DKA – Diabetic Ketoacidosis Nursing Care NCLEX® Review |

Nursing Care NCLEX Review | Okay, so let s talk about Diabetic Ketoacidosis.This is something that you may see in your time in the hospital. If “youre working in” an ICU, general medical ICU, you re gonna see this often as it is fairly common but it requiresvery intensive monitoring labs, frequent lab outlines, cardiac observing, electrolyte monitoring, so there s a good deal that goes on that is involved with taking care of a Diabetic Ketoacidosispatient.So, tell s talk about it really quickly and we re gonna break it down very simplywith our nurse and what we need to know to understand these patients and take careof them. So, first of all, this is gonna occur withtype I diabetic patients. You remember with Type I, it is an autoimmune disorder whereour immune system destroys these beta cells produced insulins, so, we have extreme insulindeficiency or no insulin at all and this should contribute to, what happens is this ends up leading tothe breakdown of fat into glucose which results in ketone torsoes which are acidic. Okay. Thats very simply, we re gonna get in this a little bit more now. So, we have severe insulindeficiency or no insulin at all which leads to breakdown of fatty into glucose for energyand that results in acidic ketones in their own bodies. So, briefly, we re gonna tell you the assessmentand then we re gonna go over it a little bit really quick.So, what happens is, it is asudden onset, it is usually associated with infection or stress. You re gonna notice fruitybreath on your patient and that is result of those acid mass which have kind of thatfruity smell. Ketones are gonna be released into the urine. You re gonna have severe hyperglycemia, generally in like the 400 – 600 array with DKA. You re gonna have dehydration and thisis due to osmotic diuresis which we will go a little bit more in the next move. You realso gonna have acidosis, okay. What is acidosis? Acidosis is pH of less than 7.35, right? Andthen, it s gonna be also a HCO3 of less than 22. Okay. So, we re gonna have a decreasein pH and we re gonna accompany a decrease in Bicarb because of this acidosis.The reason acidosisoccurs, is because these fatties are broken down into glucose. These ketones are a by productto the solid disturbance, ketones are very acidic and potassium begins to leave the cell asa result of this acidosis. You re too gonna examine these Kussmaul s breathings in yourpatient, and like we said, this hyperkalemia. Hyperkalemia is associated with this acidosis.You re likewise gonna watch an hoisted BUN and creatinine and that s a decision to this osmoticdiuresis. As you begin to put out all these urine, you accompany an hoisted creatinine associatedwith that renal flop. You re also gonna want to monitor level of consciousness, cerebraledema can occur due to this fluid shifting as we become highly osmotic and your patients height of consciousness. Okay. So, cause s look at it one more time reallyquick. So, what happens is, we have a decreased stage of insulin or basically, what happensis, the body is no longer develop insulin, okay. So, because we do not have insulin, alright, so our cadre can use glucose and fatty acids to produce energy, right? And so, within the mitochondria, itcan breakdown glucose, it can break down fatty acids to produce ATP, right? But, in orderto use glucose, it has to have insulin, right? Okay, so, now s our cell.Glucose is outsidethe cell. We ve once talked about this before, that in order to get into the cell, it needs insulin. So, without the presence of insulin, glucose is unable to get intothe cell. So, glucose is going to remain outside the cell, alright? But the cadre has anotherway that it can use energy. It are truly break down fatty acids. Okay. So, when thesefatty acids broken up, we get enough energy to kinda to be implemented by cellular metabolismbut we still remain with this glucose outside the cadre, okay.So, what happens when we donot have insulin, is the cell starts to breakdown fatty battery-acids, okay. This leads to acidosiswhich is our pH less than 7.35 and a Bicarb of less than 22. Okay , now it s gonna be ananion gap acidosis. If you wanna learn more about that, there s actually some really goodvideos on youtube by MedCram about what anion gap is, but for our purposes, we just needto understand this is going to lead to acidosis. Due to this acidosis, we re also gonna seehyperkalemia. Okay , now, it also leads to, when we don t have insulin, this is also gonnalead to an high glucose tier, right? So, glucose is not able to get into the cell.So, glucose is rising within our blood.So, our glucose continues to grow, continues torise because we are not attract it into the cell to use it, it s the above reasons these fattyacids. So, as that glucose rises, this is going to lead to osmotic diuresis, okay? Orsimply means that our osmotic pres becomes so great, that the kidneys begin to dump itoff. Okay. And this is gonna lead to the renal downfall and the raised creatinine. Okay.So, that s kinda what s happening here. Two things are happening and that is what we needto understand.Two things are happening, we re breaking down fatty battery-acids, and that s leadingto acidosis. We re too not exerting glucose and that s leading to hyperglycemia. Okay.So , now that we have those two things understood, okay , now, you understand it very simply now, right? It s particularly very simple formerly we break it down like this. We are not, we is not haveinsulin accessible, so, out form has to get that force from somewhere, right? The placethat is gaining that vigour is from breaking down these fatty battery-acids. And, we just saidright there, these are fatty battery-acids. So, we re going to develop acidosis. Okay. And becauseof that, we re going to develop hyperkalemia.Now, the other thing that s happening here, “weve had” these glucose circulating in the cells, or in the blood. So, we still havethese glucose distribute in the blood that s leading to hyperglycemia, at the same time, we re developing this acidosis. So, we re Diabetic Ketoacidosis. Okay. So, our bloodsugars are gonna rise, and again, they re not gonna rise as high as they are in likeHNS because we re apply a little of this vigour, okay? So, how are we gonna treat these patients, okay. We re gonna treat these patients with very intensive insulin therapy. What insulinis gonna do for us, is it s gonna do a couple of things. Insulin is going to help to correctthis acidosis, okay? It s likewise going to help to lower the glucose, okay? What our goalhere with Diabetic Ketoacidosis is to correct this acidosis.That s our primary concernhere, it s chastising this acidosis. As we compensate that acidosis, our potassium is goingto improve, right? We know that insulin is one of the regimen for hyperkalemia, right? With insulin, we can pull potassium back into the cell. And, with insulin likewise, we can correctacidosis, okay? So, the other thing that is going to do at the same time, however, isit s going to correct our glucose stage. So, as we re rectifying our acidosis, we re alsocorrecting our glucose height. Remember, our case is also extremely dehydrated, and so, whatare we gonna get for dehydration? We re gonna do flowings. So, we re gonna get liquids toour patient, that s gonna correct dehydration due to this osmotic diuresis.So, we correctthat osmotic diuresis by giving flowings and that helps to correct that patient there.Then, we contribute our insulin to correct acidosis and that likewise brings down our blood sugars. Okay, so, we re gonna give dehydration, were gonna place the patient in intensive insulin rehabilitation, we re gonna check potassium andwe re going to access for and treat acidosis. If you wanna learn more about this anion gapacidosis, you can check out the Merck Manual, it s one aid you can check out there.But, that s genuinely kind of the basics. But if you can draw this diagram, you get DKA, okay? And if you get DKA, you get the managements and you re understanding better ABG and everythingthat s going on there.Okay? Okay, so that s certainly what s going on with DKA and thats how you can understand why it pertains exclusively, well, most commonly to type I Diabetics andwhy it s different from HNS. Okay. So, that s what we need to understand here. 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