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PCL200 > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

what are the neurons for pain called

A

nociceptors

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2
Q

what is pain

A

the emotional experience of the nociceptors being activated

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3
Q

the nociceptor neurons send the signal to the brain via

A

the spinal cord

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4
Q

what is the thalamus

A

think about it as a filter for all of the neuron information
- filters all sensory information before sending it to the rest of the brain

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5
Q

algesia is

A

pain

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6
Q

what is hyperalgesia

A

means that there is more pain than usual

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7
Q

what is allodynia

A

means you are now experiencing a sensation that is painful which is normally innocuous

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8
Q

for pain there is an (pathways)

A

ascending and a descending pathway

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9
Q

two ways to reduce pain

A

reduce the ascending pathway or augment the descending pathway

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10
Q

what is the ascending pathway

A

the system of neuron signals (nociceptors) that send pain information to the brain

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11
Q

what is the descending pathway

A

the system of neurons that attempt to inhibit the pain being experienced so that the affected area can keep functioning

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12
Q

name for pain medicine

A

analgesics

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13
Q

local anesthetics

A

drugs that stop all action potentials
- block voltage gated sodium channels of all neurons
- they are antagonists of the sodium channels and will block all neuron transmission

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14
Q

what was the first local anesthetic

A

cocaine

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15
Q

what are NSAIDs

A

non steroidal anti inflammatory drugs

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16
Q

what do NSAIDs do

A

block the production of prostaglandins
- inflammation means redness, swelling, pain, fever which is all called by prostaglandins
- inhibiting this will reduce symptoms

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17
Q

acetominophen

A
  • unknown mechanism of action
  • does not affect prostaglandin production
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18
Q

opioids (origin)

A

○ Opiates are derived from poppy (morphine, heroin, opium)
§ Two molecules of morphine attached together becomes heroin (which is why its called a semi-synthetic)
§ Fentanyl is fully synthetic and is easier to produce
○ Opioids are drugs that activate the mu opioid receptor

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19
Q

how do prostaglandins contribute to symptoms of inflammation on the ascending pathway

A
  • Prostaglandins facilitate firing of peripheral nociceptors.
  • Prostaglandins facilitate firing of central neurons in ascending pathway
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20
Q

Process for prostaglandins (three steps)

A
  • When there is an injury, an enzyme called cyclooxygenase 2 (COX2) is activated. COX2 makes a chemical called prostaglandin (PGE2).
  • Prostaglandins cause swelling and increase blood flow. They bind to prostaglandin receptors on the sensory nerves (nociceptors). When prostaglandin binds to those receptors, they fire more often. This activates the ascending pathway.
  • Non-steroidal anti-inflammatory drugs act as antagonists of COX2 – they prevent the enzyme from making prostaglandins. Therefore they block pain and reduce swelling and redness. They also reduce fever by preventing prostaglandin production in the brain.
21
Q

what are some common NSAIDs

A

ibuprofen, naproxen, aspirin, diclofenac (over 20 NSAIDs)

22
Q

benefits of NSAIDs

A

reduces pain, swelling, redness, fever
- used for rhematoid arthritis and reduces blood clotting (low dose aspirin)

23
Q

side effects of NSAIDs

A

stomach / gastrointestinal ulceration (prostaglandins protect the stomach and intestinal lining)
- can reduce kidney function if used in high doses
- can exacerbate asthma
- some people are allergic

24
Q

acetaminophen is not

A

a NSAID
- it reduces pain and fever
- but it does not reduce redness or swelling and is not an anti inflammatory

25
Q

what is a ligand

A

a molecule that sticks to a receptor

26
Q

opioids are agonists of which receptor

A

the mu opioid receptor

27
Q

endogenous ligands (agonists) for the mu receptor are

A

endorphins and enkephalin

28
Q

where are mu opioid receptors located (MORs)

A

located in brain areas that control pain sensation and emotional response to pain
- thalamus and descending pain pathway

29
Q

when the MORs on a neuron are bound by an agonist

A

then the result is less firing of that neuron
- opioids are depressants
- the descending pathway is engaged by morphine
- depressants will also cause sleepiness and reduced consciousness

30
Q

naloxone is an

A

antagonist of the MOR
- naloxone and other MOR antagonists are antidotes for opioid overdose

31
Q

oxycodone is a

A

prescribed opioid that can be formulated as a slow release medicine

32
Q

oxycodone story

A
  • Physicians were told by Purdue that oxycodone was not addictive because it was slow-release. This was a lie.
  • Like other opioids, oxycodone is addictive. It is also abused by crushing the pill, snorting or injecting intravenously.
  • In 2012, regulations to reduce access to oxycodone were put in place, and the pill was made harder to crush and solubilize.
  • became cheaper to buy heroin than oxy
33
Q

fentanyl is a

A

synthetic opioid that is 100 times more potent than morphine. it can be found in other street drugs and is the primary cause of overdose

34
Q

what is codeine

A
  • tylenol 3 (acetominophen and codeine)
  • codeine is converted to morphine in the liber
  • morphine is the active drug
  • some people are fast metabolizers and some are slow due to differences in genetics
  • it is not a pain reliever but the body converts it into morphine
  • 0.1x as potent as morphine
35
Q

what is morphine

A
  • active ingredient in the poppy plant
  • source for many other semi synthetic opioids
36
Q

how much more potent is oxycodone and hydrocodone than morphine

A

1.5x

37
Q

how much more potent is hydromorphone (diluiad) than morphine

A

5x

38
Q

how much more potent is diamorphine than morphine

A

10x

39
Q

what does potency mean

A

how much of a drug you need to get the desired effect

40
Q

what does affinity mean

A

refers to the goodness of fit between the drug and the receptor (how hard is it to pull it off)

41
Q

what does selectivity mean

A

refers to the range of receptors a given drug prefers

42
Q

t/f drugs that have a high potency are usually selective for just one type of receptor

A

true

43
Q

t/f drugs with high potency have a better affinity for the receptor than drugs with a low potency

A

true

44
Q

what is receptor desensitization

A

when an agonist binds to a receptor it causes the receptor to internalize into the neuron and stop the signal
- this is a feature of all G Protein coupled receptors - even if morphine is still circulating, the receptors get internalized so the morphine stops working

45
Q

opioids work

A

for a few hours, but then the effects begin to fade

46
Q

what is the reason for the gap between doses of opioids

A
  • The drug is still in the body, but the receptors that mediate the feeling of pain have been desensitized to the drug
  • They don’t give you more drugs because other receptors, like receptors for breathing, but they are still affected
47
Q

why are opioids addictive

A
  • they inhibit the neurons that usually inhibit dopamine
48
Q

methadone treatment

A
  • Nothing that is effective at addressing the addiction
    ○ Instead replace the opioid with something else to help them survive the withdrawal symptoms
    § It treats the symptoms of withdrawal but does not give them the same high
  • Methadone is also an opioid. It also activates mu opioid receptors.
  • It is given in tapered doses to lessen withdrawal from heroin. However, methadone withdrawal is as aversive as heroin withdrawal.
  • Methadone is not effective to reduce heroin use relapse rates unless it is accompanied by other interventions like counseling.
49
Q

Buprenorphine Treatment

A
  • Buprenorphine is also an opioid. It also activates mu opioid receptors but it is a partial agonist.
  • It is given in tapered doses to lessen withdrawal from heroin. Because it is a partial agonist it doesn’t fully activate the mu receptor. It is less rewarding and causes less withdrawal than methadone.
  • Buprenorphine is not effective to reduce heroin use relapse rates unless it is accompanied by other interventions like counseling.

PCL200 (6 decks)

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