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PSYC 302 > Lecture 8 > Flashcards

Lecture 8 Flashcards

1
Q

what are the 4 neurotrophins?

A
  • NGF
  • Brain derived neurotrophic factor (BDNF)
  • N 4/5
  • N 3
  • These neurotrophins bind to one of 3 receptors (Trk A B or C)
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2
Q

how does NGF work? (increasing pain)

A
  • In periphery: causes peripheral sensitization
  • In Dorsal root ganglion: can increase substance P, CGRP, Na channels, bradykinin receptors
  • In CNS: cause central sensitization
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3
Q

explain the biology of inflammation (simpler terms)

A
  • inflammation is body’s response to wound
  • Wounds cause bacteria to enter body
  • Inflammation is how our immune system recognizes where to act
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4
Q

when immune system is activated, what does it bring in?

A

brings in macrophages, mast cells, platelets

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5
Q

why do histamine, serotonin, prostaglandin, ATP, etc hurt when they’re injected?

A

hurts when injected because they activate nociceptors

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6
Q

what are algogens?

A
  • things that activate nociceptors
  • Algogens released during inflammation are known as “inflammatory soup”
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7
Q

what are the important ions channels in the inflammatory soup?

A
  • TTX - resistant sodium channels
  • TRPV1
    These ion channels cause neuron firing
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8
Q

what can change the number of receptors?

A

gene regulation

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9
Q

The firing of a nociceptor is dependent on:

A

amount of excitatory/inhibitory receptors

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10
Q

function of aspirin

A

Aspirin interferes with algogens of inflammatory soup
- works entirely in the periphery

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11
Q

how was aspirin discovered?

A

Aspirin arose from discovery that willow tree bark helps w pain
** willow bark tree is hard on stomach

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12
Q

difference between aspirin (ASA) and salicylic acid

A

ASA has same effects of salicylic acid but isn’t as hard on the stomach

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13
Q

what is COX?

A

COX: cyclooxygenase
- Turn arachidonic acid into PGH2

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14
Q

explain PGE2 and EP receptors

A
  • PGE2 binds to a type of receptor called EPs
  • EP receptors are found in brain, kidney, vascular smooth muscle cells, platelets, mast cells, nociceptors
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15
Q

how do NSAIDs work? (and what do they stop)

A

NSAIDs work by blocking production of PGE2 because NSAIDs are inhibitors of COX1 and COX2
- NSAIDs stop pain and inflammation but have many side effects and have ceiling effects

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16
Q

which inhibitors are more COX 1 / COX 2 specific?

A

COX1: naproxen, ibuprofen
COX2: rofecoxib, celecoxib

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17
Q

explain coxib controversy

A
  • latest data suggest that coxibs may not actually reduce risk of serious GI events over standard NSAIDs
  • Merck execs didn’t want to fund a study to test vioxx (associated with heart problems)
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18
Q

how does chemical transduction work?

A

conversion of energy in environment or molecule environment into neural firing

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19
Q

what are TRP channels?

A

TRP channels are expressed by sensory fibres (not all nociceptors, but they are all primary afferents)
- Sensory fibres express molecules and allow us to know what temperature our skin is
- Evolutionarily, we have TRP channels for temperature
* plants evolve ability to activate these TRP channels

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20
Q

which TRP channel is most activated with cold?

A

TRPA1

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21
Q

which TRP channel is most activated when skin temp reaches level of painfully hot?

A

TRPV1

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22
Q

what is capsaicin?

A

makes chili pepper hot
- topical cream (TRPV1 helps with pain)

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23
Q

what is resiniferatoxin?

A

lab drug

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24
Q

what is anandimide?

A

endogenous cannabis

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25
Q

what are protons?

A

acid

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26
Q

explain TRPV1 channels

A

discovered by David Julius
- TRPV1 channels can be opened up indirectly by many other things

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27
Q

decrease in pH is associated with:

A

inflammation

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28
Q

what side effects did TRPV1 antagonists produce?

