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PSYC-2920 > Chapter 11: Opioids > Flashcards

Chapter 11: Opioids Flashcards

1
Q

two main traits of a narcotic analgesic

A

makes you sleepy and produces analgesia (less pain)

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2
Q

main plant as opiate source

A

poppy Papaver somniferum

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3
Q

2 main active ingredients in opium

A

1) morphine (makes up 10%)

2) codeine (makes up 0.5%)

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4
Q

is heroin a natural opioid

A

no, it is synthetic, made by adding two acetyl groups to morphine

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5
Q

is morphine more lipid soluble than heroin

A

no, heroin is more lipid soluble than morphine, allowing it to get to the brain a lot faster.

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6
Q

medical name for heroin

A

diacetyl morphine

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7
Q

another name of a paramorphine that is used in oxycodone

A

thebaine

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8
Q

main incredients of percocet

A

thebaine (oxycodone) and acetaminophen

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9
Q

oxycontin is just concentrated ____

A

concentrated oxycodone.

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10
Q

what is percodan

A

oxycodone mixed with aspirin

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11
Q

is demerol synthetic or natural. comment on its half life

A

synthetic, shorter acting

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12
Q

synthetic opioid used as a maintenance drug for heroine addicts

A

methadone

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13
Q

what drug causes “frozen addict” symptoms? Why?

A

the designer drug MPTP, created when trying to make meperidine. MPTP destoys the SUBSTNATIA NIGRA and EXTRAPYRAMEDAL MOTOR SYSTEM, which provides dopamine stimulation to the basal ganglia. This results in parkinson-like symptoms.

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14
Q

why was heroin originally created?

A

tried to create a “safer” drug to morphine, one with less respiratory depressive effects and less likelihood to get addicted

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15
Q

T/F: Heroin is banned for medical use in Britain

A

False. Heroin can be used for medical use in Britain, but it is illegal in all forms in the states and Canada

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16
Q

who founded heroin?

A

Henrich Dreser

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17
Q

why was heroin more appealing for morphine users in the early 1900s?

A

because it didn’t cause as much nausea and the effects were more stronger.

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18
Q

is morphine acidic or basic, does this mean it can be taken in pill form?

A

basic, pka of 8. not as effective in pill form because the molecules are ionized and thus NOT LIPID SOLUBLE, there is also significant first pass metabolism

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19
Q

bioavailability of morphine versus methadone after first pass metabolism via ingestion

A

morphine gets subjected to significants amounts of first pass metabolism if it is injested orally. Bioavailabiltiy of only 15%. On the other hand, methadone hass 80-90% bioavailability after first pass metabolism.

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20
Q

benefit of taking an opioid orally despite large first pass metabolism and slow absorption because of basic pka?

A

the slow absorption allows long-time affect due to constant blood levels of morphine. good for clinical analgesic-use

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21
Q

competitive opioid receptor antagonists.

A

nalorphine and naloxone

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22
Q

T/F: heroin, but not morphine, can be inhaled through the nose

A

true. heroine is more lipid soluble and can pass through the mucus membranes better than morphine.

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23
Q

organs in which opioids are concentrated in

A

the lungs, liver, spleen and some blood proteins. NOT THE BRAIN

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24
Q

T/F: opioids can pass through the placental barrier

A

true.

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25
Q

T/F: opoids are slow getting through the blood brain barrier. Why or why not? exception to this rule?

A

slow getting through the blood-brain barrier because they have poor lipid solubility. Heroin can pass quickly because it has higher lipid solubility than morphine

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26
Q

What is heroin metabolized to in the brain? is it heroin or its metabolites that produce the intended effects?

A

heroin is INACTIVE, but it is metabolized in the body to MORPHINE, which creates effects. heroin thus effectively allows morphine to cross the lipid membranes faster.

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27
Q

what allows the brain to keep opoid level at a lower concentration than the rest of the body?

A

the brain has an active transport mechanism that removes the opoid from the brain.

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28
Q

where in the brain are opioids relatively concentrated that allows for decreased pain sensation

A

opioids are affecting the PERIAQUADUCTAL GRAY, allowing for analgesic effects. Also concentrated in the basal ganglia (VTA) and amygdala, allowing better mood state and reinforcing effects (affecting pain tolerance)

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29
Q

T/F: opoid antagonists such as naloxone enter the brain quicker than morphine

A

true

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30
Q

how are most opioids excreted?

