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Pharmacology > Module 6 Pain > Flashcards

Module 6 Pain Flashcards

1
Q

what are eicosanoids

A

a damily of inflamayory molcules that are dervied from arachidonic acid

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2
Q

where does arachidonic acid comr from

A

obtain in diet and stored in an esterifed form in membrane phospolipids

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3
Q

how is arachidonic acid released

A

it is released from the membrane phospholipids though the activity of the enzyme phospolipase a2

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4
Q

arachidonic acid serves as the prcursoe for what

A

all the eicosanoids

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5
Q

arachodonic acid is broken down into what

A

leukotrienes bt lipooxgenase enzyme and is metabolized by cyclooxygenase 1 and 2 enxymes ot proata glandin h2

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6
Q

prostaglanisn h2 is the precursoe to what

A

to all the other prostaglandins and thromboxane a2 which stimualtes paltelet agreggation

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7
Q

how do prednisode and dexamethosone work

A

they inhibit the phospholiupase a2 molecule which shuts down the whole pathway

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8
Q

what happens when prdnisode is used chronically

A

when used chronically there are a number of side effects such as bone and muscle breakdwon and cause hyperglycemia

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9
Q

what do aspirin and ibuprofen do

A

inhibit the cox 1 and cox2 enzymes that are expressed throughout the body inhibitng syntheiss of prostaglnaidns and thomboxanes

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10
Q

acetaminophen does what

A

inhibits cyclooxygenase enzyme expressed in the brain

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11
Q

what does cox 1 do

A

constintutive expression, physioloical housekeeping through production of prostaglandins
there is a constant level of prostagmadins that are needed for physiological housekeeping
ex prostaglamdinsm that protect gastric mucosa from stomach avcid

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12
Q

what does cox 2 do

A

inducible expression, pathological production of prostaglandins (injury and infelmmation stimuli)

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13
Q

what are patholoical actions of prostaglandins

A

-vasodilation and increase in vascular permiability - release of proinflammatory mediators
-activation of nociceptors - pain pathways
-stimulation hypothermic regulartory centers - fever

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14
Q

drugs taht inhibit the cox enzymes do whayt

A

they ahve antiinfalmmatory, analgesic and antipyretic effects

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15
Q

what is the mechanism of action for nsaids

A

inhibition of cyclooxyganse
non selective inhibition of cox 1 and cox 2

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16
Q

what does nsaid stand for

A

nonsteroidal antiinflammaotry drug

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17
Q

what are examples of nsaids

A

aspirin, ibuprofen and naproxen

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18
Q

salicilic acid dereviates include what and what do they do

A

aspirin
irreversable inhibition of cox 1 and cox2

aspririn covalently modifed both cox1 and cox2 causing an irreversible inhibition of these enzymes

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19
Q

propionic aids include what and what do they do

A

ibuporfen and naprozen
reversible inhiibition of cox 1 and cox2

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20
Q

aceitic acids incldue

A

indomethoacin

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21
Q

what drug does selective inhibtion of cox2

A

celecoxib

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22
Q

at normal doses celecoxib does what

A

it does not inhibit cox1 so there is no effect on house keeping prostaglansins mad eby cox 1

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23
Q

what is the pharmacology of aspirin

A

irreversable inhibition of cox 1 and cox 2
requires new platelet syntheiss for enzyme activity since inhibits abilitty of cells to make thromboxane a2 (incrase bleeding time for several days)
analgestic antiinflammatory and antipyrectic effects

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24
Q

what are therapeudic uses of aspirin

A

decreases in prostaglandins
mild to moderate pain - post operative, dental pain, back pain etc but other nsaids are now preferred
rheumatoid arthritis
osteoarthritis
dysmenorrhea

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25
Q

what si teh clotting use of aspirin

A

inhibitionof platelet aggregation
acute corononary syndrome (mi)
transient ischemia attacks

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26
Q

what are the side effects fo aspirin

A

salicylism: tinnitus, nausea and vomting (activation of chemorecetpor trigger zone)
associated with teh development of reyes syndrome in chiclren with febile viral illness but this is nwo less common bc we use acetominophen

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27
Q

what are side effects of both aspirin and other nsaids

A

hypersensitviity reactions similar to anaphylatic shock ebcause of increases leukotrienes
gastric ulcerations, excecerbation of peptic ulcer symptoms, gi hemorrhage, erosive gastritis
prolongationof bleeding time
caution in patinet swith asthma, gi ulcers and hemophilia

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28
Q

if pt has hyeprsensitivity to any nsaid then what

A

then all nsaids are contraindicated

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29
Q

hypersensitivity is particularly a problem if pt has what

A

if pt has asthma bc increase in leukotrienes results from inhibtion of cox enzyme
now there is more arachidonic acid that can be synthesized to leukotrienes

