate previous PK/PD concepts into this reflection?

A

Younger bodies are more susceptible to damaging effects as their body cannot handle adult-levels

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7
Q

Who is the highest consumer of caffeine?

A

Males
Youths 17-18

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8
Q

Caffeine absorption: oral

A

Low pKa = not ionized
Highly lipid soluble = easy pass through membrane
Peak blood levels: 45-75 min
Slowed by presence of food

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9
Q

Distribution: caffeine

A

Complete absorption (20 min) into bloodstream from stomach/small intestine
Travels to stomach, kidneys, liver, heart, brain, quadriceps, skin, urine, blood
Passes blood-brain and placental barriers

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10
Q

Elimination: caffeine

A

Metabolized in liver
CYP1A2
Broken down into metabolites
Steady individual half life
Variable population half life
Average half life: 5hr

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11
Q

What metabolizes caffeine? What are the caffeine metabolites?

A

CYP1A2
Theobromine, Paraxanthine, Theophylline

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12
Q

What factors affect CYP1A2 metabolism?

A

Genetics (slow/fast)
Food: alcohol and grape juice slow, broccoli speeds
Medications
Hormones
Pregnancy: slows
Age: slows

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13
Q

What is the neuropharmacology of caffeine ? How does it interact with the body?

A

Adenosine receptor blocker
Effects sleep cycle
Inhibits the inhibiter: adenosine builds up throughout the day, acting as a signal to sleep when later released
Effects on GLu, NE, 5HT, DA

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14
Q

What receptors does caffeine bind to?

A

Adenosine receptors: A1 and A2a

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15
Q

When is the best time to consume caffeine, so that it does not negatively affect sleep?

A

Early-late afternoon

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16
Q

Explain the sleep cycle, how is it affected by caffeine?

A

Motivation, stress, hunger inhibit adenosine binding, causing it to build up throughout the day
When released, it binds to A2a - inhibiting arousal, A1 receptor - promoting sleep states
Caffeine blocks these receptors, increasing arousal and inhibiting sleep

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17
Q

Summarize reasons for/against adding Caffeine use disorder to DSM

A

FOR
- Can produce intoxication and withdrawal syndromes
- Some continue use despite physical and psychological effects
- Tolerance = increased use
AGAINST
- Most people use moderately
- No major effects on social, work, interpersonal life

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18
Q

How might the placebo effect or expectancy affect the cognitive effects of caffeine?

A

People expect caffeine to give them a boost, thus their expectation will give them cognitive boosts

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19
Q

What does it mean for caffeine preference to show task-dependence?

A

When a task is relaxing, most people do not prefer caffeine, whereas if a task is demanding, people prefer caffeine

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20
Q

What are the benefits of caffeine consumption, at what dose? Include research limitations

A
  1. Lower risk of type 2 diabetes - also seen with decaf - may be other ingredient
  2. Weight loss / prevent weight gain
  3. Reduced risk of cancer - may be other ingredient
  4. Reduced risk of heart problems - most likely with moderate consumption
  5. Protective effects against neurodegenerative disease (Parkinsons)
  6. Protect against accumulation of protein clumps linked to alzheimer’s
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21
Q

What are the harmful effects of caffeine on reproduction? Experimental and observational research

A

Experimental
- Reduced blood flow to placenta
- Slowed embryonic/neonatal growth
Observational
- Decelerated fetal growth
- Increased risk of miscarriage

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22
Q

How does caffeine / pregnancy cause conditioned taste aversion? Identify US/CS/CR (Classical conditioning)

A

US: morning sickness
CS: coffee
CR: vomiting
Pregnant person has coffee, is sick due to morning sickness, associates coffee and being sick, gets sick from coffee

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23
Q

What are the effects of caffeine on cardiac disease? What are the limitations of research?

A
  1. A study found that 6+ cups of coffee/day doubled risk of heart attack - contradictory follow up research
  2. Boiled coffee raises cholesterol
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24
Q

How is the peak concentration of substances affected by the route of administration?

A

Certain routes have more direct access to the bloodstream, whereas other routes may get metabolized before reaching the blood
EX: oral - some breakdown in saliva, then stomach and intestines as they absorb
Injection: straight into bloodstream

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25
Q

What are the pros and cons of using Modafinil for stimulant addiction?

A

Pro
- Limited abuse potential
- Encouraging but inconclusive results for cocaine treatment
- Greater affinity for DA transporters
Cons
- Noncompliance makes results for meth addicts disappointing

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26
Q

What are the pros and cons for using Bupropion for stimulant addiction?

A

Pro
- Enhance DA may reduce craving and cognitive deficits of withdrawal
Cons
- Only effective for light users

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27
Q

What are the pros and cons of using Methylphenidate for stimulant addiction?

