For instance, there is Oxycontin, which is pure Oxycodone with no Tylenol in it. Why is there no Hydrocodone with no Tylenol or other binding agent? I take hydrocodone for pain and the Tylenol in it always worries me and anything stronger makes me too sleepy to function. I know there is Vicoprofin, but I mean pure hydrocodone.
Anyone, Bueller? Bueller?
Tylenol potentiates the action of the hydrocodone, meaning you need far less hydrocodone if you take a bit of Tylenol with it. This, of course, lessons the unwanted effects of large doses of hydrocodone.
Ibuprofen, incidently, is also potentiated by Tylenol. Taking an Advil and a Tylenol together works better than two of either by itself. (Check with your doctor, avoid prolonged use of Tylenol unless under a doctor’s care, do not drink alcohol with Tylenol on a regular basis, void in Lesser Zimbabwe.)
The interesting thing about this is that toxicity in overdoses is generally not the fault of the hydrocodone, but the Tylenol. While the LD50 for Tylenol is around 7000 mg and the LD50 for hydrocodone only 800 mg, the normal dosage in a Vicodin or generic APAP/hydrocodone tablet is 500 mg acetaminophen/5 mg hydrocodone. It would take 160 tablets to reach the LD50 for hydrocodone and only 14 to reach the LD50 for Tylenol.
I have often suspected that the Tylenol is in there to prevent abuse. It’s pretty cynical to assume the FDA would place poison in prescription drugs to prevent misuse, but there you have it. I guess it says something about my character.
I’ve wondered about the OP’s question myself. If you’re trying to manage your pain with Tylenol or a similar drug, but need something stronger occasionally, then when you take the Vicodin, you’ve got a double dose of Tylenol. And too much of that can’t be good.
Oh, it’s manufactured by itself. But then it’s a schedule II drug, same as oxycodone with or without acetaminophen.
But first you have to find a doc to prescribe plain hydrocodone, and most probably won’t be that eager to do so. If I’ve got a patient who needs more than 40 mg of hydrocodone a day (the max amount to take of the hydrocodone/APAP 5/500 mix, in terms of max APAP dose), perhaps there’s another problem, or I should be using a stronger pain killer.
Then you’d have to find a pharmacy that stocks it. Not much call for it. Just another schedule II drug to keep an inventory on, and not much used.
So there you go.
Qadgop, what would it be called? The name brand, that is?
It is just hydrocodone, as it is a generic. There are several trade names, including Hycodan. It is not a great pain reliever, that’s why mostly it is used with acetaminophen. If you are needing greater pain relief, I’m not offering medical advice but what we use around here is a long acting opiod with a short acting one for PRN breakthrough (oxycontin + PRN oxycodone, for example). You should really seek advice from a qualified pain expert, though.
Yeah, I’ve tried percocet, oxycontin and they just make me too sleepy. Hydrocodone is the only thing that doesn’t make me crash out during the day. It sucks, too. I’ll talk to my doc about compound hydrocodone, though. Thanks !
Ask your doctor for Oxycodone IR, and be prepared to discuss it with him/her. I have it for breakthrough pain. I can take or not take Tylenol with it, as seems appropriate at the time. I have liver worries, so I watch my Tylenol intake closely.
Hycodan (hydrocodone without any Tylenol or ibuprofen) is usually prescribed for cough, not pain. It’s not used that frequently; the hospital I work for doesn’t carry it.
I have had Hycodan prescribed for me some years ago when I had a severe bronchitis with a cough that kept me up all night. It worked pretty well, especially at night, when sleepiness wasn’t a real issue. The Tylenol is useless for cough, so the manufacturer (Dupont, I think) left it out.
Theobroma, R.Ph.
One thing to remember about hycodan: Homatropine methylbromide is included in a subtherapeutic amount to discourage deliberate overdosage. Take a lot of homatropine and it will discourage you from doing so again.
That’s how hycodan can get away with being schedule III, not schedule II.
Hydrocodone is an extremely popular drug of abuse, with a stronger euphoriant effect than codeine for the typical individual.
Out of curiousity, what are the effects of Homatropine methylbromide. I guess I could google, but I’m super lazy right now.
Sorry to chime in so late, and this is a slight hijack since the OP’s had his question answered by Whynot and Qadgop the Mercotan, but I had to go to work to look up the answer I wanted to this question.
I was a little puzzled by Bill Door’s statement above about the toxicity in OD’s. Because I sign the death certificates on maybe three hydrocodone deaths a month, and one acetaminophen death a year. So why do his sources say so much of the toxicity is due to acetaminophen?
Then it hit me. He’s probably talking about living people who OD’d but survived. Since as is well known, acetaminophen toxicity (this is acute overdoses we’re talking about, not chronic toxicity) comes on about a day or two after you attempt suicide on that handful of pills. You don’t really watch your liver die for four to ten days.
