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Autoimmune gastritis (type A chronic) is related to auto-antibodies to parietal cells, but in pathoma it says the pathogenesis is mediated by t-cells (referring to it as Type 4 HSR),
In FA immuno section pernicious anemia is a type 2 HSR

Is first aid just referring to pernicious anemia alone is a type 2, but chronic gastritis is a type 4 HSR that leads to pernicious anemia (type 2)?
 

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Autoimmune gastritis (type A chronic) is related to auto-antibodies to parietal cells, but in pathoma it says the pathogenesis is mediated by t-cells (referring to it as Type 4 HSR),
In FA immuno section pernicious anemia is a type 2 HSR

Is first aid just referring to pernicious anemia alone is a type 2, but chronic gastritis is a type 4 HSR that leads to pernicious anemia (type 2)?
Keep it simple. Its actually a mixed hypersensitivity. For the boards, consider it as Type 2, where antibodies are made against the Parietal cells, and they get destroyed.

Later in the course of the disease, Cell-mediated takes over. This is true for many diseases that start as Type 2, and end up as Type4 (Like Hashimoto, but that is mostly Type4). You look at the INCITING event that leads to hypersensitivity. Who came first? The Antibodies or the T-Cells? And thats the convention. Otherwise, most diseases aren't solely antibody or cell-mediated. There is a mixture.

Bottom line, decide on the intitating event. For Pernicious anemia, the initiating, and the first response is Type 2. Hence, select type 2 for the boards.

Hope that helps!
 

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CH. Gastritis

According to Dr. Sattar, in Chronic gastritis , the damage is mediated by T-cells which is type iv hsr. As a consequence of which you get autoantibodies in the blood which are against parietal cells and intrinsic factor, so its useful for diagnosis.

Also in Robbins it says,

"It was initially thought that the autoantibodies to parietal cell components, most prominently the H+,K+-ATPase, or proton pump, and intrinsic factor were involved in the pathogenesis of autoimmune gastritis. However, this is unlikely because neither secreted intrinsic factor nor the luminally oriented proton pump are accessible to circulating antibodies, and passive transfer of these antibodies does not produce gastritis in experimental animals. It is more likely that CD4+ T cells directed against parietal cell components, including the H+,K+-ATPase, are the principal agents of injury. This is supported by the observation that transfer of H+,K+-ATPase-reactive CD4+ T cells into naive mice results in gastritis and production of H+,K+-ATPase autoantibodies. There is no evidence of an autoimmune reaction to chief cells, suggesting that these are lost through gastric gland destruction during autoimmune attack on parietal cells. If autoimmune destruction is controlled by immunosuppression, the glands can repopulate, demonstrating that gastric stem cells survive and are able to differentiate into parietal and chief cells."

But i think if we are considering Pernicious anemia, we should say its type 2 and ch gastritis is type 4.
 

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agreed with the above. it is a type IV HSR that produces anti-parietal Ab.

also i think you could argue that pernicious anemia =/= autoimmune chronic gastritis by strict definition.

autoimmune gastritis is the T-IV HSR against parietal cells (thus producing anti parietal cell and *Anti-IF* Ab).

pernicious anemia is any anemia caused by B12 deficiency not related to something like ileum resection. so autoimmune gastritis leads to pernicious anemia due to the 1) lack of IF production in damaged parietal cells and 2) the anti-IF Ab made against any IF still made.

at least this is my understnading.

http://emedicine.medscape.com/artic...AnRvMZQgTLPauXVYxAX8MwC0EECwzp432Skuf9qw==#a5

http://emedicine.medscape.com/article/204930-overview
 

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as far as the IV vs II thing, i think this is akin to priamry bilary cirrhosis in which there is an autoimmune desctuction of the intrahepatc bile ducts that *causes* the antimitochondrial Ab to become present.

or by the same token celiacs is a type IV that causes anti-endomysial Ab to form.

its a very common theme to see type IV HSR producing auto-Ab.
 

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PA

Goljan says,

PA is most common cause of Vit B12 def. But has findings not present in other causes of vit B12 def, which are:
- antibodies against Proton pump in parietal cell (85-90%)
- antibodies that block binding of Vit B12 to IF (60-75%)
- antibodies preventing binding of vit B12-IF complexes to Ileal Receptors (30-50%)

Antibodies that attack parietal cells in body/fundus (type 2 HSR) produce a chronic atrophic gastritis that is assoc. with achlorhydria and loss of IF

Looks like in his sentence its the type 2 leading to type 4. also it kind of contradict what Sattar said and also what robbin says that these AB cannot reach the parietal cells.
Still confused what follows what here
 
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