scott@vtx-cpd.com

Replying to Julia C. 14/09/2022 - 12:51

Welcome Julia!

Thanks you so much for joining us.

I have only ever visited Norfolk once… to do my pig farming EMS when I was in vet school! I remember it being very beautiful.

Let me know if you have any questions.

Scott 🙂

Replying to Holly D. 17/09/2022 - 22:14

Welcome Holly.

Thanks so much for joining us! Let me know if you have any questions!

Scott 🙂

Replying to Felipe M. 15/09/2022 - 21:38

Felipe!

Thank you so much for joining us. It is such an honor to have you be involved with the course.

Scott 🙂

Replying to sara h. 15/09/2022 - 21:18

Really lovely to meet you!

Thank you so much to everyone for your brilliant contribution!

Scott 🙂

Replying to Amy Arbuthnott 12/09/2022 - 17:59

I know… poor puppy!

Interesting case though.

Scott 🙂

Replying to Andrea Scott 12/09/2022 - 20:55

Brilliant!

We will know where to direct all of our bacteria related questions!

Scott 🙂

Replying to Victoria Rubasinska 13/09/2022 - 10:56

Hey.

I do think this is possibly most relevant at initial catheter placement. This is a good opportunity to get some blood and this is something we have been doing more routinely. I am also less sure about doing it when the IV line has been in and had fluids etc. going in. I suppose it is good to know it is an option in really tricky cases.

Scott 🙂

Replying to scott@vtx-cpd.com 12/09/2022 - 17:46

All great questions Kelly!!!!

There are indeed live Q&A sessions which are recorded to watch back. Would be lovely to see you live if you can make it!

Regarding the coagulation and proteinuria. Again, not straightforward. Because emboli may be difficult to detect, the prevalence of thromboembolism in dogs with glomerular disease may be higher than indicated. The risk of thromboembolism is highest in dogs with nephrotic-range proteinuria and hypoalbuminemia. Pulmonary thromboembolism is most common, but emboli may also lodge in other arteries (e.g., mesenteric, renal, iliac, brachial, coronary) or the portal vein. Although urinary loss of antithrombin (AT) has gained the most attention in veterinary medicine, the pathogenesis of the hypercoagulable state is multifactorial. AT is a serine protease inhibitor that modulates fibrin generation; heparin catalyzes these reactions. AT (65,000 Daltons) is similar in charge and size to albumin (69,000 Daltons); serum AT activity closely correlates with the serum albumin concentration. Prior studies have suggested that this close correlation can be used to predict thromboembolism when the serum albumin concentration is <2 g/dL, when serum AT III activity would be expected to be less than 75% of normal. Albumin binds to arachidonic acid, which, if unbound, would stimulate platelet aggregation through the generation of prostaglandins (i.e., thromboxane B2); hypoalbuminemia is associated with increased platelet aggregation. Hypercholesterolemia contributes to platelet hypersensitivity by influencing membrane-associated enzyme and receptor activity through alteration of the membrane composition. The role of platelet hypersensitivity in the development of hypercoagulability may be enhanced by thrombocytosis, which occurs in many animals with glomerular disease. Increased fibrinogen concentrations (i.e., above 300 mg/dL), which are often present in patients with NS, lead to increased fibrin complex formation and platelet hyperaggregation. The risk of thromboembolism may be further enhanced by increased concentrations of alpha2 macroglobulin; alpha2 antiplasmin; procoagulant cytokines; coagulation factors V, VII, VIII, and X; increased plasma viscosity and interstitial pressure; decreased plasma plasminogen concentrations; decreased plasma volume and blood flow; endothelial injury; and infections.

I hope that helps.

Scott 🙂