Errors in First Aid for the USMLE (2007): Immunology

As always, this comes from an email sent to the First Aid team.


  1. P.191, Complement
    1. “Membrane attache complex” should be “Membrane attack complex.”
  2. P.191, Complement
    1. “Deficiency of C1 esterase inhibitor leads to angioedema (overactive complement).” The angioedema is due to overactive bradykinin as C1 Inh is responsible for inhibiting this pathway. The parenthetical remark should instead be ” (overactive bradykinin pathway).”
  3. P.194, Diseases caused by hypersensitivity
    1. Several texts list auto antibodies as a finding and alternative cause to IDDM (against islet cells) and Hashimoto’s Thyroiditis (against thyroglobulin, thyroid peroxidase), but these are both classified as strictly Type IV hypersensitivity reactions. This is inconsistent with P.196, where auto antibodies to “antimicrosomal elements” are mentioned.
    2. Rheumatoid arthritis is listed as a Type III hypersensitivity disorder. Most medical texts agree that the likely pathogenesis of RA involves CD4+ cells sensitive against the synovium that begin releasing cytokines. The Rheumatoid factor (anti-IgG IgM) is absent in 20% of patients and is a byproduct of the type IV hypersensitivity, not the cause itself. Because Rf does contribute to the vasculitis and subcutaneous nodules characteristic of the disease, RA should be listed as a Type IV with Type III characteristics. SLE represents another mixed hypersensitivity reaction with characteristics of Type II and Type III. I suggest a separate section for mixed hypersensitivity reactions to avoid confusing this issue.


Return to First Aid Errors page.


11 Responses to Errors in First Aid for the USMLE (2007): Immunology

  1. smalley says:

    hello topher……… regarding all the errors in first uve made out……have ya confirmed that they are indeed errors?
    hope ya prep is goin on well………how many hours are ya puttin in?

  2. There are times where I’ve called something an error only to later find that I am wrong, and both times that has happened, I have noted it (e.g. acetazolamide, captopril). Everything else, I’ve called an error for being incomplete or conflicting with other texts (e.g. Merck Manual).

    When things have been especially ambiguous, I’ve gone through PubMed to find the answer.

  3. kumalo says:

    p 196 Transplant rejection. It says that chronic rejection is antibody-mediated, but I believe this is a T-cell mediated Type IV hypersensitivity reaction.

  4. word says:

    pg 190. il-4 and il-5 entries should say switch TO Ig_, not switch FOR Ig_. Also, can’t find anywhere that says that il-5 stimulates isotype switching to IgA. il-5 is primarily an eosinophil activator for helminthic immune responses, and has little to do with mucosal immunity, which is IgA mediated.

  5. word says:

    Also, just wanna say: Topher, great site.

  6. word says:

    page 195, pathophysiology of SCID lists several possible etiologies, the last of which is “adenosine deaminase” this should say “activation-induced deaminase” (Abbas 2nd edition page 136)

  7. word says:

    p190: it is not il-5, but TGF-beta that stimulates isotype switching to IgA. (Abbas 2nd edition page 156)

    p191: C3 convertase in the classical and lectin-dependent pathways of complement activation is C4b2a, not C4b2b as written in FA. (Abbas 2nd edition page 150)

  8. Nelson says:

    Regarding hereditary angioedema (p191) – it appears that there is uncertainty regarding the ultimate cause of the swelling–some texts say it’s the complement cleavage products with anaphylactic activity, and some (eMedicine) says that bradykinin may be important too.

  9. Shining says:

    In regards to IgA and IL-5, IL-5 is a post switch secretion factor for IgA.

  10. Canadian says:

    p. 188 – diagram of antibody structure has light chains medial to heavy chains – light chains should be drawn laterally.

  11. ZedX says:

    Response to word’s entry :March 10th, 2007 at 6:25 am

    According to Lange Microbiology, C1 cleavage of C2 and C4 produces “to form C4b2b. The latter is an active C3 convertase.” Has anyone else come across this difference?

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