NB7-5 - Pain and DLA Flashcards

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1
Q

How are nociceptors and their neurons structurally different from other somatosensory receptors/neurons?

A

The nerve endings of somatosensory receptors are typically encapsulated or associated with some other structure while nociceptors are simply free nerve endings. Somatosensory neurons are typically well myelinated while nociceptor neurons are unmyelinated or very lightly myelinated.

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2
Q

List the types of nociceptors by the stimuli they respond to. How are these receptors activated?

A

Mechanical Nociceptors - respond to strong pressure or sharp objects which stretch/bend the nociceptor thereby activating mechanically gated ion channels to trigger an AP.

Thermal Nociceptors - respond to heat above 43C which opens heat sensitive ion channels to trigger an AP.

Chemical Nociceptors - respond to histamine, pH extremes, and other chemicals (capsacin) which will open ligand gated or pH sensitive ion channels to trigger an AP.

The majority of nociceptors are polymodal.

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3
Q

List some internal stimuli that can activate nociceptors.

A

Histamine (usually from mast cells), Potassium (from damaged cells), Substance P (edema), Bradykinin (from blood), Lactic acid, and more

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4
Q
A

D

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5
Q

Explain what first and second pain is and how that pain is mediated.

A
  • First pain is the immediate sharp pain felt after a trauma and it is mediated by faster Aδ fibers (somewhat myelinated)
  • Second pain is the delayed, longer lasting, duller, throbbing pain that occurs after a trauma and it is mediated by slower C fibers (not myelinated)
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6
Q
A

C

Touch is always faster than pain

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7
Q

List the important referred pain areas we need to know.

A

Heart attack refers pain to the upper chest wall and left arm

Appendicitis refers pain around the abdominal wall and navel

Pancreatitis refers pain to the upper left quadrant, extending to the back

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8
Q
A

E

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9
Q
A

C

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10
Q

Describe the gate control theory. Provide an example of when the effects of this are seen in nature.

A

The gate control theory is that the touch pathway can inhibit the pain pathway via an inhibitory interneuron that releases enkephaline at the synapse within the substantia gelatinosa where the primary pain neuron syanpses on the secondary pain neuron. This has the effect of cancelling out the signal. This is often observed in nature when a human rubs an injury for temporary pain relief. There are also descending pain control fibers that project down form emotional centers to influence these inhibitory neurons. This is why it seems that a persons attitude can affect their pain perception

Refer to image

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11
Q

From which centers in the CNS do the descending pain control fibers originate and what NTs are released by these fibers?

A
  • Periaqueductal Gray center in the midbrain whose fibers will release Enkephaline
  • Locus Coeruleus in the pons whose fibers will release noradrenaline
  • Nucleus raphe magnus in the medulla whose fibers will release serotonin
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12
Q
A

C

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13
Q

What are the two principal ways that pain is managed?

A
  1. By inhibiting the agents that sensitize the pain receptors (substance P, prostaglandins, leukotrienes)
  2. By inhibiting the pain pathway itself
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14
Q

How do NSAIDS and Opioids manage pain? List the major NSAIDS and Opioids we need to know and their major risks.

A
  • NSAIDS manage pain by inhibiting COX enzymes, thereby decreasing the synthesis of prostaglandins which are sensitizing agents. The NSAIDS we need to know are the nonselective COX inhibitors Aspirin, aka acetylsalicylic acid, and Ibuprofen (Advil & Motrin); and the selective COX-2 inhibitors Celecoxib (Celebrex) and Vioxx (withdrawn from market). Since COX-1 has a protective role in the GIT lining, the nonselective COX inhibitors can cause a GI bleed. The selective COX-2 inhibitors increase the risk for stroke
  • Opioids manage pain by mimicing opioid peptides (ie - enkephalin) and activating opioid receptors on the primary and secondary pain fibers. This activates the inhibitory interneurons of the gate control circuitry. The opioids we need to know are codeine, morphine, and heroin. These are highly effective analgesics but are also highly addictive.
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15
Q

List and provide a brief description of the way a person may experience more pain than is normal in response to a given stimulus. Provide examples.

A

Hyperalgesia - increased sensitivity to a painful stimulus (ie - a painful stimulus is more painful if applied to an already injured area)

Allodynia - a previously painless simulus becomes painful (ie - a touch to a sunburn is painful)

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16
Q

Draw out (or picture in your head) the pain sensation vs stimulus intensity graph and mark where allodynia and hyperalgesia occurs.

A
17
Q

Describe the cause of hyperalgesia after a skin wound.

A

After a skin wound, many endogenous chemicals that act to sensitive nociceptors are released:

  • Prostaglandins from damaged cells (from membranes of ruptured cells)
  • Potassium from damaged cells
  • Substance P released by primary afferents in response to edema
  • Histamine from mast cells
18
Q

What is primary and secondary hyperalgesia? What causes them?

A

Primary hyperalgesia is hyperalgesia within the area of damaged tissue to the release sensitizing agents

Seconday Hyperalgesia is hyperalgesia surrounding the area of damaged tissue due to the release of sensitizing agents.

19
Q

What is believed to be the purpose of hyperalgesia

A

It persuades an organism to take greater care of a wound and not disturb it during the healing process.

20
Q

What causes Allodynia?

A

Allodynia after trauma is thought to have similar causes as hyperalgesia after trauma.

Neuropathic allodynia (no obvious injury) is not completely understood but is likely NOT caused by nociceptor sensitization. The leading theory is that there is sensitization of the CNS by regular Aβ touch fibers converging, via interneurons, with C-fibers of the pain pathway leading to the interpretation of touch activity as pain.