A

Pros
- Lower abuse potential
- Reduce craving
- Increase treatment retention rates
Cons
- Has an abuse potential

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28
Q

What are the pros and cons of using Oral D-Amphetamine for stimulant addiction?

A

Pros
- Oral is safer: dampens blood fluctuations
- Increased duration of treatment retention
- Decreased severity of dependence among meth abusers

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29
Q

What are the pros and cons of using Naltrexone for stimulant addiction?

A

Pros
- Reduce reaction to self-administration cues
- Effective in reducing amphetamine use

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30
Q

Amphetamines: Plant/Synthetic, Generic name, street name, mixture or isomer, use, effects?

A
  • Plant derived: ephedrine, pseudoephedrine
  • Synthetic substitute: Amphetamine
  • Generic: Adderall, Dexedrine, Vyvanse
  • Street: Pep pills, uppers
  • D and I isomers
  • Effects: improved mood, attention, wakefulness, weight loss,
  • Use: Treat ADHD, pleasure, self medication
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31
Q

Cathinone:
Plant/Synthetic, Generic name, street name, mixture or isomer, use, effects?

A
  • Plant derived: Khat
  • Synthetic: methcathinone, bupiron
    Generic name: Wellbutrin, Zyban
  • Street name: bath salts, meow meow, bubbles
  • Mixture
  • Use: anti depressant, smoking cessation
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32
Q

Cocaine:
Plant/Synthetic, Generic name, street name, mixture or isomer, use, effects?

A
  • Plant: cocoa leaves
  • Generic: Ritalin, Concerta
  • Street: coke,
  • Use: ADHD, narcolepsy, chronic fatigue, depression, rituals
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33
Q

Why would Indigenous people in the Andes mix coca leaves with wood ash?

A

Ritualistic purposes, for meeting and gatherings
Mambe: paste made from cocoa leaves and ash, to be put into cheek (chew and spit)

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34
Q

What is a prodrug? Give an example

A

Lisdexamfetamine
An inactive compound that is rendered pharmacologically active through metabolism

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35
Q

What are the unconditioned behaviours observed following psychomotor stimulant administration

A

Low-intermediate: Increased spontaneous locomotion and exploration
High: Increased locomotion turns into stereotyped behaviours (head bobbing, sniffing, rearing, biting)
Khat/Cathinone: enhance aggression in ISOLATED rats
Monkey: automutilation
Decreased food and water consumption

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36
Q

What DA pathway is linked to the psychomotor effects of stimulants?

A

Mesolimbic DA pathway

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37
Q

What is punding? Under what conditions is it displayed?

A

The repetition of complex motor behaviours such as collecting or arranging objects

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38
Q

What is the rate dependency effect? Why is it important?

A

The effect of a drug on the frequency of a behaviour varies depending on baseline
EX: increased responding on fixed interval, decreased responding on fixed ratio
Importance: drugs interact dynamically with ongoing behaviour

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39
Q

What behaviours are linked to the rate dependency effect? Which ones are not linked?

A

Linked: Motor activity
Not: Behaviour suppressed by punishment

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40
Q

What are the subjective effects of cocaine use?

A

Increased heart rate and BP
Increased body temp
Vasodilation
Pupil dilation
Bronchodilation
Decreased food consumption

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41
Q

How do the subjective effects of IV administered cocaine compare to amphetamines?

A

IV will hit faster and harder (straight to bloodstream), produces greater rush

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42
Q

What are the harmful effects of cocoa leaves / cocaine?

A

Jaundice + liver disease, Inflammation and ulceration of nose membrane - holes, Blurred vision, Weight loss, poor attention and concentration, paranoia, hallucinations, cravings

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43
Q

What are the harmful effects of ADHD medications?

A

Headache, dizziness, drowsiness, sleep distrubance, irritability, abdominal pain, nausea, vomiting, diarrhea, cough, motor tics, increase BP and heart rate

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44
Q

What are the harmful effects of oral amphetamines in low and high doses?

A

restlessness, confusion, dizziness, paranoia and psychotic behaviour, lack of sleep, punding, irrational thinking

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45
Q

What are the harmful effects of methamphetamines?

A

Chest pain, tachycardia, cardiac illness, hypertension, intracranial hemorrhage, deterioration of skeletal muscles, loss of vision, harm to organs, repetitive skin picking, dental decay, depression, suicidal ideation, anxiety, psychosis, anger, violence, death

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46
Q

Which drug is most harmful:
Cocaine
amphetamines
ADHD meds
Methamphetamines

A

Methamphetamines

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47
Q

Define rush

A

Intense feelings of euphoria and pleasure

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48
Q

Define crash / comedown

A

Depressive episode following drug intake, as it wears off

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49
Q

Define caine reaction

A

Cocaine overdose in 2 phases
1. Initial excitement followed by severe headache, nausea, vomiting, convulsions
2. Loss of consciousness, respiratory depression, and cardiac failure leading to death

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50
Q

What is cocaine sudden-death syndrome?

