Diabetes 15, Diabetic Ketoacidosis (DKA)
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- čas přidán 15. 07. 2013
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In addition to occurring in previously undiagnosed patients, ketosis may occur if insulin therapy is interrupted. This is another good reason why insulin therapy should never be stopped in type 1 DM. If no insulin is available, most tissues will switch to fat metabolism as they are unable to metabolise carbohydrates. It is this fat metabolism by the mitochondria, mostly in the liver, which generates the ketone bodies. Increased levels of acetone are formed in ketosis and accumulate in the blood. Acetone is a volatile substance and some of it is blown off in the expired air from the lungs. This causes the breath to smell of acetone; a smell usually described as being like 'pear drops'. Like most smells, once you have experienced it the first time you will immediately recognise it again.
This is the simplest way of explaining the concepts of DKA.I loved it Dr John.Thanks a lot
Dear Dr Campbell. Every evening, after all my chores are done, I watch your lectures. Your explanations are always the best, they supplement my nursing textbook reading so well. Thank you very much!
me too
Thank you , simplified and put together all the bits I needed. Thank you again and you are for a good cause sending funds to less advantaged people. Thanks again.
Thank you, Dr. Campbell. What a wonderful explanation!
absolutely loved the way you explained this, thank you so much!
Thank you. I have an important exam in a few days and your explaining makes me feel alot more calmer.
Dr.John I would love to thank you for this great explanation for this topic, and I subscribed to your channel.
This is really helpful.
Thank you Dr. John. It will help me a lot for my research assignment.
thank you Dr. John. this video is very nice!
Excellent Dr Campbell 👍
I am a new nursing grad about to take my RN nclex and I wish I would have found you years earlier. I love the way you teach and explain things. It really makes sense and I thank you for posting your lectures and lessons. I will continue to use your lessons throughout my nursing career and will highly recommend you.
Thanks Mcangie, best wishes for the NCLEX.
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You described this SO WELL.
thank you for explaining so clearly!
thank you very much, Dr great work
Thank you!! just what i needed so simplified and straight forward.
thank you. you explain simply in one what I need.God bless you!!!!
Thanks a lot... helped me to understand
you are the BEST , Thank you 😍❤
Thank you, it helped me a lot.
One word... Brilliant!
i need to do alot more work but you made it so simple thank you
Very organized and helpful explanation!
Just awesome sir
Thank you sir.
Thankyou doctor
Thanks. Well done and helpful.
Thank you sir
What causes delirium? In a dka patient. I know this is ages ago. I am watching your new content but have found this very useful at present.
thank u senior
from somalia
woow.. thanks a lot
I had diabetic ketoacidosis yesterday.
Blood glucose: >33.3 mmol /l consistently all day, and i became very dehydrated. In addition to that i had a rapid pulse, acetone breath and felt quite cold.
I went to the GP, he put me on a drip, the drip attached to the top of a lamp (he had to improvise) lol.
I want to ask, when you say fatty acids and ketones are used by the cells, i notice my muscles felt "lactic" was that the ketones and fatty acids?
Are ketones acidic in solution... ? Or does the cells metabolise them into acid? But ketones resist mild oxidation.... so it confuses me slightly.
cha gya boss
Wonderful
Thank you for your great videos. Also have been following the COVID series☘️☘️☘️🌹🌹
Thanks for the videos
What is DKA rare in type 2 diabetic
U are talented
I can remember my ketoacidosis like a Nightmare. I was so tired and thirsty. But if I drank some Water, I've spilled it out almost instandly.
i too remember that nightmare.
Thank you Dr. Campbell! I really enjoyed this video! I wish you explained a little bit more about K inside the cell and outside the cell, and how K can be extracellularly elevated but depleted intracellularly.
Thank you!
John shouldn't we give titrated oxygen also to help with the acidosis, Kussmals breathing, the patient's gaseous exchange is not controlled due to hyperventilation. O2 will help correct the acidosis? I'm not 100%
Thanks
Hello Dr. Campbell, thanks for the video, it is very helpful. My question is about the treatment for DKA. A text I was reading stated that ..."if a patient is hypokalemic, insulin administration will further decrease the potassium level leading to life - threatening hypokalemia." In this case, what should be done -hold off for the insulin-?
You are correct. Insulin gates both glucose and potassium into the cell cytosol from the tissue fluids and blood. Giving insulin will therefore lower glucose and potassium serum levels. It will therefore be usual to give insulin and potassium together, according to local protocols. This must of course be done very carefully, as rapid changes in potassium can lead to ventricular fibrillation.
