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scott@vtx-cpd.com

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  • scott@vtx-cpd.com
    Keymaster
    20:17 19/07/20

    Indeed… spread the word!

    It is a nice paper.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    19:18 19/07/20

    It seems cost is the biggest issue.

    That is such a shame because it is so much easier! I still have nightmares about having to give them that powdered form!

    I wonder why is costs so much?! I would heave thought the active ingredient was quite cheap!

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    19:16 19/07/20

    It is indeed.

    It is that back and forward motion.

    This is also the first time someone has posted a video in the forum… it works really well. Thank you for that.

    I do like to have my patients a bit more sedated than this for liver FNA’s. I think especially if you are going it for the first time, it helps if they are still and not reactive!

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    19:11 19/07/20

    Great question Sara and great points Simon.

    There are a couple of studies in dogs where both drugs are used. Problem is that most involve maropitant being given and then around an hour later the apomorphine is given:

    https://pubmed.ncbi.nlm.nih.gov/28042152/
    https://pubmed.ncbi.nlm.nih.gov/19000276/

    I think the main point is due to the timing of the drug administration and how long to peak effect. If we are giving the maropitant SC after the apomorphine, it is probably starting to work after the emetic effect of the apomorphine has passed. I think it probably has little effect.

    Makes us feel better for sure.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    18:18 19/07/20

    I think that is a really good point.

    I definitely use them in a cumulative way. If maropitant id not effective enough. I will add in metoclopramide and then ondansetron. I really do think some cases need all three.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    18:11 19/07/20

    Interesting!

    Have you often given it IV?

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    18:10 19/07/20

    Hello.

    Thank you so much for your question. I am so glad you are enjoying the course.

    Electrolyte abnormalities also commonly occur as a complication of diuretic treatment. The normal physiologic response to increased sodium and water loss is the stimulation of homeostatic mechanisms that attempt to more vigorously retain sodium and water. Predominant among these mechanisms is the RAAS. Less commonly—although significantly—vasopressin release is sometimes also stimulated by a marked fall in blood pressure secondary to heart disease or diuretic treatment. One of the effects of the stimulation of these homeostatic mechanisms is altered handling of electrolytes. Increased activity of aldosterone will tend to favour sodium retention and potassium loss in the distal nephron. This leads to one of the more commonly observed consequences of loop diuretic administration: hypokalaemia. Hypokalaemia is less likely to be observed in patients if they are concurrently receiving treatments that tend to counteract the RAAS. More widespread use of angiotensin-converting enzyme inhibitors and spironolactone, in addition to loop diuretics, mean that hypokalaemia now is seen less frequently. The situation in which it is now probably most likely to be encountered is during the emergency stabilization of patients where they are likely to receive large doses of furosemide and might not yet have been started on other agents.

    Hypokalaemia can contribute to the development, or worsen the symptoms, of hepatic encephalopathy. Hypokalaemia increases proximal tubule ammoniagenesis. Approximately 50% of proximal tubule ammonia production is returned to the systemic circulation via the renal veins.

    Hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    15:30 19/07/20

    Hello.

    Thank you so much for you great questions. I wanted to start by discussing gallbladder sludge. “Sludge” in the gallbladder is defined as nonshadowing echogenic material in the gallbladder which is dependent on gravity and a commonly seen ultrasonographically during the investigation for hepatobiliary diseases. The clinical significance of this finding in small animal patients is not well established. The reported prevalence of the gallbladder “sludge” is 53- 57% in clinically healthy animals. Bromel et al. (1998) showed prevalence in clinically healthy animals is not significantly different from that in patients with hepatobiliary disease or other diseases “Sludge” seems to most commonly affect Labrador retrievers, Yorkshire terriers, Miniature Schnauzers, Beagles, Cocker spaniels, Poodles, and crossbreeds. Fewer studies have been performed to investigate prevalence and significance of gallbladder “sludge” in cats, but a lower prevalence of 14% is reported. In both dogs and cats, increased age is positively correlated with the prevalence of “sludge” but sex seems to have no effect. DeMonaco et al. (2016) identified healthy dogs with gall bladder sludge remained asymptomatic for 12 months. Biliary sludge was mild in 50%, moderate in 36%, moderate to severe in 9% and severe in 5% of this population and persistent in 88% and recurrent in 10%. Furthermore, there is no correlation between increases in liver enzymes or total bilirubin and the prevalence of “sludge” in dogs. Recently, a small study reported that the detection of immobile “sludge” had a 70% sensitivity and 100% specificity for diagnosis of bactibilia. Overall, the presence of “sludge” is not necessarily clinically significant. This finding needs to be considered in combination with clinical signs and other laboratory findings.

