LA.txt

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emm64
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164499
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LA.txt
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2012-07-30 20:40:35
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LA pt
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LA pt 1
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  1. ´╗┐Briefly describe the history of injections/LA
    • 1850s hypodermic needle, cocaine isolated
    • 1884 Freud cocaine, cocaine in medicine, LA by Halsted & Hall
    • 1905 Procaine (Einhorn)
    • 1921 Cartridge syringe
    • 1947 Aspirating syringe
    • 1948 Lidocaine
    • 1959 Disposable needle
  2. What is Local anesthetics?
    • drugs that reversibly block gen & propagation of nerve impules
    • depress conduction in all exciteable cells
    • sensory/motor periph, ANS ganglia, CNS, NMJ, cardiac & smooth muscle
  3. What did descartes discover in 1664?
    pain in brain.
  4. What did gate control theory 1965 imply?
    rubbing can interrupt pain transmission
  5. What is the IASP definition of pain?
    unpleasant sensory & emotional experience associated w/ actual or potential tissue damage or described in terms of such
  6. What are the 2 aspects of pain?
    • sensory: detection threshold, ID/loc, reproducible, intensity
    • affective: escape threshold, reaction, variable, unpleasantness
  7. What are the processes of pain experience?
    • transduction: physical to electrical
    • transmission: to CNS
    • modulation: endogenous opiods
    • perception: experience
  8. What is nociception?
    potentially tissue damaging thermal or mechanical energy impinging upon specialized nerve endings (A-delta & C fibers)
  9. Describe tranmission pathway of nociception.
    • nociceptor-> dorsal root of spinal cord-> decussation to ascend via anterolateral system to thalamus and cortex vial spinothalmic and reticulothalmic tracts
    • LA blocks nociceptors
  10. Which nerves are responsible for head pain sensation?
    • CN (V,VII, IX, X)
    • C (1,2,3)
    • Sympathetic nervous system
  11. What are the different nuclei of the trigeminal?
    • main sensory: non-nociceptive
    • spinal trigeminal nucleus: nociceptive info, nucleus cauadalis
    • mesencephalic nucleus: proprioception
    • rostral to caudal (center of face to outside therefore central face is harder to block with anesthesia than outside face)
  12. What are the types of LA applications?
    • topical: skin & mucous membranes
    • infiltration: direct injection
    • regional nerve block: injected proximal to nerve supplying area
    • spinal: injection to lumbar subarachnoid CSF
    • epidural, peridural or extradural: inject to extradural space where nerve roots pass, less likely to rise to higher segment then intended
    • IV: distal to point and interrupted by tourniquet
    • Sympathetic blocks: reflex symp dystrophies or intractable pain such as carcinoma
  13. What is the difference between spinal and epidural,peri or extradural?
    spinal is in subarachnoid CSF which may rise to higher parts
  14. Explain some of the Complex regional pain syndromes that are addressed by sympathetic blockades.
    • Stellate ganglion: CRPS upper arm, herpes zoster of H&N
    • Celiac plexus: pancreatitis pain
    • Lumbar sympathetic: CRPS lower legs: acute herpes zoster of legs
  15. What are peripheral nerves?
    mixed population of nerve fibers w/different diameters and rates of conduction.
  16. Explain the axon organization.
    • axon: individual cell
    • endoneurium: surrounds ind axon
    • perineurium: bundles into fascicles
    • epineurium: invests fascicles (vessels, fat cells)
    • Core(deep) vs. Mantle(peripheral) fibers
  17. What factors speed nerve conduction.
    • myelination: saltatory conduction
    • diameter: directly (larger=faster)
  18. What is a A-alpha peripheral nerve?
    • innervate skeletal muscle
    • biggest, fastest
  19. What is a C perpheral nerve?
    smallest, slowest nociceptor
  20. What fibers transmit nociception?
    A-delta and C
  21. Describe the various types of peripheral nerve fibers.
    • A-alpha: skeletal (15um, 100m/sec)
    • A-beta: touch/pressure (8um, 50 m/sec)
    • A-gamma: muscle spindles (6um, 20 m/sec)
    • A-delta: nocicpetors (3um, 15 m/sec) (sharp acute myelinated)
    • B: symp preganglionic (3um, 7 m/sec)
    • C: nociceptors (1um, 1 m/sec) (unmyelinated
    • Symp post (unmyelinated)
  22. Describe the ionophores of the nerve membrane.
    • very selective Na+, regulated or gated by membrane potential
    • closed(resting)->depolarize->open(ion-conducting)->inactive->repolarized to closed(recovery)
    • Na+ influx makes intracelluar more positive
  23. What are the permeabilities of the nerve membrane?
    • Na+: impermeable, high extracellular (1:14)
    • K+: selectively permeable, high intracellular (27:1 in:out)
    • Cl-: 1:11 in:out
    • gradient = -70mV (inside is negative)
  24. What is the firing threshold?
    • magnitude of decrese in negative transmembrane potential that is necessary to initiate an action potential(impulse)
    • about 15mV
    • ALL or none: anything less will not initiate
  25. Explain the Na channel gates.
    • m gate: activation, initial depolarization opens
    • h gate: inactivation, rapid depolarization closes
    • 4 alpha subunits, 1 beta holds alphas in membrane
  26. With regard to the Na channels what do LA do?
    • prevent closed->open
    • binds to transmembrane segments IS6, IIIS6, and IVS6
    • S4 segments unwind to open channel, LA prevents unwinding
    • induce reversible/dose-dependent reduction in rate of rise and height of action potential
    • causes an elevation of firing threshold and slowing of spread of conduction as conc of LA inc
