Nociception and Pain Flashcards

1
Q

What occurs in primary hyperalgesia?

A

Local tissue damage heightens sensation of pain to subsequent stimulus.

-Occurs at site of tissue damage

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2
Q

WHich receptors become more sensitive in primary hyperalgesia?

A

Nociceptors

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3
Q

What are some examples of chemical mediators that are released by damaged tissue that can result in increased sensitivity?

A

1) K+
2) 5-HT, serotonin
3) Histamine
4) Bradykinin (most potent nociceptor known)
5) Prostaglandins

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4
Q

What can substance P cause?

A

1) Histamine release from mast cells

2) Vasodilation (flare) around area leading to release of proteins and other factors

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5
Q

What occurs in secondary hyperalgesia?

A

It is centraql sensitization in which C fibers are persistently active and the EPSPs on the dorsal horn neurons progressively increase.

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6
Q

What type of hyperalgesia is associated with “wind-up” and what is it caused by?

A

Secondary hyperalgesia

Casued by glutamate released from C fiber endings acting on NMDA receptors on the dorsal horn cells. It is very similar to Long-term potentiation (LTP). NMDA receptor activation also induces supersensitivity and hyperexcitability in the dorsal horn neurons

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7
Q

What is Allodynia?

A

A pain in response to a stimulus which does not normally produce pain. It results from mechanoreceptors projecting to neurons in the nociceptive pathway.

1 ). normally mechanoreceptor input too small to activate
nociceptive neuron
2). after injury, central nociceptive neurons become sensitized (central sensitization) and now mechanoreceptor input excites second order nociceptive neurons

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8
Q

What fibers innervate the pulp and the rest of the oral cavity and face?

A

A-delta and C fibers whose cell bodies lie in the trigeminal ganglion

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9
Q

Nociceptive fibers synapse on cells in the __________________________ nucleus which is arranged much like the dorsal horn of the spinal cord.

A

Spinal trigeminal nucleus

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10
Q

The axons of the spinal trigeminal cells cross over and project to the contralateral _______________.

A

Thalamus

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11
Q

Nociceptive fibers enter the spinal cord through the _____________ part of the dorsal root.

A

Lateral

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12
Q

__________ produces fast EPSP on dorsal horn neurons in spinal cord.

A

Glutamate

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13
Q

What fibers release substance P?

A

C fibers

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14
Q

__________________ produces slow EPSP on dorsal horn neurons in spinal cord.

A

Substance P

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15
Q

What tract of neurons is the most prominent and best studied tract?

A

Spinothalamic

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16
Q

_____________________________ is the cutting of the spinothalamic tract for relief of intractable pain. This provides initial relief but often the pain returns indicating other pathways are involved

A

Anterolateral cordotomy

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17
Q

Where do the axons of the spinothalamic tract project to in the brain?

A

Thalamus (reticular formation)

18
Q

Where do third order thalamic neurons project to?

A

Cortex

19
Q

Does extensive damage to somatosensory cortex result in loss of pain?

A

NO - bc there’s no orderly arrangment of nociceptive inputs to the somatosensory cortex.

20
Q

What is the most common and usual type of pain?

A

Nociceptive pain - caused from activation of nociceptors

21
Q

What is causalgia?

A

Peripheral nerve injury - also known as reflex sympathetic dystrophy syndrome

22
Q

Causalgia is described clinically as “sympathetically mediated pain” and can be reduced or abolished by blocking sympathetic activity or depleting ______________________.

A

Catecholamines

23
Q

What is the most painful disease in all of medicine and is also referred to as suicide disease?

A

Trigeminal Neuralgia

24
Q

What is another name for trigeminal neuralgia?

A

Tic douloureux

25
Q

What is trigeminal neuralgia described as by patients?

A

A stabbing or electric shock-like pain usually felt only on one side of the face that maybe triggered by brushing teeth, talking, touching the face, and chewing.

26
Q

What are the causes of tic douloureux?

A

1) Most common - enlarged looping artery or vein pressing on the trigeminal nerve root at the brain stem. The repeated pulsations of the vessel eventually produce irritation and abnormal signals
2) Multiple sclerosis
3) Tumor

27
Q

Often trigeminal neuralgia can be mistaken for what?

A

Tooth pathology - often results in loss of one or more of the patients natural teeth before a correct diagnosis is made

28
Q

What is a referred pain associated with tic douloureux?

A

Classic referred pain is visceral pain that is felt as pain in some distant somatic structure for ex: cardiac pain that is felt as pain in the left arm

29
Q

What is the mechanism for the referred visceral pain in trigeminal neuralgia?

A

Pain fibers from the visceral structure and the somatic structure to which the pain is referred, enter the same spinal cord segment. The visceral and somatic pain fibers converge on the same population of nociceptive neurons in the spinal cord and since somatic pain normally predominates, the brain interprets the activity in this pathway as arising from the somatic source even though it is from a visceral structure.

30
Q

What are some examples of referred pain involving the trigeminal nerve?

A

1) Tooth pain from one tooth is felt as pain in another
2) Pain from actual tooth is felt as a headache
3) Infections of the ears and sinuses can cause the sensation of a toothache
4) Angina is felt as a tooth ache or jaw pain

31
Q

What is the gate control theory?

A

Perception of pain is not simply due to activation of nociceptors, but is the outcome of modulation of both nociceptive and non-nociceptive inputs. According to the gate theory of pain, inhibitory interneurons regulate the transmission of ascending nociceptive information at the level of the second order neuron, allowing modulation of the signal (both increases and decreases in activity are possible). This modulation can explain phantom limb pain, as well as the success of TENS treatment and the actions of opioid analgesics.

32
Q

Stimulation of certain brain regions, especially the __________________________________, produces profound analgesia with no loss of tactile sensibility.

A

Periaqueductal gray

33
Q

What is analgesia?

A

Loss of pain

34
Q

T/F - Analgesic action of IV injected or ingested opiates is due to direct action on the CNS not peripheral receptors even though peripheral nociceptive endings do express opiate receptors.

A

True

35
Q

What are the 3 classes of endogenous opioid peptides?

A

1) Beta-endorphin from proopiomelanocortin precursor of pituitary
2) enkephalins from proenkephalin precursor
3) dynorphin from prodynorphin precursor (least potent analgesic)

36
Q

What are the 3 major classes of opiate receptors?

A

Mu, delta, and kappa

37
Q

Nearly all the clinical effects of opiates are mediated by ___ receptors.

A

Mu

38
Q

______________ is a potent agonist of the mu receptor.

A

Morphine

39
Q

The most clinically used opiate antagonist is ______________ which binds specifically to mu receptors.

A

Naloxone

40
Q

T/F- Opiate action is probably due to disinhibition of the periaqueductal grey neurons.

A

True

41
Q

Injections of __________ into subarachnoid space of the spinal cord (intrathecal injection) alleviates labor pain.

A

Opiates

42
Q

Descending serotonergic and noradrenergic fibers synapse directly on spinothalamic neurons and on _______________-containing interneurons.

A

Enkephalin-containing

  • Directly suppresses spinothalamic neurons
  • Indirectly suppresses spinothalamic neurons through activation of enkephalin-containing interneurons