    So, I would use ursodeoxycholic acid in cases of “sludge” if there were clinical signs/biochemical changes consistent with hepatobiliary disease. It may not be necessary to use in every case where “sludge” is detected if the animal is having ultrasound for a completely unrelated reason.

    SAMe is a very safe product generally and can be used long term if necessary. I will use in cases of acute hepatitis for as long as the animal is being treated for. In these cases I will use until the point of resolution. This is normally the point where all biochemical abnormalities go back to normal. I will definitely use longer term in chronic cases. This could be lifelong if required.

    I would always try and confirm inflammation with biopsy and exclude infection as you have mentioned. The evidence about what drugs to use in inflammatory/immune medicate hepatitis cases is variable. Some specialists combine corticosteroids with another immunosuppressive drug (either azathioprine or cyclosporine) to enable more rapid tapering of the corticosteroid administration to every other day anti-inflammatory doses. For most, maintenance on the second drug alone was the goal. For other specialists, single agent cyclosporine twice a day was used as first-line treatment to avoid the adverse effects of corticosteroids. Cyclosporoine is tapered to once a day as soon as remission is established.

    Sorry for the long answer! I hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    15:05 19/07/20

    Hello.

    Hope you are well and having a lovely weekend.

    Thanks so much for your question. We will indeed be recording the live sessions and will pop them on the website the same way that we do the other webinars.

    Please feel free to send me any cases you would like us to chat about in advance and I can include them.

    Thanks.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    15:01 19/07/20

    Hey.

    I think the paste option is definitely helpful in some patients, particularly cats. It is a shame that it does not contain SAMe. I keep meaning to look in to other possible paste options that have SAMe in too.

    You are right to contact the manufacturer. I think it is really important to be confident with what exactly is in these supplement.

    Hope you are having a nice weekend.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    16:54 16/07/20

    Hahaha!

    I am trying to make you less scared. When it comes to FNA’s, generally these are very safe. As long as there is a normal number of platelets, I am happy to perform this procedure.

    The only cases that I would have blood products on stand by for would be when we are taking actual large surgical tissue biopsies in cases that are at higher risk of bleeding.

    I have never had significant bleeding post liver FNA.

    Definitely go for it!

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    16:42 16/07/20

    Hello.

    Yes. I think when thinking about liver function you have to consider all the parameters that you have mentioned. Relying on BAS as a marker of liver function as a stand alone value has limitations.

    It is still useful… but has to be part of the bigger picture.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    16:35 16/07/20

    Hello.

    Hope you are well. There is not a definite multiple of normal that would make me withdraw treatment. It depends on a number of factors. I would definitely be taking more notice when the ALT and ALP are getting greater than 3x the reference.

    Hepatotoxicosis from phenobarbital appears to be dependent on cumulative dose, with possible individual modulating factors. Signs typically develop after a year or more of phenobarbital treatment, and the duration of administration is associated with the degree of histologic injury in epileptic dogs. Presentation can range from subclinical increases in serum bile acids to fulminant liver failure. Typical histologic findings in dogs with clinical signs are bridging portal fibrosis, bile duct hyperplasia, and nodular regeneration. Higher phenobarbital dosages or serum drug concentrations have not been correlated with the development of abnormal serum bile acids across epileptic dogs; however, individual dogs with phenobarbital hepatotoxicosis can improve clinically following phenobarbital dosage reduction. For dogs with hepatotoxicosis during chronic phenobarbital treatment, phenobarbital should be discontinued, or the dosage minimized, by adding another anticonvulsant. For example, potassium bromide (KBr) can be substituted at a maintenance dosage of 40-60 mg/kg PO q 24 h, and phenobarbital can then be discontinued with a rapid taper over 1-3 weeks.

