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5 items that do nociceptive activation and sensitization (in addition to various ions and other biochemical mediators that do this)
- substance P,
Substance P is made by cells of the spinal ganglia, and found at peripheral terminal of unmyelinated primary afferent fibers. Plays a role in ...?
increasing pain from GI, ureters, and urinary bladder
C fibers conduct what pain, how
- dull and burning pain
- slow conduction velocity, bc they're unmyelinated
A fibers conduct what pain, how?
fast, sharp, -- they're myelinated
from muscles, joints, bone
A and C ascending nociceptive fibers synapse with neurons where?
Dorsal horn has neurons that get hyperexcited by distinct types of stimuli from primary afferent nociceptors (A and C). There are 3 classes of cells responding here. What are they, what do they respond to?
- class I - respond to low threshold mechanical and thermal impulse
- class II - have a wide dynamic range
- class III - respond to stim only from tissue damage
anterolateral pathway transmits what kind of sensory info?
temp, pain, crude touch, tickle, itch
does sensory that doesn't require speed, precise localization, or fine gradations of intensity from signal source
anterolateral fibers originate where? then do waht?
- dorsal horns
- then cross in the anterior commissure to the opp. ant and lat white columns
upper terminus of anterolat pathway
- throughout the reticular nuclei of brainstem
- ventrobasal and introlaminar nuclei of thalamus
5 classes of pain meds
- non-opiate analgesics
- steroidal anti-inflam
- opiate analgesics
- local anesthetics
- skeletal muscle relaxants
when to use opioids? what do they mix well with and why?
- in refractory cases or pts w severe pain
- use with NSAIDs bc they can enhance opioid analgesia and produce "dose sparing"
acetylsalicyclic acid, aka __
how does aspirin/ acetylsalicylic acid exert its therapeutic effect?
inhibit synth of eicosanoides
4 basic effects of eicosanoides (prostaglandines, thromboxanes, leukotriens)
- inflam (increase local blood flow, capillary permiability, and effects of histamine)
- pain (increase sensitivity of receptors)
- thrombus formation
4 times to use aspirin or other NSAIDs
- mild to mod pain
- vascular disorders (nsaids inhibit thrombus formation)
- certain cancers (decreases risk of GI cancer)
aspirin side effects
- Reye's syndrome (brain and liver damage)
- irreversible inhibition of platelet aggregation
choline magnesium trisalicylate (an NSAID) - side effects?
- minimal bleeding
- peptic ulcer potential
diflunisal (NSAID) 2 notes
- antacids may decrease absorption
- convenient dosing
ibuprofin -- what type of drug? does what?
- reversibly inhibits platlet aggregation
- same gastric effects as aspirin but w less severity and incidence
- same mechanism as acetaminophne
- reversibly inhibits platlet aggregation
- same gastric effects as aspirin but with less severity
what pain killer irreversibly inhibits platelet aggregation? what 2 do it reversibly?
- ibuprofen and naproxen
indomethacin -- pain killer with higher risk of what
GI sie effects
4 potentitial adverse effects of nonopioids
- renal failure
- hepatic dysfunction
- gatric ulceration
use nonopioids cautiously in these populations
- renal, heart, liver porblems
- elevated angiotensin II or catecholamine levels
what do aspirin and aspirin like drugs do that acetaminophen does too? what doesn't acetominophen do? advantages of aceto?
- both are analgesic and antipyretic
- acetaminophen doesn't do anti-inflam or anticoagulant
- aceto has minimal bleeding risk, no GI irritation, no Reye's, doesn't decrease uric acid secretion
acetaminophen, 5 points
- low anti-inflam activity
- low plasma protein binding
- minimal bleeding / peptic ulcer potential
- doesn't ecacerbate volumen overload
- synergistic w narcotic analgesics
histamine's impact on inflammation
prostaglandine's impact on inflammation
leukotrien's impact on inflammation
vasoactive properties (affects diameter of vessels)
lymphokine's impact on inflammation
chemotactic properties (causing cells to exit the blood stream and enter tissue?)
main category of corticosteroid drugs used for inhibition of inflammatory process
- decrease of pain receptor activation
5 jobs of glucocorticoids (the main category of corticosteroid drugs)
- inhibit fibroblast activation (prevent walling off of infection)
- inhibit phospholipase A2 and reduce release of arachidonic acid from phospholipids
- reduce formation of eicanosides - leukotriens (high conc are found in synovial fluid in RA) thromoxanes, and prostaglandinsstabilize lysosomal membrane and inhibit breakdown of lysosomes
- inhibit rel of interleukin-1
downsides of glucocorticoids
- they treat the symptoms but don't address the disease -- could mask the severity of the disease, leading to serious or fatal delay in diagnosis
- inhibit body's own production of glucocorticoids from adrenal cortex
does the body produce glucocorticoids?
adrenal cortex (can atrophy and shut down in response to taking to much of the drug)
side effects of glucocorticoids
- skin atrophy
- muscle weakness
- weakening connective tissues
- reduced wound healing
- increase susceptibility to infection
- peptic ulcers
- hyperglycemic reactions (esp troublesome for diabetics)
how to administer glucocorticoid drugs?
orally for short term episodes or directly by injection into the inflamed tissue or joint
3 conditions where you'd use glucocorticoid drugs?
- inflammation in ankylosing spondylitis
- soft tissue inflam
how to administer dexamethasone?
- iontophoresis, pushing it into inflamed areas with the negative electrode
- (it's a glucocorticoid)
acting at the different levels of the CNS, system opioids induce analgesia by
- mimicking the actions of endogenous neurotransmitters at the opioid-receptor binding sites
- specific receptors in the encephalon and spinal cord are activated by the interaction with opioid agent --> stim or depression of diff neurons
at level of spinal cord, opioids do what?
inhibit transmition of nociceptive impulses from periphery to CNS
at level of basal ganglia, opioids
activate the descending antinociceptive pathway by interaction btwn opioids and recepters in the periaqueductual gray matter of the brain stem
mu opioid receptor effects include
kappa opioid receptors mediate
- spinal analgesia
delta opioid receptors mediate
- may potentiate morphine analgesia
morphine binds to what opiate receptor?
- but also kappa and delta