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PSYC 302 > Lecture 8 > Flashcards

Lecture 8 Flashcards

1
Q

who discovered ngf

A

rita levi montalcini

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2
Q

what are the hallmarks of inflammation

A

-heat
-redness
-swelling
-pain
-loss of function

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3
Q

true or false: steroids are inflamatory agents

A

false, they are anti inflammatory

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4
Q

what are the side effects of steroids

A

-blurred vision
-weight gain
-depression
-bloody stoo;l

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5
Q

what are allogens

A

Algogens are substances that can induce pain when they come into contact with tissues in the body. Some examples of algogens include capsaicin, which is found in spicy foods, and acetic acid, which is found in vinegar. These substances can activate pain receptors in the body, leading to the sensation of pain.

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6
Q

what is one of the main drawbacks of willow bark

A

salicylic acid is rough on the stomach

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7
Q

what is aspirin made of

A

acetylsalicyclic acid

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8
Q

what do nsaid do?

A

they block cox1 and cox2 which usually turn pgh2 into a bunch of things

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9
Q

what does cpges and mpges?

A

they make more pge and this acts on mast cells and nociceptors

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10
Q

true or false: nsaids are mid efficacy

A

false they are wuite a slay

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11
Q

what is cox 1

A

-constituteky expressed enzyme
-side effects: platelets, stomach, intestine and kidney
-normal cell functions aka housekeeping functins

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12
Q

what happens to cox 2 under nsaids

A

-inducible enzyme
-kills pain and helps marophages
-inflammation, regulation of electrolyte balance and fertility, vasoprotection and cardioprotein

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13
Q

true or fase: coxibs are a slay

A

no they are not, they got yeeted out

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14
Q

what is another name for acetaminophen

A

paracetamol

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15
Q

sensory transduction can be activated by:

A

-heat
-cold
-touch
-cell lysis
-chemicals

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16
Q

TRPA1 is for

A

-cinnamon
-horseradish
-garlic

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17
Q

TRPM8 is for?

A

-mint

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18
Q

TRPV4 is for

A

BAA

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19
Q

TRPV3 is for…

A

camphor

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20
Q

TRPV1 is for

A

spicyyyyyy

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21
Q

what is TRPV2 for

A

we dunno

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22
Q

who discovered TRPV1

A

david julius

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23
Q

what can activate trpv1

A

a lot of things like capsaicin

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24
Q

clinical trial of TRPV1 antagonists

A

-they were supposed to block reception
-all had a small fever but it went away
-they all still had to drop it out

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25
Q

capsaicin analgesia: how does trpv1 agonist kill pain

A

-it will hurt but then it will be fine
-it will overstimulate the ion channels and they will be desensitized

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26
Q

what are the channels that are in charge of transduction of mechanical pain

A

-tacan
-piezo which is a big slay

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27
Q

who found piezo

A

ardem ratapoutian

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28
Q

what happens to iion channels when there is pain

A

there is the naK pump
-na in and k out
-there is always the k+overshoot aka hyperpolarization

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29
Q

which channel do you wanna block for analgesic

A

-wanna block na+ channel
-or enhance K+pump

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30
Q

what does lidocaine do

A

-block the local Na channel which means no ap which means numbness

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31
Q

what is the mist important mammalian voltage gated sodium channel gene

A

nav1.7
the others are 1.8 and 1.9

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32
Q

what are the inherited disorders of the scn9(nav1.7) gene

A

-HSAN aka they feel nothing;loss of function mutation
-paraxysmal extreme pain disorder aka only in babies and makes red patches on their assesand it also causes pain and erythema’;gain of function mutation
-primary erythromelalgia causes pain and erythema on hands and feet caused by gain of function mutation

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33
Q

true or false: gene expression in the drg changes after nerve injury

A

true

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34
Q

central terminal of primary sensory neuron; thc

A

THC blocks CB1 which means less release of glutamine

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35
Q

central terminal of primary sensory neuron; pregabalin

A

pregabaline blocks voltage gated calcium channel which means that it will block the release of glutamate because no ca+ means no fusion of the bubbles

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36
Q

dorsal horn neuron; morphine

A

morphine blocks GIRK which means no signal is gonna get transduced

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37
Q

dorsal horn neuron; ketamine blocks….

A

ketamine blocks NMDA, AMPA and mGluR which means no inhibition which means excitTION

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38
Q

true or false; pregabalin and gabapentin are antidepressants and how do they work

A

false they are anticonvulsants
they reduce seizures by blocking ay subunit of Ca+ channels

39
Q

how old is opium

A

we have clay tablets dating back to 5000bc that reference it as the joy plant

40
Q

true or false: heroin is 100% synthetic

A

false: it is semi synthetic

41
Q

what is the definition of an opiate

A

They are derived from the opium poppy plant or synthetically produced to mimic the effects of natural opioids. Opiates work by binding to opioid receptors in the brain and spinal cord, which can result in pain relief, sedation, and a sense of euphoria.