A

through the urine and feces. 10% of morphine is extcreted as morphine, the rest as metabolized products..

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31
Q

why does methadone have a much longer half life than other opioids such as meperidine (demerol)?

A

because methadone becomes bound to BLOOD PROTEINS which are not available for breakdown. the methadone that does get excreted is excreted as methadone, it is not metabolized into something prior to being peed out.

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32
Q

Why does antagonist naloxone have a shorter half life?

A

because it is lipid soluble and the drug gets rapidly redistributed into body fat. Thus, if you are trying to use this drug as a opioid overdose, you might need to administer it repeatedly.

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33
Q

what are the endogenous ligands that bind to the body’s opioid receptors

A

endorphines.

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34
Q

how does lipid solubility contribute to addiction?

A

the faster the drug can cross a membrane (increase solubiltiy) the faster and stronger the positive affects are. therefore, it has higher reinforcing effects because the affects are more instantaneous

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35
Q

rank these with highest to lower potency: heroin, fentanyl, morphine

A

fentanyl>heroin> morphine

fentanyl is 200 times stonger than morphine
heroin is 10 times stronger than morphine

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36
Q

T/F opioid receptors are ionotropic receptors

A

false, they are metabotropic

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37
Q

what kind of receptor are opioid receptors

A

metaboropic receptors

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38
Q

what kind of proteins are opioid receptors coupled to?

A

INHIBITORY G-protein receptors which release second messengers.

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39
Q

how do G proteins activate and inhibitory response?

A

stimulation of G proteins activates the OPENING of K+ channels, cause K+ TO LEAVE THE CELL, making the cell MORE NEGATIVE.

the G proteins also inhibit CALCIUM, meaning that the prevent the cell from firing. Ca2+ CANNOT ENTER THE CELL, it makes the cell more negative.

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40
Q

what does activation of the opioid receptors do to the presynaptic cell? the post synaptic cell?

A

presynaptic: they inhibit the relase of neurotransmitters because Ca2+ ion channels are blocked

post synaptic: they open the K+ ion channels, making the cell extremely hyperpolarized (more negative) and thus transmitters that do happen to bind to the postsynaptic side do not provide any effect.

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41
Q

because the opioid receptors operate on both pre and post synaptic cells, what does this make the opioids?

A

opioid drugs themselves are thus INHIBITORY neurotransmitters (open K+ channesl) and INHIBITORY neromodulators (block ca2+ channels)

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42
Q

what secondary messenger is inhibited by opioid receptor activation?

A

cAMP

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43
Q

how does opioid receptor stimulation result in changing gene expression?

A

because the receptor-ligand complex can move inside the neuron and react with KINASES, altering the activity of TRANSCRIPTION, changing the expression of genes in the cell nucleus.

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44
Q

When a drug has agonistic effects on two or more receptor types

A

mixed agonist drug.

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45
Q

activation of all types of opioid receptors has the___ effect on all cells, but the ____ of the cell determines what effect the opioid will have in the brain and on behavior.

A

activation of all types of opioid receptors has the SAME effect on all cells, but the LOCATION of the cell determines what effect the opioid will have in the brain and on behavior.

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46
Q

where is the mu receptor primarily located?

A

throughout the limbic system (hippocampus and amgydala), throughout the locus coeruleus and the VTA.

this receptor is primarily known for its reinforcing effects when stimulated

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47
Q

where is the delta receptor primarily located

A

also in the limbic system but IT DOES NOT OVERLAP WIth thE MU RECEPTOR

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48
Q

Where is the kappa receptor primarily located?

A

in the Nucleus accumbens, the VTA and hypothealamus, some in the thalamus.

known for producing aversive effects when stimulated.

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49
Q

generally, the effects of a drug are stronger when its binding affinity to the opioid recpetor is ___

A

WEAK. thats why morphine has a weak binding affinity to the mu receptor and is potent, but naloxone has a high bindign affinity to the receptor and is less potent.

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50
Q

if a drug with a high binding affinity is mixed with a drug with a low opiate receptr affinity, which would bind? which would act as an antagonist to the other?

