Damage to the kidneys may cause signs of acute kidney failure such as increased thirst, increased urination, vomiting, diarrhea, loss of appetite, lethargy and dilute urine (lighter in color).
Symptoms associated with damage to the liver include jaundiced skin, gums, inside of ears, and sclera (whites of the eyes) as well as vomiting, diarrhea, loss of appetite and lethargy.
Here's some info I found on Rimadyl toxicity. Since your dog threw up so quickly, I would say he'll probably be OK.
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Rimadyl® toxicity generally occurs as the result of one of the following:
Accidental ingestion of excessive quantities of the drug
Administration of the incorrect dose of medication by the owner (overdose)
Idiosyncratic reaction – the pet is unusually susceptible to the side effects of the drug and the reaction is unrelated to dose.
Generally, a high serum creatinine level means that the kidneys are not working well. Causes include kidney failure (acute or chronic), kidney infection, drug toxicity, dehydration, high blood pressure (hypertension), and high sugar levels (diabetes). It is possible to have acute renal failure and still have normal-sized kidneys. Renal atrophy may result from chronic renal disease or infection, as well as other conditions such as narrowing of renal arteries or obstruction of urinary tract.
“Unintentional acetaminophen poisoning is responsible for 13,000 emergency department admits every year, 2,200 acute hospitalizations, and 100 deaths. It is also the number one cause of acute liver failure requiring a liver transplant. Making the active ingredient more obvious and giving clearer warnings may help reduce those numbers.”
Acetaminophen toxicity poses two dangers. One is genetic.
Is there a normal course of action for a patient complaining of an acute exposure to an unknown noxious gas/fume? Symptoms include irritation to the upper respiratory tract, watering eyes, noxious exhaled gas after exposure, possible lesions on lung.
What should a doctor do to investigate this patient? What lab tests could be performed? What treatments might aid the body in ridding itself of related toxicity?
Thank you!
I dont see much about it in these posts but I have been taking oxymorphone(OPANA) for FBS.I have been addicted to Meth cocaine and alcohol in the past but have been free from those chains for 10 years.My disease has resurfaced with this Opana though.I have cut my intake from 20 mg a day to 10 mg a day for the past three days.I have been blessed to avoid the terrible sickness of opiate withdrawl that I went through last year with this **** when I went CT off of it.
Scientists have learned a great deal about how THC acts in the brain to produce its many effects. When someone smokes marijuana, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to the brain and other organs throughout the body.
THC acts upon specific sites in the brain, called cannabinoid receptors, kicking off a series of cellular reactions that ultimately lead to the "high" that users experience when they smoke marijuana.
I was actually dehydrated and could not pee for my UDtest so they took blood and it came back positive for oxymorphone, noroxycodone, and noroxymorphone at low levels but on a zero tolerance test any amount is a positive. Are these items that could be from just taking the oxycodone and my body coverts it to this or is the test flawed.
I’ve been taking 5mg oxymorphone extended release pills for 8 years. I recently had to switch primary care doctors because mine moved away. The first urine drug test I was asked to do was last Friday and they called today and said the drug didn’t show up in my system, and dropped me as a patient. I should start withdrawals tomorrow & I’m scared out of my mind. I’ve never failed a drug test, asked for an early refill, nothing like that.
I have built up a tolerance to oxycodone IR that I have had to take 3 times my dose just to get my pain to get down to a moderate level. The research I have done is that oxymorphone is stronger and less mg. I have several questions. Are taking less mg easier on the body? How do I ask my doctor to switch, I don't want to seem like just another patient trying to get high.
I've just been switched from Fentanyl 25mcg every 48 hrs to Oxymorphone 10mg every 12hrs. I feel way worse (pain) & was wondering if anyone knows what the equivalence is between the 2. I have a feeling I've just been decreased in pain relief. My dr & the pharmacist told me to wait a few days to "feel it's working" & in the meantime I'm in excruciating pain. Can anyone help with what I can do here? Btw...
there are trials already i posted in the past, also the effect of sim on liver was reviwed by liver researchers and they said it has no toxicity the elevations of alt that can happen on few are due to a balance of lipids not toxicity because the alt elevation is transient and resolve itself
the only serious side effect of sim that can happen is muscle damage or mitocondrial discorder, very rare
statins cause acute liver failure in chronic hbv patients?
I am going through serious withdrawal. I suffer chronic back and hip pain and my doctor can't seem to find the source of the pain. So I started to medicate myself. I started off with oxy 30s. then I started dating a guy who also is in chronic pain and when I would start getting "sick" from not being able to get the 30s he gave he some of his oxymorphone, opana, and I don't want to continue taking his meds anymore.
Oxycodone is metabolized by the liver into oxymorphone. Oxymorphone is about 2 times stronger than oxycodone based on pharmacology. When I was first switched to Opana, the drowsiness and tiredness were unreal! It was a real struggle for me at first and I also have a desk job. However, the sedation effects only lasted for a month at the most. Now I don't get sedated anymore and in fact I am more alert than I was on Morphine.
Was on Tramadol for the past 7 months, up to 400mg a day for severe neck/back injury/pain due to a car accident 8 months ago. My pain management doc gave me this Oxymorphone 5mg. up to 3 times daily yesterday. Doc said try this, but if that doesn't work, its epidural cervical injections and possible surgery. I'm worried about addiction now, w/ all these pills they throw at me.
A couple of months ago, I ended up in ER with acute symptoms relating to overmediation with synthroid. I was on 175 mcg. I was having severe tremors, palpitations, blood pressure and pulse rate were sky high, and of course then the anxiety kicked in. Luckily I had some low dose Ativan - took 2 tablets and got to the hospital. My ECG was normal, but showed some PVC's (from the anxiety I was told). My TSH was 0.1 mU/L (Normal 0.3-5.
No it is not unusual but is your pain acute or is it on going? If you have acute pain you may need something for what they call breakthrough pain the Dr's call it "resque meds" Also Dr's now like to prescribe opana (oxymorphone) because it has very little to none euphoric or high feelings unless abused like snorting,plugging etc! I take opana er 10mg 2-3 times a a day along with percocet 10/325 tablet 3x a day!
will it show up if being tested for opioids or just synthetic opioids? i came up positive on a drug screen for oxymorphone and i was perscribed to percocet.. can u please explain?
my son was treated for an acute anxiety attack in his university ER with risperdal 4 days ago. he has not been the same ever since. he has had all of the classic signs of toxicity from this drug. he was treated in our local ER (2 days later) with benedryl and adavan and he seemed fine following the treatment. but the dystonic reactions, disorganized thinking, anxiety, all symptoms continue.
Stands to reason that:
2 x 5mg Percocet = 1 x 10mg Oxycontin
Don't quote me on that though. I know Percocet has both Oxymorphone AND Acetaminophen in it, and Oxycontin has Oxymorphone only. I'm not certain what the Acetaminophen brings to the table as far as drug-interactions go, but your statement that the Perc and the Oxy are the same (2x5mg vs. 1x10mg) sounds about right.
Maybe someone in the Pain-Management Community would know.
It is likely the patient had acute colchicine toxicity brought on by the addition of erythromycin and superimposed on chronic colchicine intoxication secondary to renal and hepatic impairment. The patient improved with supportive therapy and intensive hemodialysis and was discharged on day 70 of hospitalization. Another report describes two fatal cases of agranulocytosis due to presumed interaction between colchicine and clarithromycin, a potent CYP450 3A4 inhibitor.
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