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Addiction > Test 2 > Flashcards

Test 2 Flashcards

1
Q

How much of the adult population consumes caffeine

A

80%

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2
Q

How much caffeine is in a regular cup of coffee on average

A

100mg

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3
Q

How much caffeine is in a can of pop

A

40mg

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4
Q

What is excedrin and how much caffeine is in it

A

It is a drug that contains caffeine that is used to treat headaches. It contains 65mg of caffeine.

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5
Q

What is caffeine

A

a xanthine alkaloid

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6
Q

What are the names of three cousins of caffeine

A

guaranine, mateine and theine

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7
Q

When does caffeine reach peak plasma content

A

after 45 minutes

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8
Q

How much of caffeine is excreted unchanged

A

2-3%

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9
Q

What are the three metabolites of caffeine

A

paraxanthine, theobromine, theophylline

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10
Q

What is the largest metabolite of caffeine

A

theobromine

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11
Q

What does the metabolite of caffeine called paraxanthine do

A

increases lipolysis (decreases fat)

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12
Q

What does the metabolite of caffeine called theobromine do

A

dilates blood vessels and increases urine volume

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13
Q

what does the metabolite of caffeine called theophylline do

A

relaxes smooth muscles and bronchi in the lungs. It can be used to treat asthma

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14
Q

What enzyme is caffeine metabolized by

A

CYP1A2

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15
Q

What is an example of a drug that is an inhibitor of CYP1A2

A

Fluvoxamine (SSRI)

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16
Q

What is the half life of caffeine

A

2.5-10 hours

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17
Q

In what populations is the half life of caffeine extended

A

infants, pregnant, and elderly

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18
Q

What are the side effects of heavy consumption (15 cups of coffee a day)

A

Agitation, anxiety, tremors, insomnia

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19
Q

What is considered a lethal dose of coffee

A

10g or 100 cups of coffee

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20
Q

What is caffeinism

A

a clinical syndrome characterized by overuse of caffeine, CNS effects like anxiety/agitation/insomnia and PNS effects like hypertension/tachycardia/ and gastrointestinal issues

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21
Q

What does it mean to say that caffeine increases cardiac contractibility and output

A

your heart pumps harder in terms of power

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22
Q

Does caffeine constrict or dilate coronary arteries

A

dilates

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23
Q

Does caffeine constrict or dilate cerebral blood vessels

A

constricts

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24
Q

Why does ephedrine work to help headaches

A

it has caffeine which reduces cerebral blood flow. Which means less oxygen in the brain and more room between the brain and the skull

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25
Q

What are three physical actions of caffeine

A

bronchial relaxation, increases secretion of gastric acid, increases urine output

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26
Q

What two physical actions of caffeine make the drug a good digestion aid

A

it relaxes your bronchi, and increases the secretion of gastric acid in your stomach

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27
Q

How is caffeine an adenosine antagonist

A

it is a competitive inhibitor of adenosine

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28
Q

Explain the typical outcome of adenosine activation and explain what happens when caffeine inhibits adenosine`

A

adenosine typically releases GABA in the dopamine reward pathway. This makes more GABA in the rear pathway than dopamine. Caffeine blocking adenosine receptor reduces the release of GABA and allows for more dopamine in the reward system instead. But only in the prefrontal cortex

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29
Q

What is the caffeine intake of canadian adults broken down into

A

60% coffee, 30% tea, and 10% chocolate, cola, and energy drinks

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30
Q

What is the caffeine intake of canadian children aged 1-5 broken down into

A

55% cola drinks, 30% tea, and 14% chocolate

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31
Q

What do the broad canadian guidelines suggest the maximum daily caffeine intake be

A

400 mg or 4 cups of coffee

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32
Q

What is the safe daily intake of caffeine for kids aged 4-5 years

A

45 mg

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33
Q

What is the safe daily intake of caffeine for kids aged 7-9

A

62.5mg

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34
Q

What is the safe daily intake of caffeine for kids aged 10-12

A

85 mg

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35
Q

What is the maximum safe daily dose of caffeine for pregnant woman

A

300mg of caffeine

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36
Q

At reasonable dosages of caffeine use from pregnant woman what can the results on the fetus be

A

a modest degree of fetal growth restriction

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37
Q

At high doses of caffeine while pregnant what are the associated fetal outcomes

A

can increase the risk of miscarriage (no other effects)