A

feeling hot, nausea, headache, fatigue, hyperthermia (small fever, very important, mainly why it was dropped)
- didn’t work better than the NSAIDs

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29
Q

TRPV1 agonists cause pain, so why would we put them on our skin? (capsaicin cream)

A
  • Desensitizes the TRPV1 ion channel
  • Ion channel is closed and will stay closed until the
    channel is recycled
  • Overuse of a channel can kill the channel until it’s
    recycled
  • Stops TRPV1 channels for a few hours bc receptors cant be activated
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30
Q

what is piezo?

A

transducer of mechanical touch

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31
Q

what does pain need to propagate?

A

Need both transduction and propagation of action potential for it to make it to the spinal cord

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32
Q

blocking/enhancing which channels has analgesic effects?

A

Blocking Na channels and enhancing K channels has analgesic effects

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33
Q

local anesthetics prevent:

A

Na channels from opening (inhibit action potentials, therefore inhibiting somatosensation

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34
Q

explain xylocaine

A
  • Really really works
  • Nerve blocks are v effective temporarily
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35
Q

explain Inherited Disorders of the SCN9A (Nav1.7) Gene

A

Caused by mutations of SCN9A gene (gene that produces NAV1.7 type of sodium channel)

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36
Q

what is Hereditary sensory autonomic neuropathy
type 4?

A

feel no pain and have no other effects
* NAV1.7 doesn’t work

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37
Q

what is paroxysmal extreme pain disorder?

A

-pain and erythema
-rectum
-usually only in babies
-gain-of-function mutation

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38
Q

what is Primary Erythromelalgia?

A

-pain and erythema
-hands and feet
-gain-of-function mutation
- NAV1.7 works too much (more active than it should be)
* Causes pain for no reason

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39
Q

what’s unexplainable about Inherited Disorders of the SCN9A (Nav1.7) Gene?

A

Why would gain of function be localized? (Place on body and time period of onset/disappearance)

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40
Q

explain Gene Expression in the DRG Changes After Nerve Injury (+ what genes are expressed more/less)

A
  • DRG is where cell bodies of nociceptors are
  • After nerve injury, some genes will be expressed more or less in nociceptor cell bodies
  • Genes that are expressed more: neuropeptide Y, galanin
  • Genes that are expressed less: CGRP, substance P
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41
Q

what is the potential analgesic strategy for Gene Expression in the DRG Changes After Nerve Injury?

A

reduce levels of genes that were expressed more after injury, and/or increase levels of genes that were expressed less after injury

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42
Q

opioid receptors exist in:

A

periphery and in dorsal horn

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43
Q

THC binds to:

A

CB1

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44
Q

presynaptic and post synaptic AKA:

A

pre: primary afferent
post: dorsal horn neuron

45
Q

what does pregablin do?

A

blocks voltage gated calcium channels, causing analgesia
* Nothing released if Ca channel is inhibited

46
Q

Glutamate acts on 3 diff types of receptors:

A
  • ampereceptors
  • MGluRs
  • NMDA
    (NMDA involved in learning)
47
Q

what is ketamine?

A

ketamine is NMDA receptor blocker (therefore ket is
analgesic)

48
Q

in the Spinal Cord Neurochemistry of Pain, which activity is analgesic and pro-algesic?

A

analgesic: inhibitory (top)
pro-algesic: excitatory (bottom)

49
Q

Gabapentin and pregabalin are:

A

anticonvulsants

50
Q

Gabapentin (and pregabalin) blocks:

A

a subunit of Ca channel: alpha delta
- 2 subunits
* need subunit to make working calcium channels

51
Q

why does pregabalin exist if gabapentin works just as well?

A
  • pregabalin works at lower doses
  • Patent on gabapentin ran out
52
Q

what could be a target to develop a drug that could be an analgesic?

A

anything downstream of a glutamate receptor or opioid receptor

53
Q

why is Thalamocortical Neurochemistry of Pain studied so little?

