Exam 4 scores are up! And thank you.


Exam 4 scores are up and on Moodle – you guys did AMAZING – I’m so proud of you!! The mean was 52 (out of 63), or 84%. EVERYONE PASSED, and by a very generous margin.

With the changes in our schedule in the last two weeks – including one lecture that you guys had to watch online – this is great news. It shows how dedicated you are to working hard and doing your best, even in something that doesn’t directly impact your future practice as much as your other courses do. You are also a very kind, empathetic, and all-around stand-up group of people. I loved coming to class and seeing so many smiling faces. So many of you asked how I was doing and showed such genuine concern that it makes me tear up. You have lots of way more pressing stuff to deal with – but you took the time to smile, or say something positive, or send an email. I’m proud we get to send people like you out into the world to do good; it makes me happy to think of how much your patients will love you.

Thanks for a great semester! I’ll see you a few more times in oral pathology, so it’s not goodbye 🙂

Developmental Path summary

Hand 1

Here’s a summary of the developmental path lecture from Tuesday. Questions will only come from this summary – if it’s not in the summary, it’s not testable.

I thought I’d post a couple photos of my uncle’s hand. He has Marfan syndrome and was kind enough to do a little hand modeling for us. In the photo above, you can see how long and thin his fingers are (the official term is arachnodactyly).

He also shows two classic signs of Marfan syndrome. One is the overlap of thumb and finger as he encircles his wrist:

Hand 2

The other is the way his thumb sticks out when he makes a fist (that’s my hand on the left for comparison):

Hand 3

For a long time, it was thought that Lincoln suffered from Marfan syndrome. He was well over 6 feet tall, which was highly unusual for a male in the mid 19th century. He also had long limbs, an abnormally shaped chest, and loose (lax) joints.


However, a 2007 study alleges that Lincoln actually suffered from MEN IIB. Patients with MEN IIB often have a Marfanoid habitus (meaning they look like they have Marfan syndrome – but they don’t). If it is true that Lincoln had MEN II, maybe the early deaths of his mother and three of his sons were not random bad luck (maybe the deaths were due to cancer). And maybe he was not as physically vibrant and healthy as we assume; he may have been suffering from advanced cancer at the time he was shot.

Pemphigus vulgaris vs. bullous pemphigoid


Here are two disease names that are maddeningly similar: pemphigus vulgaris and bullous pemphigoid. Both diseases have bullae (big blisters), and both are mediated by antibodies – but they are different diseases that you have to learn separately. Here’s a post I wrote on the main differences between these two disorders. There is actually some logic behind the naming of each disease, and once you learn that little trick, the rest of the disease features fall into place.

Questions on brain tumors and thyroid stuff

Q. In the nervous system lecture, under the “tumors of the brain” section, I am confused on if they are benign or malignant. Gliomas are malignant? While the rest are benign?

A. We don’t really use the terms benign and malignant a lot when talking about brain tumors. For one thing, brain tumors don’t metastasize (which as you know is one measure of malignancy). For another thing, they ALL can cause serious problems (even death) if they’re in the wrong spot – even if they are small. In general, though, we consider most brain tumors, with the exception of meningioma, to be malignant. Meningiomas have a good prognosis – they grow in a non-injurious way (they sort of push the normal tissue to the side rather than invading), and they are generally in places where they can be resected easily – so they are generally called benign.

Q. For Graves disease, I do not understand how ANTI-TSH receptor antibodies stimulate thyroid growth.

A. Yeah it’s weird. There are anti-TSH-receptor antibodies in both Hashimoto and Graves disease, and they work in opposite ways: in Hashimoto disease, they block the receptor, and in Graves disease, they stimulate the receptor. I don’t know the molecular mechanisms of how that works (and that’s probably not what you’re asking anyway) – but for some reason, the antibodies have opposite effects. They must bind to different epitopes on the receptor or something. For some reason, the antibodies in Graves must act enough like TSH that the receptor thinks its being stimulated – and the antibodies in Hashimoto probably just block the receptor so TSH can’t bind.

Q. For the non-neoplastic diseases, are only some associated with hyper or hypothyroidism? As in they all are some abnormality of the thyroid, and one of the symptoms of the abnormal thyroid can be hypothyroidism (Riedel Thyroiditis, Hashimoto) or hyperthyroidism (Grave’s)?

A. Some non-neoplastic diseases present with hypothyroidism, some present with hyperthyroidism, and some present with neither (they just show up as an enlarged thyroid). To make matters worse, some diseases can present with hyperthyroidism and then progress to hypothyroidism (DeQuervain thyroiditis, for example, can have hyperthyroidism early on, as the follicles are busted open and the colloid leaks out – and then hypothyroidism later as the disease heals). Goiters are usually hypothyroid – but they can also be hyper or euthyroid.

I think the ones you really need to remember hypo/hyper for are Hashimoto disease (most common cause of hypothyroidism in the US) and Graves disease (most common cause of hyperthyroidism in the US). The others are not so clear-cut, and it’s probably not worth trying to memorize what the thyroid hormone levels are at presentation and as the disease progresses. I doubt anyone will ask you about that.

No class Monday, 12/5

We had a change in our schedule for next week. Dr. Dolan’s lecture on Developmental Pathology will now be on Tuesday, December 6. I would normally just do my Skin Pathology lecture on Monday – but I need to be out of town that day. So we’re going to do the skin lecture as an independent study. You can watch last year’s lecture here (put it on 2x…I talk really slow!), and here are the lecture notes: part 1, non-neoplastic skin diseases (ppt, color pdf, and grayscale pdf) and part 2, neoplastic skin diseases (ppt, pdf color, and pdf grayscale). I apologize – this isn’t a great way to do it, but it’s the best solution we could come up with. I hope to be in class on Tuesday for Dr. Dolan’s lecture – so please catch me then (or email me at any time) if you have questions.