Acetaminophen or paracetamol is a common over-the-counter analgesic and antipyretic drug for humans. Often, well-meaning pet owners may give it to their sick pets. This will do more harm than good. Here’s why.
Acetaminophen toxicosis acetaminophen is also known as paracetamol or n-acetylpara-aminophenol it is a common over-the-counter analgesic and antibiotic drug for humans it is very rarely if at all used in veterinary medicine here’s why acetaminophen metabolism involves these biochemical pathways glucoronidation where the drug is conjugated by two coronal transferase
Into acetaminophen glucoranide sulfation to a lesser degree where it is acted upon by sulfur kinase to become acetaminophen sulfate both of these are non-toxic metabolites however when these pathways are saturated that is when there is too much acetaminophen for the enzymes to act on acetaminophen then goes through another pathway the cytochrome b450 oxidase
System where it is biotransformed into n-acetylpara-benzoquinone or napkin a reactive toxic metabolite napkin can be detoxified by glutathione into a more water-soluble less toxic acetaminophen mercaptorate however this is short-lived as glutathione stores can be rapidly depleted before proceeding to the toxic effects of napkin it must be pointed out that cats
In particular are deficient in glucoronal transferees and their sulfation pathway is also less efficient than that of other species thus only a small amount of acetaminophen is needed to saturate these two pathways resulting in a large amount of napki being produced dogs on the other hand although they have this enzyme may have these pathways saturated at doses
Of acetaminophen formulated for humans furthermore repeated exposure at low doses may also cause toxicity it is important for pet owners to know that they should not self-medicate their pets always consult your veterinarian when you are concerned about your pet’s health toxic effects of napkin or red blood cells are extremely susceptible to the oxidative damage
Brought about by napkin ferrous iron in the heme is oxidized into ferric iron turning the bright red hemoglobin into a brownish methymoglobin methemoglobin is much poorer at carrying oxygen than hemoglobin thus methemoglobinemia brings about respiratory distress tachycardia weakness and cyanosis its brown color makes the mucus membranes and urine dark brown
Too cats also have a deficiency in methymoglobin reductase an enzyme that converts methemoglobin back to hemoglobin thus making cats more likely to and more quickly manifest these clinical signs capped erythrocytes also have more sulfhydryl groups than dogs and humans making their hemoglobin more likely to denature and precipitate as heinz bodies this results in
Increased osmotic fragility and lead to hemolytic anemia this adds to the respiratory distress tachycardia weakness and cyanosis experienced by the animal hepatocytes suffer from centrilobular necrosis power shall lead you to the decreased oxygen carrying capacity of the blood and because of direct oxidative damage that occurs as acetaminophen from the portal
Vein is metabolized into napkin closer to the central vein this acute liver injury results in increased alp asd and total bilirubin as well as ignorance abdominal pain and vomiting facial and slash or paw edema may also occur the mechanism of which is not fully understood depending on the severity of the case clinical signs can progress to shock coma and even
Death diagnosis clinicians must look out for history of access to and ingestion of acetaminophen note that many human medications contain a combination of acetaminophen and some other drugs it is important to obtain an accurate description of what was ingested during history digging matching clinical signs can also point to the diagnosis complete blood count
May reveal methamoglobinia and slash or highest body anemia and the serum chemistry profile may show increased alt asd and total bilirubin treatment if presented within 2 hours of ingestion mss may be induced followed by administration of activated charcoal with cathartic this is to reduce absorption of the offending agent thereafter the following may be given
An acetylcysteine the drug of choice for acetaminophen toxicosis it serves as a glutathione precursor increasing the levels of glutathione to conjugate with nauki it has three sulfhydryl groups that can bind directly to napkin too it can also increase levels of freeze serum sulfate making the sulfation pathway less saturated it is important to note though that
N-acetyl cysteine can be absorbed by activated charcoal thus they must be given at least two hours apart from each other ascorbic acid promotes the reduction of methemoglobin back to hemoglobin and cementidine an h2 receptor antagonist usually uses an anti-ulcer drug but in this case it is used for its effect as a cytochrome p450 inhibitor thereby inhibiting
This part of the pathway that produces neptune supported care of course such as intravenous fluid therapy supplemental oxygen and blood transfusions should be given as needed prevention this is to be reiterated do not self-medicate your pets a settlement event may be an over-the-counter drug often taken by humans that feel ill and well-meaning pet owners may give
It to their sick pets this will do more harm than good always consult your veterinarian for the proper treatment of your pets all medications whether for humans or for animals should be stored properly and out of your pet’s reach you
Transcribed from video
Acetaminophen Toxicosis – metabolism, toxicology, pathophysiology, diagnosis, treatment, prevention By Vet Skye
