Forgive me a moment, or a series of moments, to talk about something personal, rather than the world of literacy. It's the thing I tried to post a few weeks ago, which kept going wrong. It's going to take a while, because I'm not sure how much I can type and post in here. And it upsets me a lot, and it takes ages to type as is. I'll write these in themes too, and hopefully my reasons why will become apparent.
This first post will be about the bare facts and figures. The next postings will be my personal experiences, pre-, during, and post-. I'm mainly doing this to be cathartic, but also to clear up what I was talking about when I posted about Stefenie Meyer. A justification for my reaction, if you will.
For a full title, I suffered from Thrombotic Thrombocytopenic Purpura caused by pancreatitic gallstones. It's three different things at once, a chain reaction, but the last part of the chain can cause the first. Does that make sense? The ultimate vicious circle. Forgive me now for anything I spell incorrectly, I'm going to try and show off with my basic medical know-how. I'll break it down into its component parts.
First of all, gallstones. I was told medical staff look for 'the four F's' in gallstone patients (Fat, Fair, Fertile, Forty. And since 60% of gallstone sufferers are wormen, I consider it the five F's with Female). If I were a blonde, middle-aged woman when having my son, and a few stone heavier, I would have been the prime candidate. Instead, I was size 10-12 before having my son (who I had at 22), and am now size 12-14, and a brunette. So one established characteristic (even a year after pregnancy, you're incredibly fertile).
However, there are other things that can trigger gallstones. Eating disorders (and I went through a period in university where I ate a bowl of porridge a day because I couldn't afford anything else), pregnancy, the contraceptive pill, sudden increase in animal fats (I've been vegetarian since the age of 11, I gave up during pregnancy ... though looking back I was showing symptoms before starting university, so who knows?) as well as the four F's.
You can live with gallstones by the way. The only consider removal when the stone becomes too large, or if you have many, and one slips into a duct between the gall bladder and the bowel or the pancreas. That can turn your gall bladder septic, and cause complications like pancreatitis. Then you'll usually be given a laparoscopic cholescystectomy (or key hole surgery. They rarely open people all the way up any more, there's like a 10% chance they'll need to). They perform around 500,000 lap chol's in the US per year.
Gallstones are the most common cause for women of a certain age who get pancreatitis. I was not that age. The second most common cause, and the most common in people in their early/mid twenties, is alcoholism. As far as I'm aware, pancreatitis is usually caused by an inhabitant. It's not the same as diabetes, it's shorter lived but just as potent. It has a survival rate of 80% and most hospital treatment involves 'nil by mouth' (no eating, drinking, or taking medication orally. Intravenous city!) When the pancreas has reduced in size again, and they know the cause, they'll take action then.
Thrombotic Thrombocytopenic Purpura (or, as I'll call it in the rest of this, and all other posts on the subject, TTP) has a survival rate of 80%, should you be properly diagnosed and treatment given within a very short time frame. Without, survival rates are more like 0-5%. So basically, if you get it, you need treatment or you'll die. TTP occurs when the ADAMTS-13 enzyme is inhibited, normally by an anti-body which sits on the ADAMTS-13. Sometimes there is no antibody, and the inhibition is from something else, like AIDS/HIV virus, combine contraceptive pill, interferon, quinnine (malaria treatment, also found in tonic water and irn bru). The ADAMTS-13 is meant to control certain things in the bloodstream, hormones and such. One of its jobs is to break down a substance called the Von Willebrand Factor (I mentioned it before, in my Stefenie Meyer post).
The Von Willebrand Factor is this long strand, like a protein, that is used to knit together cuts, scrapes and bruises. Like the glue pasting white blood cells and platelets together. In it's organic form, it's extremely sticky. The ADAMTS-13 basically stops it from causing blood clots, by reducing it into a managable form. With the ADAMTS-13 inhibited, the Von Willebrand Factor remains long and sticky, and of course causes blood clots. It normally causes kindey failure, multiple organ failure, or strokes, if you don't bleed to death first. NB-It only attracts white blood cells and platelets. They build up, and white blood cells come to the site like they do to any infection or cut or bruise, to heal. And when it gets big enough, the red blood cells get shredded up. On a blood test, the red blood cells and platelets are reduced in number, white blood cells have increased. Leukaemia blood tests show the same (except for the fact with leukaemia, it's the white blood cells thinking there's an infection there isn't and turning on the blood as a result).
They analyse TTP in two different ways, you either have congenital TTP (you're born with it, or discover it during pregnancy, and suffer it frequently from there on in) or acquired TTP (caused by the antibody, or another source. Those with the antibody have a 50% chance of having TTP repeat, other sufferers have a reduced likelihood). TTP affects 1-4 in a million. Based on that figure, there are 60-240 TTP sufferers in the UK. 15 of those people have congenital ttp. 80% have the antibody. That leaves roughly 15% of TTP sufferers in the UK at least, to have another factor cause their TTP. From what I know of TTP from pancreatitic gallstones, in the past 5 years there have been 7/8 other patients with pancreatitic TTP, and only one of them had gallstones. 5 of them had the antibody present anyway. My branch of TTP is therefore incredibly rare.
TTP affects people more in their 30's/40's, and women more than men. A typical person has a count of 12-16 RBC, 8-10WBC and 150-400 platelets in a blood sample. I've heard of TTP patients with no platelets, but most have maybe 7/8.
Treatment for TTP is usually using an aphaeresis machine, this machine that looks a little like a 1950's tape recorder with hooks everywhere, crossed with a washing machine. It has 4 different G-force settings, according to different blood products, and will spin at the required speed, taking in someones blood and seperating blood, adding donated blood products, combining it again,and putting it back into a person's blood stream. These machines can hold around 40 pints of blood product, or as far as I've seen they can. Straight transfusions, from packet to blood stream, feed TTP, rather than curing it, and can speed up the process.
ttpnetwork.org.uk has more information, if anyone was interested in reading. It's probably a lot more cohesive than me. That's about all the facts I can retain and recall, so my next post on the subject will be the start of my experiences. Bear in mind all I've said here, because parts of it will come into play as I talk.
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