Pharm Exam 4 General/local anesthetics & muscle relaxants

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Pharm Exam 4 General/local anesthetics & muscle relaxants
2013-03-15 20:57:39

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  1. What are the 4 "goals" of general anesthesia?
    • 1. amnesia
    • 2. analgesia
    • 3. "muscle relaxation"
    • 4. inhibition of autonomic reflexes
  2. What is the most common IV general anesthetic?
  3. What is the target of general anesthetics and why?
    Brain--> want to block perception of pain
  4. What are a couple differences between the newer and older general anesthetics?
    • Newer--> no longer volatile, "low" lipid solubility
    • Older--> had "high" lipid solubility--> took longer to reach brain because uptaken by tissue first
  5. What are inhaled agent dosing based on?
    Minimal alveolar concentration (MAC)--> dose required to inhibit moving in 1/2 of patients during surgical stim
  6. What is the suspected MOA of inhaled agents?
    -Inhibits AP around CNS and ultimately PNS
  7. What are the effects of inhaled agents on CNS, CV, Resp, Renal, & liver system?
    • CNS: ⇑ cerebral blood flow, ⇓ CMRO2
    • CV: inhibit CV and vasodilates
    • Resp: reduce normal min ventilation
    • Renal: ⇓GFR, barely
    • Liver: minimal ⇓ hepatic blood flow
  8. KNOW: Is HR efffected by inhaled gases?
    NO--> because gases decrease CV function, but may increase HR indirectly b/c of vasodilation
  9. What receptor is responsible for Malignant Hyperthermia?
    Ryanodine receptors (L-type Ca channel) in the SR
  10. What triggers Malignant Hyperthermia?
    • 1. Inhaled anesthetics
    • 2. Succyincholine
  11. What is the patho behind Malignant Hyperthermia?
    Exagerrated release of Ca+--> muscle contraction--> increased metabolic demand--> hyperthermia
  12. What are the 4 general effects of inhaled anesthetics?
    • 1. Decrease SVR
    • 2. Decrease contractility
    • 3. Increase cerebral blood flow
    • 4. Minimal metabolism and excreted primarily in lungs
    • **Patients w/ Low EF may not tolerate well
  13. KNOW: MOA of propofol
    -Activation GABAa--> increase CL- conduction across neuronal membrane--> hyperpolarizes cell--> decrease neuronal transmission
  14. What are the effects of propofol on the CNS< CV, Rest?
    • CNS: ⇓metabolic demand (CMRO2), ⇓ cerebral blood flow--> decrease ICP
    • CV: Vasodilation--> hypotension, Inc HR
    • Resp: Apnea
    • **has some anti-emetic properties
  15. What is the MOA of barbiturates?
    -Activation of GABAa (like propofol)
