Anes MT II

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HLW
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139550
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Anes MT II
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2012-03-04 15:05:22
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Anes MT II
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Anes MT II
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  1. which 2 LAs are licensed for use in some animals?
    lidocaine and mepivicaine
  2. What is in EMLA creams that are not licensed but used topically in animals?
    lidocaine and prilocaine
  3. What is mechanism of action for LA's?
    direct blockage of sodium channel to prevent Na influx --> prevents response to membrane depolarization
  4. Is absolute analgesia provided with LA's?
    yes since painful stimulation cannot be transmitted to the spine/brain to induce response
  5. Is higher concentration needed to block motor or sensory fibers? why is this advantageous?
    • higher needed to block motor
    • allows sensory anesthesia without motor paralysis
  6. which type of fibers are blocked first?
    • smaller, unmyelinated
    • so autonomic B fibers first
  7. After B fibers are blocked, what is next? Myelination? What function is blocked when they fibers are blocked?
    • Adelta (light myelination) blocks fast pain, will see increased skin temp.
    • C (none) blocks slow pain, see loss of skin sensation/pain
  8. Which nerve fiber is 3rd to be blocked and is moderately myelinated? What is its function? what do you see with block?
    • A gamma: function is motor to muscles and proprioception
    • see loss of proprioception
  9. Which fiber is responsible for sensory detection so that blocked patients lack response to touch and pressure?
    A beta (moderate myelination)
  10. What is the final fiber to be blocked? Myelination? Function and sign of blockage?
    • A alpha: heavy myelination
    • motor to skeletal muscle --> see loss of motor function
  11. Are LA's weak acids or bases? Highly or poorly soluble?
    • weak bases
    • poorly soluble
  12. how are LA's formulated to improve their stability and solubility?
    formulated with acidic hydrochloride salts
  13. What are two classifications of LA's?
    esters and amides
  14. Amide or esters? Lidocaine, bupivicaine, mepivicaine, ropivicaine, prilocaine, etidocaine.
    amides
  15. Amide or ester? Procaine, cocaine, tetracaine, amethocaine.
    Esters
  16. Do esters or amides produce more allergic reactions? Why?
    esters: PABA metabolite
  17. Amide or ester: short duration of action and degraded by plasma pseudocholinesterase?
    esters (procaine, tetracaine)
  18. Amide or ester: very stable and metabolized by hepatic microsomes to active compounds that are inactivated and excreted by kidney?
    Amide (lidocaine, bupivi, mepivi, ropivi)
  19. what property effects potency and contributes to speed of onset?
    lipid solubility (more lipid soluble --> more potent/ faster onset)
  20. What property has main effect on duration of action?
    • protein binding (higher bound --> lasts longer)
    • * lipid solubility and vasodilation contribute also
  21. What property is main determinant of speed of onset?
    • pKa (ionization) unionized form passes
    • closer pKa to physiologic pH --> faster onset
  22. Since LA's are weak bases, is there more ionized or unionized form at alkaline pH?
    more UNionized in BASE
  23. As pH decreases, what happens to proportion of unionized drug?
    decreases (acid environment decreases amount of available effective drug)
  24. Which LA has the most notable vasodilator effect? Which is the only one to cause vasoconstriction?
    • lidocaine
    • cocaine = constricts
  25. What is added to LA to delay systemic absorption and removal from action site? How does this addition accomplish this?
    epinephrine --> vasoconstriction
  26. When is it inappropriate to use epinephrine with LA?
    • ring block (teat block, declaw)
    • LA in distal extremities (digit, ear, tail --> potential for ischemia)
  27. What are some advantages/reasons to use LA in adjunct to general anesthesia?
    • versatile (various routes of admin)
    • effective/reliable analgesia
    • easy w/minimal equipment
    • minimal systemic effect
    • red. sympathetic response if given before sx
    • improved post-op analgesia
    • prevents central sensitization (blocks enhanced pain sensitivity)
  28. Why may CRI of lidocaine be indicated in a horse?
    prokinetic activity (promotes GI motility)
  29. Is lidocaine given systemically MAC sparing?
    yes
  30. Does lidocaine given systemically modulate or enhance inflammation during acute trauma or multiple organ dysfunction?
    modulates/protective
  31. IV lidocaine infusion is used in horses and dogs but is usually avoided in which species?
    cats (possible higher risk of systemic overdose)
  32. What are 5 factors that contribute to systemic toxicity?
    • total dose given
    • rate of systemic absorption
    • acidosis increases risk of toxicity/reduced seizure threshold
    • rate of metabolism
    • presence of epinephrine
  33. Where is highest rate of systemic absorption after injection? slowest rate?
    intercostal > epidural > brachial plexus > subcutaneous

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