Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
29 Cards in this Set
- Front
- Back
|
What are the types of peripheral pain neurons? |
1. Ad-- fast 2. C-- slow |
|
|
What is the NT used by all nociceptive neurons? |
1. Glutamate |
|
|
What glutamate receptors are activated in the 2o nociceptor in a pain impulse? |
1. AMPA 2. +/- NMDA 3. Leads to production of EPSP |
|
|
What is the duration of acute pain? Chronic? |
1. <3-6 mos 2. Chronic=>3-6 mos. |
|
|
What causes nociceptive pain? What are its characteristics? |
1. Noxious stimuli activating pain fibers 2. Intense pressure, high temperature, extreme low temperature, chemicals 3. Sharp, aching, throbbing 4. Tissue injury apparent |
|
|
What causes inflammatory pain? |
1. Inflammatory mediators activating pain fibers 2. Sharp, aching, throbbing 3. Redness, warmth, and swelling |
|
|
What causes neuropathic pain? What are its characteristics? |
1. Nervous system malfunction resulting from injury to PNS or CNS 2. Compression, transection, ischemia, or metabolic injury 3. Burning, tingling, shooting and/or electric 4. +/- apparent tissue injury |
|
|
From where does somatic pain arise? |
1. Bone or muscle |
|
|
From where does visceral pain arise? |
1. Internal organs |
|
|
What does noxious heat activate? |
1. TRPV channels |
|
|
What does noxious cold activate? |
1. TRPA1 channels |
|
|
What does acid activate? |
1. Acid sensitive ion channels (ASIC) |
|
|
What does strong pressure activate? |
1. Mechanosensitive ion channels |
|
|
What are some inflammatory agents that can mediate inflammatory pain? |
1. TNFa 2. ILs 3. Bradykinin 4. ATP 5. Histamine 6. Prostaglandins |
|
|
How can inflammatory agents act to induce pain? |
1. Can activate silent nociceptors to produce pain 2. Can act as positive modulators of noxious nociceptors--- hyperalgesia |
|
|
How is hyperalgesia induced? |
1. Inflammatory mediators activate PKC and PKA 2. TRPV, MA channels, and NaV channels are phosphorylated to enhance activity |
|
|
What mediators can induce both inflammatory and nociceptive pain? |
1. Acid 2. Heat 3. Pressure |
|
|
What are silent nociceptors? |
1. Not activated by noxious stimuli 2. Cause pain when activated by inflammatory mediators |
|
|
What changes can occur at a neurologic level in chronic nerve damage? |
1. Increased NaV channel levels--- enhance nociceptor excitability 2. Increased levels of CaVa2d--- enhances glutamate release 3. Decreased KV channels |
|
|
What causes the change in ion channel levels in chronic pain? |
1. Altered gene activity |
|
|
What is allodynia? |
1. Pain resulting from a non-painful stimulus |
|
|
What will phosphorylation of TRPV, MA, and NaV channels lead to? |
1. Increased ability of these channels to enhance pain signaling |
|
|
How can short-term sensitization be achieved? |
1. Increase size of depolarization produced by TRPV and MA channels 2. Reduce threshold for activation of these channels |
|
|
What is the effect of phosphorylation on KV channels? |
1. Decrease activity--- higher frequency of AP generation in nociceptor |
|
|
What intracellular signals are involved in long-term peripheral sensitization to pain? |
1. Ca activation of PKC 2. Signals alter gene transcription to upregulate channel levels to increase excitability 3. KV channels downregulated |
|
|
How does sunburn produce allodynia? |
1. Activation of PKA |
|
|
What is gate-control of pain? |
1. Non-nociceptors contact secondary nociceptors indirectly via inhibitory interneurons 2. Block pain signaling
|
|
|
What is the mechanism of gate-control pain? |
1. GABA inhibits secondary nociceptor interneurons activated by Merkel cells 2. Primary nociceptors release glutamate onto interneurons, leading to an excitatory impulse that inhibits secondary nociceptors
|
|
|
What is the basis for TENS? |
1. Gate-control 2. Electrical stimulation activates AB touch receptor axons, which activate inhibitory interneurons |