  16. Which drug can cause pain, vasoconstriction, and tissue injury if given intra-arterial?
  17. Which drug can provide a significant "hangover" effect?
  18. What is the MOA of benzos?
    MOA: Activation of GABAa
  19. Which drug metabolism requires transformation to water soluable compound first, Barbiturates or Benzos?
  20. What are benzos used for in anesthesia?
    • 1. anxiolysis
    • 2. sedation
    • 3. decrease in seizure activity
  21. What are the CNS, CV, and Resp effects of Benzos?
    • CNS: decrease CMRO2 & cerebral blood flow
    • CV: decrease SVR
    • Resp: minimal min volume reduction; CO2 right shift
  22. What is the MOA of etomodate?
    Activation of GABAa
  23. What are some adverse effects of Etomodate on the CNS?
    Myoclonus--> precipitate seizures
  24. T or F. Etomodate has minimal effect on the CV?
    True--> as long as they are normovolemic--> must decrease dose if hypovolemic
  25. What is an endocrine side effect of Etomodate with continuous infusion?
    Adrenocortical suppression w/ repeated or continuous infusion
  26. What is the MOA of Ketamine?
    Activates the NMDA receptor
  27. What are the CNS, CV, and Resp effects of Ketamine?
    • CNS: Increase CBF, increase ICP
    • CV: Sympathomimetic
    • Resp: potent bronchodilator
  28. Which IV anesthesia med may be best for patients with significant blood loss?
    Ketamine--> bronchodilator, sympathomimetic so don't have decrease of BP, HR
  29. Which IV anesthetic does not use GABAa as a MOA?
  30. What is the MOA of local anesthetics?
    • Bind w/ Na channels and reduces AP (called Na Channel blockers)
    • -Lack of NA influx and K efflux causes HYPERPOLARIZATION
  31. What part of the Na channel receptor do local anesthetics bind to?
    Diffuse across membrane and bind with a receptor on the inner surface--> inhibiting action
  32. What are the 2 sites/ways local anesthetics are use?
    • 1. Discrete sites--> limit pain/sensory input
    • 2. Systemically (lidocaine) to induce neuroleptic anesthesia (numb the brain)
  33. What are the 2 classes of local anesthetics?
    • 1. Esters
    • 2. Amides
  34. What is the effect of epi in combo with a local anesthetic?
    Epi--> prolongs LA by constricting vessels at site and keeping LA near site of administration
  35. What areas of the body are at higher risk of systemic absorption with LA?
    ribs, trachea
  36. Where are Amide LA's converted to water soluable metabolites?
  37. Where are Ester LA's converted to water soluable metabolites?
    Plasma (increase incidence of allergic reaction)
  38. T or F.  In LA, potency is proportional to lipid soluability?
  39. LA are weak acids or weak bases?
    weak bases (7.5-9.0)
  40. Cations or anions are the most active form of LAs?
  41. What is the effect of LA on infected tissue?
    Less analgesia--> infections usually acidic so a weak base is less active in an acidic environment
  42. Which nerve fibers are blocked first with LAs?
    C-fibers: pain and SNS
  43. What is the blockade order of nerves? (SNS)
    • 1. Temp first
    • 2. Pain
    • 3. Touch
    • 4. Motor
  44. What are the systemic toxic effects of LA on the CNS and CV?
    • CNS: low concentration--> depression, sedation, tinitus
    •   -high concentration--> seizure
    • CV: (bupivicaine)--> highly selective for cardio na channels--> lethal
  45. What is the effect of LA  toxicity on the Nervous system?
    -repeated exposure--> chronic nerve injury
  46. How many grams is in Lidocaine 2%?
    2%--> 2gm in 100ml solution
  47. How many gm of Lidocaine are in a 0.5% solution?
    500mg/100--> 5mg/1ml
  48. Where do neuromuscular blocks act on?
    Peripherally NS--> interfere w/ nerve transmission at the NMJ
  49. Where do spasmolytics act on?
  50. Which 2 spasmolytics do NOT act centrally?
    Dantrolene and botulism toxin
  51. How are spasmolytics used?
    To reduce muscle spasm ADLs (MS, CP, SCI)
  52. What are the 2 major classes of neuromuscular blockades and provide a drug example?
    • 1. Depolarizing--> succinylcholine
    • 2. Non depolarizing--> Roc/Vec
  53. What happens when a neuromuscular blockade is given without adequate sedation?
  54. What is the NMJ innervated by?
    PSNS (Ach--> N2)
  55. What is MOA of depolarizing agents?
    Acts like Ach--> causes depolarization--> muscle contraction--> prolonged repolarization
  56. What is the onset and duration of action of succyincholine?
    • Onset--> 30-60sec
    • duration--> 7-10min
  57. What is a common side effect after surgery complaint after use of succyincholine?
  58. What are the adverse effects of depolarizing agents? (4)
    • 1. Increased intraocular pressure
    • 2. increased gastric pressure (aspiration)
    • 3. muscle pain
    • 4. prolongation of duration (w/ aminoglycosides)  Some antibx reduce prejunctional ACh and reduce evoked potentials
  59. What side effect can occur w/ depolarizing agents used in children?
    bradycardia (vagally mediated & airway manipulation--> vagal stim)
  60. What effect can severe burns or UMN diseases have on depolarizing agents?
    • -Desensitize ACh--> b/c of up-regulation of extrajunctional receptors so increase Na/K channels
