mdeast

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There's probably an answer for this somewhere on here, but thought I would post anyway. Re-reading Pathoma and came across pernicious anemia. Dr. S states that it's actually T-cell mediated (i.e. Type IV hypersensitivity reaction), while First Aid has it listed as a Type II hypersensitivity reaction. Dr. S mentions that the antibodies are just a consequence of destruction (aka Hashimoto's). This sort of makes more sense to me, given that IF is usually intracellular anyway...so this seems like an unlikely target that would actually end up contributing to parietal cell destruction.

So...is First Aid wrong?
 
Apr 11, 2012
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There's probably an answer for this somewhere on here, but thought I would post anyway. Re-reading Pathoma and came across pernicious anemia. Dr. S states that it's actually T-cell mediated (i.e. Type IV hypersensitivity reaction), while First Aid has it listed as a Type II hypersensitivity reaction. Dr. S mentions that the antibodies are just a consequence of destruction (aka Hashimoto's). This sort of makes more sense to me, given that IF is usually intracellular anyway...so this seems like an unlikely target that would actually end up contributing to parietal cell destruction.

So...is First Aid wrong?
if I find where exactly in Goljan pathology I saw it I'll write it down, but I remember that pathogenesis of pernicious anemia includes both II and IV types of HR


Edit: I guess it was in Goljan audio lectures because I can't find it in his RR book.
But I found in Immunology RR: Mechanism: II type - a/b to intrinsic factor, IV type - reaction against gastric parietal cells
 
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Morsetlis

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Big Robbins says:

It is believed that an autoreactive T-cell response initiates gastric mucosal injury, triggering the formation of autoantibodies, which may exacerbate epithelial injury. CD4+ T cells are involved. There are three types of antibodies recognized: Type I ab that blocks binding of B12 to IF, Type II ab prevents binding of the IF-B12 complex to ileal receptor, and Type III ab recognize the alpha and beta subunits of the gastric proton pump (these most likely result from gastric injury, rather than cause it). 75% of patients have Type I and 85% of patients have Type III abs.

Buuuut in the Table of Type II HSR it lists Pernicious Anemia as Type II.
 
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mdeast

mdeast

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Big Robbins says:

It is believed that an autoreactive T-cell response initiates gastric mucosal injury, triggering the formation of autoantibodies, which may exacerbate epithelial injury. CD4+ T cells are involved. There are three types of antibodies recognized: Type I ab that blocks binding of B12 to IF, Type II ab prevents binding of the IF-B12 complex to ileal receptor, and Type III ab recognize the alpha and beta subunits of the gastric proton pump (these most likely result from gastric injury, rather than cause it). 75% of patients have Type I and 85% of patients have Type III abs.

Buuuut in the Table of Type II HSR it lists Pernicious Anemia as Type II.
Hmmm....yeah. I still don't get how this is Type II then in any form. The Type I/II abs shouldn't cause damage to the parietal cells. They'll just knock out the function of IF. Type III ab I could see causing cell damage (but it says it doesn't cause this?). This just seems like a Type IV only to me (like Hashimoto's...where there are antibodies, but they don't actually cause tissue damage).

In other words....does Type II include a definition of damage to circulating protein complexes? In other words, I just don't see how these antibodies are penetrating parietal cells to cause cellular destruction. Their main effect seems to be extracellular without a real effects on the actual parietal cell.
 
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According to Dr. Goljan, antibodies in Type II hypersenstivitiy can cause recruitment of inflammatory cells like neutrophils which can release damaging substances. He discusses all the varieties of Type II rxns in his immunopath chapter.
 
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May 9, 2014
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Did you guys find anything conclusive?

UWorld also says type 4, but everything else I'm seeing says type 2
 

StraightOuttaBrooklyn

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Cell Mediated Immunity destroys the parietal cells; consequently, you develop anti-IF antibodies. The anti-IF antibodies are a byproduct of the pathogenesis - they are not pathogenic themselves.
 
May 9, 2014
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Cell Mediated Immunity destroys the parietal cells; consequently, you develop anti-IF antibodies. The anti-IF antibodies are a byproduct of the pathogenesis - they are not pathogenic themselves.
Yeah that's how Pathoma explained it, but we learned it differently in class (what we learned lines up with FA), so I figured I'd ask. Thanks