A

Sudden death caused by self administration of a lethal dose of cocaine

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51
Q

What does it mean for antidepressant use if there is a 5HT deficiency?

A

Antidepressants could cause extreme deficits, leading to or contributing to widespread dysregulation of 5HT system function

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52
Q

What are the symptoms of major depressive disorder?

A
  1. Sadness, despair, hopelessness, emptiness, feeling down
  2. Significant lack or total loss of interest in activities (anhedonia)
  3. Unintentional change in appetite / body weight
  4. Sleep disturbances
  5. Excessive or lack of motor activity
  6. Lack of energy
  7. Worthlessness
  8. Inability to focus
  9. Frequently occuring thoughts of death/suicide
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53
Q

What are the main projections involved in antidepressants (13.2.1)

A

NE: medial forebrain bundle - locus coeruleus
5HT: raphe system
DA: VTA - mesocortical and mesolimbic

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54
Q

Summarize the evidence supporting and refuting the original monoamine theory of depression

A

Support:
- Enhanced monoamine transmission = feel good
- Decreased transmission = depression
- Ridding body of tryptophan = depression
Against:
- Despite immediate action, must be taken regularly for relief
- Not everyone is affected by tryptophan levels

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55
Q

Explain what is meant by: the increase in serotonin transmission produced by antidepressants appears to be a necessary but not sufficient condition for alleviating depression

A

Acute administration of SSRIs/reuptake inhibitors does not cause an immediate increase in conduction at 5HT synapses

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56
Q

Why do antidepressants take so long to take effect?

A

It takes a while before the body starts to full react to them and adjust to new levels

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57
Q

How are the modern monoamine hypothesis and the glucocorticoid hypothesis “two sides of the same coin”

A

Many things can be contributing to causing depression, stress hormones in HPA axis and monoamine transmitters both linked to stress and developing depression

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58
Q

What kind of drug is Mirtazapine? How does it work? Who is it best for? (13.5.2)

A

Antidepressant, second or third generation, best for those who struggle to fall and stay asleep

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59
Q

How do the different types of antidepressants work?

A

MAOI: degrades free-floating monoamine molecules, increasing DA, NE, 5HT
TCA: anticholinergic, block MAChR
SSRI: block 5ht and NE reuptake, increasing action
SNRI: block 5ht and NE and sometimes DA reuptake, increasing action

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60
Q

What are the discriminative stimulus properties of antidepressants?

A

MAOI/TCA = not generalizable
Antidepressants that block 5HT and NE substitute for citalopram/reboxetine
SSRI: generalize to citalopram
Stimulus properties of citalopram blocked by 5HT2C receptor blockers

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61
Q

Do any antidepressants share the same mechanisms? How do we know?

A

SSRI and SNRI - named because they both block serotonin

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62
Q

Do any antidepressants have reinforcing properties? How do we know?

A

Tricyclics (TCA)
- Decreased avoidance behaviour
- Decrease punishment-suppression behaviour
- Increases rates of ICSS

63
Q

What is serotonin syndrome? What are the symptoms?

A

A dysregulation of the autonomic nervous system functioning (Fight/Flight - Rest/Digest)
Disorientation, confusion, agitation, hypertension, rapid/irregular heart beat, pupil dilation, flushing, shivering, diarrhea, headache, loss of motor coordination, shock, seizure

64
Q

What circumstances lead to serotonin syndrome? How can a washout period help?

A

Results from and acute. dramatic increase in serotonergic transmission, commonly caused by the co-administration of multiple 5HT enhancing drugs
Completely eliminating drugs from the body would reduce adverse effects

65
Q

What are the effects of antidepressants on sleep?

A

MAOI: insomnia or sedation
TCA: drowsiness
Reduce REM sleep time
Increase dream vividness
SSRI: insomnia in some cases
Third gen with antihistamine: sedation and sleepyness

66
Q

What are the pros and cons of antidepressant use in childhood/adolescents?

A

Pro
- Relieve depression, anxiety, OCD
Cons
- Increased suicide rates
- Worsened depression
- Agitation, restlessness
- Serotonin syndrome

67
Q

Which is the most likely antidepressant class to lead to overdose? Is overdose common with antidepressants?

