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Mechanism of action Monday: Xylitol
Xylitol is a sugar substitute in human foods and a potent toxin in dogs.
Here's the pathophysiology of xylitol ingestion in dogs:
1. Rapid Absorption: Xylitol is quickly absorbed from the canine gastrointestinal tract.
2. Insulin Release: Xylitol then leads to a rapid and pronounced insulin release from the pancreas. This is due to xylitol's ability to stimulate insulin secretion directly in the pancreas.
3. Hypoglycemia: The significant release of insulin leads to hypoglycemia. The syxmptoms of hypoglycemia can manifest within 10-60 minutes following xylitol ingestion and include vomiting, loss of coordination, lethargy, incoordination, tremors, seizures, and in severe cases, coma.
4. Liver Toxicity: Apart from the hypoglycemic effects, xylitol has been associated with acute hepatic necrosis in dogs. The exact mechanism for this liver toxicity is still not well-understood. Increased liver enzymes can be detected on blood tests, and in severe cases, it can lead to complete liver failure.
5. Other Effects: Xylitol can lead to potassium release into the bloodstream, resulting in hyperkalemia (increased potassium levels), which can affect cardiac function.
6. Species Differences: In cats, the available evidence to date suggests they might not experience the rapid insulin release and subsequent hypoglycemia that dogs do.
Given its potentially fatal consequences, it's vital for pet owners to be aware of xylitol-containing products in their households and to keep them out of reach of their pets. Immediate veterinary attention is necessary if xylitol ingestion is suspected in a dog.
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There's usually one in every practice. They give the best of care, but definitely have their preference if pushed...
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🎼Don't be suspicious 🎶
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🫠
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Mechanism of action Monday:
Lidocaine is a local anesthetic that also has antiarrhythmic properties.
Here's how it works:
1. Voltage-Gated Sodium Channel Blockade:
Lidocaine's primary antiarrhythmic mechanism is its blockade of voltage-gated sodium channels in cardiac myocytes. By binding to these channels, it inhibits the rapid influx of sodium ions into the cell during the depolarization phase.
2. Fast-Dissociation:
Unlike some other antiarrhythmic drugs, lidocaine quickly associates and dissociates from the sodium channel. This allows it to preferentially affect cells that are abnormally depolarizing more frequently than they should, such as those undergoing repetitive depolarizations seen in ventricular arrhythmias.
3. Shortened Refractory Period:
By blocking sodium channels and prolonging the refractory period, lidocaine prevents cells from being re-excited prematurely, which can help stop the arrhythmia.
4. Decrease in Abnormal Automaticity:
Ventricular arrhythmias can arise due to increased automaticity (abnormal spontaneous firing of electrical impulses). By blocking sodium channels, lidocaine can reduce or eliminate these abnormal impulses.
5. Focus on Ischemic Tissues:
Lidocaine has a particular affinity for ischemic tissues, this makes lidocaine especially effective in treating arrhythmias that arise in the context of certain toxicities.
Lidocaine is often used as an emergency drug to treat ventricular arrhythmias, especially in the perioperative period or in cases of toxin ingestion. It's one of the first-line drugs for this purpose due to its rapid onset of action when given intravenously.
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Sometimes it costs time and money to save time and money.
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I don't know how anyone researched medicine before online journals were published.
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They really needed this win. ❤️🩹
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Makes up for lost time by doing the spay in 4 minutes.
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Do you think the clients will notice my sweat patches?
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I'm sure my husband wouldn't mind one more pet?
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Wait until the hear qulaity pet food isn't free either
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