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Hypertrophic Actinic Keratosis with perfect "flag sign" (dermatology pathology dermatopathology)
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- Опубліковано 23 січ 2022
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This video is geared towards medical students, pathology or dermatology residents, or practicing pathologists or dermatologists. Of course, this video is for educational purposes only and is not formal medical advice or consultation.
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You’re the best, I’m surviving med school because of you.
So happy to help! Check out #pathTwitter also. Lots of good pathology education plus a really friendly welcoming environment. You might like my Twitter 101 guide: pathinfo.wikia.com/wiki/Social_Media_Guide_for_Pathologists
A lot of useful things I have learned in only one case and just a few minutes that’s awesome
Thank you for that lucid explanation ...
You are the best! Thank you!
I would like to know your opinion.
I had eczematous dermatitis two years ago.
I did a skin biopsy.
Outcome (bx): sloughed superficial epidermis with marked solar elastosis and eczematous change.
p53: not increase
is it Actinc keratosis?
Hi Jerad. I respectively disagree with the diagnosis of HAK. In my view, this is squamous cell carcinoma in situ. Full-thickness intraepidermal squamous dysplasia, with or without maturation, is squamous cell carcinoma in situ. The present case is well-differentiated SCCIS, and would be expected to show maturation, just as you might see in the often associated underlying/contiguous invasive WD SCC. This histology is in contrast to PD SCCIS (aka bowenoid CIS, and sometimes exhibiting the "eyeliner sign"), which does not show maturation, and often shows associated HPV cytopathic changes (koilocytosis, coarse hypergranulosis, binucleation). It seems to me that there is a school of thought in dermatopathology that well-differentiated intraepidermal squamous dysplasia=AK, with moderately/poorly-differentiated intraepidermal squamous dysplasia=SCCIS. This view, I believe, is flawed. If invasive SCC may exhibit varying degrees of differentiation, doesn't it follow that the overlying surface dysplasia, which often precedes the invasive component, would also do the same? I would observe that the degree of differentiation of invasive SCCs often/usually mirrors that of the overlying SCCIS. Indeed, if you were to take one of the cystic lobules of invasive WD SCC, open it up, and spread it flat on an imaginary skin surface, it would be a good example of what WD SCCIS may look like. Anyway, just my 2 cents. I truly appreciate your content, and all of the effort that you take in creating it. Keep up the strong work!
Thanks for your comments. It’s always interesting to see different perspectives and schools of thought in dermpath. For as common as they are, it’s amazing how tricky and controversial keratinocytic lesions can sometimes be. Although I don’t hold to the idea, I have started to understand why Bernie Ackerman claimed that all AK are actually SCC. The line between the two can be quite subjective and arbitrary in some cases.
Thanks dr i am preparing for master degree in derm from egypt i just need to speak alittle slow
👏🏻👏🏻👏🏻👏🏻👏🏻👏🏻
Alternating ortho and para are also seen in pityriasis rubra pilaris where there are called checkered board, how is that different from this??
AK has keratinocyte atypia and disorganization. Also the parakeratosis here is sharply demarcated from Ortho much more than the so called “checkerboard” of PRP. To be honest I don’t really think PRP looks much like a checkerboard. Because it’s not geometric squares. It’s more like musical notes on a scale… Parakeratosis drifting up and down in the midst of background ortho keratosis. The final thing is that clinically actinic keratosis is a solitary lesion and PRP is a rash.
@@JMGardnerMD musical notes on a scale - that's an awesome analogy. Thanks