A

Trycyclics (TCA)
Generally safe, not MUCH risk of overdose - but not 0

68
Q

Classify these antidepressants, give their trade name: Iproniazid, moclobemide, imipramine, amitriptyline, desipramine, fluoxetine, citalopram, escitalopram, paroxetine, sertraline

A

MAOI: Iproniazid (Euphozid), Moclobemide (Aurorix)
TCA: Imipramine (Tofranil), Amitriptyline (Elavil), Desipramine (Norpramin)
SSRI: Fluoxetine (Prozac), Citalopram (Celexa), Escitalopram (Lexapro), Paroxetine (Paxil), Sertraline (Zoloft)

69
Q

Give the trade name, what mechanism of action is at play?
Venlafaxine, desvenlafaxine, reboxetine, trazodone

A

Venlafaxine: Effexor, 5HT and NE reuptake blocker
Desvenlafaxine: Pristiq, 5HT and NE reuptake blocker
Reboxetine: Norebox/Edronax, NE reuptake block
Trazodone: Desyrel, 5HT reuptake block

70
Q

How does mirtazapine work? What is the trade name?

A

NE α2 autoreceptor and 5-HT1A autoreceptor blockade; 5-HT2–3 receptor antagonist; histamine H1 receptor antagonist
Remeron

71
Q

How does Bupropion work? What is the trade name?

A

DA reuptake blocker, partial NE reuptake block, NAChR antagonist
Wellbutrin/Zyban

72
Q

What are the different types of pain? Which kind of opioid is best for each one?

A

Thermoreceptive pain: δ agonist
Mechanical pain: δ agonist
Visceral pain: K agonist

73
Q

Do some opioids act primarily in a specific region?

A

Yes
Spinal cord, thalamus

74
Q

What properties affect the absorption of opioids mentioned 11.3.1

A

First pass metabolism enzymatic breakdown
Extended-release
Lipid-solubility

75
Q

What is the best route of administration for fentanyl, morphine, codeine, methadone, heroin

A

Fentanyl: transdermal
Morphine: Injection
Codeine: Oral
Methadone: Oral
Heroin: Injection

76
Q

What is a poppy straw? How does it differ from opium? What are the extracted actives?

A

The opium that remains after seed pods have been harvested - dried stalks, stems, leaves
Morphine, codeine, paramorphine

77
Q

Morphine: Street name/Generic name/trade name, treatment uses, drug combinations?
Typical administration?

A

Generic name: Morphine sulfate
Use: pain
Legal admin: oral, suppository, Parenteral (IV)
Illegal admin: injection, swallowed, smoked

78
Q

Codeine: Synthesis, Street name/Generic name/trade name, treatment uses, drug combinations?
Typical administration?

A

Semi-synthetic
Street name:
Use: pain killer, cough meds
Combinations: codeine+alcohol - lean
Legal admin: oral, parenteral
Illegal admin: injected, swallowed

79
Q

Heroin: Synthesis, Street name/Generic name/trade name, treatment uses, drug combinations?

A

Semi-synthetic
Trade: Diamorphine
Street: Black tar,
Use: treat opioid addiction

80
Q

Hydrocodone: Synthesis, Street name/Generic name/trade name, treatment uses, drug combinations?
Typical administration?

A

Semi-synthetic
Use: Cough suppressant, pain relief
Trade: Vicodin (with acetaminophen), Vicoprofen (with ibuprofen), Alor (with acetylsalicylic acid)
Legal admin: oral
Illegal admin: injected, swallowed, snorted

81
Q

Oxymorphone: Synthesis, Street name/Generic name/trade name, treatment uses, drug combinations?
Typical administration?

A

Semi synthetic
Trade: Opana, Numorphan
Use: pain
Legal admin: oral, suppository, parenteral
Illegal admin: injected, swallowed, snorted

82
Q

Oxycodone: Synthesis, Street name/Generic name/trade name, treatment uses, drug combinations?
Typical administration?

A

Semi synthetic
Trade: Percocet/Endocet (with acetaminophen), Percodan/Enodan (With acetylsalicylic acid), Oxycontin
Use: pain
Legal admin: oral, suppository, parenteral
Illegal admin: injected, swallowed, snorted

83
Q

Fentanyl: Synthesis, Street name/Generic name/trade name, treatment uses, drug combinations?
Typical administration?

A

Synthetic
Street: White persian, China white
Use: pain
Combination: Methylfentanyl
Legal admin: oral, intranasal, parenteral, transdermal
Illegal: injected, snorted, smoked

84
Q

Methadone: Synthesis, Street name/Generic name/trade name, treatment uses, drug combinations?
Typical administration?

A

Synthetic
Trade: Dolophine
Use: treat heroin addiction
Use: pain
Legal admin: oral, parenteral
Illegal admin: injected, swallowed

85
Q

Buprenorphine: Synthesis, Street name/Generic name/trade name, treatment uses, drug combinations?
Typical administration?

A

Semi synthetic
Use: maintenance therapy
Legal admin: oral, parenteral, transdermal
Illegal admin: injected, snorted, sublingual

86
Q

What factors contribute to the variability in effectiveness/subjective effects of opioids?

