Ten
to twenty minutes into my first day, I saw my first patient. The experience was
relatively short as the older woman declared something to the effect of, “I don’t
like so many people in my room.” I could see her point. The small room was
occupied by myself, Dr. Lane, his fellow, a visiting orthopedic surgeon from
Texas, and her husband. As I walked out almost soon as I walked into the room,
I felt a little disheartened at the prospect of getting kicked out from future
visits but that has yet to be the case.
In
three days of clinic (Monday, Tuesday, and Thursday), I mostly saw patients
with osteoporosis, either pre- or post-fracture. I was forced to quickly google
drug names between observations to keep up with the comments made by Dr. Lane. I’ve
learned that there are 3 key players. Forteo (common name, teriperatide) is a
recombinant form of parathyroid hormone. When given intermittently, the drug
activates osteoblasts more than osteoclasts, resulting in a net gain in BMD and
decrease in fracture healing time. However, chronic Forteo will deplete calcium
in the bone and can dangerously increase its concentration in the blood serum.
Prolia (common name, denosumab), is a RANKL inhibitor which inhibits osteoclast
maturation. This drug is very nice compared to bisphosphonates such as Fosamax,
because it can be cleared from the body within 2 months rather than 60 years.
I
also observed several unique visits that were unrelated to osteoporosis. For
example, there was a gentleman who is the only US adult to have been implanted
with a magnetically expanding prosthesis (Stanmore). These cases are usually
reserved for children who need a prosthesis to accommodate their growth after
bone has been resected. This individual required similar accommodation due to
prior surgeries to attack a synovial sarcoma. His follow-up visits were for
expansion of the prosthesis in 4-6mm increments with a large magnet that
surrounds his leg. He will need to return 10-15 times to achieve the proper
re-alignment of his anatomy. Another gentleman had a very high bone mineral
density but an extremely low trabecular bone score, indicating that his bone
was very poorly distributed. X-rays confirmed that he had an abnormally thick
cortex and almost no trabecular bone. It was clear that he was either not forming
enough bone or removing too much. Some potential diagnoses proposed by Dr. Lane
were cathepsin K deficiency, sclerostin disfunction, and an osteopetrosis
(overly dense bone) variant. These suggest an inability to digest collagen,
problems with the Wnt pathway, or the need for a bone marrow transplant,
respectively.
I was
not able to attend surgeries this week. The Wednesday/Friday schedule presented
me with issues as I was unable to acquire scrubs by Wednesday and the weekly
meeting conflicted with start of surgery Friday. In lieu of surgery, I did
attend several unique meetings which highlight the procedures and outcomes for
clinical research. One such meeting was Arthroplasty, in which fellows
presented their year research projects.
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