pharm pain

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  1. 5  items that do nociceptive activation and sensitization (in addition to various ions and other biochemical mediators that do this)
    • histamine,
    • substance P,
    • prostaglandins,
    • serotonin,
    • bradykinin
  2. 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
  3. C fibers conduct what pain, how
    • dull and burning pain
    • slow conduction velocity, bc they're unmyelinated
  4. A fibers conduct what pain, how?
    fast, sharp, -- they're myelinated

    from muscles, joints, bone
  5. A and C ascending nociceptive fibers synapse with neurons where?
    dorsal horn
  6. 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
  7. 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
  8. anterolateral fibers originate where? then do waht?
    • dorsal horns
    • then cross in the anterior commissure to the opp. ant and lat white columns
  9. upper terminus of anterolat pathway
    • throughout the reticular nuclei of brainstem
    • ventrobasal and introlaminar nuclei of thalamus
  10. 5 classes of pain meds
    • non-opiate analgesics
    • steroidal anti-inflam
    • opiate analgesics
    • local anesthetics
    • skeletal muscle relaxants
  11. 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"
  12. acetylsalicyclic acid, aka __
  13. how does aspirin/ acetylsalicylic acid exert its therapeutic effect?
    inhibit synth of eicosanoides
  14. 3 eicosanoides
    • prostaglandines
    • thromonxanes
    • leukotriens
  15. 4 basic effects of eicosanoides (prostaglandines, thromboxanes, leukotriens)
    • inflam (increase local blood flow, capillary permiability, and effects of histamine)
    • pain (increase sensitivity of receptors)
    • fever 
    • thrombus formation
  16. 4 times to use aspirin or other NSAIDs
    • mild to mod pain
    • fever
    • vascular disorders (nsaids inhibit thrombus formation)
    • certain cancers (decreases risk of GI cancer)
  17. aspirin side effects
    • Reye's syndrome (brain and liver damage)
    • irreversible inhibition of platelet aggregation
  18. choline magnesium trisalicylate (an NSAID) - side effects?
    • minimal bleeding
    • peptic ulcer potential
  19. diflunisal (NSAID) 2 notes
    • antacids may decrease absorption
    • convenient dosing
  20. ibuprofin -- what type of drug? does what?
    • nonopioid
    • reversibly inhibits platlet aggregation
    • same gastric effects as aspirin but w less severity and incidence
  21. naproxen
    • same mechanism as acetaminophne
    • reversibly inhibits platlet aggregation
    • same gastric effects as aspirin but with less severity
  22. what pain killer irreversibly inhibits platelet aggregation? what 2 do it reversibly?
    • aspirin
    • ibuprofen and naproxen
  23. indomethacin -- pain killer with higher risk of what
    GI sie effects
  24. 4 potentitial adverse effects of nonopioids
    • renal failure
    • hepatic dysfunction
    • bleeding
    • gatric ulceration
  25. use nonopioids cautiously in these populations
    • geriattrric
    • renal, heart, liver porblems
    • hypovolemia
    • elevated angiotensin II or catecholamine levels
  26. 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
  27. 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
  28. histamine's impact on inflammation
  29. prostaglandine's impact on inflammation
    platelet aggregation
  30. leukotrien's impact on inflammation
    vasoactive properties (affects diameter of vessels)
  31. lymphokine's impact on inflammation
    chemotactic properties (causing cells to exit the blood stream and enter tissue?)
  32. main category of corticosteroid drugs used for inhibition of inflammatory process
    basic role?
    • glucocorticoids
    • decrease of pain receptor activation
  33. 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 prostaglandins
    • stabilize lysosomal membrane and inhibit breakdown of lysosomes
    • inhibit rel of interleukin-1
  34. 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
  35. does the body produce glucocorticoids?
    adrenal cortex (can atrophy and shut down in response to taking to much of the drug)
  36. side effects of glucocorticoids
    • skin atrophy
    • muscle weakness
    • weakening connective tissues
    • osteoporosis
    • reduced wound healing
    • increase susceptibility to infection
    • peptic ulcers
    • hyperglycemic reactions (esp troublesome for diabetics)
  37. how to administer glucocorticoid drugs?
    orally for short term episodes or directly by injection into the inflamed tissue or joint
  38. 3 conditions where you'd use glucocorticoid drugs?
    • inflammation in ankylosing spondylitis
    • RA
    • soft tissue inflam
  39. how to administer dexamethasone?
    • iontophoresis, pushing it into inflamed areas with the negative electrode
    • (it's a glucocorticoid)
  40. 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
  41. at level of spinal cord, opioids do what?
    inhibit transmition of nociceptive impulses from periphery to CNS
  42. 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
  43. 5 opioid receptors
    • mu
    • kappa
    • delta
    • sigma
    • epsilon
  44. mu opioid receptor effects include
    • analgesia
    • nausea
    • vomiting
    • constipation
  45. kappa opioid receptors mediate
    • sedation 
    • spinal analgesia
  46. delta opioid receptors mediate
    • analgesia
    • may potentiate morphine analgesia
  47. morphine binds to what opiate receptor?
    • mu
    • but also kappa and delta
Card Set:
pharm pain
2013-11-04 15:47:48

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