Invokana Euglycemic Dka

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What is DIABETIC CARDIOMYOPATHY? What does DIABETIC CARDIOMYOPATHY mean? DIABETIC CARDIOMYOPATHY meaning - DIABETIC CARDIOMYOPATHY definition - DIABETIC CARDIOMYOPATHY explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... Diabetic cardiomyopathy is a disorder of the heart muscle in people with diabetes. It can lead to inability of the heart to circulate blood through the body effectively, a state known as heart failure, with accumulation of fluid in the lungs (pulmonary edema) or legs (peripheral edema). Most heart failure in people with diabetes results from coronary artery disease, and diabetic cardiomyopathy is only said to exist if there is no coronary artery disease to explain the heart muscle disorder. One particularity of DCM is the long latent phase, during which the disease progresses but is completely asymptomatic. In most cases, DCM is detected with concomitant hypertension or coronary artery disease. One of the earliest signs is mild left ventricular diastolic dysfunction with little effect on ventricular filling. Also, the diabe

A Case Of Euglycemic Diabetic Ketoacidosis Due To Canagliflozin Complicated By Takotsubo Cardiomyopathy

A Case of Euglycemic Diabetic Ketoacidosis due to Canagliflozin Complicated by Takotsubo Cardiomyopathy Muzammil Khan , Shaza Khalid, Asghar Marwat, Hassan Mehmood American Journal of Medical Case Reports. 2018, 6(1), 1-3. DOI: 10.12691/ajmcr-6-1-1 Sodium-glucose co-transporter-2 (SGLT-2) inhibitor is the latest class of anti diabetic medication that improves glycemic control in insulin independent fashion by increasing urinary loss of filtered glucose. Since its introduction in 2013, several cases of euglycemic DKA have been reported in patients being treated with SGLT-2 inhibitors. Blood glucose levels in range lower than expected for DKA makes the diagnosis challenging if clinical suspicion for euglycemic DKA is not high. We report a case of a patient being treated with canagliflozin who presented with DKA, AKI and mild hyperglycemia that was complicated by stress-induced cardiomyopathy. Keywords: sodium-glucose co-transporter-2 (SGLT-2) inhibitor euglycemic DKA In March 2013, first Sodium-glucose co-transporter-2 (SGLT-2) inhibitor, canagliflozin, was approved for the treatment of type 2 diabetes mellitus by the US food and drug agency (FDA) (1). SGLT-2 inhibitors reversibly i Continue reading >>

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  1. Kevin Gormley

    I have been in nutritional Ketosis for 4 months now. I GET that I am not as hungry as before due to being "fat adapted". Some days I do not feel like eating much at all. But, my question for the group is there science around "Does you body have the ability to store extra calories from fat into adipose tissue when insulin is low?" That is... when someone is Keto adapted (protein is appropriate and carbs are very low) if I DO eat too much cream cheese and whipped cream one night- what happens to that energy? I have done this a couple of times (binged on whipped cream) and it has not seemed to ruin anything. Are there alternative mechanisms other then insulin for your body to store excess calories from "fat bombs" when you are fully Keto- adapted? BTW, I am not looking for permission to gorge myself- just the science how how our bodies deal with too much fat calories! I have been curious since the second month on Keto.

  2. Fiorella

    I believe that yes it is possible to eat too much. However, the fat typically allows you to have satiety signals that naturally stop you from over eating.

  3. carolT


    "Does you body have the ability to store extra calories from fat into adipose tissue when insulin is low?"
    I think the key to this is the definition of "low". I take that to mean normal basal insulin plus whatever insulin response you get from stomach signaling upon ingestion. Then yes, it is sufficient to store fat in adipose tissue. Take, for example, a type-1 diabetic. They do not store fat well at all. Also, a severely insulin resistant person has damaged fat cells in adipose tissue that can no longer absorb fat. This is when visceral fat accumulates and leads to NAFLD. Most of us with normal to elevated basal insulin are quite adept at fat storage. It's getting the fat back out again [and using it for fuel] bit that's the problem.

