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Integrated Drug Structure, Action, and Therapeutics > Initiation of Pain > Flashcards

Initiation of Pain Flashcards

1
Q

What is the difference between analgesia and anesthesia?

A

Analgesia only blocks nociception and leaves proprioception untouched. Anesthesia blocks proprioception, nociception, and the perception of environmental cues.

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2
Q

What are the four pieces of pain signaling?

A

Initiation
Transmission
Perception
Reaction

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3
Q

What does initiation of a pain signal entail?

A

Initiation takes place at the peripheral terminal of the primary afferent nerve. This is outside the CNS and will bring the signal to the nervous system.

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4
Q

What are the most effective inhibitors of initiation?

A

Local anesthetics. The problem is that they are the least selective.

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5
Q

Are sensory primary afferents the same?

A

They share some but not all structural aspects.

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6
Q

What is the pathway of a pain signal in initiation?

A

Starts in the periphery; signal goes through dorsal root and in through the dorsal horn. Synapse takes place here.

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7
Q

What nerves fibers are we most interested in?

A

A-alpha, A-beta (fast conduction - lots of myelin. Motor and proprioception). Signal jumps further and faster.
A-delta and C fibers going into dorsal root (interested in for pain conduction). Also temperature and touch.

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8
Q

A-delta

A

Smaller diameter, less myelin than A-alpha and A-beta. Slower conduction.

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9
Q

C fibers

A

No myelin. Slow conduction.

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10
Q

What are the key concepts for nociceptive activation?

A
  • Selective for stimulus
  • facilitate sodium/Ca2+ entry
  • sensitivity and receptive field can change with pathology
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11
Q

What are pseudo unipolar neurons?

A

Cell body off to the side, axons in both directions. We can traffic any neurochemical (neuropeptides) being made in that cell body in both directions. Important in terms of being able to transmit a pain signal. Traffic it periphery or into dorsal horn.

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12
Q

Glutamate, substance P, CGRP are what?

A

Important neurochemicals in pain transmission.

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13
Q

What is disinhibition?

A

When pathways normally under tonic inhibition are released.

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14
Q

How can we block nociceptors?

A

Wildly unsuccessful. If we try to block one nociceptor, the others pick up the slack.

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15
Q

Which receptor can we look at for blocking nociception?

A

TRPV1

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16
Q

Which drug can we look at for blocking nociception?

A

Capsaicin… it is an agonist at TRPV1 receptors, causing calcium overload. Huge disgorgement of substance P. Screws up mitochondria, which makes the neuron dysfunctional. Can no longer transmit signal.

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17
Q

Hyperalgesia?

A

Painful stimulus as consequence of some pathophysiologic change. Ex) Sunburn plus poking equals extreme pain.

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18
Q

Allodynia?

A

A stimulus that is not usually painful is painful. Ex) Diabetic neuropathy and gout have extreme pain with things that aren’t normally painful.

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19
Q

Where does receptor sensitization occur?

A

Centrally and peripherally.

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20
Q

What does it mean for sensitization to be a self-reinforcing process?

A

As a result of immune-competent cells (mast cell, leukocyte) releasing inflammatory mediators. This makes is easier to depolarize a primary afferent. Primary afferent is loaded with pain neurochemicals that conduct the pain signal. Dump some of those back into the periphery. Peripheral release of substance P and PGRP. Facilitate vasodilation and leakage and make it easier for inflammatory cells to cause depolarization of pain neurons.

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21
Q

Is sensitization as a self-reinforcing process a good thing?

A

It is a good thing within the context of cell repair. If regulation is lost, then it keeps cycling and causing chronic pain that is difficult to interrupt.

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22
Q

Is sensitization as a self-reinforcing process a good thing?

A

It is a good thing within the context of cell repair. If regulation is lost, then it keeps cycling and causing chronic pain that is difficult to interrupt.

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23
Q

What part of the spine are we interested in for sensory pathways?

A

The dorsal horn.

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24
Q

What part of the spine are we interested in for pain pathways?

A

The substantia gelatinosa.

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25
Q

What rex lamina are part of the substantia gelatinosa

A

Named for functional and shape of the cell as you look through the layers. II and III constitute this. Huge area for interactions of neurons conducting pain.

26
Q

What are the most important secondary neurons that project pain from the dorsal horn through the spinal cord?

A

Wide Dynamic Range neurons (WDR)

27
Q

What are the oldest fibers evolutionarily?

A

C fibers

28
Q

What do C fibers activate?

A

Paleospinalthalmic polysynaptic pathways

29
Q

What is the difference between the speed of action of the excitatory neurotransmitters glutamate and substance P/CGRP?

A

The speed.

30
Q

What is the difference between the speed of action of the excitatory neurotransmitters glutamate and substance P/CGRP?

A

The speed.

31
Q

What is sympathetically maintained pain?

A

Neurons that are normally involved in proprioception are now involved in nociception. They dysfunctionally start conducting pain signals.

32
Q

What is the dosage that when a patient passes without having adequate pain relief, the patient has to seek a consult from a pain specialist?

A

If they pass 120mg MME (morphine mg equivalents)

33
Q

What is are the 2010 CDC recommendations in seeking a balance in pain management?

A
  • Use opioids only after determining that alternative therapies do not work.
  • Consider random urine screens for those taking opioids for more than 6 weeks
  • If they pass 120MME without proper coverage, consult a pain specialist
  • Do not prescribe long-acting meds for acute pain
  • Monitor PDMP
34
Q

What is concerning about the slope of the line in overdoses since 2010?

