Term
| how is nociception modulated? |
|
Definition
| Can modulate at several levels of afferent sensory pathways before pain is perceived or can occur with efferent inhibitory pathways |
|
|
Term
| What is primary hyperalgia? What mediates this? |
|
Definition
| An enhance response or newly acquired response to a wider range of stimuli (including non-noxious stimuli)mediated by histamine, serotonin, bradykinin, and prostaglandins release from damaged tissue |
|
|
Term
| How do analgesics affect primary hyperalgia and relieve pain? |
|
Definition
| Produce analgesia by decreasing the frequency and intensity of stimuli firing |
|
|
Term
| What is secondary hyperalgia? What is the "triple response"? |
|
Definition
| neurogenic inflammation driven by a neuron; the triple response is flushing, edema, and hypersensitization of the local tissue to noxious stimuli |
|
|
Term
| Are local anesthestics effective to relieve secondary hyperalgia? Is secondary hyperalgia seen in denervated tissue? |
|
Definition
|
|
Term
| What are the 3 mechanisms responsible for central modulation? Describe them. |
|
Definition
1. Wind-up sensitization of 2nd order neurons: wide density receptor neurons increase frequency of discharge w/same stimuli and exhibit prolonged discharge even after stimulus has stopped
2. receptor field expansion: adjacent neurons respond to stimuli that they previously did not respond to (join the fun)
3. hyperexcitability of flexion reflexes: enhancement of flexion reflexes occurs |
|
|
Term
| What role does calcium play in the pain response? |
|
Definition
| Calcium causes neurotransmitter vesicles to fuse to receptor and release substances - specifically, calcium causes glutamate vesicles to fuse to the n-methyl-d-aspartate receptor to cause a pain response (this is why ketamine produces analgesia - it blocks glutamate at the NMDA receptor) |
|
|
Term
| At what level do COX inhibitors work? |
|
Definition
| Peripherally AND centrally |
|
|
Term
|
Definition
In the spinal cord itself (regional) or via a descending pathway
We can increase inhibitory neurotransmitters (ie. GABA or glycine) or via the gate theory (ie. TENS units produce pain in different, otherwise nonpainful, location and signals are divereted here/away from actual painful site) |
|
|
Term
| What is another name for the descending pain pathway? |
|
Definition
| the supraspinal inhibition pathway |
|
|
Term
| Why do antidepressants have analgesic effects? |
|
Definition
| They prevent the reuptake of serotonin and norepinephrine, which are then able to exert their effect as inhibitory neurotransmitters in the CNS |
|
|
Term
| Where do endogenous opiates act? What is the effect of enkephalins and endorphins? |
|
Definition
| Endogenous opiates act centrally; presynaptically they hyperpolarize afferent neurons and inhibit the release of substance P; they also act postsynaptically |
|
|
Term
| Where do exogenous opioids act and on what specifically? |
|
Definition
| Act postsynaptically on 2nd order neurons or interneurons in the substantia gelatinosa (lamina II) |
|
|
Term
| Give an example of a pain modulating neurotransmitter that is excitatory and one that is inhibitory |
|
Definition
| there are a few choices - Gayle wants us to know Glutamate is excitatory and Substance P is inhibitory |
|
|