A

it’s a lot more complicated, we don’t know enough

54
Q

opium is a component of:

A

the milk of opium poppy

55
Q

difference between opium and opiates

A
  • opioids: things in your body
  • opiates: anything that is similar to opium in
    structure and function (some compound you would ingest)
56
Q

what are agonists?

A

substances that bind to and activate a receptor in the same way that an endogenous transmitter would

57
Q

what are antagonists?

A

substances that can “fit in the lock but not turn the key”

58
Q

what is potency?

A

how much drug in mg do you need to start getting effects (study graph in slides)

59
Q

what is PVG (PAG)?

A

grey matter around ventricles in midbrain
- area where if electrode is placed and stimulated, most likely to cause stimulation-produced analgesia
- Sometimes reversed by naloxone

60
Q

can get analgesia from either electrical stimulation or from morphine/other opioids in:

A

◦PAG
◦RVM
◦Directly into the spinal cord

61
Q

why would there be descending system from
midbrain to spinal cord?

A

so that stress-induced analgesia can work

62
Q

what are opioids acting on, and what are they endogenously activated by?

A

Opioid receptors
* mu
* Delta
* Kappa

63
Q

explain the difference of rats in cold vs warm water

A
  • Rats in warm water: produces naloxone-reversible stress induced analgesia
  • Rats in cold water: produces naloxone-insensitive stress induced analgesia
64
Q

explain the results of tail flick and exposure to cats

A

Eliciting tail response (stress response) with shock
* When exposed to a cat, almost triples amount of shocked required for rat to show stress response

65
Q

explain the results of intruder vs resident rat test

A
  • loser of rat fight becomes analgesic
  • Intruder rat usually loses
  • X axis - number of bites the intruder gets from the resident
  • More bites/longer experiment goes on: tail flick delay of intruder goes up (analgesic)
  • “Defeat stress”
66
Q

Descending inhibition can become descending facilitation:

A
  • if stress is mild
  • if stress is chronic
  • after injury
  • after prolonged exposure to opioids
67
Q

Opioid-Induced Hyperalgesia is _____ demonstrated in animals but _______ to show in humans

A

Easily; harder

68
Q

T or F: after opioids, can become more sensitive to stimuli

A

true bishhh

69
Q

does Morphine increase time amount to return to normal threshold?

A

yes

70
Q

Opiates can bind to opioid receptors, but receptors are designed for _________________

A

endogenous ligand

71
Q

all 3 subtypes of opioid receptors are:

A

G protein coupled receptors + inhibitory

72
Q

Essentially all of the analgesic effects of analgesic drugs occur on:

A

mu receptors
- but acting on mu receptors also cause most side effects

73
Q

kappa used to be used for:

A

labour pain

74
Q

what are kappa agonist side effects?

A

dysphoria, pupil constriction, analgesia (spinal level), respiratory depression

75
Q

what do opioid receptors in the intestines do?

A

cause constipation

76
Q

difference between peptides and receptors

A

Peptides: short amino acid chains formed by gene expression
Receptors: proteins (many amino acids)

77
Q

what is POMC?

A

POMC produces wide variety of important peptides (AlphaMSH)

78
Q

what is peculiar about endomorphins?

A

no evidence these are being produced because cannot find gene associated with peptide

79
Q

what is the RVM?

A

Rostroventral medulla

80
Q

explain the off-cell vs on-cell

A
  • off-cell: when analgesic, goin crazy (ex: stops when heat starts)
  • on-cell: when analgesic, doesn’t fire (ex: starts when heats starts)
81
Q

what is most efficacious complementary modality?

A

acupuncture

82
Q

explain how Acupuncture analgesia is naloxone-reversible

A
  • naloxone: opioid receptor antagonist
    If something is naloxone reversible, implies that opioid receptors must have been involved
  • If opioid receptors are involved, what could be activating them? -> endogenous opioids
83
Q

what is amitrimptyline?

A
  • Lowest NNT for neuropathic pain
  • Old school antidepressant
84
Q

what is the problem with depression?