    @richard and @erdoke can get more technical and sciencey than I can.

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To watch the full lecture visit: https://bit.ly/2GCpykW About this lecture: Covering reviews of cardiovascular outcome trials, Professor Andrew Krentz focuses on glucose lowering in clinical trials. Professor Krentz discusses updates on hypotheses concerning the mechanism of benefits and risk of EMPA-REG OUTCOME and CANVAS studies, and considers the clinical implications of these trials. This lecture was filmed at the RSM in London for the event 'an update on lipid and glucose lowering clinical trials' on Friday 23rd of February 2018

Euglycemic Diabetic Ketoacidosis With Prolonged Glucosuria Associated With The Sodium-glucose Cotransporter-2 Canagliflozin

Euglycemic Diabetic Ketoacidosis With Prolonged Glucosuria Associated With the Sodium-Glucose Cotransporter-2 Canagliflozin Neda Rasouli, MD, University of Colorado Denver, Mail Stop 8106, 12631 East 17th Avenue, Aurora, CO 80045, USA. Email: [email protected] Received 2017 Mar 15; Revised 2017 May 5; Accepted 2017 May 9. Copyright 2017 American Federation for Medical Research This article is distributed under the terms of the Creative Commons Attribution 4.0 License ( ) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( ). Sodium-glucose cotransporter-2 (SGLT2) inhibitors improve glycemic control by a reversible inhibition of the sodium-glucose cotransporters in the renal proximal tubules resulting in increased urinary glucose. This unique mechanism, independent of insulin secretion and beta cell function, has made this class of medication desirable in patients with type 2 diabetes. However in May 2015, the US Food and Drug Administration issued a safety warning pertaining to the development of diabetic ketoacidosis (DKA) with the use of SGLT2 Continue reading >>

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  1. Babybeastte

    So I have looked high and low. Is there a list out there of supplements (i.e BCAA, L-carnitine, creatine etc etc ) that have the potential of kicking you out of keto. Or maybe should I be looking for a particular ingredient other than the obvious (i.e sugar or sugar derivative)?
    My urine ketones seem to drop dramatically after a heavy weight session (which involves supplements as noted above). I always bounce back very quickly, but its good to be in the know.
    Facts: current weight 110, BF 17%, height 5'2", sex F, age 48 soon to be 49. 6 weeks out from my 1st grand master figure comp & excited as heck!! Keto since May 1, 2015 and luv'g it.

  2. anbeav

    Put the ketostix away, you can make no conclusions from the level on the stick. Embrace it, as discussed yesterday, don't second guess what's clearly working for you

  3. rickamore

    Nutritional ketosis relies on empty liver glycogen. That's it. I don't know why people think things like caffeine will "Kick them out of keto". Is it a substantial amount of carbs? No? Then unless it's something that will kill you already (thus halting ketosis) it won't do anything other than at most reduce the amount of circulating ketones in the blood. Which doesn't matter, you'll still produce them as needed unless you start carbs again.

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DKA diabetic ketoacidosis nursing management pathophysiology & treatment. DKA is a complication of diabetes mellitus and mainly affects type 1 diabetics. DKA management includes controlling hyperglycemia, ketosis, and acdidosis. Signs & Symptoms include polyuria, polydipsia, hyperglycemia greater than 300 mg/dL, Kussmaul breathing, acetone breath, and ketones in the urine. Typically DKA treatment includes: intravenous fluids, insulin therapy (IV regular insulin), and electrolyte replacement. This video details what the nurse needs to know for the NCLEX exam about diabetic ketoacidosis. I also touch on DKA vs HHS (diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic syndrome (please see the other video for more details). Quiz on DKA: http://www.registerednursern.com/diab... Lecture Notes for this video: http://www.registerednursern.com/diab... Diabetes NCLEX Review Videos: https://www.youtube.com/playlist?list... Subscribe: http://www.youtube.com/subscription_c... Nursing School Supplies: http://www.registerednursern.com/the-... Nursing Job Search: http://www.registerednursern.com/nurs... Visit our website RegisteredNurseRN.com for free quizzes, nursing care plans, salary