A

Genetic differences, medical conditions, history of opioid use

87
Q

Rank the routes of administration for methamphetamines:
- peak concentration the fastest-slowest
- Bioavailability highest-lowest
- First subjective effects fastest - slowest
Peak subjective effects fast-slow
Smoke-snort-oral-IV

A

Peak conc.: Smoked, oral, snorted
Bioavailability: IV, smoked/snorted, oral
First subjective: IV, oral
Peak subjective: snorted, smoked, oral

88
Q

Factors of the distribution of methamphetamine administration

A

Amphetamines, coke, and other stimulants pass the blood-brain and placental barrier easily
Highest concentration in kidneys, lungs, then stomach, pancreas, liver, spleen, then heart and brain

89
Q

Describe the elimination of methamphetamines/stimulants

A

30-50% unchanged, 15% metabolite, 10% amphetamine excreted from urine
Reabsorbed and re-metabolized in liver
Eliminated in sweat and saliva
9hr half life (IV, oral)
11-13hr half life (snorted, smoked)
Active metabolites
Cleared from brain the fastest

90
Q

Describe the factors of absorption of orally administered antidepressants

A

Degradation in GI tract
First pass in liver
Low bioavailability
Alcohol inhibits metabolism (dangerous)
TCA peak conc.: 1-3hr
SSRI/SNRI peak conc.: 4-8hr

91
Q

Describe the factors of distribution of antidepressants

A

Easily cross blood-brain and placental barriers
Concentrated in lungs, kidneys, liver, brain
Sometimes found in breast milk

92
Q

Describe the factors of elimination of antidepressants
What is the exception?

A

MAOI: 2-4hr half life, irreversible and reversible effects
TCA: 24hr half life, reach a steady stated in 5 days
SSRI: 15-25hr half life, reach a steady state after 1 dose
Fluoxetine: 4day half life, norfluoxetine active metabolite - 7-15day half life, steady state after 75days

93
Q

Describe the factors of absorption of opioids

A

Less effective when taken orally
Ionized in GI tract, not lipid soluble = not easily absorbed
Easier to maintain steady state

94
Q

Describe the factors of distribution of opioids

A

Concentrated in: Basal ganglia, amygdala, periaqueductal grey, heart, lungs, kidneys, liver, spleen, muscles
Lipophilic: have long half life, rapid distribution, stored in fat - ex: heroin
Less lipophilic: shorter duration of action, slower BBB pass, ex - morphine

95
Q

Describe the factors of elimination of opioids

A

Metabolized in liver and GI tract by CYP3A4, CYP2D6 + more
Excretion through kidneys - urine, feces, sweat, tears
Inactive and hyperactive metabolites

96
Q

Describe the factors of absorption and distribution of antipsychotics

A

Typically oral administration
Readily absorbed in GI tract
Cross BBB and placental barrier
Stored in fat + protein bound = slow release
High half life
safe - no LD50

97
Q

Describe the factors of elimination of antipsychotics

A

Excreted through urine and feces
High individual variability in metabolism: genetics, medications
Typicals: 11-58hr half life
Metabolized by the cytochrome P450 family

98
Q

What are the routes of administration of cannabis?

A

Buccal/sublingual
Oral
Transdermal
Inhalation

99
Q

Describe the factors of absorption for orally administered cannabis

A

Weak acid = not ionized = passes easily
Extensive protein binding
Extensive first pass
low bioavailability

100
Q

Describe the factors of absorption of inhaled cannabis

A

Readily absorbed in lungs
70% of THC destroyed by burning
Lung first pass metab.
Volume of puff changes concentration
Vaporized = higher THC absorbed

101
Q

Describe the factors of distribution of cannabis

A

Rate depends on blood flow
Highly concentrated in lungs, kidneys, heart, liver
Stored in fat = slow + random release
Crosses placental barrier and BBB
Can be found in breast milk

102
Q

Describe the factors of elimination of cannabis

A

Metabolized in liver by CYP2C9, CYP3A4
30hr-4day half life - individual variability
Excreted via urine and feces (liver and kidneys)

103
Q

Describe the factors of ADME for PCP

A

Lipid soluble - stored in fat
Taken as: liquid, tablet, capsule, powder, injection, snorted, smoked
Powdered form dissolves in alcohol/water
First effects 2-5 mins (inhaled)
Peak effects: 10-90mins
Duration: 4-8hr

104
Q

Describe the ADME for ketamine

A

Lipid soluble
Taken as liquid, powder, oral, injection, snorted, smoked
Extensive first pass metabolism
Duration: 30-60 mins - short, rapid anaesthetic
Lethal dose 40x higher than effective dose

105
Q

What might affect the elimination of opioids?

