Last lecture for 1st term

Today, we had an integrated lecture. One professor from each of our courses was there. We were given a case study and we had to use all the knowledge from all our classes to solve the case. This wasn't for a grade and the lecture was optional. In fact, many people did not show up or left because they wanted to study for final exams instead. I stayed because I was curious to see what case study they were going to give us.

As soon as I saw the picture, it was clear it was ascites. There was a clear swelling in the abdomen, which is the definition of ascites. Now, the question is what caused it. It was an adult, so it couldn't be an embyrological defect. I also couldn't see any superficial veins near his umbilicus, so it couldn't be a porto-cavo anastomosis problem. That left me with only two options - hypoalbunemia or a pleural effusion with a CDH defect. There are probably other causes, but this is all I remember from what they taught us. Pleural effusion would be more of a thorax problem though, not an abdomen, so the most likely cause was hypoalbunemia. This is what I got from just looking at the picture of a patient with a swollen abdomen in 1 min.

Next, we had to go through the algorithm that most docs have memorized. Ask patient history, lab tests for blood, CT, etc. Eventually, they got the lab tests for serum albumin and it was low, confirming my hypoalbunemia. They later showed the picture of his eyes, which had a brown ring around his iris -->Wilson's disease b/c of Kayser-Fleischer rings. In this disease, there is an abundance of copper and it forms rings around the eyes. Though I would never correlate this with ascites in my wildest dreams. So if they didn't show me his eyes, I would've never guessed it. Anyways, mystery was solved and I left the class because there was no more reason to stay. The Anatomy professor discussed about using CT, the Histology professor pointed out the cells in the sclera with copper deposition, the Biochemistry professor talked about hypoalbunemia, and lastly, the ethics professor talked about um - ethics.

I left when the ethics lecture started. The diagnosis was over and I knew the pathophysiology. The only thing that didn't make sense was the fact that Wilson's disease was a genetic disorder, so why are the manifestations only now? The patient was in mid 30s. In real life, ascites would have happened a lot sooner. In Wilson's disease, there is a defect in a gene that codes for a transport protein that transports copper-->hence no copper is transported to the right places-->copper build-up in liver-->liver can't make albumin-->hypoalbunemia-->oncotic pressure goes down-->hydrostatic pressure is still high so-->ascites. They didn't say all of this stuff however. There was still 30 mins in the lecture, so I'm pretty sure they explained later. Though most of the time was just spent talking about the patient history, which really revealed nothing.

Anyways, it was a nice fun lecture, even though I didn't stay for all of it.