iqqi said:
Thanks for the concern. My only question regarding that is wouldn't there be other signs, if I was having liver failure? I don't have any other food sensitivities.
Also, 3 drinks might be a lot... if it was every day or for a lengthy amount of time. Whenever I would drink, it would be on the weekends, and it was only for a few months here and there, I wasn't a heavy drinker regularly throughout my 20's. I just really doubt that the drinking I did was excessive, simply because I see so many other people's drinking habits, and mine were nowhere near theirs. To this day there are still some people who don't believe I drink, because I don't do it often, or because there have been years where I just didn't drink at all (no particular reason... just didn't feel like it.)
Could hormonal changes play a part in this? It all seemed to start when I began taking a certain pill birth control pill, which I stopped taking after 2.5 months when I noticed how sick it made me feel. That was almost a year ago.
Just a tip iqqi, don't take advice on your hepatic health from someone who can't spell "cirrhosis" properly haha... Alle_gory no offense dude, nothing you said was really fundamentally incorrect, but a lot of it was misleading.
I'm a CCRN (critical care registered nurse). I have 8 yrs of post secondary education, including a degree in molecular bio as well as a B.ScN. I have around 1.5 years of ICU experience working in a large med/surgical ICU in a level 1 trauma center. The hospital is also the largest organ transplant center in Western Canada. We do our shares of liver transplants, and I see LOTS of liver failure. I'm not a hepatologist/GI doc, but I think I do know more about hepatic health, and general metabolic physiology than most guys who post on a certain teenage "how to pick up chics" forum.
Iqqi, in short, yes, if you truly were in liver failure you'd have tons of other symptoms. Not only would you be grossly jaundiced (assuming your total bilirubin was high), but you'd also have problems w/ blood clotting, and your level of consciousness would be all phucked up. All in all, you'd be at a VERY high risk for decompensation and death if you didn't get immediate medical treatment.
There are simple LFTs (liver function tests) you can do if you wanna see how your liver's doing. When liver cells are damaged the enzymes in them leak out into the blood. The levels of these enzymes can then be measured. The more enzyme that is present, typically, the worse the hepatic injury is. I'm willing to bet your LFTs are probably normal. Namely these enzymes are:
AST/ALT - alanine/aspartate transaminase
LDH - lactose dehydrogenase (not super specific for hepatic failure)
ALP - alkaline phosphatase.
you can also quantify T.bili (total bilirubin), albumin, GGT, etc etc.
If you're worried about your liver, get these numbers checked out, and they'll give you a good picture of what's up. The AST/ALT/LDH/ALP/T.bili combo are a sure bet. In my opinion, your liver enzymes are probably within normal ranges. I still standby my "CTZ-sensitivity/GI mucosal sensitivity leading to nausea" theory.
Allegory, several things you're saying are misleading. I'll address a few of them:
* Although heavy drinking of high glycemic load drinks can increase risk for DM (diabetes mellitus), there are many other risk factors involved. Its wrong to be this reductionist.
* Surgery is not always an option for cirrhosis. When a pt has substantial cirrhosis, and hepatic dysfunction, their blood coagulation factors won't be produced in appropriate amounts. Most surgeons don't wanna operate on someone who won't stop bleeding. Furthermore, if your electrolytes are outta whack and you're acidotic, you're MUCH more likely to have adverse complications, like PEA (pulseless electrical activity) arrest, from surgery. Liver resections are often done for things like HCA (hepatocellular carcinoma)... but not typically for cirrhosis/liver failure.
* The liver doesn't truly "filter" anything (unless you're talking about the reticuloendothelial system of the liver). You're probably thinking of drug metabolism. Any pills you eat will pass through the portal circulation. Your liver will basically try and do stuff to it to make it less toxic, and make it easy to get rid of. I'm not gonna get into phase I/phase II reactions and the P450 cytochrome system... just look it up. You're correct in that some chemical reactions of the liver can cause harm of liver cells, typically by production of harmful ROS (reactive oxygen species). Great analogy about the TI (therapeutic index), when you said that the difference between medicine and poison is the dose.
* You're correct in that cirrhosis and the resultant liver failure is typically slow and progressive, however, this is not always the case. There's lotsa badass things out there like death cap mushrooms that can really mess up your liver, and put you in acute liver failure. Liver failure secondary to tylenol poisoning is notoriously common.
Regarding your question cocaine:
Cocaine is an alkaloid that is a very powerful central nervous system stimulant. A portion of the molecule also has local anesthetic properties. Here's a cool 3D molecular model... God I'm such a NERD:
http://www.3dchem.com/molecules.asp?ID=279
An alkaloid is a naturally occurring chemical that has basic nitrogen atoms. As you know cocaine is naturally present in coca leaves, and has been concentrated. Usually, "street cocaine" will be a HCl (hydrochloride salt) of the base molecule, so yes, there is some minor modification. Lotsa OTC (over the counter) drugs are HCl salts of the active compound. Its just easy and convenient to store and administer drugs like this. I think crack or "free base" is the cocaine molecule w/o the hydrochloride salt... I'm not sure about this though.
With regards to cocaine metabolism by the liver, as far as I know there isn't significant damage to the liver w/ cocaine metabolism. Obviously there's other health risks, like cardiac arrhythmias, but I don't think you'd usually see elevated LFTs from cocaine use (unless of course there was some underlying pathology). This is probably because cocaine metabolites at "normal dose" are not damaging to hepatocytes. Usually, compounds that are damaging to hepatocytes are the reactive ones that induce oxidation, and produce ROS. For example, there's a very reactive tylenol metabolite abbreviated "NAPQI" that brutalizes hepatocytes, and causes a shiite load of oxidative stress. This is the molecular basis for tylenol poisoning.
Although cocaine by itself isn't super hard on the liver, mixing it with alcohol is whole different ball game...
Hope I answered your question.