A

the drug with the high bindign affinity (nalorphine) will bind to the receptor stronger than the one with the low affinity (morphine). thus, it will push morphine out of the way and bind, and the person would see the less-severe effects of the naloxone (stronger binding affinity=less effects)

the naloxone thus acts as an ANTAGONIST to morphine because it blocks morphine from working. this is why naloxone is called a PARTIAL AGONIST because it binds to something AND CAUSE ITS OWN EFFECTS, while blocking something else.

partial antagonists-agonists will terminate the activity of more potent agonist drugs and at the same time have a milder effects of their own.

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51
Q

is nalorphine a partial or complete opioid antagonist? what about naloxone?

A

nalorphine is a partial antagonist, naloxone is a complete antagonist of mu, kappa and delta receptors.

52
Q

why is naloxone a compelte atagonist?

A

because it will completely block all opioid receptors without exrerting any agonistic effects on its own, unlike nalorphine which creates mild effects when it binds and prevents other things from binding to the opioid receptors.

53
Q

naxolone is typically used to treat___, causing ___

A

opioid overdoses. it causes immediate withdrawal symptoms because it blocks all receptors instantly.

54
Q

thermoceptive pain

A

pain caused by heat or cold

55
Q

mechanical pain

A

pain caused by damage to muscle and skin

56
Q

visceral nociception

A

pain associated with organ damage.

57
Q

which type of opioid is good to treat thermoceptive and mechanism pain?

A

delta agonists

58
Q

which opioid is good to use if you are disembowled but are not burnt?

A

kappa agonists. their effective at blocking visceral nocicpetive pain, but not thermal pain

59
Q

why are opioids good at relieving pain

A

because majority of opioid receptors are found in the periaquaductral gray, the area which activates during pain, and they are alos found in the limbic system, which dereases the emotional significance that comes with pain.

60
Q

activity in what parts of the brain is responsible for the reinforcing properties of opioids?

A

increase in activity in the mesolimbic (VTA AND Nucleus accumbens) systems

61
Q

which neurotransmitter is effected by mu receptor agonists in order to cause the rewarding effects?

A

mu agonists in the VTA INHIBIT GABA release from the interneurons. therefore, because interneurons are inhibited, dopamine can freely be released into the nucleaus accumbens. (since there is no inhibitory GABA stopping them)

62
Q

which neurotransmitter is effected by kappa agaonists that cause rewarding effects?

A

kappa agonists appear to directly INHIBIT dopamine release inthe nucelus accumbens. KAPPA DOES NOT HAVE ANY REINFORCING PROPERTIES

63
Q

which opioid receptor does not produce reinforcing properties when stimulated

A

kappa, because it inhibits dopamine release completely. (hyperpolaization of dopamine neurons via G protein)

64
Q

3 important centers in the brainstems that contribute to “vvital life functions” that opioids depress.

A

1) they depress the respiratory center
- causes death due to respiratory failure
2) they depress the vomiting center
3) they depress the coughing center
- prevents coughs. Opioids were once used in cough medicine.

65
Q

Which receptor is typically associated with dependence upon it’s angonization?

A

mu opioid receptor agonists

66
Q

Injecting mu opioid receptor agonists into the _____, but NOT the ____ will cause the development of physical dependence.

A

Injecting mu opioid receptor agonists into the PERIVENTRICULAR GRAY, but NOT the VTA will cause the development of physical dependence.

  • strange because most people get dependent due to stimulation of the mesolimbic reward system.
67
Q

which receptors do endorphins have affinity for?

A

mu, delta, kappa

68
Q

which receptors do enkephalins have affinity for?

A

mostly delta

69
Q

which receptors do DYnorphins have affinity for?

A

mostly kappa

70
Q

which receptors do nociceptin have affinity for?

A

ORL1 receptors

71
Q

What zone triggers vomiting and nausea when opioids are administered to a person for the first time? why does this go away?

A

first time administration triggers the chemoreceptor trigger zone, which detects impurities in the blood and stimulates a center that causes vomiting. these symptoms decrease because opioids also depress the center that causes vomiting, so even though the chemoreceptor zone is triggered, the vomiting center is now inactive.

72
Q

what happens to the pupils in opioid users?

A

they become smaller “pin point” pupils.

73
Q

Why does a person become flushed and sweaty while on methadone or opioids?

A

because it causes dilation of PERIPHERAL blood vessels, increased blood flow.

74
Q

T/F: opioids can treat diarrhea

A

true, but it also causes constipation.

75
Q

what happens to fertility and sex hormones in opioid users?