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38
Q

What are three fruits/vegetables that nicotine is found in

A

tomatoes, eggplant, and potatoes

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39
Q

How many cancer deaths does smoking account for

A

30%

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40
Q

How fast does cigarette smoke (nicotine) diffuse through the blood, lungs, heart, brain, and exert an effect

A

7 seconds

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41
Q

What is the half life of nicotine

A

2hours

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42
Q

What is the maximum amount of nicotine the body wants before it shuts it down

A

1-2mg of nicotine

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43
Q

How much of nicotine from cigarettes actually gets absorbed into the body

A

20% or 0.5-3 mg

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44
Q

What enzyme metabolizes nicotine

A

CYP-2A6

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45
Q

What is the metabolite of nicotine and is it active or passive

A

cotinine and active

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46
Q

How long does the metabolite of nicotine called cotinine stay in the blood

A

48 hours

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47
Q

What receptor does nicotine bind to

A

nAChR or alpha4 beta2 nicotinic acetylcholine receptor

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48
Q

Where are the nAChR receptors that nicotine binds to found

A

presynaptic nerve terminal on dopamine neurons, acetylcholine neurons, and glutamate neurons

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49
Q

What neurotransmitter is released when nicotine binds to a receptor

A

either acetylcholine, glutamate, or dopamine depending on which type of neuron the receptor was on

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50
Q

What makes nicotine positively reinforcing

A

it increases dopamine levels in the limbic system

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51
Q

How much already bounded molecules (previous nicotine, or acetylcholine etc) does nicotine displace after 3 cigarettes

A

75%

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52
Q

What are 6 effects of nicotine in early stages of use

A

Nausea, vomiting, stimulates the hypothalamus which releases ADH, decreases muscle tone, appetite suppressant, increased blood flow to arousal/reward centres, and anti depressant effects

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53
Q

What does the release of ADH do

A

makes you less likely to pee, and feel bloated. Causes fluid retention

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54
Q

What does nicotine use during pregnancy lead to

A

a 2-3 fold increase in being small for gestational age, paediatric asthma, SIDS, various immunological diseases, fetal hypoxia which leads to lower IQ’

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55
Q

When nicotinic acetylcholine receptors are activated elsewhere in the body happens (3)

A

Increase of blood pressure and heart rate, causes release of epinephrine, and gastrointestinal enhancement

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56
Q

What are 5 treatments for nicotine addiction that include nicotine

A

transdermal patch, nicotine gum, nicotine nasal spray, nicotine inhaler, and e-cigarettes

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57
Q

Why are e-cigarettes that contain nicotine banned

A

health canada and other bodies don’t know enough about them or inhaling the PG that is in them

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58
Q

What are 3 pharmacotherapies used for treating nicotine addiction

A

bupropion (like wellbutrin and zyban), Varencline (champix), and CBT

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59
Q

How did Buproprion become a treatment for nicotine addiction

A

was originally an anti-depressant. It was a crappy anti-depressant but they noticed that the depressed people who were taking it stopped smoking.

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60
Q

What is the history of Varencline or Champix

A

It was a drug to stop smoking that was effective but increased violence and aggressive behaviours. So people have to be screened for violent tendencies before taking this

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61
Q

Why is the patch the best treatment option for nicotine addiction

A

Maintains a level of nicotine in plasma so there are less highs and lows/cravings. It also reaches the highest amount of nicotine in plasma relative to a normal cigarette.

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62
Q

What does THC stand for

A

Tetrahydrocannibal

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63
Q

What is the most common illicit drug in the world

A

Cannabis

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64
Q

What are the three main reasons/goals for the cannabis law in Ontario

A

Legalize, restrict and regulate sale of cannabis, restrict sale to youth, limit the illicit cannabis trade

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65
Q

What are the three psychoactive compounds in weed

A

Delta 9 Tetrahydracannabinol, cannabinol, cannbidiol

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66
Q

What is the main psychoactive ingredient in weed (not thc)

A

Delta 9 tetrahyrdycannibinol

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67
Q

What is hashish and how potent is it

A

Dried portions of the female plant. High potency-10-20% thc

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68
Q

What is ganja and how potent is it

A

Dried tops of the female flower, medium potency 5-8% thc

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69
Q

What is marijuana and how potent is it

A

The remainder of the weed plant- low potency 2-5% thc

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70
Q

What are 5 routes of administration for THC

A

Pipe, cigar, cigarette, bong, and edibles

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71
Q

What does a weed cigarette(joint) have in it

A

Dried marijuana buds and tobacco

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72
Q

What does a weed cigar(blunt) consist of

A

Taking out whatever was originally in the cigar and replacing it with marijuana

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73
Q

What is a reason someone would use a pipe for thc

A

There is a higher level of drug entry

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74
Q

Why are bongs used for weed

A

The water pipe increases the concentration of thc. It is less harsh than other methods while being the most concentrated form