A

St John’s wort: induce CYP3A4 activity - faster metab.
Antibiotics, antipsychotics hormonal therapies, grapefruit juice - affect
Genetics: fast/slow metabolizer

106
Q

What is the neuropharmacology of psychomotor stimulants ? How does it interact with the body?

A

Competitive reuptake inhibitors
Impact monoamine transmission - DA, NE, 5HT
Concentrated in DA reward path
DA, NE, SE continues to bind to receptors

107
Q

What is the neuropharmacology of opioids ? How do they interact with the body?

A

Binding on MOR, KOR, DOR - mainly target MOR
Metabotropic - G protein coupled
Various actions - inhibitory and excitatory
Found widely in brain and spinal cord
Primary effects: analgesia (pain), sedation, respiratory depression, cardiovascular changes, decreased GI mobility, lowered body temp
Rewarding and euphoric properties

108
Q

What is the neuropharmacology of antipsychotics ? How do they interact with the body?

A

Typical: D2 receptor antagonists, BUT also affects many other receptors
Second gen: 5HT antagonist and inverse agonist

109
Q

What is the neuropharmacology of cannabis ? How does it interact with the body?

A

2-AG: full agonist at CB1R and CB2R
AEA: partial agonist at CB1R
CB1 found throughout body (axons, presynapse), GPCR, inhibits CA2+ channels - hyperpolarization
CB2 found mainly in periphery and microglia, role in immune function
Main effects on GABA, Glu (+DA, NE, 5HT, ACh, histamine, opioids)

110
Q

What is the neuropharmacology of classic hallucinogens ? How do they interact with the body?

A

Reuptake inhibitor (SERT)
Substrate-releasing agent - disrupts H+ gradient - effects SERT
5HT2 agonist - stimulant and euphoria - indirect via DA increase
Neuroendocrine effects - increased oxytocin - social bonding

111
Q

What is a mixed agonist opioid? A mixed agonist-antagonist opioid? A partial agonist opioid?

A

Mixed agonist: Exerts an agonistic effect on two or more receptors
Mixed agonist-antagonist: partially agonizes bot MOR and KOR - mild pain relief
Partial agonist: Agonizes receptor to lesser degree than endogenous ligand

112
Q

How does the binding affinity of an opioid drug for its receptor affect potency and efficacy? Are there exceptions?

A

Lower affinity typically means less potency and lower efficacy
Oxycodone and fentanyl have lower affinity but are much more effective and potent

113
Q

What is partial generalization? How do you use this paradigm to determine the mechanisms of action

A

When drugs have similar effects but not fully the same, can be discriminated partially
Use a drug you know the mechanisms of, against a new drug, if there is discrimination, they work at the same mechanism

114
Q

How are MOR and DOR involved in establishing conditioned place preference?

A

MOR: produces a reward, mediates sensitization to conditioned reward (drive craving)
DOR: promote contextual learning

115
Q

What supports the theory that KORs mediate the effects that oppose MOR/DOR?

A
  • Agonists increase brain reward thresholds (ICSS)
  • Animals will learn to respond to avoid M+K agonists (Cancel out)
  • KOR enhances drug-motivated beh., causes dysphoria and stress (bring down)
  • Antagonism ok KOR reduces self-admin of ethanol, cocaine
116
Q

What is the chemoreceptor trigger zone? Why is it important in relation to opioid drugs?

A

Area of the brain, not protected by BBB, that monitors for toxins and sends signals to initiate vomiting
Opioids stimulate by binding to MOR and DOR receptors in the CTZ

117
Q

What are the effects of opioids on cognitive performance?

A

Inattention, difficulty concentrating, perceptual distortions, memory deficits, executive dysfunction, psychomotor impairment, hallucinations, delirium, coma

118
Q

Relate the cognitive effects of opioids to pharmacokinetic, pharmacodynamic, behavioural

A

PK: body is better able to metabolize drug - lower peak, shorter duration
PD: adjustments in body to compensate - smaller effect - circuit dependent
Beh: Learning based/conditioned to have lower effect

119
Q

Summarize the associations between opioid drug dose and reward
How does this relate to liking and how can you eliminate it?

A

Drugs become more reinforcing when administered in moderately high doses and quickly via IV
If a dose is highly euphoric and reinforcing, there will be a greater degree of liking, can be eliminated using smaller doses/withdrawal

120
Q

Why is eliminating physical dependence not enough to cure addiction?