A

problem is imbalance of monoamine transmitters
(norepinephrine, serotonin, dopamine)
- Antidepressants are used to increase the levels of these transmitters

85
Q

what are SNRIs?

A

selective norepinephrine reuptake inhibitor
◦Cymbalta

86
Q

what is tramadol?

A

a combination opioid/SNRI

87
Q

Antidepressants are thought to amplify:

A

the descending inhibitory effect of the descending inhibitory system

88
Q

what is the end result of antidepressants?

A

To inhibit the second order spinothalamic neuron (projection neuron) from firing through release of norepinephrine (locus cerulius) or serotonin (RVM) in spinal cord
* antidepressants act as agonists so that more serotonin/norepinephrine is released or has longer action

89
Q

what is CB1?

A

receptor that gets you high

90
Q

why is the analgesic drug development graph inaccurate?

A
  • patent ran out on Lyrica
  • Oxy isn’t making as much due to lawsuit
91
Q

explain the market share of certain types of drugs

A
  • strong opioids: 29%
  • NSAIDs: 28%
  • anti-convulsants: 13%
  • anti-depressants: 11%
  • weak opioids: 7%
92
Q

explain drug development process

A

PHASE 0: animal testing
- in vitro screening
- molecular biology studies
molecule discovery and characterization
PHASE 1: assess toxicity
- evaluate route of administration
- determine safe dosage
PHASE 2: evaluate effectiveness
- determine side effects
PHASE 3: validate effectiveness of treatment
FDA APPROVAL

93
Q

___ % of drugs fail because they lack efficacy

A

46%

94
Q

what is the file drawer problem?

A

when your study doesn’t work/failed, you’re less likely to publish it

95
Q

what is the receptor for substance p?

A

NK1

96
Q

explain the failure of NK1 antagonists

A
  • all trials failed except one
  • problem may be with the trials themselves
97
Q

explain cone snails venom

A
  • venom is very deadly
  • it’s an omega conotoxin - blocks calcium channels (works like gabapentin)
  • without calcium channels, you don’t get vesicle migration
  • got improved as analgesic (beat placebo by 7%)
  • BUT, Elan (the company) lost money bc you can only give it through an intrathecal pump
98
Q

explain tanezumab

A
  • it’s an antibody that blocks nerve growth factor
  • had a huge effect (beat placebo by a lot)
  • some patients arthritis got worse
  • FDA put a stop on the trials
  • some thought it alleviated OA pain so well people over used their joints (dancing in the streets hypothesis)
  • REAL problem was when tanezumab was combined with NSAIDs (interaction)
  • without NSAIDs it doesn’t beat placebo as much (10 points as usual)
  • due to worry about side effects and reputation, drug wasn’t approved
99
Q

how do you know that something is a monoclonal antibody?

A

when it ends with mab

100
Q

what are prophylactic drugs?

A

prevent the thing from happening

101
Q

what is glutamate?

A

major excitatory NT

102
Q

what is NMDA?

A
  • involved in learning
  • affected very much by depolarization
  • ketamine blocks it
103
Q

what happens if you block voltage-gated calcium channels?

A

glutamate or substance p aren’t released
(action potential already happened)

104
Q

name strong, moderate, and weak opioid agonists

A

strong: morphine
moderate: codeine
weak: tramadol

105
Q

explain what drugs bind in the spinal neurochemistry

A
  • Substance p —> NK1
  • Glutamate —> AMPA, mGluR, NMDA
  • Ketamine —> NMDA (blocks)
  • THC –> CB1
106
Q

what are mu receptor agonist effects?

A
  • analgesia
  • respiratory depression
  • nausea
  • miosis
  • euphoria
  • reduced gastrointestinal motility
107
Q

what is naloxone?

A

opioid antagonist

108
Q

explain where different NTs (serotonin and norepinephrine) in anti-depressants work in the body

A

serotonin: RVM
norepinephrine: locus cerulius

PSYC 302 (9 decks)

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