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75
Q

What are THC receptors called and when were the found

A

CB1 and CB2 in the 90’s

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76
Q

What 3 things do G protein coupled receptors do in relation to thc

A
  1. Inhibit adenylate cyclase
  2. Binds thc
  3. Binds other cannabinoids
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77
Q

Where are CB1 receptors found

A

On the presynaptic nerve terminal

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78
Q

What endogenous neurotransmitter is meant to bind to the receptors that THC binds to

A

Anandamide

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79
Q

What does activation of the THC receptor do in terms of charge and what does this result in

A

inhibits calcium (positive) and facilitates potassium (also positive, slightly less though). Because potassium is considered the “off” binding of the THC receptor makes a cell less likely to fire on the presynaptic side.

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80
Q

By THC decreasing the likelihood that the presynaptic neutron will fire what results

A

decrease in overall neurotrasnmitters including GABA. Leads to overall neuronal inhibition.

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81
Q

Is THC a weaker or stronger agonist than endogenous anadmide

A

stronger agonist

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82
Q

Is THC potent

A

not overly. There are not a lot of places for the drug to bind to in our bodies. There are just enough to feel an effect.

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83
Q

What type of agonist are anandamide and THC

A

partial agonists

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84
Q

What percent of available receptors does anandamide bind to

A

50%

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85
Q

What percent of available receptors does THC bind to

A

20%

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86
Q

What are 4 major brain regions that THC effects

A

basal ganglia, cerebellum, frontal cortex, and the hippocampus

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87
Q

What are the results of THC binding to receptors in the basal ganglia or the cerebellum

A

Movement slows down and posture changes

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88
Q

What are the results of THC binding to receptors in the frontal cortex

A

Changes in senses and perception of time. (The psychoactive effects of the drug)

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89
Q

What are the results of THC binding to receptors in the hippocampus

A

Memory being affected and memory storage

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90
Q

How much THC is in a joint and how much THC is available in smoke and how much of the available THC in the smoke actually gets absorbed into the blood stream

A

75mg, 25 mg, and 5-10 mg

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91
Q

What drug is an oral way to take THC

A

Dronabinol (marinol)

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92
Q

Why would someone take dronabinol for a dose of THC (3 reasons)

A

Slower onset, goes through first pass metabolism, and helps with nausea

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93
Q

How much THC gets into the blood stream when taking dronabinol

A

10-20%

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94
Q

What is the active metabolite of THC

A

11 Hydroxy-delta-9-THC

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95
Q

What is the half life 11 hydroxy-delta-9-THC

A

4-6 hours

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96
Q

What is the effect of hydroxy-delta-9-THC

A

It is very similar to the effect of THC

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97
Q

How long does the effect of THC last when it is smoked

A

2-3 hours

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98
Q

Is THC lipid or water soluble or readily does it pass through the blood brain barrier and placental barrier

A

it is highly lipid soluble and readily passes through the blood brain barrier and placental barrier

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99
Q

What is the inactive metabolite of THC called and what is the half life

A

carboxy-thc and this has a half life of 30-60 hours

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100
Q

What are the pharmacological effects of THC (6)

A

Analgesic properties, decreases body temperature, calms aggressive behaviour, temporal distortions, memory impairments, increased appetite (weight gain)

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101
Q

The decreased blood flow that is a result of THC leads to which psychoactive effect

A

memory impairments

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102
Q

How long does it take frequent marijuana users to go back to their original selves once they stop using

A

1 year

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103
Q

When chronic marijuana users over 10 years stop smoking what percentage of their original state do they get back

A

90%

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104
Q

What are the two mechanisms of tolerance or dependence for THC

A

Down regulation of cannabinoid receptor (most common mechanism) and receptor internalization

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105
Q

What are 4 withdrawal symptoms when stopping THC use

A

depressed mood, insomnia, lower food intake, irritability

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106
Q

What are the purposes of cannabinoid antagonists (3)

A

They block the marijuana induced intoxication and assists in abstinence. They enhance learning and memory. They can control eating and obesity.