A

People are conditioned and have cues they associate with use, mental rewiring is also required

121
Q

Summarize the procedures, important success factors, pros and cons of methadone maintenance treatment

A

Pros: easy, safe, painless, longer duration prevents withdrawal symptoms for 24hr, blocks action of heroin - reducing euphoria if relapsed
Cons: non-compliance, pressures to fully detox, discrimination in housing/insurance/employment, travel to clinic may interfere with schedule, uncomfortable side effects
Success factors: with therapy,

122
Q

Summarize the procedures, important success factors, pros and cons of buprenorphine maintenance treatment

A

Pros: Longer half life, less frequent dosing, less expensive, less sedation and dysphoria, les risk of respiratory depression and OD death, suppress stress, home administration, mixed with naloxone
Cons: Capped effect on reducing craving and withdrawal - more symptoms, less reinforcement, discontinued rehab,
Success factors: taken as prescribed, with therapy

123
Q

Summarize the procedures, important success factors, pros and cons of heroin-assisted maintenance treatment

A

Pros: Safe source, safe location, highly effective in alleviating symptoms, reduces use of heroin and other substances, lower mortality rates, less crime, boosted physical/mental health/QOL,
Cons: short half life = 2/3x daily, high abuse risk, costly
Success factors: mut be done in clinic, 2/3x daily

124
Q

Pros and cons and success factors of antagonist therapies (opioids)

A

Pros: Blocks euphoric/reinforcing effects of opioids,
Cons: Does not reduce craving, does not re-balance stress, non compliance, high dropout, lengthy,
Success factors: motivation, family support, have careers, court ordered

125
Q

What are some myths about harm reduction and drug use that were presented in class? Which addiction models are these myths most congruent with?

A
  • Harm reduction activities encourage people to use
  • Safe injection sites are just drug dens
  • Safe inj. sites have made drug use worse

Model: drug use as a result of deficient character/low moral fiber/poor willpower and self control - addicts as sinners/criminals

126
Q

How does Oviedo-Joekes (video) explain the addiction treatment program? Who is this program best for?

A

Supervised injections of heroin with hydromorphone pain reliever added
This treatment is for “those we are leaving behind”

127
Q

What is the dopamine hypothesis of schizophrenia?

A

The theory that dopamine is involved in psychosis symptoms, based on the fact that d-amphetamines can cause psychosis symptoms and antipsychotics target dopamine systems

128
Q

Trade name, side effects, First/second gen of: Clozapine, risperidone, ziprasidone, quetiapine, olanzapine, aripiprazole, chlorpromazine, raclopride, reserpine, haloperidol

A

Clozapine - second gen - clozaril
Risperidone - second gen - Risperdal
Ziprasidone - second gen - Zeldox
Quetiapine - second gen - seroquel
Olanzapine - second gen - Zyprexa
Aripiprazole - second gen - abilify
Chlorpromazine - first gen - Thorazine
Raclopride - second gen - Dogmatil
Reserpine - first gen - Serpasil
Haloperidol - first gen - Haldol

129
Q

What are the dopamine and glutamate hypotheses?

A
  1. The theory that imbalanced dopamine contributes to symptoms of schizo.
  2. Theory that hypoactive glutamate transmission contributes to symptoms of schizo.
130
Q

What are the three names for antipsychotics and their principle effects?

A

Typical: D2 receptor blockers, treats positive symptoms - tremors, slurred speech, dystonia
Atypical: 5HT antagonism/partial antag, D2 partial agonism
Third-gen: DA partial agonist, increased DA action

131
Q

What is the depot injection method? What type of antipsychotic patient would benefit from it

A

The drug is dissolved in a high concentration in a viscous oil (ex:sesame) which is then injected into a muscle (butt). Drug slowly diffuses from oil over long period
Best for those who may not take their meds - schizo - need long lasting

132
Q

What impact could antipsychotic-induced dissociation have on treatment?

A

Could be a cause of treatment-resistant schizo - psychotherapy is beneficial but will not work is dissociated

133
Q

How and why do antipsychotics change ED50 in ICSS paradigms? 12.6.3

A

There are likely adverse effects from antipsychotics, attributed to their ability to antagonize D2 (block)

134
Q

Why is the ratio of THC to CBD important?

A

The natural ratio is 1:1, more THC increases the abuse potential

135
Q

What are the effects of a high THC content? How does CBD counter this?

A

High THC: psychoactive pain relieving, antiemetic, and appetite stimulation
CBD decreases the psychotropic activity of THC, producing anticonvulsant, anti-inflammatory, neuroprotective, pain relief, anxiolytic, and antipsychotic effects

136
Q

How do the effects of synthocannabinoids differ from phyto/endocannabinoids?
Do they have a higher or lower affinity for receptors?

A

Synthocannabinoids are often blended, increasing the risk of toxicity, as they have been found to interact in unpredictable ways
Synth. metabolites retain their high affinity for CB1+2 receptors, resulting in greater or prolonged effects

137
Q

Would increasing the metabolism of synthocannabinoids help decrease their effect? why/why not?

