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Is pain a conscious or unconscious experience?
Which autonomic system does pain stimulate? Does pain increase or decrease metabolism? Protein/carb catabolic or anabolic? Water balance?
- increases metabolism
- sodium and water retention
What is another word for physiologic pain? is this conscious?
What is another term for pathologic pain? Is this conscious?
Physiologic v. pathologic pain: which is considered useful and aids to prevent tissue damage?
Physiologic v. pathologic pain: which is NOT useful and is pain felt in tissues that are damaged?
Is inflammation part of peripheral or central sensitization? does inflammation increase or lower stimulus threshold?
- peripheral sensitization
- lowers stimulus threshold
What are two characteristics of peripheral sensitization? Does this happen at the site of injury?
- primary hyperalgesia
- yes, at tissue
What contributes/what is central sensitization?
severe prolonged discharge of afferent neurons due to peripheral stimulation and neuropathic pain
What fibers are first order? Where are these fibers?
- what/where are second order fibers?
- 1st: A-delta and C in periphery to dorsal horn
- 2nd: excitatory ascending neurons in dorsal horn
In central sensitization, 1st order stimulates 2nd order which activates which receptors?
NMDA receptors --> exacerbates response to peripheral stimulus
What are 2 characteristics of central sensitization?
- secondary hyperalgesia (AWAY from tissue)
- allodynia (at tissue)
What are the 4 parts of pain process?
Do nociceptors have hi or low threshold for stimulus? What are 3 types of stimuli nociceptors respond to?
- hi threshold
- thermal, mechanical, chemical
How are silent/sleeping nociceptors activated?
only by inflammatory mediators (not tissue damage)
Which nociceptor is responsible for 1st pain? How is this pain described?
- sharp, discriminative
Which nociceptor is responsible for 2nd pain? How is this pain described?
- C fiber
What percentage of A-delta fibers act as nociceptors? What about C fibers?
Where are silent/sleeping nociceptors found?
terminal end of A-delta and C fibers
How do silent nociceptors contribute to hyperalgesia?
only stimulated by inflammatory mediators --> once activated, very sensitive to stimulus --> hyperalgesia (peripheral sensitization)
Are A-delta or C fibers non-myelinated so slower discharge rate?
what part of pain process involves stimulating nociceptors to initiate action potential?
What part of pain process is when AP travels 1st order neuron to dorsal horn to projection/2nd order neurons?
What part of pain process occurs in dorsal horn and nociceptive input can be reduced or increased, depending on release of neurotransmitters?
Do neurotransmitters like GABA, serotonin, and norepinephrine reduce or enhance nociception?
Do neurotransmitters like glutamate, prostanoids, acetylcholine, and substance P reduce or enhance nociception?
What receptors are activated with central sensitization?
What part of pain process occur in post-synapse of 2nd order neurons to relay modulation to brain?
What part of pain process integrates, processes, and produces autonomic/motor/endocrine response?
What are some differences between nociceptors in viscera v. somatic tissue?
- viscera has greater distance/fewer fibers, more K-opioid receptors, and stimulated by inflammation/ischemia/dilation
- viscera has sympathetic/parasymp fibers that transmit nociception