Does this have anything to do with how the body is affected by a Keto diet?
awesome :D
Thanks Dr John
wow think you so much it have important for no Diabetes 15, Diabetic Ketoacidosis in other country that there are some people have it. can lost it.
Good video, nice flow diagram haha! One thing I don't get is the K+ situation; I thought K+ was pumped into the blood in order to balance the high H+ being produced, so you were HYPERkalaemic? I'm obviously wrong, but could you maybe explain this part of it a little bit more? Thank you!
I share your thoughts. I guess it is really a relative thing. Some patients might develop hyper or hypokalemia depending on how much K+ is being lost in the urine and how much is going from the cells to the blood to trade that H+
Guess we'll only know for sure with arterial gasometria
Thanks Dr. Campbell, I had a question about the treatment if the patient has cerebral edema, in the use of manitol or hypertonic saline, which one has better outcome or it's better to use manitol and if the patient is not responding to treatment use the hypertonic saline?
Pedro Cardoza I don't know, you ask a good question.
In the words of Kamel H1, Navi BB, Nakagawa K, Hemphill JC 3rd, Ko NU writing in
Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials.
'We found that hypertonic saline is more effective than mannitol for the treatment of elevated intracranial pressure. Our meta-analysis is limited by the small number and size of eligible trials, but our findings suggest that hypertonic saline may be superior to the current standard of care and argue for a large, multicenter, randomized trial to definitively establish the first-line medical therapy for intracranial hypertension.'
Thanks Dr. Campbell!
Pedro Cardoza I think monitol is better I have seen it used much
Acidosis causes vomiting very often, you didn't mention that doctor?
hi Dr... u really astonished doctor... why there is ketoacidosis in type 1 but no in type 2 as u say in another videos TKu so much. ..
Because the ketosis is caused by insulin lack and in type 2 DM, there is still some insulin in the system. However, in type 1 DM, there is an absolute deficiency of insulin, leading to ketogenesis.
Doctor you are amazing :)
i would like to say that at first metabolic acidosis causes HYPERKALEMIA bc due to the acidosis protons (H+) leak into the cells and Kallium out .But in continuity we will give potassium as treatment as a result of insulin substitution which will reduce the potassium in blood . So at first there is hyper or hypokalemia ?
at first there is hyperkalemia and once they recieve insulin they will have hypokalemia so they will recieve KCL
I am a big fan of your presentations - really really appreciate the amount I have learnt from you - but I have a few questions about the flow - my understanding is - insulin will shut off movement of glucose in the muscles and fat cells - muscles will then have no choice but to switch to glycolysis (relying on small glycogen stores it has) and/or fat utilisation as energy source (which is a slow process) - this causes ketone bodies to form in the blood and in extreme cases DKA, liver has no problem getting glucose in cause it has two-way insulin independent GLUT-2 pump, brain is fine too cause it has just like RBC (GLUT-2) insulin-independent GLUT-1 but the glucose it is producing is not getting to the muscles and that is the problem. So I am entirely sure how liver is a contributing factor to formation of ketone bodies. Insulin shut off gluconeogenesis so really it is the glucose and hyperosmotic effects it will have and various other problems (glycated products etc) which is the issue. I would appreciate if somehow you find some time somehow to let me know what am I missing - thank you for all your excellent excellent presentations.
I'm not sure i quite understand your doubt here. But what i think is the key to the pathophisiological process is the complete (or near complete) absence of insulin, resulting in no negative feedback with the counterregulatory hormones (glucagon, cortisol, even cathecolamines). Because of the complete absence of the negative feedback, your body interpretates as if your in a state of fasting. Hope i helped you somehow !
That is why even though the liver and brain are being able to use glicosis just fine, the liver still induces glicogenolisis, gliconeogenesis and beta oxidation of the fatty acids. Because of the counterregulatory hormones effect on the liver, wich are very high in DKA.
Hi Dr Campbell. Does the resulting free fatty acids transferred into the blood result in an increased level of LDL and HDL lipids? if so does this result in an increased likelihood of thrombus formation and Cardiovascular pathology in patients with T1DM?
Jordan,NZ Nursing Student
Hello Jordan, Patients with DM 1 or DM 2 are prone to diabetic dyslipidaemia. There is a tendency for protective HDL to go down, while at the same time harmful, atherogenic LDL goes up. Triglycerides can also be raised. These dislipidemic factors will certainly predispose to deposition of atheroma in the process of atherosclerosis. If atheromatous plaques become unstable, thrombus formation will develop leading to stroke or MI.