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107
Q

What are psychedelic drugs

A

a class of drug in which hallucinations and out of body experiences occur

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108
Q

What are the the two types of produced psychedelics

A

naturally produced and synthetically produced

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109
Q

What were psychedelics historically used for

A

religious ceremonies

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110
Q

What are 4 different classes of psychedelics

A

anticholinergics, catetchlominelike, seroton like or monoaminergic, and glutaminergic NMDAR antagonists, Opioid kappa receptor agonists

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111
Q

What time of psychedelic drug class does scopolamine fall under

A

anticholinergic

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112
Q

What does scopolamine do at the receptor level

A

it blocks the acetycholine receptor so actual acetylcholine or other active molecules cannot bind to it

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113
Q

Where does scopolamine come from

A

the plant atropa belladonna

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114
Q

Is scopolamine potent? Toxic?

A

It is a highly potent drug and at high doses it can be poisonous

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115
Q

What is cholinesterase?

A

An enzyme that breaks down choline

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116
Q

What happens when you take cholinesterase inhibitors

A

a buildup of choline which leads to over excitation- up to death

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117
Q

What is atropine

A

a molecule that reverses cholinesterase inhibitors

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118
Q

What drug is an important source of atropine

A

scopolamine

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119
Q

What was scopolamine originally used for

A

women used to put it in their eyes to constrict the muscle in eyes for beauty purposes.

120
Q

Does scopolamine work on the CNS or PNS

A

The PNS

121
Q

Is scopolamine an antagonist or an agonist (which type) and at which receptor

A

scopolamine is a competitive antagonist at the muscarinic receptor

122
Q

What kind of syndrome can scopolamine lead to

A

anticholinergic syndrome

123
Q

What are the characteristics of anticholinergic syndrome (5)

A

Dry mouth, reduced sweating, dry skin, increased body temperature, and tachycardia (irregular heartbeat)

124
Q

What do low doses of scopolamine lead to (4)

A

drowsiness, profound amnesia, mental confusion, absence of REM

125
Q

What happens to your sleep when you stop taking scopolamine

A

very vivid REM

126
Q

What do high (toxic) doses of scopolamine lead to (3)

A

Delirium, coma, respiratory depression

127
Q

What makes a certain psychedelic a catechlomine psychedelic

A

these drug are structurally similar to catechlomine neurotransmitters (norepinephrine, epinephrine, and amphetamines)

128
Q

What type of psychedelic has amphetamine like properties (as well as other effects)

A

Catechlomine like psychedelics

129
Q

What are 4 types of catechllomine like psychedelics

A

MDMA, Mescaline, Myristin, and Elemicin

130
Q

Which catechlomine like psychedelics come from nut meg

A

Myristin and Elemicin

131
Q

What neurotransmitter receptors do catechlomine psychedelics interact with

A

dopamine receptors and the 5-HT2A receptor

132
Q

What is the result of catechlomine psychedelics binding to the 5-HT2A receptors

A

The psychedelic actions of the drug

133
Q

Where does Mescaline come from and how is it made

A

it comes from the peyote cactus. The crown of the plant is cut, and dried to a hard brown disk referred to ask mescal buttons.

134
Q

How is Mescaline taken

A

it can be chewed or soaked to make a drink

135
Q

What is the common use of mescaline

A

for religious services in the native community.

136
Q

Describe the pharmacokinetics of of mescaline

A

effects are ramped up slowly and last a long time (10 hours)

137
Q

What time of action does mescaline have on the 5ht2a receptor

A

agonistic action

138
Q

How long does it take for mescaline to reach peak plasma content

A

1-2 hours

139
Q

What kind of high does mescaline cause

A

it alters the visual system and causes an acute psychomimetic state (like a psychosis- you’re in an altered state)

140
Q

What drug is ecstasy structurally similar to

A

Mescaline

141
Q

What usage shift occurred with ecstasy

A

it went from being a rave or club drug to a normal night thing

142
Q

Is ecstasy more or less potent and toxic than mescaline

A

it is much more potent and toxic

143
Q

Why is ecstasy so dangerous

A

it causes serotinergic neurotoxicity

144
Q

What drug was made famous by the Dallas gay club

A

ecstasy

145
Q

What is the typical street price for an ecstasy high

A

$5-10

146
Q

What are some of the symptoms you experience while on ecstasy

A

Hyperthermia, Tachycardia, convulsions, kidney failure, cardiac arrhythmia, and death

147
Q

What drug reverses the effect of ecstasy and when or why would you take it

A

Dantrolene is used to reverse the effect of ecstasy when you have a fatal syndrome called malignant hypothermia.

