Usual Interstitial Pathologist

  I gave a talk on AI/ LLM (aka ChatGPT and its cousins) in medical education at the UMEDS section of the Association of Pathology Chairs meeting July 17, 2023.  https://www.apcprods.org/apc2023 Some highlights. With respect to LLM, any literature from before 2022 is irrelevant. Forget the IBM Watson debacle. Generative LLM should be thought of in a different context than the various black box algorithms that predict patient outcome or classify images. I find those problematic as they distract from understanding the underlying biology. But LLM is different technology for different uses. With respect to education, there are two major categories of use cases. One is that the instructor can use LLM to generate an indefinitely large number of clinical scenarios and various questions for formative and summative learning exercises / tests. The system can generate harder or easier questions as needed. The material can be based on pasted in reference works or based on the LLM’s existi...

 Thoughts on pathology hypersensitivity pneumonitis from the newish ATS, ACCP consensus statement, and a review article by Andrew Churg  https://pubmed.ncbi.nlm.nih.gov/34531525 https://pubmed.ncbi.nlm.nih.gov/35738345 https://pubmed.ncbi.nlm.nih.gov/32706311 These criteria are designed primarily to provide a uniform language for clinical trials.   Nonetheless, they provide a platform to air general problems with current approaches. Both ATS and ACCP emphasize that HP should be thought of as non-fibrotic vs fibrotic rather than acute, subacute or chronic. This seems like a good thing but is basically relabeling how I (and presumably others) always thought of them with a more logical label. A precedent would be acute (cellular only) vs chronic/fibrotic interstitial nephritis. No attempt though is made to define how much fibrosis is needed to be labeled fibrotic e.g. is one reticulation on HRCT enough?  Lack of quantitation for all criteria is a problem throughout...

  I had to do it. My Yale ancestors created UIP/DIP and the like (although they got those largely wrong, see my previous blog posts). So it is now my turn. While Tom Colby long ago relegated the wedge biopsy from gold to a silver standard, such biopsies are still considered potentially helpful. But how do we assess even a silver standard?  A few years ago, I felt frustrated that the biopsies I was looking at seemed difficult to classify and wanted additional input. I recruited an international group of pathologists with interest/expertise in ILD to review a series of cases using both fixed and whole slide images to see if we could improve our criteria. We have recently published this work (no paywall). https://bmcpulmmed.biomedcentral.com/articles/10.1186/s12890-021-01522-6 For the truly curious, all the images used in this study are available online.   http://pathmodule.org/PathCamp/virtualslideshare/ The approach we took paralleled that taken by Carol Farver (a mem...

In my previous post, I suggested a central dogma for students of pathology. After injury, a physiologic response maintains homeostasis without loss of function while a pathologic response leads to reduced function, even if a new homeostatic set point is reached.  With that in mind, let us turn to the first figure in the textbook that most of us consider the “standard of care” for pre-clinical instruction, Robbin’s textbook of pathology. The first figure is an opportunity for pathology to state the central dogma of the field.  Unfortunately, this figure is terrible.  The figure lists various names such as cell injury and death, homeostasis and adaption, reversible and irreversible injury. The relationship of these to each other seems arbitrary, ignoring definitions or time course. At most, one learns that some how a cell at rest maintains homeostasis, but that the cell can be injured, that sometimes this injury is mild and can be repaired, sometimes there is something call...

 Pathology has been a central pillar of allopathic medicine since the dawn of scientific medicine. However, with respect to medical education, pathology no longer is a stand alone course.  Pathologists must therefore make the underlying message of pathology as clear as possible or get lost in the firehose of information that medical students are subject to from their first day of classes. The central dogma of molecular biology as enunciated by Crick in 1958 is that information required to run an organism flows from DNA to RNA to protein. It represents the entire field as a flow of information, rather than as a series of molecular interactions. For the student, this is a very attractive proposition, rather than considering molecular biology as a series of endless organic chemistry reactions.  Pathology needs something similar or will forever be viewed at random (uninterpretable) histologic images. I was taught that “all disease occurs as a response to injury”. Unfortunatel...

In a previous blog post, I noted that the term “usual interstitial pneumonia”, coined by Leibow and Carrington and long considered the “sine qua non” of idiopathic pulmonary fibrosis (IPF), was originally used by them to describe what we would now call organizing phase diffuse alveolar damage (DAD), essentially the direct opposite to today’s approach. I left open the question of where the modern definition arose.   While multiple older articles describe small series on histology of IPF, the histologic language of those papers is hard to interpret in the modern era.  The earliest reference I can find to a relatively modern description is Crystal’s 1976 series of 29 patients seen at NIH (1) .  Fortunately, this paper includes color illustrations allowing us to actually see the disease under consideration. By any criteria, these images are instantly recognizable as classic idiopathic pulmonary fibrosis / usual interstitial pneumonia.  The most important concep...