42
Q

what are the three main classes of opiates

A

-agonists
-mixed abonis-antiagonist(buprenorphine, nalbuphine)
-antagonis ex: naloxone and naltrexone

43
Q

what are some some example of strong opiate agonists

A

morphine
methadone
meperidine

44
Q

what are some examples of moderate opioid agonist

A

codeine
oxycodone

45
Q

what are some examples of weak opioid agonist

A

propoxyphene and tramadol

46
Q

what exactly does strong/weak of the opioid refer to

A

the potency of the drug so like how much mg do I need to get the effects

47
Q

descending modulation of pain: stimulation produced analgesia: what was the experiment you can do

A

you can stimulate a part opf a rats brain so that it is analgesic

48
Q

descending modulation of pain: stimulation produced analgesia: what parts of the brain will cause SPA?

A

PVG
grey matter surrounding ventricules in mid brain

49
Q

which drug will stop SPA

A

naloxone since it blocks morphine

50
Q

what can cause SPA

A

morphine and electrical stimulation

51
Q

who found opioid receptors

A

pert and snyder in 1973

52
Q

who found endogenous opioids like enkephalin

A

hughes and kosterlitz

53
Q

descending modulation of pain: stress induced analgesioa

A

it is when your body is so stressed that it produces analgesia

54
Q

which sport causes the most SIA

A

track

55
Q

can naloxone block SIA

A

true

56
Q

can the body also enhance pain?

A

yeah it can, it is called SIH: stress induced hyperalgesia

57
Q

descending inhibition can become descending facilitation if:

A

-stress is mild
-stress is chronic
-after injury
-after prolonged exposure to opioids

58
Q

what are the opioid receptors

A

-mu (u)
-delta(weird g)
-kappa (k)

59
Q

which type of receptors are the opioid receptors

A

gpcr

60
Q

what is the antagonist of the u receptor

A

naloxone

61
Q

what is the main opioid receptor

A

u

62
Q

true or false: opioid receptors are in the brain

A

false: they are everywhere

63
Q

what is the main amino acid sequence of 3 genes endogenous

A

-POMC, PENK and PDYN
tyr gly gly phe

64
Q

true or false: all endogenous opioids amino sequence starts with tyr gly gly phe

A

false there are some genes that code for endomorphin 1-2 they code for tyr pro trp phe and try pro phe phe

65
Q

pomp encodes for and binds to

A

b endorphin u>g
-mu (u)
-delta(weird g)
-kappa (k)

66
Q

penk encodes for and binds to:

A

leu enkephalin and met enkephalin
binds to g>u

67
Q

pdyn encodes for and binds to:

A

dynorphin A and binds do kappa

68
Q

what are on and off cells?

A

they are cells that are turned on when there is pain or cells that are turned off when there is pain

69
Q

does acupuncture works

A

we dunno but we know that acuelectrivity works since it can get blocked by naloxone

70
Q

do antidepressants work for pain?

A

yeah they do
-amitriptyline which is a tricyclic antidepressants
-cymbalta which is a cymbalta which is for norepinephrine

71
Q

do we know if canabinoids work for pain

A

nahhh they don’t work

72
Q

what is the share of the strong opioids in the analgesic drug development

A

29%

73
Q

what is the share of the nsaids in the analgesic drug development

A

28%

74
Q

what is the amount of money in the analgesic drug development

A

27 billion

75
Q

what are all the steps for drug development

A

-phase 0: animal trials
-phase1: assess toxicity, evaluate route of administration and determine safe dosage
-phase2: evaluate effectiveness of treatment to see if it beats placebo and determine side effects
-phase 3: validate the effectiveness of treatment

76
Q

preclinical lenght

A

6-10 years

77
Q

lenght for clinical

A

8.5 y

78
Q

approval lenght

A

1.7 years

79
Q

approval % phase 1

A

56%

80
Q

approval % phase II

A

20%

81
Q

approval % phase III

A

12%

82
Q

approval fda approval

A

11.6%

83
Q

cost phase 1

A

11 billions

84
Q

cost phase 2

A

23 billion

85
Q

cost phase 3

A

66 billion

86
Q

what are the main reasons drugs are not getting approved

A

-lack of efficacy
-animal toxicity
-adverse effects in men

87
Q

what are the meds that ate getting the less being under development

A

-womens health
-oncology
-cns

88
Q

what are the meds that ate getting the most being under development

A

-cardio vascular
-opioids
-infectuous diseases

89
Q

what is the file drawer problem

A

basically the studies that did not work will never be published because mostly successful studies get published

90
Q

what is the receptor for substance P

A

NK1

91
Q

the failure of NK1 antagonists

A

-they are supposed to block the receptors which was supposed to create an ana;gesic effect
-all the trials failed

92
Q

what happened to Prialt

A

it works through catheters

93
Q

tanezumab

A

-blocks in periphery; analgesic in spinal cord
-antibody that blocks ngf
-for osteoarthritis
-did not slay and ended up cancelled

94
Q

what are anti cgrp monoclonal antibodies

A

-such a slay for migraines which are prevented thanks to these drugs
-ex: erenumab which is an antibody to cgrp receptors
-galcanezumab, fremanezumab and eptinezumab

PSYC 302 (10 decks)

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