Sunday, August 11, 2013

Context is everything - in the economy and in medicine

During the past week, there was the usual bickering of politicians about interest rates policies, with the RBA dropping the overnight cash rate target from 2.75% to 2.5%. As expected, Labor seized the opportunity to announce that the interest rates are lower, which makes it better for working families with home loans; directly contradicting the former coalition government's advertising campaign that interest rates "will always be lower under the coalition". To counter this, the coalition opposition mentions that "context is everything", and the only reason why the interest rates are low is because the "economy is struggling", which is a bad thing.

Now, both these arguments have some element of truth behind them. That said, if the government was to support the economy further, perhaps the only way to do this would be to increase the budget deficit even further, which is not desirable. Now, even for budget debt and deficit is context very important. The coalition talk of debt and deficit as if it is the "be all and end all". However, while it is very true that debt should not be ever increasing, and there should not be continual deficits, it is also true that temporary deficits are justified to support the economy in bad times; to be made up with surpluses when the economy is strong. As such, the government was quite justified in spending in the stimulus package at the peak of the financial crisis in order to support jobs and growth, even though this resulted in a larger deficit for the budget.


One thing I have realized though is that "context is everything" also applies to medicine. I recall an interaction with my CSC (clinical skills coach) tutor, who was quizzing the group about the effects and side effects of certain medications. The interaction was as follows:

CSC: What does aspirin do?

(At this stage, my pharmacology major instincts kicked in)

Me: Aspirin is a non-selective, irreversible cyclooxygenase inhibitor. It inhibits both COX-1 and COX-2, by irreversible acetylation of the active site. This reduces the amount of prostaglandin production. In this case, for this patient, the wanted effect is a decrease in TXA2 to decrease platelet activation, and we want an irreversible inhibitor because platelets don't synthesize new COX and other tissues can...

CSC: What you said was all true, but if you can summarize this in three words, what would you say?

Me: Stops blood clotting?

CSC: Close. "Thins the blood"

Now I was actually quite surprised that we were allowed to use this terminology, because aspirin doesn't actually decrease the viscosity of blood; it just stops the platelets from aggregating. But it seems like it was OK in this circumstance.


Another interaction was with a cardiologist in cardiology outpatients.

Cardiologist: How would you tell the difference between someone with fluid retention due to kidney failure and heart failure?

Me: Heart failure might have displaced apex beat, additional heart sounds, valvular regurgitation, murmur...

(seems like he was after investigations, rather than examination findings)

Me: BNP level...

Cardiologist: The BNP level might give you some idea. But what else?

Me: Echo

Cardiologist: Yes. An echo!


In contrast, there was a question of some similarity but also considerable differences asked in a tutorial I had later in ICU.

Intensivist: How would you assess if his heart and circulation is working well?

(I had the cardiologist experience in my mind)

Me: An echo

Intensivist: Get out. You won't have an echo everywhere you go.


Now it seems like the answer to the same question depends on the context in which it is asked. In pharmacology class, the molecular mechanism is important, but in the clinic, the CSC tutor is after the end broader effect. And in cardiology, the echo is very useful in determining heart failure, but not practical for immediate measurement of cardiac function. So as it is the case in many other things, context is everything in medicine too.

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