    • -Increase K binding can cause cardiac arrest
  61. T or F.  Succyincholine can be used in burns <12hrs.
  62. What happens when a cell depolarizes?
    Increase K+ levels--> a problem for spinal, stroke, or renal failure patients
  63. When is Sux contraindication? (5)
    • 1. CVA
    • 2. renal failure patients
    • 3. spinal cord injury
    • 4. burns
    • 5. family hx or hx of MH
  64. How do Non-depolarizing muscle relaxants work?
    Are N2 blockers--> prevent ACh from binding
  65. T or F. Non-depolarizing agents have a short elimination period?
    FALSE--> prolonged elimination
  66. What are 3 characteristics of Non-depolarizing muscle relaxants?
    • 1. highly ionized
    • 2. weak bonds to peripheral tissues
    • 3. small Vd
  67. Where are NDMR typically excreted?
  68. What is the NMDR physiologic effect of IV administration?
    -weakness that progresses to flaccid motor response
  69. Which muscle groups respond first to NDMR?
    • -small muscle groups--> hands, larynx
    • -then larger muscle groups--> diaphragm
  70. What muscle order do NMDR effects wear off?
    large muscle to small muscles
  71. Which agents are reversible? Sux or NDMA
  72. WHat is the reversal agent for NMDA?
  73. Why is the reversal agent anticholinesterases a problem?
    -affect more than N2--> effects everywhere and can cause N/V
  74. When are anti-spastic agents used and why?
    • -treat neuro disorders--> CP, MS, SCI
    • -Reduce muscle tone for therapy
    • -But may mask progression of dx
  75. When are anti-spasmodic agents used?
    • Treat MSK conditions--> back pain-
    • -can increase ROM for therapy
    • -SHORT TERM (NSAIDS first)
  76. What are the side effects of Spasmolytic agents? (3)
    • 1. sedation
    • 2. dizziness
    • 3. impaired vision
  77. How do spasmolytic agents work?
    • 1. Reduce muscle fiber tension
    • 2. Enhance inhibitory effect of neurons
  78. What is the MOA of Diazepam?
    Enhances GABAa--> hyperpolarization of neuron
  79. What is diazapam effective for?
    Effective for SCI spasms due to spinal cord mediation (sedation--> don't use long-term)
  80. How do baclofen and tizanidine work?
    -act centrally on spinal cord/brain stem--> inhibit neuronal transmission (outflow)
  81. What is the MOA of baclofen?
    Action on GABA-b--> increased K+ conductance (hyperpolarizes)
  82. Which anti-spasmodic agent limits substance P?
  83. What patients should avoid or be careful when given baclofen?
    • -Seizure disorders--> must taper off
    • -Renal disease
  84. T or F. Baclofen toxicity can cause CNS and CV effects.
    • FALSE--> only CNS effects (seizure, confusion, loss of reflexes)
    • -NO CV effects
  85. T or F. Baclofen is useful in ETOH, back pain, migraines.
  86. T or F.  Only a small portion of intrathecal baclofen reaches the CSF
    True (effective for spacicity)
  87. What is the MOA of Tizanidine?
    Alpha 2 agonist (like clonidine)
  88. T or F. Tizanidine has major effects of the CV?
    FALSE--> less CV effects than clonidine and REDUCES spasticity
  89. T or F.  Tizanidine acts by increasing post-synaptic inhibition of spinal motor neurons?
    • FALSE--> PRE-synaptic
    • **reduces presynaptic/postsynaptic signaling at SC
  90. T or F. Tizanidine reduces nociceptive transmission.
  91. What patients should Tizanidine be used with caution?
  92. What are 4 major side effects of Tizanidine?
    • 1. Sedation
    • 2. hypotension
    • 3. dry mouth
    • 4. loss of strength/energy
  93. What condition is Dantrolene often used?
    • Malignant hyperthermia
    • (also muscle spasms)
  94. What is the MOA of Dantrolene?
    • -Acts PERIPHERALLY at SR of skeletal muscle
    • -Blocks Ca release at SR reducting contraction
    • -
  95. What patients should Dantrolene not be used in?
    • -Liver
    • -COPD--> may decrease smooth muscle in airway and ribcage
  96. What patients should cyclobenzaprine (flexeril) be used with caution?
    • 1. Hx of urinary retention
    • 2. Angle-closure glaucoma
    • 3. BPH
    • ***Anticholinergic properties