A

1) decreased sex hormones–> erectile dysfunction, reduced fertility
2) stop menstruation.
3) reduction of secondary sex characteristics in men

76
Q

T/F: opioids increase sleep

A

false. they cause a sleepy sensation but acute administration of morphine or heroin actually causes INSOMNIA

77
Q

T/F: acute administration of morphine or heroin can make a person pass out and go to sleep

A

FALSE. acute administration of morphine or heroin actually causes INSOMNIA

78
Q

effect of opioids on REM sleep

A

decrease REM sleep

79
Q

What happened in the systematic studies of mood experiment?

A

heroin users were allowed to administer heroin, and their activity and agression was monitored. it was discovered that heroin INITIALLY produces positive mood effects, but AFTER TOLERANCE, duration of positive mood decreased, and people started to act more aggressivlely and anti-socially.

80
Q

How were the aggressive traits of heroin users in the systematic mood studies reversed?

A

by administering methadone and giving an opioid antagonist.

81
Q

which receptor is primarily associated with mood swings and dysphoria upon opioid injection?

A

kappa agonist opioids that have a high affinity for kappa receptors (the ones that do not trigger dopamine release because they depress dopamine receptors) seem to cuase dysphoric effects.

82
Q

difference between self administration in non users and users.

A

users wanted another hit of morphine, but only 2/20 non users said they wanted another hit of morphine.

83
Q

allodynia, causes?

A

where neuronal alterations or injury make touch that is normally pleasant feel unpleasantly painful. Caused by decreased effectiveness of opioid receptors as well as an altered role of alpha and beta fibres pain gating.

84
Q

what is opioid rotation?

A

switching from one opioid to another opioid or non-opioid when opioid-induced hyperalgesia begins to develop with the old opioid.

85
Q

T/F: acute administration of opioids have a small detrimental effect on performance, and little to know effect on cognitive performance.

A

true.
in long-time users, they are still capable of maintaining successful careers while addicted because they can still think and perform okay.

86
Q

Are opioids (morphine specifically) biphasic in their physical effects?

A

Yes. They cause INCREASES in SMA at low doses, DECREASES in SMA at high doses.

87
Q

What is catalpsy? what is this caused by?

A

seen in small animals caused by high doses of morphine. the body becomes rigid and molded into a random position. this is not normally seen in humans. at high doses, the typical effect is a depression in behavior and SMA.

88
Q

what happens to conditioned behavior at low doses of morphine?

A

opioids tend to increase response rates of most species responding for positive reinforcers at a low rate.

89
Q

what happens to conditioned behavior at high doses or morphine?

A

high doses of morphine decrease response rate in conditioned behaviours.

90
Q

effect of morphine on avoidance behavior

A

slows avoidance behavior, but does not delay escape behavior.

91
Q

T/F: morphine increases the amount of punishment-suppressed behaviors

A

false. there is no increase in behaviors that were once suppressed by punishment.

92
Q

common on discrimination of opioids and morphine

A

opioids can be discriminated easily from saline.

morphine generalizes to other opioids like codeine, but ONLY PARITALLY TO MIXED AGONIST-ANTAGONISTS like cyclazocine.

93
Q

how can you block morphine discrimination?

A

by using a mu receptor blocker.

94
Q

why are the effects of cyclazocine, a mixed-agonist, only partially blocked by mu receptor blockers?

A

because it has affinity for two receptors. it is a mized agonist drug. this drug also works at the kappa receptors, which is why blocking only the mu receptors will only partially block cyclazocine’s effects.

95
Q

mechanism of acute tolerance to opioids

A

because opioid receptors that get bound to by a ligand will move into the cell via endocytosis, resulting in less membrane receptors. this means less activation of the receptors, showing less sensitivity (more tolerance) to the opioids.

96
Q

what is opioid induced hyperalgesia?

A

increased sensitivity to pain. chronic opioid administration and tolerance may cause opioid-induced hyperalgsia, allodynia and a decrease in its affects in its ability to reduce pain.

97
Q

T/F: opioid with drawal can be fatal

A

false

98
Q

T/F: opioid withdrawal mimics a severe stomach flu

A

true.

99
Q

how can you prevent withdrawal symptoms?

A

1) give a mu agonist drug–> alcohol helps prevent withdrawal by partially binding to mu receptors
2)

100
Q

how can you induce withdrawal symptoms?

A

by giving an opioid receptor antagonist (blocks opioid receptors)

101
Q

which part of the brain is activated that causes physical dependence

A

periventricular gray.

