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Neuro 3

The flashcards below were created by user ariadne9 on FreezingBlue Flashcards.

  1. hypotonia
    decreased muscle function, flaccid
  2. hypertonia
    spastic
  3. hyperkinesia
    excessive movement
  4. hypokinesia
    decreased movement
  5. paresis
    weakness
  6. UMN injury
    • -injury btw brain and SC
    • -or injury with the SC itself before the anterior horn synapse
    • -result is spastic paralysis (lack of inhibitory input)
    • -ex: CP
  7. LMN injury
    • -injury below the SC (below L1)
    • -injury btw SC and the muscle or below synapse at anterior horn
    • -primary muscle or peripheral nerve injury
    • -result is flaccid paralysis
  8. Injury to what areas would cause an UMN injury?
    Motor cortex, brain stem, internal capsule, SC
  9. Injury to what areas would cause a LMN injury?
    Anterior horn cell, primary muscle, myoneural junction, bulbar area
  10. Bulbar palsy
    • LMN injury (even though it's in the brainstem)
    • injury to CN 9, 10, and 12
    • s/sx paresis or paralysis of the jaw, face, tongue, and pharynx
  11. Is damage to the extrapyramidal tract considered UMN or LMN?
    LMN
  12. What 2 types of motor function make up extra pyramidal syndromes?
    • 1) basal ganglia (imbalance btw Ach and dopamine)
    • 2) cerebellum (difficulty coordinating voluntary movement and gait)
  13. What effect does excess Ach in the basal ganglia have?
    hypokinesia or akinesia
  14. What effect does excess dopamine in the basal ganglia have?
    hyperkinesia
  15. How does injury to the extra pyramidal tract differ from injury to the pyramidal tract?
    • Extra pyramidal tract injuries cause movement disturbance WITHOUT paralysis
    • Get hypo or hyperkinesia