+Dr. John Campbell
how TAG will accumulate and lead to dyslipdemia if there is breaking down for the lipids in body and as a result from it weight loss. .... .. clear that to me...TKU so much
in 7:58 you say hypoglycaemia, but you write down hyperglycaemic, low insulin levels cause hyperglycaemic as in diabetes
Is it possible to have DKA with low blood sugar?
Is this only possible after having high blood glucose and then injecting to lower blood sugar but still being in DKA?
There will always be a degree of hyperglycaemia associated with DKA as both are causes by insulin lack.
Theres also euglycemic dka with some diabetic drugs,but I think the glucose is still a bit high.
Very nice video but 1 thing that always confuses me. what is the stimulus of glucagon? If a person has an insulin deficiency is it the intracellular glucose or the serum glucose which stimulates glucagon? cause if it's the serum glucose why on earth would glucagon be secreted when there is already a high glucose in the blood( if it's the intracellular then it may make sense ). Does insulin have a direct inhibitory effect on insulin or not? thnx for the answer in advance.
+Georgios Spartan Low blood glucose levels are directly detected by the alpha cells, which then respond by secreting glucagon. Therefore the direct stimulus for glucagon secretion is relative hypoglycaemia. This mechanism works, independently of insulin. Stimulation for insulin secretion, from the beta cells, is raised level of glucose in the blood. In both cases, it is the levels of glucose in the blood plasma which is detected.
+Dr. John Campbell : thank you but you have partly answered my question. When you have an insulin deficiency or resistance in diabetes then the sugar in the blood is high--then why does is glucagon secreted? since you say the stimulus is relative hypoglycemia. Glucagon should not be secreted is sugar is high!! except if there is an another stimulus or for some reason glucagon regulation /secretion in diabetics malfunctions.
+Georgios Spartan Yes, there is always an extra layer of complexity. Secretion of glucagon has a U shaped secretion pattern, as stimulated by glucose. So, low levels of serum glucose will stimulate glucagon secretion, this is well established. Then as plasma concentrations of glucose rise, the secretion of glucagon is inhibited by this rise. However, as glucose levels rise still further, into the pathological hyperglycaemic ranges, this hyperglycaemia, paradoxically, but for definite, stimulates glucagon secretion. Therefore glucagon secretion is stimulated by low, and very high plasma glucose concentrations. This is because the body needs to use ketones, when insulin lack prevents the use of glucose as a metabolic fuel substrate. So the very high levels of glucose are detected by the alpha cells as pathological, this is how the alpha cells 'know' the body is in need of ketones as an emergency substrate. The alpha cells will then release the glucagon to stimulate the required ketogenesis.
+Dr. John Campbell Brilliant!) Now i got you)) now its all clear) thnx a lot , i appreciate it)) have a nice day!)
Does DKA occur in type 2 dm?
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Yes, it can happen to Type 2 as well, this video needs to be updated.
so very low insulin levels (almost none) causes hypoglyceamia and very high levels causes hypoglyceamia, the 2nd one called hyperglycaemic hypoglyceamia
low insulin levels causes hyperglycemia
What is the cause for the vasodilation?
+Graham Taylor I think its the acidosis. The acidosis interferes with the ably of the peripheral arterioles, and their neuronal innervations to function. Without neuronal innervation, peripheral vessels with dilate on their own.
+Dr. John Campbell Thanks Dr. Campbell, I have a nursing exam on Tuesday, your videos have been extremely useful as well as your books! Wish me luck!
+Graham Taylor I do, train hard, fight easy.
+Graham Taylor Ketoacidosis causes an autonomic type of neuropathy(damage to nerves) including faulty regulation of innervation of blood vesels leading to vasodilation.
+Georgios Spartan Thank you! I aced the exam too thanks to these videos and a great deal of revision :)
My Boyfriend died he was a achoic and he was tiie 1 dibeatic he would drink alot do you think he died of the drink as well????
Hello Leanne,
Its hard to tell by what you have said here, but certainly drinking too much and poorly controlled diabetes are both risk factors. It may have been that the drinking interfered with his ability to care for his diabetes, so his levels of diabetic control were not as good as they could have been. If his levels of diabetic control were poor, this would make it more likely he would develop complications, such as heart disease. Whatever the precise cause of his death, I am sorry for your loss. John
thanks we was told he died from KETOACIDOSIS
Thank you sir