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30
Q

what is the pharmacology of the propinonic acid derivateves

A

ibuprofen adn naproxen
reversible inhibition of cox1 and cox2
antiinflammatory, analgesic, antipyriectic effects
preferred ove aspirin for chronic treatment - rheumatoid arthritis, osteoarthritis, etc
better side effect profile than aspirin

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31
Q

naproxen is often combined with what

A

a proton pump inhibitor - esomeprolze

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32
Q

why is proton pump inhibitor used with naproxin

A

prostaglandin 2 stimualtes the epitheltial cells of the gasttric tract to secrete mucus and bicarbonate into gastric lumen which protects against protons secreted from parietal cells but naproxen decreases teh prostaglandin E and then there is less protection which becomes destructive to gi lumen

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33
Q

what is the half likfe of aspirin

A

2 hours

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34
Q

what is the half life of ibuprofen

A

2-3 hours

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35
Q

what is half life of naproxen

A

12-14 hours

36
Q

what is the pharmacology of celecoxib

A

inducible expression, patholoical produiction of prostaglandins (injury, inflammatory stimuli etc)
so it has antiinflammatory, analgesic and antipyreetic effects
no effects on gi tract or plateltes
treatmetn of rheumatoud arthritic, osteoarthritis and dysmenorrhea

37
Q

what are side effects of celecoxib

A

caution in pt with hypersensitiveity to nsaids
good choice for pt with gastric ulcers
cardiovascualr conerns with long term sue

38
Q

what is the pharmacology of acetominophen

A

acts on teh cox enzume expressed in teh brain
analgesitc and antipyretic actiosn
no antiinflammatory
used for mild to moderate pain

39
Q

what are the side effects and consideratiions of acetaminophen

A

limited risk of hypersenstivity reactions
not assocaited with reyes syndrome
absense of gi disturbances
hepatic toxicity is major concern especially at high doses

40
Q

acetophinohen undergoes what

A

both phase one metabolism via cyp 450 enzyme and phase 2 metabolism via glucotrhinone congugation

41
Q

phase 1 of acetaminophen metabolism dose what

A

produces a highly reactive metabolite
at normal doses of acetaminophen this metabolite is congutated with glucathione and excreted from the body
with high doses of acetophnophen the glucothione becomes depleted and the reactiive metabolite can cause liver damage/necrosis

42
Q

how is liver necrosis from acetaminophen treated

A

pt is given n-acetylcysteine which the body uses to restore free glucoathione thus emliminating the metabolite

43
Q

opioids can be obtained in what 3 ways

A

opitates - from juice of opium poppy
semisynthetic - comes form morphine, codien, thebaine
synthetic - other chemical precursors

44
Q

what are the opiates

A

morphine, codine, thebaine

45
Q

what are the semisynthetics

A

heroine, hydrocodone, oxycodone

46
Q

what are the synthetics

A

fetanyl, methadone, meperidine

47
Q

the synthetic opiods do what

A

these opioids mimic the action of endogenouse opioids such as endorphiens and kephalones and dimorphins

48
Q

what is the mechanism of action of opioids

A

opioids bind to 3 opioid receptors that include the mu, kappa and delta receptors
all opioid recetpors are gpcrs signaling through GI protein
binding of opioid to mu receptor inhibits neuronal pain pathways by producing presynaptic inhibition
opioids produce post synaptic inhibtionn by activating potassium channels and inhibtinig adenylylcyclase

49
Q

the mu receptor is invloved in what

A

involved in pain release
also responsible for the side ffets of opidods

50
Q

when the mu receptor produices presynaptic inhibtion what happens

A

this results from the inhibtion of calcium influx into the presynaptic neuron and the inhibtion of neruo transmitter release

51
Q

what happens in the ascending pain pathway

A

glutamatergic neuron in the ascending pain pathway
opiod receptors are presetn at both the presynapic and postsynaptic membranes
normally when an electircal signal reaches the presynaptic neuron, voltage gated calcium channels open allowing calcium ions to move into the neruon
the calcium causes the synaptic vessicles to release glutamate into the synaptic cleft
glutamate then binds to glutamate recetpros (ligand gated channels) on the post synaptic membrane allwoing dosium ions to move into the neuron
the influx of sodium into the neurons causes membrane depolarization and the electrical signal continues along the neuronal pathway

52
Q

what ahppens to teh ascenigng pain pathway in teh presence of opiods

A

opiods bind to the mu recetpors present in both the pre and postsynaptic membranes
first binding to the presynaptic recetpor stimualtes the G inhibitory protien that then inhibtis the calcium channel
without an influex of calcium, the vessicles do not release glutamate and the glutamate does not bind to the glutamate receptor
this is called presynaptic inhibtion
second the binding of opioids to the post synaptic recetpor causes the gihibitiory protein to open membrane potassium channels that allow k+ ions to leak
this loss of positive charge cayes membrane potential to become more negative or hyperpolar
the gi protiein inhibits the proidiction of camp
these 2 effects then prevent the eelctrical signal from continuing along the pathway