148
Q

What age group is the design of ecstasy pills aimed to appeal to

A

ages 12-17

149
Q

What is an example of a serotinergic or monoaminergic psychedelic

A

LSD

150
Q

What does LSD stand for

A

lysergic acid diethylamide

151
Q

Where is LSD found

A

in the Ipomoea purpurea plant seeds

152
Q

what kind of action does LSD have on the 5HT2A receptor

A

agonistic action

153
Q

Is LSD a safe drug

A

relatively speaking yes. It has very low toxicity

154
Q

What two areas of the brain does LSD activate

A

The prefrontal cortex and the anterior cingulate cortex

155
Q

What are some of the effects of LSD (4)

A

Alterations in perception, temporal changes, visual alteration, and euphoric mood

156
Q

What is HPPD

A

Hallucinogen persisting perception disorder. Where a person will experience flashbacks of a visual hallucination after the drug action has passed.

157
Q

What are the three phases of LSD-induced psychedelic experiences

A

Somatic phase- CNS stimulation and autonomic changes
Sensory (perceptual) phase- sensory distortions and pseudo hallucinations
Psychic phase- maximum drug effect. “bad trip”

158
Q

What are two examples of glutaminergic NMDAR antagonist psychedelics

A

ketamine and phencyclidine

159
Q

What odd setting are glutaminergic NMDAR antagonist psychedelics used in

A

vet settings

160
Q

What were ketamine and phencyclidine originally used for

A

anesthesia

161
Q

What kind of symptoms do glutaminergic NMDAR antagonists resemble

A

schizophrenia symptoms

162
Q

What receptor types do Glutaminergic NMDAR antagonists not have an effect on

A

5-HT, ACh, or DA

163
Q

what kind of antagonistic action do Glutaminergic NMDAR antagonists have on the NMDAR

A

competitive antagonistic action

164
Q

Where is the ketamine binding site found

A

IN the NMDAR

165
Q

How does ketamine work

A

it blocks an open channel from sites within the receptor. also binds on the outside

166
Q

Overall what does ketamine do

A

disassociates people from their environments

167
Q

What are the characteristics of the psychotic state induced by ketamine (5)

A

rigid, unable to speak, appear very drunk, amnesia, coma/stupor (at high doses)

168
Q

What is opium

A

the juice that comes from the opium poppy plant

169
Q

What does is an opiate

A

the drug that is made with opium

170
Q

what is an opioid

A

a broad descriptor for any drug that binds to the opioid receptor

171
Q

What are the four main causes of acute pain

A

a trigger, soft tissue damage, infection, inflammation

172
Q

What is the process of detecting pain called

A

nociception

173
Q

what does the process of nociception refer to

A

the system that carries signals of damage and pain to the brain.

174
Q

What are nociceptive neurons

A

specialized neurons that focus on detecting pain

175
Q

Where do nociceptive neutrons have cell bodies

A

in the dorsal root ganglia

176
Q

What are 3 types of pain that nociceptive neutrons can pick up on

A

mechanical, thermal and chemical

177
Q

Where do the axons of nociceptive neutrons synapse

A

axons synapse in the dorsal horn of the spinal cord.

178
Q

Do opioids remove pain

A

no they simply modulate the symptoms of pain

179
Q

What endogenous molecules mimic opioids

A

endorphins and enkephalin

180
Q

Are opioids or endogenous pain killers stronger

A

opioids

181
Q

Why is it bad that opioids are stronger than our endogenous enkephalin and endorphins

A

we have lowered our internal ability to manage our pain

182
Q

Why is it good that opioids are stronger than our endogenous enkephalin and endorphins

A

we can control our pain/ manage our experience of pain

183
Q

The natural method of getting opium through poppy plants is utilized for which three types of drugs

A

Morphine, codeine and thebaine

184
Q

What are 3 examples of semi synthetic opioids?

A

Heroin, oxycodone and hydromorphone

185
Q

What are 2 examples of fully synthetic opioids

A

Fentanyl and methadone

186
Q

What is a papaver somniferum

A

An opium poppy that means sleep bringing poppy.

187
Q

What is the extraction technique for opium

A

Workers will scratch a whole bunch of plants and then return to them to scoop up the liquid.

188
Q

What are the three types of opium receptors

A

Mu, Kappa and Delta

189
Q

Up to how many subtypes of opioid receptors have been found?