102
Q

how was self administration of opioids in non humans enhanced?

A

by giving them cocaine at the same time

103
Q

T/F: all mu agonists are self-administered. Which types of opioids arent?

A

true. all mu agonists are self-administered, but kappa agonists are not.

104
Q

T/F: non-experienced opioid users inject morphine readily

A

false. non-experienced users will only use opioids as reinforcers only in the presence of pain. this is most likely due to the fact that opioids cause nausea the first time someone does it.

105
Q

T/F: patterns of use of opioids follows an intake-abstinence cycles, when they use heroin for a period of time and then stop

A

false. the daily dose continues to increase until it reaches a peak and remains steady. they do not follow any sort of abstinence patterns.

106
Q

T/F: naloxone and cyclazocine are self administered.

A

false. naloxone is a complete antagonist and cyclazocine is a partial agonist and kappa agonist, which do not increase dopamine levels and are thus not self administered.

107
Q

how does high levels of opioid administration cause death

A

from respiratory depression and convulsions.

108
Q

1 cause of death in heroin addicts

A

heroin overdose- not their lifestyle choices like unclean needles or poor nutrition.

109
Q

how is overdosing related to environment?

A

there is a sudden drop in toelrance if the heroin is administered in a new environment.

110
Q

harmful effects to the brain after chronic use of opioids?

A

decrease CNSflow. decreased activity in the anterior cingulate gyrus, prevents risk calculations and proper risk assessment.

111
Q

What task is used to assess risk calculations?

A

cambridge risk task.

112
Q

which part of the brain is compromised in opiate users which prevent them from assessing risky situations properly?

A

decreased activity in the anterior cingulate gyrus.

113
Q

method of reporting fatalities that emphasizes the tragedy of deaths in younger people from opiate use

A

Years of Potential Life Lost

114
Q

what is the taper approach to treating opioid addiction

A

giving a slight opioid agonist like methadone or buprenorphine and then tapering the dose so that withdrawal symptoms are alleviated.

115
Q

examples of taper drugs

A

methadone, buprenorphine, LAAM, suboxone.

116
Q

Examples of abrupt approach of opioid treatment

A

using an opioid antagonist to trigger withdrawal symptoms instantly and get them out of the way. Is more intense but is faster. Uses naloxone

117
Q

methadone’s relationship with heroin

A

methadone is an opioid agonist that is a heroin antagonist. it is thus an agonist-antagonist mixed drug. it can prevent withdrawal for up to 24 hours, which is longer than heroin.

118
Q

why does methadone prevent relapse by acting as a heroin antagonist?

A

by acting as a heroin antagonist, it is better because it blocks the euphoria heroin gives if they choose to relapse back to heroin with methadone in their system. Methadone thus does not allow heroin to produce the intense rush and rewarding effects.

119
Q

how does methadone act as a heroin antagonist?

A

by occupying mu opioid receptors, preventing heroin from binding. it is a FULL mu opioid agonist, unlike buprenorphine, which is partial mu agonist.

120
Q

which areas of the brain does methadone act on?

A

thalamus, caudate, anterior cingulate gyrus, and PFC.

121
Q

process of antagonist therapies

A

1) detoxify from the drug (7-10 days), intense physical withdrawal
- high drop out rate
2) give mu receptor antagonist.
- if they try and use heroin while on an antagonist, it will not produce any pleasureable effects because the mu opioid receptors are bound to the antagonist drug.
3) continued support

122
Q

why can you not overdose on brprenorphine

A

because buprenorphine is only a partial mu agonist, which means that it is quickly bound to mu receptors, slow to detatch and only has a partial effect.
because there is a CEILING EFFECT with buprenorphine, it is safer than methadone.

123
Q

fibers and gate control theory

A

Normally, activation of nerves which DO NOT transmit pain signals, called nonnociceptive fibers, can interfere with signals from pain fibers, thereby inhibiting pain.

non-pain normal touch fibers can inhibit pain by interfering with pain signals, “closing the gate”

124
Q

nerves that do not transmit pain signals

A

non-nociceptive fibers

125
Q

which type of fiber conducts messages of acute and intense pain?

A

Aδ” fiber

126
Q

Which type of fiber conducts messages of throbbing and chronic pain

A

slow “C” fiber that carries the longer-term throbbing and chronic pain.

PSYC-2920 (15 decks)

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