Whereas, if you die from hydrocodone overdose, you die within hours of use. You go into a very deep sleep in which your breathing is so shallow that you don’t get enough oxygen to your heart or your brain. Any condition which lowers the threshold for your heart to go into an arrhythmia will bring on your death faster – such as enlarged heart, cardiomyopathy, diabetes with small vessel disease of the myocardium, or concomitant use of cocaine, amphetamiines, or alcohol.
(Not everyone knows that alcohol decreases the ventricular threshold for arrhythmias just as it decreases the brain threshold for seizures. And benzoylecgonine is also a fairly strong arrhythmogen, though not as strong as the mother compound cocaine.)
I got the following data from the Red Book, formally known as Baselt’s Disposition of Toxic Drugs and Chemicals in Man, third edition.
Hydrocodone. One dose. Peaks two hours later at 0.011 mg/L (that’s drug level in the bloodstream). One high dose. Peaks two hours later at 0.024 mg/L. Fatal doses. 11 people in 6 studies died from levels varying between 0.13 (that’s about eleven pills!) and 7.0 (that one was a suicide who emptied the bottle down her throat); in eight of them, the fatal blood level ranged from 0.013 to 0.60.
Tylenol. One dose (one standard pill, 325 mg). Blood level maximum, 4.2 mg/L.
Tylenol. One dose of 1000 mg. Blood level maxes out at 9 mg/L.
Tylenol. One dose of 1300 mg (four standard pills). Blood level, 4.8 to 13 mg/L.
Tylenol. One dose of 1800 mg. Blood level, 5.6 to 52 mg, mean 26.
One hundred and thirty-nine people who died from a combined overdosage of acetaminophen and at least one other drug, any other drug. Acetaminophen blood levels ranged from 90 to 300 mg/L, mean 170. Six people who died from acetaminophen alone, range 160 to 367 mg/L, average 248.
Obligatory reference to the Rumack nomogram.
So you got a little more room to make mistakes with Tylenol. Your wiggle room with hydrocodone is measured in hundredths of a mg per liter. Your wiggle room with acetaminophen is in tens of grams.
gabriela
Typo. The fatal blood level ranged from 0.13 to 0.60.
Oops!
Definitely a hijack here, but the part about alcohol lowering the seizure threshold caught my eye. Why would it decrease the seizure threshold?
If I recall correctly, EtOH has a very similar mechanism to barbiturates–ie it binds to and increases conductance through the GABA-Cl ion channel, resulting in hyperpolarization of the neuronal membrane. If this is correct, why wouldn’t EtOH raise the seizure threshold the same way that barbiturates do? Or is there another effect of EtOH that I am not considering?
I have NO IDEA at all if this is what QtM was referring to, but back in the experimental college days, when I was doing reseach on robotripping (I always did reseach before trying something) I read something about bromide poisoning. That may or maynot be what Qadgop was talking about. I don’t remember how much you had to injest to do it or any of the complications though.
No, homatropine is an anti-muscarinic:
Mad as a hatter
Red as a beet
Dry as a bone
Hot as a hare
Blind as a bat
Bowel and bladder lose their tone
And the heart runs alone
It is quite an unpleasant toxicity – CNS disturbance, hyperthermia, dry mouth, hyperthermia, miosis, urinary retention, gastric ileus, tachyarrhythmias.
I’m sorry to say I don’t know why, Hirundo82. I only know that it does.
I can try to find out for you. One reason may be the difference between neuronal and myocardial membranes. Myocytes have some extremely specific calcium and other ion channels. As you no doubt know well.
As a consideration: The myocardium lives chiefly off short-chain and medium-chain fatty acids. EtOH as a very short-chain fatty acid interferes with the mechanism of production of energy in heart mitochondria. I read that in the NEJM about fifteen years ago.
It would seem likely to me that it’s from interference with the use of fatty acids as food rather than from any direct neuron-like effect.
I haven’t followed this subject in a decade, but isn’t EtOH also believed to operate by mass-effect random disruption of the lipid bilayer in susceptible cell types? I realize that this seems a crude mechanism, but it’s to be expected: not too many substances (much less drugs) are routinely ingested in such large quantities.
(While there is no real “standard” dose, I’ve seen .both 75 g/kg and a single US beer [~10 grams EtOH] cited as “standard” in recent studies. Three beers has as much alcohol as the acetominophen in 100 tablets. At that dose range, raw physico-chemical effects can be quite significant, compared to the more specific biochemical effects. Of course, for a lot of people, 3 beers (or equivalent) is a daily thing, and much higher doses are not uncommon]
er - make that “not may single chemicals” (not substances) “are routinely ingested in such large doses” (not quantities).
You might consume 10-30g of sucrose in a sitting, or perhaps some proteins or starches in a given meal, but the list tails off rapidly. Take table salt, ubiquitous in most of our diets: while many people ignore the federal RDA of under 2400mg/day of sodium, You’d have to eat 10 lbs of potato chips to get 30g.