Is this a UW error?

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agranulocytosis

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I had this question on Crohn's disease and the question stem asked what overexpression NF-kB is associated with. Well I got it wrong because I didn't know what NF-kB does. Anyway, after reading through the explanation I came to the understanding that NF-kB stimulates cytokine production, leading to the exaggerated immune response typical of Crohn's which is treated by corticosteroids.

But, then I go on to read the final summary and UW states that Crohn's is associated with a DECREASED NF-kB protein activity, allowing prolonged chronic infection without resolution of symptoms. I think that's a mistake in the summary. Anyone care to shed some light on this or has my mind gone completely nuts?

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I had this question on Crohn's disease and the question stem asked what overexpression NF-kB is associated with. Well I got it wrong because I didn't know what NF-kB does. Anyway, after reading through the explanation I came to the understanding that NF-kB stimulates cytokine production, leading to the exaggerated immune response typical of Crohn's which is treated by corticosteroids.

But, then I go on to read the final summary and UW states that Crohn's is associated with a DECREASED NF-kB protein activity, allowing prolonged chronic infection without resolution of symptoms. I think that's a mistake in the summary. Anyone care to shed some light on this or has my mind gone completely nuts?

IMHO They often have mistakes in the summaries which say the opposite of what the explanation says
 
I had this question on Crohn's disease and the question stem asked what overexpression NF-kB is associated with. Well I got it wrong because I didn't know what NF-kB does. Anyway, after reading through the explanation I came to the understanding that NF-kB stimulates cytokine production, leading to the exaggerated immune response typical of Crohn's which is treated by corticosteroids.

But, then I go on to read the final summary and UW states that Crohn's is associated with a DECREASED NF-kB protein activity, allowing prolonged chronic infection without resolution of symptoms. I think that's a mistake in the summary. Anyone care to shed some light on this or has my mind gone completely nuts?

This one seems a bit strange. As I understand it, the theory is that since NF-kB stimulates cytokine production it should mobilize the immune system to fight non-welcomed bacteria. Therefore, an underproduction of NF-kB allows chronic infections to hang around and exacerbate or perhaps directly cause some Crohn's symptoms. But it still seems a bit confusing, since you would think the inflammatory response should be doing the damage, not the infection. I've marked that as something that (1) probably won't be on USMLE and (2) something to look up in a more complete reference just in case. Let me know if you find something. ;)
 
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This one seems a bit strange. As I understand it, the theory is that since NF-kB stimulates cytokine production it should mobilize the immune system to fight non-welcomed bacteria. Therefore, an underproduction of NF-kB allows chronic infections to hang around and exacerbate or perhaps directly cause some Crohn's symptoms. But it still seems a bit confusing, since you would think the inflammatory response should be doing the damage, not the infection. I've marked that as something that (1) probably won't be on USMLE and (2) something to look up in a more complete reference just in case. Let me know if you find something. ;)

Ha, I hope it does now that I know what NF-kB is involved in! I also thought that Crohn's was not involved with bacteria or any causative agent per se, but more of a hyper-inflammatory reaction secondary to genetics.
 
UW does have some minor errors, but in this case, both the explanation and the educational objective say that the activity of NF-kB are reduced in Crohn's.
 
I also thought that Crohn's was not involved with bacteria or any causative agent per se, but more of a hyper-inflammatory reaction secondary to genetics.
I as well. We were taught extensively about the immunology of Crohn's, and it came up in our practical pathology labs about a thousand times, and I never remember anything about infections playing anything other than a very minor ancillary role. Perhaps the UWorld explanation just didn't make that clear? I've noticed that UWorld occasionally asks something about ten notches down the totem pole of importance for certain diseases, drugs, etc.
 
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