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  1. trophic changes
    • due to interruption of nerve supply
    • pes cavus
    • kyphoscoliosis
    • loss of hair
    • charcot joints (neurogenic arthropathy)
  2. sensation that suggests neuropathy
    • vibration/proprioception (large myelinated axon)
    • temp/pain (small myelinated axon)
  3. chronic
    over one month
  4. why is it a polyneuropathy?
    • motor and sensory
    • symmetrical (or more than one limb)
    • non-length dependent
  5. what percentage of patients had class triad?
    30% in patients who all had proximal and distal weakness and in whom 95% had improvement with treatment
  6. classic triad
    • slow nerve conduction velocity
    • elevated CSF protein
    • demyelination on nerve biopsy
  7. american academy of neurology criteria says must have three of four
    • conduction block
    • decreased conduction velocity
    • increased distal latency
    • increased F-wave latency
  8. what characteristics in CSF support CIDP
    • WBC<10
    • VDRL neg
    • elevated protein
    • criteria by aanc is not sensitive and may miss more than 50% of the patients
  9. protein level is increased in how many patients?
  10. demyelinating neuropathy
    • multifocal conduction block or temporal dispersion of CMAP
    • prolonged distal latencies
    • variable conduction slowing to less than 70% normal
    • absent or prolonged F wave latencies
  11. histological findings
    • interstitial and perivascular infiltration of endoneurium with T cells and macrophages
    • segmental demyelation and remyelation (onion bulb)
    • neutrophil infiltration
    • axonal damage/loss of myelinated nerve fibers
  12. histology on picture of CIDP
    • decreased density of nerve fibers
    • demyelinated fibers
    • fibers undergoing active macrophage mediated demyelination
  13. what is the prevalence of the disease?
    1-7.7 per 100,000
  14. pathophysiology (the disordered physiological process associated with the disease)
    • gradual onset (difficult to document)
    • respiratory and gastrointestinal infections have been cited, no causative organism identified
    • GBS (Campylobacter) most common preceding infection
  15. IgM
    produced by B cells is the first antibody to appear in response to antigen
  16. phenotype of CIDP
    • proximal and distal weakness
    • large fiber sensory loss and areflexia
  17. MS
    CNS white matter changes in patients with CIDP
  18. CIDP associated conditions
    • diabetes mellitus predispose patients to CIDP
    • pregnancy (3rd trimester or postpartum)
  19. goal and course of treatment
    • goal: block immune process
    • course: continue until maximal improvement then maintain
  20. treatments
    • immunosuppressants
    • interfereons 
    • decoy molecules
    • t cell vaccination (destroy population of autoimmune T cells)
  21. how many percentage of patients have sustained remission after initial treatment
  22. early treatment why?
    prevent axonal and motor neuron loss
  23. what is the first line therapy
  24. agents used for refractory patients?
    • cyclosporin 
    • cyclophosphamide
    • azathioprine
    • mycophenolate
  25. anti-epileptics
  26. tricyclic antidepressants
  27. common treatment regime for plasma exchanges
    3 per week for first 2 weeks
  28. IVIg
    composed of heterogeneous human IgG and smaller amounts of IgA and IgM
  29. mechanism of IVIg
    • random set of antibodies to neutralize immune factors causing damage to peripheral nerve
    • activate complement cascades and antibodies against toxins, etc
    • provide immediate passive immunity
    • seen at day 10 continues to day 42
  30. serum half life
    • 21-29 days
    • patients require repeated treatments to maintain remission or treat recurrences
Card Set:
2015-11-05 01:39:13

exam 2
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