A

17

190
Q

What does it mean to say that there is differential distribution of opioid receptors in the brain

A

there are some parts of the brain that have a higher density of these receptors

191
Q

Which side of the synapse are opioid receptors

A

they can be found on both depending on which interaction between neutrons you are looking at

192
Q

How do opioids exert their effect on their receptors

A

they bind to the receptor which blocks other neurotransmitters from binding to their receptors

193
Q

What 6 brain regions will you find Mu receptors

A

The thalamus, striatum, spinal cord, periaqueductal grey, brainstem nuclei and nucleus accumbens

194
Q

What are two main effects of opioids binding to Mu Opioid receptors

A

analgesic effects and altered respiration

195
Q

What are 5 brain regions you will find Kappa Opioid receptors

A

Basal ganglia, nucleus accumbens, hypothalamus, periaqueductal grey and deep cerebral cortex.

196
Q

In terms of opioid receptors which receptor(s) are the gas and which receptor(s) are the breaks?

A

Mu is the gas and Kappa is the main break and delta is also a milder break

197
Q

What two effects of Mu are antagonized by the binding of opioid on Kappa receptors

A

the analgesic effects and the respiratory depression

198
Q

What additional effect can binding on a Kappa receptor lead to

A

dysphoria

199
Q

What three brain regions would you find delta receptors?

A

Nucleus accumbens, limbic system and spinal cord

200
Q

What are the effects of opioid binding to a Delta receptor (3)

A

Effects emotional states, modulates the activity of mu receptors and relatively poor analgesic effects.

201
Q

What opioid receptor is the main driving force for the analgesic effects seen when opiates are taken?

A

Mu

202
Q

What are the 4 types of opioid receptor actions? (antagonists versus agonists)

A

Pure agonists, pure antagonists, mixed agonist-antagonist and partial agonists

203
Q

What is a pure agonist opioid receptor- drug relationship and what is an example of a drug that facilitates this action

A

There is strong binding of drug to receptor. Morphine is a pure agonist on the Mu receptors

204
Q

What is a pure antagonist opioid receptor-drug relationship and what is an example of a drug that facilitates this action?

A

It is something that blocks the receptor with no activity. An example of this is Naltrexone because it binds to the Mu receptor without giving any pain relieving effects

205
Q

What is a mixed agonist-antagonist opioid receptor-drug relationship and what is an example of a drug that facilitates this action

A

These are opioids that are an agonist at one receptor while being an antagonist at another receptor. An example of this is pentazocine.

206
Q

What is a partial agonist opioid receptor - drug relationship and what is an example of a drug that facilitates this action

A

When a drug binds to the receptor but is not a great fit. It has low intrinsic activity. An example of this is buprenorphine.

207
Q

How much percent does morphine account for of the extracted liquid from an opium plant

A

10%

208
Q

What is the gold standard pain analgesic that is still the most effective today?

A

Morphine

209
Q

How is morphine administered

A

IV usually into the spinal cord. Or it can be taken orally or rectally.

210
Q

Why is morphine usually injected

A

it does not pass the blood brain barrier very well.

211
Q

How much of morphine reaches the central nervous system

A

20%

212
Q

What is the therapeutic index for morphine like?

A

It is very narrow/small

213
Q

What is the dosage of morphine in pills like? Why?

A

The dosage of morphine pills jumps vastly because patients develop tolerance very quickly. This is why it can be so addictive.

214
Q

Where is the active metabolite of morphine produced

A

liver

215
Q

How much more potent is the metabolite of morphine than morphine

A

10-20x

216
Q

What is the half life of morphine

A

3-5 hours.

217
Q

What is the active metabolite of morphine called?

A

Morphine-6-glucuronide.

218
Q

What receptors does morphine-6-glucuronide bind to

A

the same receptors as morphine itself. Mu, Kappa and Delta

219
Q

Describe the action of morphine in the reward pathway

A

It inhibits GABA in the reward pathway which ends up increases the total amount of dopamine.

220
Q

What are 8 pharmacological effects of morphine

A

Analgesia, euphoria, sedation/anxiolysis, sense of tranquility, respirator depression, suppression of the cough reflex, GI symptoms (constipation) and pupillary constriction

221
Q

What are 5 symptoms of morphine withdrawal

A

Restlessness, dysphoria, anxiety, insomnia, and diarrhea

222
Q

What is RAAD

A

it is rapid anesthesia-aided detoxification to help withdrawal from morphine where the patient is given a pure opioid antagonist (naloxone) and a sympathetic blocker (clonidine)

223
Q

Besides RAAD what is an alternative to help patients experiencing morphine withdrawal

A

patient will remain in anesthesia to sleep through the worse of their withdrawal symptoms and then will be given naltrexone when awoken.