    • in myelinated nerves only at nodes of Ranvier
  27. What is critical length?
    • smaller distance for blockage of smaller fibers
    • differential sensitivity of nerve fibers therefore smaller are more susceptible to blockacde than larger ones
  28. What is a use-dependent block?
    • LA action increased by repeated firing which allows more access and affinity for binding site (when channel is open)
    • aka freqency-dependent, use-dependent, phasic block
  29. Which fibers are more susceptible to blockade?
    • dull/sharp pain, temperature
    • less susceptible: touch, pressure, proprioception
  30. What is the structure of LA?
    • 1. Lipophilic: aromatic
    • 2. Intermediate chaing: amide or ester linkage
    • 3. Hydrophilic: tertiary amine group
  31. Lidocaine
    • amide(xylidine)
    • 7.9 pKa
  32. mepivacaine
    • amide(xylidine)
    • 7.6 pKa
  33. bupivacaine
    • amide(xylidine)
    • 8.1 pKa
  34. prilocaine
    • amide(toluidine)
    • 7.9 pKa
    • vasodilator
  35. articaine
    • amide(thiophene)
    • 7.8 pKa
  36. Esther LAs
    • procaine 8.9 pKa
    • chloroprocaine 9.0 pKa
    • tetracaine 8.2 pKa
    • cocaine
    • benzocaine
    • cyclonine
  37. Factors that affect the onset of LA action
    • concentration/volume
    • lipid solubility
    • diffusion: proximitiy
    • nerve morphology
    • pH of tissue
    • pKa of drug
  38. How is the Henderson-Hasselbalch equation used to explain ionization.
    • pKa-pH=log [ionized/un-ionized]
    • ex: lidocaine pKa = 7.9
    • 7.9-7.4 = log [ion/un-ion]
    • 10^0.5 = ion / un-ion = 3/1
    • Closer pKa to body pH = faster onset time
  39. How does infection affect onset of LA?
    tissue pH of infected tissue is lower-> more acidic therefore the ration of ion/un-ion is higher and will have a slower onset time and less efficacy.
  40. What factors affect duration of action of LA
    • concentration
    • lipid solubility
    • protein binding
    • MOST IMPORTANT: DIFFUSION (hence vasoconstrictor)
  41. What is the main factor of LA potency?
    lipid solubility: ability to move intraneuronally
  42. How are amide LAs metabolized?
    • liver
    • Lidocaine: N-dealkylated to monoethyl-glycine-xylidide(MEGX) (80% potency->sedation)
    • Prilocaine: biotransformed in plasma and kidney->orhtotoludidine->methemoglobinemia
    • Articaine: amide w/ester, ester hydrolysis more rapid
    • Bupivacain is N-dealkylated
  43. What does toluidine do in the blood?
    blocks conversion of Fe2+ to Fe3+ causing methoglobinemia
  44. How are ester LAs metabolized?
    • plasma cholinesterase (pseudocholinesterase
    • concern if atypical plasma cholinesterase (deficiency)
  45. Is metabolism of LA a concern?
    • not really unless severe liver dysfunction or pseudocholinesterase deficiency.
    • total amount more important
  46. What are the interactions of LA?
    • other LA (additive): stay below max
    • opioid and phenothiazine: increases cerebral blood flow -> predisposed to toxicity, stay well below max
  47. What are the indications for vasoconstrictors?
    • inc depth of anesthesia
    • inc duration (if LA doesn't vasodilate like prilocaine)
    • decrease peak blood levels of LA (dec systemic toxicity)
    • hemostasis: minimize bleeding (bware of CV effects)
  48. Describe the adrenergic amine structures of vasoconstrictors.
    • NE: both H, no B2
    • E: (NH-CH3), all
    • Levonordefrin: alpha-methyl-NE, decreased a1, B2
  49. How is vasoconstriction mediated?
    • a1-post ganglionic
    • a2-bare extra-synaptic in periphery, (some presynaptic inhibition too)
  50. What are the CV effects of Epi?
    • inc dysrhytmias
    • inc HR, CO!!
    • dec periph resistance -> MBP stable
    • ventricular arrhythmias
    • chest pain
    • ST-segment depression->myocardial ischemia
  51. What are CV effects of Levonordefrin?
    • inc dysrhythmia, CO, PR, MBP
    • no change in HR
  52. What are the CV effects of NE?
    • inc dysrhymia,
    • inc! PR, MBP
    • dec HR
    • no change in CO
  53. What are the systemic effects of Epi?
    • CV:
    • vasoconstriction (capacitance veins) a1
    • increased contractility and HR b1
    • vasodilation (skeletal muscle) b2
    • Respiratory: Bronchodilation (b2)
    • Metabolic:
    • decrease plasma K+ (a2)
    • increased lipolysis (b2)
    • elevated plasma glucose (b2)
  54. What are the features of epinephrine?
    • rapid onset, short duration (5-10 IV, 10-20 Intraoral)
    • exogenous epi metabolized by COMT
  55. What are the sympathetic Nervous system receptors?
    • a1: vasoconstriction, inc BP
    • b1: HR & force, inc HR
    • b2: skeletal vasodilation, dec BP
  56. What are the vasoconstricor interations?
    • Non selective Beta-blockers (hypertension & reflex bradycardia)
    • NE-reuptake inhibitors: tricyclic, SNRI, SNE-reuptake inhibitors, cocaine & amphetamines
    • COMT inhibitors

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