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IMED3002 > Pain > Flashcards

Pain Flashcards

1
Q

What is analgesia?

A

Pain relief and attenuation

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2
Q

What is hyperalgesia?

A

Increasing pain stimulus from source.

Stimulus provided by noxious mechanical, thermal or chemical input

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3
Q

What is allodynia?

A

Abnormal response to touch caused by lesion or trauma to nerve or CNS

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4
Q

What is the difference between somatogenic and psychogenic pain?

A

Somatogenic pain is associated with a known cause due to nociceptor or neuropathy.

Psychogenic is not due to a known physical cause

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5
Q

What causes nociceptive pain?

A

Mechanically gated sodium channels in the skin get opened which triggers an action potential and pain results.

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6
Q

What causes neuropathic pain?

A

Pain activated by neuron in the brain along the nociceptive pathway

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7
Q

What causes nociceptive pain?

A

Activity in neural pathways in response to potentially tissue-damaging stimuli

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8
Q

What causes neuropathic pain?

A

Primary lesion of dysfunction in the nervous system

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9
Q

What are the classes of pain?

A

Pricking, stabbing, pinching (mechanical)

Burning, freezing (thermal)

Aching, stinging, soreness (chemical)

Visceral (mechanical, chemical)

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10
Q

What does the emotional component of pain affect?

A

Pain tolerance

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11
Q

What causes sharp and well localized pain?

A

Fast pain transmitted by myelinated axons (A-delta fibers) with glutamate neurotransmitters

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12
Q

What causes dull aching pain that is not well localized?

A

Slow pain transmitted by unmyelinated axons (C fibers) [1m/s] and substance P neurotransmitter

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13
Q

What kind of pain is visceral pain?

A

Very poorly localized and referred pain

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14
Q

What receptors are responsible for cold pain?

A

TRPM8

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15
Q

What receptors are important for mechanical pain?

A

MDEG

DRASIC

TREK-1

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16
Q

Does perception of temperature come from nociceptors for heat and cold?

A

No

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17
Q

What triggers chemical nociceptors?

A

Exogenous chemicals that penetrate skin such as acid, alkali, and organic molecules.

Intracellular molecules released by cell injury such as cations, peptides/neurotransmitters, prostaglandins, histamine, and bradykinin (chemicals released by mast cells)

Pathological substances released by diseased tissue

Toxins

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18
Q

What are polymodal nociceptors?

A

Pain receptors that are receptive to all kinds of painful stimuli.

They have both slow and fast pain fibers to conduct both fast and slow pain.

19
Q

What effects do inflammatory chemicals have?

A

They cause an increase in sensitization to pain. Meaning more pain will be produced.

This is due to creation of lower threshold for nociceptor firing. (hyperalgesia)

20
Q

What tracts do pain receptors ascend through?

A

The anterior spinothalamic tract.

21
Q

Where do pain fibers decussate?

A

Immediately after synapsing on the 1st lamina of the dorsal horn of the spinal cord they enter.

22
Q

Which part of the brain does the anterior spinothalamic tract go carrying pain signals?

A

Carries information to the midbrain, thalamus, and mostly the somatosensory cortex

23
Q

What path does pain sensation take from nociceptor to brain?

A

1st order neuron carries information to dorsal horn lamina I where it meets a second order neuron that decussates immediately and goes up to the brainstem (90% of fibers continue directly to the somatosensory cortex)

24
Q

What is the name of the pain directing part of the anterolateral spinothalamic tract?

A

The neospinothalamic tract.

25
Q

What kind of pain is carried by neospinothalamic tract?

A

This tract carries fast pain (sharp pain)

A-delta fibers synapse

26
Q

Where does the paleospinothalamic tract run?

A

Through the anterolateral spinothalamic tract to the brainstem where it stimulates the reticular formation, pons, limbic system, midbrain, and PAG.

27
Q

What pathway does the paleospinothalamic tract follow?

A

C fibers synapse with neurons in 2nd and 3rd laminae of dorsal horn.

Short fibers project to lamina V and 2nd order neurons decussate.

Fibers ascend anterolateral spinothalamic tract to the brainstem and most fibers branch from the brainstem.

28
Q

Where do paleospinothalamic fibers branch at the brainstem?

A

Reticular formation

Pons

Limbic system

Mid Brain

PAG (More synapses to lower brain structures)

<10% of C fiber signals reach sensory cortex

29
Q

What kind of pain is conveyed by the paleospinothalamic tract?

A

Slow, burning pain.

30
Q

Which nuclei in the somatosensory cortex contain sharp pain?

A

Ventral pesterolateral/ventral posteromedial nuclei. (Pain is more localized to a particular body site based, sensory humunculus)

31
Q

Where does slow pain sensation from cold, heat or stab sensation go?

A

Ventromedial posterior cortex and dorsal insular cortex.

32
Q

Where does emotional reaction to slow pain take place?

A

Medial dorsal to anterior cingulate cortex

33
Q

Where does physical response and subjective memory of pain take place?

A

Hypothalamus and limbic cortex

34
Q

What regions of the brain are slowed down by efferent analgesic system?

A

Periaqueductal grey matter region (midbrain)

Locus coeruleus (pons)

Nucleus raphe magnus (medulla)

35
Q

What does the efferent analgesic system do?

A

Activates anti-nociceptive pathways

36
Q

Which part of the spinal cord is the efferent analgesic system located at?

A

Dorsal horn

37
Q

How does the efferent analgesic system diminish pain sensations?

A

It releases neurotransmitters that inhibit or block transmission of nociceptive signals (opioids (enkephalins + endorphins and neurotransmitters like serotonin, noradrenaline)

38
Q

What is the gate-control theory?

A

Pain can be suppressed in the dorsal horn level

Normally inhibitory interneurons inhibit ascending pathways for pain resulting in less pain coming up to the brain.

Strong stimulus results in inhibition of the inhibitory interneuron thus increasing the pain rising to the brain. (the inhibition of the inhibitory interneuron is caused by a branch of the neuron attached to the nociceptor.

Touching another non-painful stimulus results in another stimulatory fiber that acts on the inhibitory interneuron creating more inhibition of painful signal reaching the brain.

39
Q

What are the kinds of interventions that can act on pain signals?

A

Opiates act centrally by inhibiting neurotransmission of afferent neurons.

alpha2-adrenergic agonists act centrally and stimulate endogenous anti-nociceptive neurones

Local anaesthetics block Action Potential conduction in nociceptive nerve fibers (ion channel inhibitors)

Anti-inflammatory drugs + aspirit reduce hyperalgesia and allodynia

40
Q

How do centrally acting analgesics work?

A

Potentiating descending analgesic system.

41
Q

How can peripheral pain signals be reduced?

A

Decreasing prostaglandin production

Decreasing hyperalgesia caused by inflammation.

Or block ion channels

42
Q

What is congenital analgesia?

A

Nociceptive stimuli are not processed or integrated at level of brain (patient does not feel pain)

43
Q

What is congenital sensoric neuropathy?

A

Nociceptive stimuli are not transmitted by peripheral nerves or by spinal afferent tracts (patient does not feel pain)

IMED3002 (46 decks)

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