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PCL200 > Lec #2 Drugs for Pain > Flashcards

Lec #2 Drugs for Pain Flashcards

1
Q

how do we perceive pain?

A

painful stimulus activates the nociceptive sensory neurons and their synapses in the spinal cord and sends the pain signal to different parts of the brain. the brain integrates all the sensory information and emotional state and suppresses pain perception by activating the descending pathway

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2
Q

what activates pain sensors?

A

nociceptors and prostaglandins

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3
Q

hyperalgesia

A

condition in which a person experiences an increased sensitivity to pain or an exaggerated response to painful stimuli

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4
Q

allodynia

A

a condition in which a person experiences pain or discomfort in response to normally non-painful stimuli.

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5
Q

analgesia

A

relief or reduction of pain.

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6
Q

what is one way to relieve pain?

A

prevent the neurons of the ascending pathway

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7
Q

what is the descending pathway made of?

A
  • neurons that originate in the periaqueductal grey (PAG).
  • release of endorphins
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8
Q

how do the inhibitory neurons of the descending pathway reduce pain perception?

A
  • reduce nociceptive neuron releases
  • reduce the excitability of the ascending pathway neurons that send the pain signal to the brain.
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9
Q

what are the 2 ways that pain medicines work?

A
  • block the activation of the ascending pathway
  • mimic the activation of the descending pathway
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10
Q

effects of local anaesthetics (lidocaine, novacaine)

A
  • blocks sodium channels in the axon of pain neurons
  • blocking the action potential of the nociceptive neurons
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11
Q

effects of non-steroidal anti-inflammatory drugs (NSAIDS) (ibuprofen, aspirin, naproxen)

A
  • reduce the production of prostaglandin, produced by injury and inflammation
  • reduce mucus in the lining of the stomach
  • reduce the firing rate of nociceptive neurons in the ascending pathway.
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12
Q

name common NSAIDS

A

-ibuprofen
- naproxen
- aspirin
- diclofenac

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13
Q

what are the side effects of NSAIDS?

A
  • stomach/ GI ulceration
  • reduce kidney fucntion if used at high doses
  • exacerbation of asthma
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14
Q

acetaminophen

A

although reduces pain, is not an NSAID as it does not reduce redness and swelling and is not an anti-inflammatory

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15
Q

what is the enzyme that produces prostaglandin?

A

cyclooxygenase

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16
Q

mechanism of action of acetaminophen

A

mechanism is unknown

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17
Q

how do prostaglandins contribute to symptoms of inflammation?

A
  • they facilitate the firing of peripheral nociceptors and the firing of central neurons in the ascending pathway
  • cause swelling and increase bloodflow
    bind to prostaglandin receptors on the sensory nerves (nocicpetors), consequently activating the ascending pathway
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18
Q

what drugs act as antagonists of cyclooxygenase”?

A

non-steroidal anti-inflammatory drugs
- prevent the enzyme from making prostaglandins
- block pain and reduce swelling and redness
- reduce fever

19
Q

effects of opioids ( opium, morphine, codeine, heroine and fentanyl)

A
  • mimic endorphins (discovered by being “endogenous morphine) and bind to their receptor
20
Q

what is the drug that comes from morphine, the active ingredient in the poppy plant?

A

opiates

21
Q

name the receptor that mediates pain relief for opioids?

A

the mu opiate receptor, which reduces the amount of neurotransmitter that the nociceptive neuron releases and reduces the firing of the ascending pathway neuron

22
Q

opioids

A
  • agonists of the mu opioid receptor
  • depressants
23
Q

what is the difference between opiates and opioids?

A
  • opiates come directly from the plant
  • opioids are agonists for the mu-opioid receptor
24
Q

what are the short-term effects of heroin

A
  • euphoria
  • alternating alert and drowsy states
  • dryness of the mouth
  • warm flushing of the skin
  • slowed breathing
  • muscular weakness
25
Q

what are the long-term effects of heroin

A
  • suppression of immune response
  • downregulating the amount of mu opioid receptor
  • respiratory: pneumonia
  • circulatory: collapsed veins
  • liver: decreased function
  • systemic: abscesses
26
Q

what are the common effects of opioids, as the mu-opioid receptor is located on other neurons besides the nociceptive neurons?