The Dka That Wasn't: A Case Of Euglycemic Diabetic Ketoacidosis Due To Empagliflozin

The DKA that wasn't: a case of euglycemic diabetic ketoacidosis due to empagliflozin Nellowe Candelario * and Jedrzej Wykretowicz Department of Internal Medicine, Einstein Healthcare Network, Philadelphia, USA *Correspondence address. Department of Internal Medicine, Einstein Healthcare Network, 5501 Old York Road, Philadelphia, PA 19141, USA. Tel: +267-858-5508; E-mail: [email protected] Received 2016 May 14; Revised 2016 Jun 14; Accepted 2016 Jun 16. Copyright The Author 2016. Published by Oxford University Press. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact [email protected] This article has been cited by other articles in PMC. Sodium glucose co-transporter (SGLT-2) inhibitor is a relatively new medication used to treat diabetes. At present, the Food and Drug Administration (FDA) has only approved three medications (canagliflozin, dapagliflozin and empagliflozin) in this drug class for the management of Type 2 diabetes. In Continue reading >>

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  1. KetogenicJoseph

    What's up guys? Hope everyone is having a good day so far. Anyway's I have been doing some reading on the Ketogenic diet. I have a friend who just graduated from medical school and we were talking about the potential long term effects of being on a high fat diet. He suggested that being on a high fat diet, over time, can lead to a build up of plague in your arteries. I don't know if I necessarily believe that but after further research I discovered that many of the things that I eat on a Keto diet can, in turn, cause plague build up over a period of time. What are y'alls thoughts on this?
    Also, I started reading up on the "potential dangers" of a keto diet. One article which seemed pretty biased and not based on evidence said this: .,.. if you're on a strict low carbohydrate diet, you can say goodbye to intense weight training, track intervals, or just about any activity that would be consider “tempo”, “threshold”, or “intervals”. And this is the stuff that adds lean muscle to your body, boosts your metabolism and gets you fit fast – compared to a slow and sluggish slog in your “fat-burning zone”. This is not negotiable by your body. It is simple physiology. When you deplete muscle glycogen, there is a directly proportional increase in muscle fatigue, and also an increase in muscle catabolism (direct metabolism of your body's own muscle protein, or conversion of that protein into glucose via gluconeogenesis). Many people on a low-carbohydrate diet simply stop exercising, because it can suck so much.

    Now. I have heard that people get some really good work outs in when they are on Keto and even when they are fasting. I don't buy the fact that eating a low carb diet can lead you to not being able to work out. In fact I have seen other physical, tangible evidence of people working out with great results on Keto. What are y'alls take on this dogma?

  2. NelleG

    He suggested that being on a high fat diet, over time, can lead to a build up of plague in your arteries.
    of course he did. he just graduated from med school and that’s what he’s been taught. It’s going to be a loooong time before the fallacy of fat causing heart disease and plaque is taught in med school. How else will they be able to push statins? ( a best selling med of all time)

    Do some poking around on this site, Richard and others have posted a lot of info debunking this very thing.

  3. keehan

    He suggested that being on a high fat diet, over time, can lead to a build up of plague in your arteries.

    High fat in conjunction with high carb would be more correct IMHO. Of the dietitians and nutritionists I’ve (personally) seen, they can’t seem to get a grasp on the idea of low/zero carb, so therefore high fat automatically comes with high carb. Normal carb for them is 200-300g daily or more. Under 100g is low for them, and some will frankly tell you that you cannot survive on the <20g level of a real Keto diet.

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