Here’s a high-yield summary of the Bone, Joint, and Muscle Pathology lectures from last week. It is not exhaustive – but it covers the most important features of the most important disorders.
Exam questions will come directly from the information in this summary – so this should help you structure your studying for the exam. I would strongly urge you to cover the rest of the disorders in these lectures on your own, though, because even though they are not quite as high-yield, they’re still important!
I got an email asking about whether I had any summary videos for our pituitary and thyroid lectures – since we had to move classrooms on November 18, there’s no Mediasite recording for those two lectures.
I haven’t gotten around to making any summary videos on those lectures for our website yet – but I did dig up some short(ish) youtube videos I made for the med students a couple years ago:
Please note that although the content is pretty similar, it’s not exactly the same (in the med school, pathology gets about 3x the hours that we have in the dental school). So if you do end up watching these videos, I’d recommend having our lecture ppts open at the same time so you don’t end up trying to memorize details we didn’t cover.
Here is quiz 3! You can take it any time it is convenient for you. Feel free to use your notes and/or talk about the questions together. I’ll leave it up until Tuesday (December 3) in case you don’t want to do it over Thanksgiving.
Let me know if you run into any problems.
Have a wonderful Thanksgiving, or Friendsgiving, or stay-home-and-watch-Netflix-giving. I am so very grateful for all of you!
Total points: 34
Mean: 32.41 (seriously.)
There were 3 extra credit points – those are included in Canvas in a separate row, just to keep them out of the total # of points for the course.
I’ve entered your scores for quiz 2 – but I haven’t entered quiz 1 yet. Also – we’re still working through your answers to the SUD questions – everyone completed them, but some of you asked some questions for Dustin Chapman – so I’ll forward you those when he’s completed them, and post your scores at that time 🙂
I promised to post the story of imatinib (trade name: Gleevec), the wonderdrug for chronic myeloid leukemia (CML) that we talked about in class last week.
Before the discovery of imatinib, CML was basically a death sentence. Although CML is a chronic leukemia, and therefore has a relatively good prognosis (compared to acute leukemias), it is more aggressive than most other chronic leukemias, with an overall prognosis on the order of a few years. Before imatinib, the best treatment available was bone marrow transplant, and the results were pretty grim.
Enter imatinib. Imatinib is a tyrosine kinase inhibitor – but a really specific tyrosine kinase inhibitor, and it happens to act on the tyrosine kinase made by the hybrid bcr-abl gene in CML (the gene that results from the translocation between chromosomes 9 and 22). This is important, because you can’t just go around inhibiting any and all tyrosine kinases, because we have tons of normal tyrosine kinases in all different types of cells in our body!
So imatinib blocks the tyrosine kinase made by the malignant cells in CML, preventing it from stimulating cell growth. This means that the tumor cells no longer have the capacity to proliferate uncontrollably, and the disease is held in check. The results were so amazing in early clinical trials that the drug was released for use in record time, because it would have been inhumane to withhold the drug for bureaucratic purposes.
Now, imatinib is standard, first-line therapy for CML, and it works incredibly well in most patients. It is being used for other malignancies that have similar tyrosine kinases, with excellent results. And it has sparked interest (and research) around chemotherapeutic agents that act against unique tumor cell features like the mutated tyrosine kinase in CML. This is a whole different way of attacking tumors, and it’s so much more selective and effective than the method used by traditional chemotherapeutic agents, which involves simply killing all dividing cells.