Monday, November 21, 2016

Yes, I'm Blogging In The Middle Of A Medical Procedure

I've just been injected - barely half an hour ago - with a dye laden with technetium 99m, a radioactive tracer. Some 2 hours will have to elapse then I return for the actual imaging after the tracer has spread into my bones. What gives? Right now I am in the middle of a medical procedure, namely a bone scan,  to determine if my recurrent prostate cancer has escaped from the gland and metastasized, creating "bone mets". If so they will show up in a radiograph to be taken later today, e.g.
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The first part of the procedure was being injected using the dye laced with Tc-99m, a radioactive tracer. This can be detected by a kind of medical device known as a gamma camera. It is well suited to the role because it emits readily detectable 140 keV gamma rays.  So as the dye now courses through my veins it will - within 2 hours or so - reach the bones and enable imaging to be done to detect any mets. The  Tc-99m half-life for gamma emission is 6.0058 hours (meaning 93.7% of it decays to 99Tc in 24 hours). The relatively "short" physical half-life of the isotope and its biological half-life of 1 day (in terms of human activity and metabolism) allows for scanning procedures which collect data rapidly but keep total patient radiation exposure low.

What this means is that the radioactive medium (dye) ought to work its way out of me for the most part in 1 day, and all of it in 2-3 days.  The injection phase having been done,, the next step is the actual imaging when I have to return and remain still for an hour while the gamma camera does its thing.

Where does Tc-99 m come from? According to Wikipedia:

"Technetium-99m was discovered as a product of cyclotron bombardment of molybdenum. This procedure produced molybdenum-99, a radionuclide with a longer half-life (2.75 days), which decays to Tc-99m. At present, molybdenum-99 (Mo-99) is used commercially as the easily transportable source of medically used Tc-99m. In turn, this Mo-99 is usually created commercially by fission of highly enriched uranium in aging research and material testing nuclear reactors in several countries."

Why is this procedure being done? Recall in an earlier post I had referenced focal cryotherapy specialist E. David Crawford, e.g.

Well, last Wednesday evening I had a consultation with him at his office at the University of Colorado Anschutz campus, the Cancer Pavilion. We went over the previous test results and I discovered a number of revelations in the course of the exchange:

1) The Gleason scores for the biopsy pathology samples are virtually useless - this is inevitably the case after having had a radiation treatment especially high dose.

2) The Prolaris test result - contrary to the portrayal given me - wasn't "so aggressive"'.  Instead I had to produce a urine sample to submit for what is called an NTXPR genetic test, e.g.

3) Before even having the 3D staging biopsy done (see link to Dr. Crawford earlier) it is best to have a complete bone scan done to ensure the cancer has not escaped the capsule to the bones. If it has already done so there is no point doing the focal cryotherapy treatment- or the 3D biopsy.

Hence, what has led me to the medical screening being done today - which I am currently in the middle of.

In about 5-7 days I should know the result of today's bone scan and whether I am a candidate for the focal cryotherapy, or will now have to undergo the chemical castration route involving  one or more medications including casodex, flutamide and finestride.

The medical castration route takes advantage of the chemical-hormone pathways which begin in the hypothalamus with the secretion of luteinizing hormone-releasing hormone  (LHRH) which in turn stimulates the pituitary gland  to produce luteinizing hormone (LH) as well as follicle -stimulating hormone (FSH) . Then LH signals specialized cells in the testicles to secrete testosterone into the bloodstream. When testosterone reaches the prostrate it is converted into di-hydrotestosterone (DHT) a much more potent form of testosterone, via the action of an enzyme:5 -alpha reductase. The objective of medical castration then is to break this cycle, usually in one of two ways: 1) via  LHRH agonists or 2) LHRH antagonists.

In (1) the medication stops the testicles from making testosterone. This is achieved by inducing a continuous message from the brain to produce testosterone which over-stimulates the testes. They respond by being "overworked" so switch off.

In (2) the medication also induces the testes to stop producing testosterone but not by over stimulation (which can trigger a testosterone "flare"(or spike, including uncomfortable side effects) before the level subsides.

The differences between the assorted chemical castration agents and their effects are discussed here for those interested:

Anyway, it's now become a waiting game - after getting the imaging done in 2 more hours by the Gamma camera. Hopefully, no bone mets are found and I can proceed with the salvage treatment.

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