53
Q

the body has what 2 pain pathways

A

the ascending and descrening pathwyas

54
Q

what is the ascending pathway used for

A

used to transmit pain signals to the brain letting us know that we are heard

55
Q

what is the descending pathway used for

A

modulates the ascending pathway reducing the pain

56
Q

what are the two main effects of opioids

A

to shut down the ascening pathway and to activate the descending pathway providing pain relief

57
Q

what ahppens when you injury your finger

A

primary sensory neruons in out hand are activated and send the signal to the spinal cord wher they meet secondary neurons in the doral horn
the signal continues up the spinal cord and brain stem to reach the thalamus which processes sensory information
in the thalamus, the secondary neruon synapses with tertiary neruon that activate other regionss of the rbain such as the somatosensory cortex hwere we experience pain

this is the ascneding pathway

our body can decrease how much pain we feel by activating the desending pathwy
normally neruons in teh descending pathway are inactive becayse they recieve gaba from inhibitory inter neurons in the prain stem

58
Q

how does opioid activate the descending pathwya

A

opiod prevents and inhibitos gaba release
without gaba neurons in descrenign pathway are no logner inhibited
opioids can act directly at opioid receptors in ascenidng pathwya in spinal cord inhibtioing transmission too

59
Q

what is the basis of selection of opioids

A

onset and duration of action is most often the basis of selection of opioids

60
Q

the duration of action can range from what in opioid

A

4 to 72 hours
short or long

61
Q

what kind of pain is usually releived by opioids

A

dull, constant pain is usually releived by opioids

62
Q

what kind of pain is poorly controlled with opiods

A

sharp intermittent pain

63
Q

most opioids undergo what when given orally

A

most undergo first pass metabolism when given orally such as morphine nad heroin so not very effective orally

64
Q

what are some opioids that have reduced first pass effect adn can be given orally

A

methadone and oxycodone

65
Q

most opioids are converted to what

A

most are converted to glucuronides and excreted by the kidneys

66
Q

what opioid drugs must undergo cyp 450 metabolism

A

codine and fentanyl

67
Q

codine is a prodrug meaning what

A

it must be comverted to morephin to be effective in pain releif

68
Q

what are limitations of opioids

A

tolerance and drug dependance are big limitatiosn

69
Q

opiod receptor agonists include what

A

morphine, heroine, fentanyl, methadone, oxycodone and codeine

70
Q

what is the potency of fentanyl, heromine, morphine, metadone and codine when given ive

A

Fentylanl > heroin> morphine = methadone > codine
fentanyl is about 100 times more potent than morphine
heroine is about 2-4 times more potent than morphine

71
Q

what is used for opioid use disorder

A

methadone
can be used orally

72
Q

oxycodone is 10 time more potent than codine when given orally so what can occur

A

drug dependanct with controleld release formation more common
have to end up using higher doses of teh drug

73
Q

what is considered safer to use than opioid full agonist

A

buprenorphine is a partial agonist
it has lower efficacy than morphine
considered safer to use than full agonist

74
Q

what are the side effects of opioid drugs

A

cns - euphoria, sedation, respiratory depression, miosis and cough suppression
gi - constipation due to decrased gastric motility
pregnacy - cross fetal/placental barrier by no teratogeinc effects but can result in inflant dependance and withdrawal
facial itiching

75
Q

what is used to treat diarrhea but doesnt cross bbb

A

loperamide (imodium)

76
Q

what are opioid antagonists used for

A

used for opioid overdose

77
Q

what are the signs of overdose

A

extremely low respiratory rate, pinpoint pupils and low boody temperature

78
Q

what is a mu opioid recetpor antagonist that is not effective orally due to first pass effect

A

naloxone (narcan)

79
Q

naloxone has what kind of half life

A

has short half life so much be injected eevvry 2-4 hours
some opiods have logn half lives (over 12 hours) requiring multiple maloxone injections

80
Q

what is being used to treat opioid iduced constipatin

A

new antagnoists taht dont cross the bbb are being used to treat opioid induced constipation

81
Q

what drugs are being used to treat opioid use disorder

A

methadone which is a fill agonist and buprenorphiine which is a partial agonist are used for treatment of opioid use disorder
they produce euphoria ao dont seek other opioids

82
Q

what do drugs for opioid use disorder do

A

these drugs bind to the mu opioid receptor and rpevent abused drugs such as oxycodone and heroin from binding to the receptor
this reduces cravings for toher opioids and prevents withdrawl symptoms

83
Q

the long half life of methadone allwos for what

A

allows for once daily dosing

84
Q

what is the advantage of treatment of opioid dependence with methadone

A

less risk of overdoing and contracting blood borne diease through intravenous drug use

85
Q

what is the disadvantage of using methadone for treatment of opioid dependence with methadone

A

patients may become dependent on methadone and may neeed to use it for prolonged perioids of time - substiuting one drug for another

Pharmacology (6 decks)

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