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Euglycemic DKA and SGLT-2 Inhibitors: Mechanisms and Clinical Management (Nursing)

by Rhonda Lawes, PhD, RN

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    00:01 Now, this title, euglycemic DKA, that means you've kind of got an equal glycemic reading, right? You have a somewhat normal blood sugar, but yet they're in DKA.

    00:15 Now, this sounds crazy, doesn't it? I mean, how could this happen? Well, it comes down to one medication that the patient may be taking.

    00:23 The patient may be taking a sodium glucose cotransporter-2 inhibitor.

    00:28 Obviously this medication, and we'll call it SGLT-2 from here on out because that was a mouthful, this works through this really unique mechanism of action in the kidneys.

    00:38 So is it always important that you ask if a patient is on this medication? Absolutely.

    00:44 Will they likely know that it's an SGLT-2? No, they may not.

    00:49 So you're going to need to know the names of an SGLT-2 and make sure you get a complete medical history of all the medications that they're taking.

    00:58 So let's go back to how this medication, the SGLT-2s, cause a euglycemic DKA.

    01:05 So normally this is how your kidneys handle glucose.

    01:08 The kidneys filter about 180 grams of glucose every day through the glomerulus.

    01:12 Now remember that the glomerulus is that little tangle of capillaries, right? That's in Bowman's capsule.

    01:17 It's the first thing the blood is hitting before it starts going through the filter.

    01:21 So normally your kidneys and my kidneys will filter about 180 grams of glucose every day in the glomerulus.

    01:29 Now with an SGLT-2 transporter, these are located in the proximal convoluted tubules of your kidneys.

    01:37 So these PCTs, they're responsible for reabsorbing about 90% of this filtered glucose.

    01:45 So I'm going to go back and forth just a little bit to make sure that this is clear for you.

    01:49 Otherwise it just becomes gobbledygook.

    01:51 So we know that my kidney filters about 180 grams of glucose in my glomerulus, and I've got these SGLT-2 transporters in my PCTs, the proximal convoluted tubules in my kidneys.

    02:05 Now these guys, right, these transporters are responsible for reabsorbing about 90% of that 180 grams of glucose that my kidneys usually filter per day.

    02:19 See with us, that's how it should happen.

    02:22 Now these transporters that we're talking about, they work by coupling with sodium and glucose transport, and they move both the molecules from the tubular lumen back into the bloodstream together.

    02:32 Okay so that's what these transporters do.

    02:36 But when you're taking this medication, an SGLT-2, it's a sodium glucose cotransporter to inhibitor.

    02:45 See this stops that from happening.

    02:48 These are a class of medications that are used to treat type 2 diabetes and patients with chronic kidney disease.

    02:55 So you're likely to see a patient who's taking this type of medication.

    02:58 So when an SGLT-2 blocks the transporters in the proximal tubule of the kidney, it prevents the kidneys from reabsorbing glucose and sodium.

    03:09 Are you following me? So that's why if they're on this medication, they're going to have increased glucose excretion in their urine.

    03:19 So they're also going to have increased sodium excretion.

    03:22 Remember they go together, the glucose and the sodium.

    03:26 So they're going to be peeing out a lot of glucose, which is a big factor in why they may not have as high a blood glucose as a client who isn't taking this type of medication.

    03:38 Also keep in mind, they've got excess sodium going out, so you're really going to be extra dehydrated.

    03:44 So this SGLT-2 is going to lower the blood glucose levels independent of insulin.

    03:50 So even though your client is in DKA, if they're taking an SGLT-2, this is a reason their blood sugar might not be as high as if they weren't taking this medication, because they're going to be just dumping a bunch of glucose out of the bloodstream into the urine because you're using an SGLT-2 inhibitor that is blocking the things, their job is to reabsorb that glucose to go back into the bloodstream.

    04:14 So you're also going to have this caloric loss through glucose because you can't use that energy.

    04:20 They're going to lose weight, so you'll see a reduction in their weight, and their blood pressure will most likely be impacted.

    04:26 It's going to be lower because you've lost all that sodium and further lost all that fluid.

    04:32 Now, there's some benefits of this.

    04:34 If someone's on an SGLT-2 inhibitor, there's some real cardiovascular benefits.

    04:38 It's going to reduce cardiac preload because you're getting rid of so much extra fluid.

    04:42 If you're not in DKA, that could be a really good thing.