A

The slope of the line hasn’t changed. Although new guidelines were put into place, they do not seem to be very effective. Methadone overdoses decrease, but heroin has increased.

35
Q

What are the main points in the 2016 CDC recommendations?

A

These guidelines are best practice guideline for prescribing opioids.

1) When to initiate or continue opioids for chronic pain
2) How to select the drug, duration, discontinuation
3) Assessing risk of harm

36
Q

What are the similarities between the guideline? Differences?

A
  • Both: suggest alternatives before opioids, random urine tests, review of PDMP data
  • New guidelines: more patient-involvement in risk/benefits of therapy, and more evaluation of patient risk-factors in opioid-related harms and how to reduce them.
37
Q

How successful have the attempts been to alter activation of nociception been?

A

With only one possible exception, not very successful.

38
Q

What is primarily responsible for sensitization in initiation?

A

The neurochemistry of peripheral cells surrounding primary afferents.

39
Q

Where are A-alpha and A-beta located anatomically?

A

Afferent to and efferent from muscles and joints.

40
Q

Where are A-delta fibers located?

A

In sensory roots and afferent peripheral nerves.

41
Q

Where are C fibers located?

A

Post-ganglionic sympathetic

42
Q

Where are dorsal roots located?

A

Sensory roots and afferent peripheral nerves

43
Q

How selective are sensory neurons?

A

Very selective. They have specific receptors to the type of stimulus they are responding to. However they all can fire an action potential.

44
Q

What is the gate theory?

A

It was developed in part to rationalize the mechanism of counterirritants. Small fibers transmit pain and turn off an inhibitory pathway, while large fibers when stimulated may transmit pain but stimulate an inhibitory pathway that blocks the pain signal from being transmitted to the brain. In a painless situation, there would be a inhibitory signal being transmitted.

45
Q

What pseudo unipolar mean? What is pseudo unipolar in pain transmission?

A

It means that something that seems like it only goes one direction can actually go two. Primary afferents are an example of this because they can differentially traffic neurochemicals and neuropeptides to peripheral or central sites.

46
Q

What are examples of the neurochemicals or neuropeptides that can be differentially trafficked?

A

Substance P, glutamate, CGRP (calcitonin-gene-related peptide)

47
Q

What differentiates nociceptive pathways from other sensory pathways?

A

The receptive bodies are very specific. Nociceptive pathways are used to transmit pain through chemical, pressure, or temperature stimuli. They transmit certain neurochemicals to send the signal. They are selective for stimulus, facilitate either Ca/Na entry into the cell, and can have varying sensitivity. The receptive field can even expand with a stronger pain signal.

48
Q

What fibers are we most interested in in terms of conducting pain signals?

A

A-delta and C fibers

49
Q

What structural or neurochemical aspects are important to cells that initiate pain signals?

A

They need something to send the signal, such as a neuropeptide or neurochemical. The three most common are substance P, glutamate, and CGRP.

50
Q

How are pain signals initiated; why is initiation of neuronal activity selective?

A

A pain signal is initiated when a chemical, mechanical, or thermal stimulus goes off. Specific receptors detect the signal, and an action potential is triggered through calcium or sodium entry into the cell (through depolarization that reaches the threshold to send a signal). It is selective so that the pain signal can be recognized in a specific area and more information can be given to get rid of that pain.

51
Q

Can one differentiate mechanisms of how the first pain signal is initiated and mechanisms that cause sensitization to subsequent or ongoing pain signals?

A

They are very similar mechanisms, in that a stimulus causes an action potential through a receptor. It is easier, however to start an action potential when sensitization is occurring. Substances are released that do not bind to nociceptors, but bind to their own site and lower the depolarization threshold.

52
Q

What is capsaicin at TRPV1 receptors?

A

An agonist. It opens up the channel and allows calcium to come rushing in. Substance P is released (and with chronic stimulation, depleted) but the calcium disrupts the mitochondrial function, and therefore disrupts the neuronal function. Neuron cannot transmit the signal, and so we get an analgesic response.

53
Q

Can you feel substance P release?

A

Yes, people report it.

54
Q

What is pain due to in bone cancer?

A

Out-of-control remodeling

55
Q

What strategies can you try to manage bone pain?

A

Strontium (incorporated into the bone in place of calcium)
Bisphosphonates (stop the remodeling process)
Calcitonin
Strontium and bisphosphonates have had some success in managing bone pain.

56
Q

What is allodynia?

A

When a stimulus that is not usually painful, causes pain.

57
Q

What is hyperalgesia?

A

When you have pain, an extra stimulus is extremely more painful.

58
Q

What opportunities exist to inhibit activation?

A
  • Local anesthetics (effective, not selective)
  • Na+ channel antagonists (lamotrigine, etc. neuropathic pain) Less effective for acute pain, SE’s at higher doses.
  • NSAIDS (interrupt the process of prostaglandin synthesis, which are involved in sensitization). moderate efficacy, central and peripheral actions
  • Capsaicin (limited efficacy, slow onset, discomfort)
  • Inhibition of bone resorption
  • Opioids? (endogenous)
59
Q

Where can sensitization happen?

A

Peripherally and centrally

60
Q

Why can sensitization be a self-reinforcing process?

A

Inflammatory cells are recruited to a site that needs repair. Inflammatory mediators are triggered and released, making it easier to depolarize (drop threshold) and send pain signals. Substance P and CGRP are dumped into the periphery as well as down the neuron. This recruits more inflammatory cells.

Integrated Drug Structure, Action, and Therapeutics (20 decks)

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