A
  • euphoria
  • addiction
  • sleepiness
  • constipation
  • breathing suppression
27
Q

euphoria

A

thought to be the result of increases of dopamine. The mu opioid receptor is located on the neurons that control how fast dopamine neurons fire. They are inhibitory neurons, and they act as a brake on dopamine neurons.
When the mu opioid receptor is activated, the brake is released. Dopamine neurons fire more rapidly, and more dopamine is released. This dopamine increase is believed to be the cause of euphoria

28
Q

what are the addictive properties of opiates?

A
  • opiates silence the inhibitory neurons that keep dopamine neurons quiet.
  • a double negative - opiates indirectly cause dopamine neurons to fire because they quiet the neurons that normally keep dopamine levels low. A surge in dopamine is the brain’s reinforcing signal. It signals “whatever you just did, that was a good thing, so do that thing again”.
29
Q

why do opioids induce sleepiness

A
  • mu-opioid receptors are located on the neurons that regulate wakefulness
  • when a receptor is activated by an opiate, like morphine, those neurons will fire less. Less neuron firing = less wakefulness.
30
Q

why do opioids induce constipation?

A

Activation of mu opioid receptors slows peristalsis by reducing the activity of neurons that promote defecation. If someone needs long-term morphine for pain relief, constipation is a problem.

31
Q

why do opioids induce breathing surpression?

A

Neurons in the brainstem (medulla) regulate breathing. These neurons work even when we are unconscious to keep our breathing pattern regular. The mu opioid receptor is also present in these breathing pattern-generator neurons. When opiate levels are high, these neurons fire less. A fatal overdose occurs when these neurons stop firing.

32
Q

why are some opioids more likely to cause a lethal overdose?

A

potency

33
Q

potency

A

The amount of drug that is required to get an effect. opioids are compared to morphine for their potency
- codeine is 10X less potent than morphine, so you need 10X more codeine to get the same amount of mu receptor activation and pain relief. Heroin is 10X more potent than morphine, and fentanyl is 100X more potent than morphine.

34
Q

what is opiate overdose treated with?

A

naxolone, a drug that binds to the mu opioid receptor as an antagonist with opposite effects of opoioids
- competes with morphine or fentanyl to bind the receptor at the same spot, and when naloxone displaces the opioid, that stops the signal that reduces pain, reduces breathing, produces euphoria et cetera.

35
Q

dependence

A

the body depends on the presence of the drug to function normally. without the drug, a person experiences withdrawal symptoms

36
Q

tolerance

A

more drug is required to get the same effect. the body develops tolerance to analgesic and euphoric effects

37
Q

addiction

A

person is compelled to seek out and take more of the drug despite adverse consequences

38
Q

what are the 2 addictive drugs that contributed to the opioid crisis?

A

fentanyl and oxycodone respectively (synthetic and more potent than morphine, laces other drugs: heroin and cocaine)

39
Q

difference between morphine and codeine

A
  • morphine is more potent than codeine
  • codeine is converted into morphine in the body
  • morphine is produced by poppy plants and codeine is semi-synthetic
40
Q

what are examples of prescribed opioids?

A
  • Codeine (Tylenol-3 = acetaminophen + codeine).
    ○ Codeine is converted to morphine in the liver, the active drug
    ○ Some people are fast metabolizers and some are slow due to differences in genetics. (0.1X as potent as morphine).
  • Morphine – active ingredient of the poppy plant.
    ○ Source for many other semi-synthetic opioids.
  • Oxycodone (Oxycontin)
  • Hydrocodone (1.5X more potent)
  • Hydromorphone (Diluiad) 5X more potent)
  • Diamorphine (10X more potent)
  • Fentanyl (100X more potent)
41
Q

Affinity

A

refers to the “goodness of fit” between the drug and the receptor. How much energy is needed to pull the drug away from the recepto

42
Q

What is the correlational relationship between affinity and potency

A

Drugs with high potency have a better affinity for the receptor than drugs with a low potency.

43
Q

what is the correlational relationship between selectivity and potency?

A

Drugs that have a high potency are usually selective for just one type of receptor.

PCL200 (6 decks)

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