    04:45 It can improve your cardiac energy metabolism.

    04:47 That's also a good thing, but it also reduces stress.

    04:51 It'll decrease the oxidative stress in the body, and it also reduces the stiffness of your arteries.

    04:57 Okay, ding, ding, ding, ding, ding.

    04:58 These are all winners, right? If someone's diabetic, they also have increased cardiovascular risks.

    05:04 So this particular medication, you can see why it's a good thing, that it reduces cardiac preload because the heart's not going to have to work as hard.

    05:11 It's going to be better at metabolism.

    05:12 It's going to decrease stress, and the arteries are not going to be as stiff, which will also help bring down blood pressure and cardiovascular risk.

    05:20 So these are good drugs.

    05:22 I don't want you to get the idea that they're not.

    05:24 We give them for a very specific reason.

    05:26 You just have to be on the lookout and educate your patients if they're taking this medication.

    05:31 They can develop DKA, and their blood sugars will look fine.

    05:35 They need to come in and be seen because how this impacts the kidneys, right? You're going to have an intraglomerular pressure.

    05:42 It's going to be lower, right? Because it's acting on the kidneys and what's going on.

    05:48 You're going to decrease protein in the urine, and it's going to slow the progression of diabetic kidney disease.

    05:54 So we see why it's good for the heart, right? Reduces preload, reduces the cardiac energy metabolism.

    06:00 It decreases the stress, reduces the arterial stiffness on the kidneys.

    06:04 Not as high a pressure in the glomerulus, so that's going to help the kidneys' life be extended.

    06:09 It's not going to be banged so hard.

    06:11 It's going to decrease the albumin or the protein in the urine, which remember that's a sign the kidneys can't filter well if you have too high levels of protein in your urine.

    06:21 And this together is going to slow the progression of diabetic kidney disease.

    06:26 So why are SGLT2s used? Well, they've got lots of benefits, including cardiovascular and renal effects.

    06:33 So let's go back to the context of DKA.

    06:37 In DKA, if a patient is taking an SGLT2 inhibitor, this will, say, mask the hyperglycemia, because these drugs are causing massive dumping of the glucose through the urine, even if the patient doesn't have the insulin that they need.

    06:53 That's why they can be in DKA, but it's euglycemic DKA versus hyperglycemic DKA.

    07:01 So patients can have ketoacidosis, but still have relatively normal blood glucose levels.

    07:08 So this is why a diagnosis of DKA should not rely solely on glucose levels when the patients are on SGLT2 inhibitors.


    About the Lecture

    The lecture Euglycemic DKA and SGLT-2 Inhibitors: Mechanisms and Clinical Management (Nursing) by Rhonda Lawes, PhD, RN is from the course Diabetic Ketoacidosis (Nursing).


    Included Quiz Questions

    1. Diabetic ketoacidosis occurring with relatively normal blood glucose levels.
    2. Diabetic ketoacidosis occurring with extremely high blood glucose levels.
    3. Diabetic ketoacidosis occurring with extremely low blood glucose levels.
    4. Diabetic ketoacidosis occurring with unmeasurable blood glucose levels.
    1. Reabsorbing approximately 90% of filtered glucose in the proximal convoluted tubules
    2. Filtering approximately 180 grams of glucose daily through the glomerulus
    3. Secreting excess glucose directly into the bloodstream from the tubules
    4. Converting glucose into ketones within the proximal convoluted tubules
    5. Blocking sodium reabsorption while promoting glucose retention in tubules
    1. They block glucose reabsorption causing massive glucose excretion in urine while ketoacidosis develops.
    2. They increase insulin production leading to rapid glucose utilization and ketone formation.
    3. They stimulate excessive glucose absorption causing paradoxical ketone production in cells.
    4. They enhance glucose filtration in glomeruli while simultaneously blocking ketone excretion.
    1. Because these medications mask hyperglycemia by causing glucose excretion even during ketoacidosis
    2. Because these medications cause false glucose readings on standard blood glucose monitors
    3. Because these medications prevent ketone formation despite elevated blood glucose levels
    4. Because these medications interfere with laboratory glucose measurement techniques and accuracy

    Author of lecture Euglycemic DKA and SGLT-2 Inhibitors: Mechanisms and Clinical Management (Nursing)

     Rhonda Lawes, PhD, RN

    Rhonda Lawes, PhD, RN


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