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  1. what are clues that suggest neuropathy
    • distal (tripping over toes) and proximal (more neurons) motor neuropathy
    • sensory: pain, tingling
    • acute (tingling for a little) vs. chronic
  2. lancinating
    feel like stabbing, piercing
  3. paresthesias
  4. dysesthesias
    painful tingling
  5. hypoesthesia
    diminished sensation
  6. what are physical clues that suggest neuropathy?
    • motor strength
    • sensation: (vibration/proprioception), pain
    • trophic: imbalance of neuronal innervations in muscle of joints
  7. pes cavus
    high arch
  8. kyphoscoliosis
    backward/lateral spine curvature
  9. neurogenic arthropathy
    joint disease related to nerves
  10. what do large myelinated axons vs. small myelinated axons affect?
    • large (vibration/proprioception-spatial orientation)
    • small (pain and temp)
  11. types of neuropathy
    • neuronopathy
    • axonopathy
    • myelinopathy
  12. neuronopathy
    cell body damage of the motor neuron (movement destroyed) or dorsal root ganglion (sensation destroyed)
  13. axonopathy
    • traumatic, toxic, metabolic
    • length dependent, symmetric, distal
  14. myelinopathy
    • hereditary or inflammatory
    • non-length dependent (patchy is inflammatory, diffuse is hereditary)
  15. compound muscle action potential (CAMP)
    neuron to motor muscle (proximal to distal)
  16. sensory nerve action potential (SNAP)
    distal nuron to proximal)
  17. when stimulation is further from the muscle what is the latency?
  18. what is latency
    how rapidly nerve conducting impulse
  19. what happens to EMG in axon degeneration?
    amplitude is down, NCV is stable
  20. demyelination EMG
    • action potential is variable (signal may or may not get through)
    • when further away from the muscle stimulated, amplitude decrease and increase in latency)
    • NCV decrease
  21. orthodromic stimulus
    goes down from arm to palm
  22. antidromic stimulus
    goes to motor neuron (up), fire and depolarize and send another signal down (f-wave)
  23. possible causes of demyelination?
    • some antigen initiates immune response
    • resulting antigen receptors cross react with self-protein that mimics the antigen
    • self-protein may be inhibited or the containing cells destroyed
  24. auto antigen
    self protein that binds with bad antigen receptors
  25. what are molecular mimicry examples?
    • MS, GBS, CIDP
    • MBP, PLP
    • nodal/paranodal proteins
  26. nerve biopsy
    sural nerve
  27. how many % patients have the classic triad of CIDP
    • slow nerve condition velocity
    • increase CSF protein
    • demyelination on nerve biopsy
  28. what is the only way to see pathology of the disease?
  29. point of EMG
    whether it is truly a peripheral neuropathy and whether the neuropathy is demyelinating
  30. what happens as disease prolongs?
    patents develop secondary axonal degeneration
  31. demyelinating neuropathy
    • multifocal conduction block or temporal dispersion of CMAP/SNAP
    • conduction slowing
    • absent ro prolonged F-wave latency
  32. neuropathy in EMG
    • conduction block
    • decrease conduction velocity
    • increased distal latency
    • increase F-wave latency
  33. clinical criteria for neuropathy
    two or more months, hypo/areflexia, motor/sensory involvement, more than 1 limb
  34. per os
    by mouth
  35. azathioprine
    • cytotoxic chemo drug used as immunosuppressant
    • antimetabolite drug that interferes with the purine pathway and therefore with DNA synthesis in cell division; it causes inhibition of proliferating lymphocytes and is often used as steroid-sparing agent.
    • decrease in RBC (anemic) and WBC (susceptible to infection)
    • fibrinogens disappeared
  36. IVIg (intravenous immunoglobulin)
    • IVIg is a preparation of human polyclonal IgG obtained from plasma of several thousands of healthy donors
    • anti-inflammatory activity when used in high dose and immunomodulation
    • highly expensive
    • gamma (second therapy)
  37. Cyclophosphamide
    alkylating agent that can be given orally or by intravenous injection to deplete T and B lymphocytes
  38. pure motor CIDP treatment
    IVIg, since deterioration has been reported with steroids, as in MMN
  39. hickman line
    • catheter entered target vein but was first tunneled under the skin for a few inches
    • reduced infection risk
  40. Interferon beta 1a
    • released by host cells in response to the presence of several pathogens
    • a virus-infected cell will release interferons causing nearby cells to heighten their anti-viral defenses.
    • type of cytokine
    • Interferon beta balances the expression of pro- and anti-inflammatory agents in the brain, and reduces the number of inflammatory cells that cross the blood brain barrier
    • first study sarah was in
    • flulike side effects
  41. barbara
    • patient with cancer during sarah's plasma replaced in oncology unit
    • sarah worked at a book store
  42. EMG/NCS criteria
    • conduction block
    • decreased conduction velocity
    • increase distal latency
    • increased F wave latency
    • 3/4
  43. most common preceding infection in GBS
  44. paraproteinemia
    excessive amounts of monoclonal gamma globulin, IgM produced by b cells, it is the first to appear in response to an antigen
  45. what changes in CNS occur with patients with CIDP?
    changes in white matter
  46. treatment for CIDP
    • block immune process
    • immunosuppressants
    • interferons (activate against bad antigens)
    • decoy molecules to sop up antibody 
    • t-cell vaccination
  47. IVIg
    • random set of antibodies to neutralize immune factors causing damage
    • activates complement cascade and provides antibodies capable of neutralizing many microorganisms, toxins
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2015-10-22 19:51:45

Exam 2
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