    Damage to pyramidal tract (corticospinal tract) causes paralysis
  16. S/sx dysautonomia
    • Orthostatic hypotension
    • Labile BP
    • High resting HR
    • Cardiac conduction abnormalities
  17. Why do pts with dysautonomia require direct acting pressors?
    • There is an altered amount of NT in the presynaptic vesicle, an indirect acting drug causes an erratic response.  Ephedrine may cause a large or small release of the NT (NE).  
    • Hence we give Neo (direct acting).
  18. Patho of PD
    • Insufficient quantity of dopamine in the basal ganglia
    • Relative increase in the amount of Ach
  19. PD manifestations
    • akinesia and tremor
    • ANS dysfunction
  20. PD medications
    • levodopa to increase dopaminergic activity
    • anti-cholinergics (cogentin)
  21. PD meds intra-op- d/c or continue?
    continue!!
  22. Anesthesia drugs to avoid with PD
    Droperidol and reglan (dopamine antagonists)
  23. Huntington's chorea
    • Relative increase of dopamine in the basal ganglia
    • Relative decrease of Ach
    • Opposite of PD
  24. Patho of MS
    • demyelination of axons causes abnormal nerve conduction
    • autoimmune disease affecting the CNS
    • 2 x as common in women vs. men
  25. Progression of MS
    inflammation to demyelination to axonal damage
  26. Anesthesia considerations r/t MS
    • ANS dysfunction
    • Steroid use (stress dose steroids)
    • Concern for post-op weakness
    • Avoid temp increase!!!!!
  27. Anesthesia considerations r/t PD
    • Propofol will decrease PD tremors
    • Treat hypotension with direct acting pressor (ANS dysfunction)
    • ANS can cause venous pooling so keep pt volume loaded
  28. Considerations r/t pts with NM disorders
    • degree of weakness
    • degree of atrophy affects the number of extra-junctional receptors
    • may want to avoid succ (excess K release) if there's paralysis or significant weakness
  29. Regional anesthesia considerations r/t MS
    • Avoid spinal (maybe implicated in post-op complications 2/2 LA toxicity)
    • Caution with LA as BBB may be more permeable (myelin serves to protect the nerves)
    • Epidural anesthesia is ok
  30. charot marie tooth
    • similar to MS
    • demyelinating disease
    • hereditary
  31. ALS (amyotrophic lateral sclerosis) patho
    • motor neuron disease affecting both the UMN and LMN
    • involves both the pyramidal tract and the anterior horn of the SC
    • may also involve the bulb of the brain stem
    • most commonly affects men 40-60 yo
  32. ALS s/sx
    progressive skeletal muscle weakness, atrophy, and paralysis
  33. Anesthesia considerations r/t ALS
    • -degree of respiratory involvement
    • -aspiration risk- bulb involvement may cause dysphagia
    • -risk for hyperkalemia from such due to muscle wasting
    • -sensitivity to NDMR
  34. Regional anesthesia with ALS
    Generally avoided due to fear of disease exacerbation and medical legal risks
  35. Friedrichs ataxia patho
    • similar to ALS as it also affects both UMN and LMN
    • degeneration of spinocerebellar and pyramidal tracts
  36. Friedrichs ataxia s/sx
    • CMP in 10-50% of pts
    • Kyphoscoliosis in 80% of pts (causes a rx lung disease)
  37. syringomyella
    • slowly progressing SC degeneration
    • found in newborns
    • abn of embryological development
  38. syringobulbia
    • found in newborns
    • degeneration of the bulb in the brain stem
    • dysphagia
  39. major issue with syringomyella and syringobulbia
    • -CSF outflow obstruction from the 4th ventricle
    • -due to obstruction thru foramen of magendie and lushka into the cisterna magna
  40. GB patho
    • cause unknown
    • preceded by a virus in 70% of pts
    • LMN involvement
  41. GB s/sx
    • flaccid paralysis
    • can vary from leg paresis to total motor paralysis
    • bulbar involvement and pharyngeal muscle weakness
    • ANS dysfunction
    • may resolve or may have permanent damage
  42. Recommendations re: NMB with pts with severe NM disease
    • avoid succ!!
    • avoid NMB if possible
    • use smallest possible dose of NDMR and use peripheral nerve stimulator
  43. What drugs must be avoided with porphyria
    • barbs
    • etomidate
    • enflurane
    • methoxyflurane
  44. MG patho
    • disease of muscle, not nerves
    • chronic autoimmune disease caused by destruction of Ach receptors
    • pt develops antibodies to their own Ach 
    • origin of antibodies unknown but the thymus plays a role
    • bulbar muscles often involved
  45. If a pt is scheduled for removal of the thymus gland what disease would you be suspicious for?
    MG
  46. MG treatment
    • anti-acetylcholinesterase drugs to increase Ach levels
    • PO pyridostigmine (increases amt of Ach at NMJ)
    • pt has decreased number of Ach receptors so thus need more Ach at the site
    • immunosuppressants to decrease antibodies
  47. NMB considerations for MG
    • More sensitive to NDMR (still need neostigmine for reversal)
    • Resistant to succ (takes more to paralyze them) and long DOA
    • Avoid NMB
    • If must use NMB give 2/3 dose of NDMR and use a nerve stimulator
  48. Why is the DOA of succ increased with MG?
    Pts take anti-cholinesterase drugs which also decrease the amount of pseudocholinesterase
  49. myasthenic syndrome
    • resembles MG
    • treatment with anti-acetylcholinesterase drugs NOT effective
    • often associated with SC lung ca
  50. MD patho
    • not a nerve issue but a muscle issue
    • hereditary
    • painless degeneration and atrophy of skeletal muscle
    • ? mutation of dystrophin gene on X chromosome
    • this results in the muscle being more permeable to Ca++
    • this leads to muscle cell breakdown (resembles MH)
  51. Anesthesia considerations for MD
    Avoid triggers like succ and volatiles!!
  52. myotonia
    • contracture of skeletal muscle after muscle stimulation ceases
    • hallmark sign is inability to release handgrip
    • due to abnormal Ca++ metabolism
    • result is degeneration of skeletal muscle
  53. Steinert's disease
    • type of myotonic dystrophy
    • these pts are susceptible to MH
  54. What can precipitate muscle contraction with Steinert's disease?
    • Succ
    • anti-acetylcholinesterase drugs
    • cold T and shivering
    • cautery
    • surgical manipulation
Author
ariadne9
ID
241926
Card Set
Neuro 3
Description
Neuro lecture trois
Updated
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