Fun in Malaysia

Hello all. It has been long time since I last blogged. I passed my finals Yayyyyyy. I did my elective and it was the best 2 months in my life.  And now I am a final year medical student. It is scary a little, but so far so good. I'm liking the attention we get : Where are my medical students? Ehh didn't know such line existed.

I am doing hematology ( blood related diseases) at the moment. It amuses me how much I thought I already know about sickle cell disease, SCD, which is one of the commonest hematological disorders,  and how much I daily learn. When to start hydroxyurea, exchange transfusion and why, what is the complication of different chelating agents, what is the average life of sickled cell ( 20 days compared to 120 days in normal red blood cell), MoyaMoya ,…. How to manage an ischemic stroke in a SCD? Definitely not by antiplatelet/anticoagulation/beta blocker alone. That is a misconception. ! And according to our  consultant it is a common one! The treatment is by exchange transfusion, in which you take blood from a patient and replace it with a normal healthy blood. The idea is to decrease Hb S level, the source of the problem. Many patient retain their neurological function afterwards. (if recognized and treated early). The following paragraph explain the mechanism, so feel free to skip it.

SCD starts at the DNA level while making the building blocks of the hemoglobin (Hb: the oxygen transport in red blood cells (RBC)). A new protein formed by faulty coding: mutation. This makes The Hb less stable. Any hypoxia ( reduce oxygen pressure due to high altitude, dehydration …) will cause the Hb to precipitate, pulling the membrane along and causing leaking of potassium & water out of the RBC and calcium influx. This will result in red blood cell dehydration and the RBC loose it's biconcave disc form to a sickled one. If the hypoxia corrected in reasonable time the RBC may retain to normal shape, and it is only called pseudosickled. If not it'll take a more lunar shape and become sickled for good: sickled cell. Such cell has sharp surface and it affects it surroundings ( blood vessel, activate platelet..) and it clumps with each other occluding small blood vessels causing the famous pain. The smallest vessels are the easiest to clog, hence bone is the most common site of such crisis. The vasooccluasive crisis can happen anywhere in the body, including the brain and that is why the SCD patient has high prevalence of strokes – and at younger age-compare to the general population. Other common sites are the spleen ( which they usually lose by adulthood due to frequent infarcts, a phenomena known as autosplenectomy) and the lung, where it cause the life threatening acute chest syndrome.

Back to life as a senior medical student. Will we are expected to work like interns except we got some teaching and don't have to write stupid discharges and referrals. But we need to clerk , assess, format a plan and write it up in the hospital system. And we have a tiny tyny book that we need to fill with procedures and reflections and such.. and that reminds me I need to write my case  now and read about Hodgkin lymphoma!

See you soon.