224
Q

What is codeine used for?

A

Mild to moderate pain

225
Q

How many codeine users meet the criteria for dependence

A

40%

226
Q

What enzyme metabolizes codeine into morphine

A

CYP-2D6

227
Q

What is the active metabolite of codeine

A

morphine

228
Q

What type of drug can block the effectiveness of codeine

A

An SSRI

229
Q

How much more potent is heroin than morphine

A

3x.

230
Q

How lipid soluble is heroin and what does this mean

A

it is highly lipid soluble which means in can pass through membrane (including the BBB) easily

231
Q

What are the two types of oxycodone and what are examples of each

A

There are short period oxycodones like percodan and long acting like oxycontin

232
Q

What was oxycontin designed for

A

it was designed to help people with chronic pain without having the side effects associated with morphine (respiratory depression)

233
Q

What went awry in oxycontin use

A

The long acting ones which were supposed to last a week were being crushed a snorted or injected which lead to crazy highs and even death

234
Q

How much more potent is fentanyl than morphine

A

80-500 times

235
Q

Does fentanyl cause respiratory depression?.

A

Yes

236
Q

What are the bad areas for opioid related deaths in canada

A

The west and the north

237
Q

What was the number 1 street drug 5 years ago?

A

Oxycontin

238
Q

When oxycontin’s patent ran out what did they do

A

they made oxyneo which could not be crushed

239
Q

How did abusers originally get fentanyl

A

they would cut open therapeutic patches and sollubolize it so they could inject it.

240
Q

Where does the oral version of fentanyl come from

A

China

241
Q

How much more toxic is fentanyl than morphine

A

100 times

242
Q

How much fentanyl does it take to induce a euphoric effect

A

100-300 micrograms which is less than a grain of salt.

243
Q

What are the three reasons we eat?

A

Homeostasis, emotional state and hedonism

244
Q

What is an example of a hunger stimulating GI peptide

A

Ghrelin

245
Q

Where is ghrelin found?

A

Our stomach and pancreas

246
Q

Can sleep alter ghrelin levels

A

yes

247
Q

What interesting brain region does ghrelin activate when released

A

a portion of the dopamine reward pathway

248
Q

What are 3 different adiposity (satiety) signals

A

leptin, insulin and cholecystokinin (CCK)

249
Q

Where is leptin found

A

adipose tissues- hypothalamus

250
Q

Where is insulin found and excreted

A

blood and the pancreas

251
Q

Where is CCK found

A

In the small intestine

252
Q

What two things does leptin have antagonizing effects on?

A

Neuropeptide Y (Which is a stimulant) and anandamide (also a stimulant).

253
Q

What does leptin have agonizing effects on

A

alpha-MSH (which surpasses appetite and stimulates satiety)

254
Q

What does insulin do

A

causes cells to take up glucose from the blood. stops the use of fat as energy source by inhibiting the release of glucagon

255
Q

what is an orexigenic agent

A

something that makes you eat

256
Q

What happened in the Jackson Lab experiments

A

They caused genetic mutations to see what would happen. Ended up making a large mouse and found that it had no leptin. When they gave it leptin it would finally stop eating.

257
Q

What does the dual-centre hypothesis posit

A

there are two different regions of the hypothalamus and each regulates opposing action in terms of food consumption and food satiety. The areas are the ventromedial hypothalamus a satiety centre and the lateral hypothalamus is a hunger centre

258
Q

What are three factors that influence food consumption

A

Disrupted neurobiology, poor impulse control and environmental factors (access being the biggest component)

259
Q

When is someone considered obese

A

when their BMI is 30 or above.

260
Q

What is obesity

A

A metabolic state where excess fat accumulates in peripheral tissues including adipose, muscle, and liver.

261
Q

Are people in the west or east coast of canada slimmer and why

A

west is slimmer because they have a more active lifestyle generally.

262
Q

How many canadians are said to have an unhealthy weight

A

2/3

263
Q

What brain regions does food consumption activate? What does this mean?

A

Nucleus accumbens, prefrontal cortex, ventral tegmental area and amygdala. This hows that food addiction activates the same reward centres as a typical drug addiction

264
Q

It is said that food addiction is associated with an obsessive compulsive relationship with food… What are the symptoms (5)?

A

Frequent periods of uncontrollable binges, consume food beyond the point of satiety, feelings of guilt and depression, excessive time and thought devoted to food and preoccupation with body weight

265
Q

Trigger foods can activate the reward system and release which neurotransmitter?