A

Not likely, the metabolites are active and retain their affinity and would likely continue to interact unpredictably

138
Q

Explain the open-field test, what do the different results indicate?

A

Increased time spent in center = lower anxiety
Increased time spent in corner/edges = higher anxiety levels

139
Q

Under what conditions do rodents self-administer THC? What does this indicate in relation to abuse? What factors influence IV self-administration?

A

When THC can be delivered quickly and directly to the brain, the more likely they will self-admin.
Abuse is less likely, as it seems there are aversive effects
Factors that influence IV self-admin are the strain of rodent, motivational state, speed of injection

140
Q

How is a cannabis high formally and informally described?

A

Formal: A feeling of intoxication, with decreased anxiety, alertness, depression, tension and increased sociability
Informal: Mood swings from euphoric gaiety with hilarious laughter to placid dreaminess, a feeling of well-being and joyfulness

141
Q

How might using cannabis VS phytocannabinoid VS synthocannabinoid affect study outcomes?

A

Different strains produce different effects
Unknown synthetic mixture reactions
Inactive vs active metabolites produced
Synthetics have been produced to target specific effects/receptor regions
Synthetics can be made much stronger
Synthetics can have “hot spots” - variable doses
Synthetics, and plant sometimes laced with other drugs
Duration of action is different
Synthetics can be radiolabeled
Tolerance can persist beyond stopping use - synthetics lead to higher levels of tolerance
Withdrawal effects differ

142
Q

What are the effects of cannabis on memory?

A

Verbal and episodic short-term memory deficits
Disruption in the ability to recall / hold information
Deficits in short term memory
Distorted sense of time
Persisting impairments to learning, verbal, and working memory - long term use
Greater effort required to complete tasks

143
Q

What is dose titration? How has it impacted human self-administration studies? What other factors have helped/hindered these studies? 14.6.12

A

Increasing the dose until user finds their ‘sweet spot’
Most participants are inaccurate in their adjustments, sometimes surpassing the level they were supposed to reach
Other factors
- THC potency
- Taste
- Smell
- Size and number of puffs

144
Q

What is the common factor model? Would it classify cannabis as a gateway drug? Explain

A

The theory that drug use and the progression to addiction relies on 2 factors - person is at higher risk of drug use, they are more likely to be in situations where they can use drugs,
NO, it would not classify cannabis as a gateway drug - a person’s overall predisposition to drug use is the driving factor

145
Q

How does cannabis puffing behaviour influence respiratory health? Is it worse than tobacco? Why/Why not?

A

People take bigger and longer puffs of cannabis than tobacco
- 5x higher levels of carbon monoxide binding
- 4x higher inhaled tar + greater accumulation in lungs
Increased risk of toxicity of cannabis over tobacco - BUT people tend to share joints

146
Q

What pharmacological factors can contribute to the development of cannabis tolerance? How does this relate to synthocannabinoids?

A

Fast onset of effects, short duration of action, high efficacy at target receptor
Synthetics can produce higher levels of tolerance than natural product

147
Q

How can cannabis disrupt brain maturation in childhood and adolescence? 14.9.2

A

Increase likelihood of initiating underlying genetic predispositions for psychosis
Can affect synaptic pruning, myelination, and activity-dependent strengthening/weakening of neural connections
Disrupts development of hippocampus and cerebellum

148
Q

What did Siegel surmise about the nature and structure of hallucinogens? What 3 points help determine this? 15.1.4

A

The nature and structure of hallucinogens must be determined by the nature and structure of the visual system of the brain, not the drug
a. hallucinatory experiences are similar among vastly different drugs
b. experiences resemble the effects produced by other non drug hallucinations like from fever/migraine/etc
c. experiences are similar between cultures

149
Q

What is emergence delirium?

A

When recovering from a drug, a person experiences a state of delirium, disorientation, and agitation

150
Q

What is hallucinogen persisting perception disorder? Symptoms, frequency of occurance

A

After the drug wears off, a user may experience perceptual changes similar to those experienced when intoxicated
Symptoms: geometric visual images. false perceptions of movement, flashes and/or intensification of colour, trailing phenomena, palinopsia (smearing), halos around objects, macropsia (appear larger), micropsia (appear smaller)
24-60% of users experience HPPD symptoms

151
Q

What hallucinogen type is HPPD most associated with?

A

LSD

152
Q

What evidence is presented to suggest the existence of a biological predisposition to compulsive MDMA use?

A

Animals that, over time, develop tolerance to the locomotor stimulating effects of MDMA also escalate their self-admin, exhibit s cue-induced reinstatement of MDMA seeking

153
Q

What are the “midweek blues”

A

THe psychiatric symptoms, including depression, that occur during a recovery period from MDMA

Drugs and Behaviour (3 decks)

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