    b) It may actually be helpful to include the phenobarbitone levels in your monitoring. Clinically significant hepatotoxicosis can be preempted in most dogs by serial monitoring of serum bile acids, phenobarbital concentrations, and a liver panel, ideally every 6 months. Serum phenobarbital concentrations >40 mcg/mL should be avoided, as this can be a risk factor for hepatotoxicosis. In addition, the presence of hyperbilirubinemia, new hypoalbuminemia, or discordant increases in serum ALT > ALP is clinically significant. This would definitely be a trigger to consider dose reduction/withdrawal. Newly noted sedation on a stable dosage of phenobarbital might also indicate impaired hepatic clearance of the drug, and is an indication for bile acids testing.

    This little table is also useful:

    Phenobarbitone-Monitoring

    Let me know if you have any other questions.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    14:32 14/07/20

    Hello.

    Yes, if there are elevations in liver enzymes and you are pretty sure it is primary liver then ultrasound would be a next good step.

    It is important to remember that the liver may appear sonographically unremarkable even in the presence of severe disease. While an unremarkable ultrasound exam was statistically significantly associated with the absence of histopathologic liver disease (in one study), 63% of these cases had abnormalities on histopathology in a study comparing hepatic ultrasound findings with histopathology. An normal ultrasound would not mean that FNA’s/biopsies would not be carried out.

    While bile acids are quite useful for the diagnosis of PSS in dogs and cats and cirrhosis in dogs (sensitivity of essentially 100%), their value is limited for the screening of most other hepatobiliary diseases (sensitivity 54-74%). Higher pre- than postprandial values may occur secondary to interdigestive gallbladder contraction or due to variations in gastric emptying, intestinal transit, or response to cholecystokinin release. This has no clinical significance, and whichever value is highest is used for interpretation. Falsely elevated postprandial values can occur with lipemia. Falsely decreased postprandial values may result from failure of cholecystokinin release to result in gallbladder contraction if the meal is inadequate in fat or protein content or an insufficient amount is consumed. Severe ileal disease or previous resection of the ileum can decrease bile acid reabsorption, thus decreasing postprandial bile acids. When used as a test of hepatobiliary function, the magnitude of elevation in serum bile acids does not allow differentiation of the category of disease, with the exception that patients with vacuolar hepatopathy rarely have marked elevations (greater than 75-100 mcmol/L).

    I really only find BAS useful in cases where I suspect a vascular abnormality of the liver.

    I hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster
    11:18 13/07/20

    Hello.

    I hope you are well. I am so glad you are enjoying the course. Thank you for the excellent questions!

    The pathogenesis of hyperbilirubinemia in systemic infections and sepsis is multifactorial. The development of jaundice may occur from an aberration in the processing of bilirubin by hepatocytes or from other effects on the liver that lead to the accumulation of bilirubin in the body. Such processes include increased bilirubin load from haemolysis, hepatocellular injury, and cholestasis from the septic state and from various drugs used for the treatment of sepsis. The cytokine profile will change in the body and this will alter the handling of the bilirubin.

    Regarding the increased cortisol levels which will contribute to PUPD, the cortisol levels will be increased because the liver metabolism of the cortisol will be effected/reduced.

    As for the microcytosis! The cause of the microcytic anaemia is not fully understood, although studies suggest a defective iron-transport mechanism, decreased serum iron concentrations, decreased total iron-binding capacity, and increased hepatic iron stores in Kupffer cells. This could suggest iron sequestration. Microcytosis has been reported with or without anaemia in 60-72% of dogs, but only in ≈30% of cats with portosystemic shunts.

    Hope that helps.

    Scott 🙂

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