A

Serotonin

266
Q

Why is food like medicine for addicts

A

Food addicts tend to have lower levels of baseline serotonin and dopamine and eating something that they like will give them a boost of serotonin and dopamine that they need

267
Q

What are the withdrawal symptoms of food in addicts (6)

A

Mood swings, agitation, faintness, headaches, dysphoria and hypoglycemia

268
Q

What are some diagnostic criteria for addiction and how does it relate to food addiction

A

tolerance- increased consumption of food
Withdrawal- there is dysphoria and other withdrawal symptoms
Investments- time spent eating and costs
Social change- Fear of rejection

269
Q

What is an example of a drug that was created and modified to have the effect of steroids without being detected in sports

A

Methandrostenolone or dianabol

270
Q

What gonads in testosterone secreted from

A

Ovaries and testes but barely any in ovaries

271
Q

What does testosterone consist of

A

Tested, sterol and ketone

272
Q

Describe the process of testosterone release

A

hypothalamus releases GRF. Once the pituitary glands detect a certain amount of GRF it releases FSH follicle stimulating hormone and LH the luteinizing hormone. This releases activates two structures testicles which are the seminiferous tubules which releases sperm and sperm containing substances and the leading cells which release testosterone

273
Q

When you take testosterone what happens to the normal system of testosterone release

A

Blocks all natural testosterone and the whole system that results in release of leydig cells

274
Q

Why do testes shrink in people who use steroids

A

They aren’t producing endogenous testosterone and it isn’t needed

275
Q

When are the shrunken testes from steroid use reversible when are they not

A

Non reversible anytime after 12 weeks of continuous use on average

276
Q

What are the 6 main effects of excessive steroid use

A

Blocks regular testosterone release, reduce spermatogenesis, decrease male fertility, increase muscle mass, more masculine appearance, and more aggression

277
Q

What are the 4 anabolic effects of steroid use

A

Increased protein synthesis, increased appetite, bone remodeling and growth, increase production of red blood cells

278
Q

What are 5 androgenic effects of steroids

A

Increased hair growth, increased vocal chord size, increased libido, growth of clitoris, increased breast size in men

279
Q

What five things can happen when you take supratherapeutic doses of steroids

A

Increased tonic and burst of muscle, better strength and endurance, hypogonadal state, lower high lipoproteins and increases low density lipoproteins, increased the risk of liver disorders

280
Q

What are 4 therapeutic uses for steroids

A

TS replacement for hypogonadism, certain blood anemia, muscle loss after trauma, muscle loss due to disease

281
Q

What is the active metabolite of steroids

A

Androstanolone

282
Q

What are some withdrawal symptoms from steroids

A

Fatigue, loss of appetite, decreased libido, suicidal ideation, insomnia

283
Q

What are three phases of gambling in the compulsive gambling decline

A

Winning, losing, desperation

284
Q

What are the three phases of gambling in the recovery from compulsive gambling

A

Critical phase, rebuilding phase, growth phase

285
Q

What neurotransmitters do gamblers tend to have a lower baseline level of

A

Norepinephrine and serotonin

286
Q

What’s the problem with the south oaks gambling screen

A

Over estimates false positives

287
Q

What is the focus of the Canadian problem gambling index

A

Harm and consequences of gambling

288
Q

Why would you use medication to treat gambling addiction

A

A lot of addicts have combined psychiatric disorders

289
Q

What are methods of psychotherapy used to treat gambling addiction and why are they better then meds

A

Counselling, step by step programs and peer support groups. They are better because they foster self awareness

290
Q

Why would rates of sex addiction be off?

A

Low self report, social and cultural views on discussing sexual behaviours, is it really bad?, our inability to define normal and abnormal

291
Q

What are the three compulsive components of sex addiction

A

Compulsivity, continuation despite consequences, obsession

292
Q

What are some mental issues associated with sex addiction

A

Bi polar disorder, narcissistic personality disorder and OCD

293
Q

What are the four components of the behaviour cycle of sex addicts

A

Preoccupation, ritualization, compulsive sexual behaviours, despair

294
Q

What are 4 components of Patrick cranes sexual addiction screening

A

It is a secret, it is abusive or degrading to you or others, it is used to avoid painful feelings, it is not part of a caring committed relationship

295
Q

What are 4 potential causes for sex addiction

A

Trauma, impaired neuro chemistry, developmental impairments, early life exposure to sexual experiences

Addiction (2 decks)

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