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Diabetes 15, Diabetic Ketoacidosis (DKA)

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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.


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  1. thank you very much, Dr great work

  2. πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’™β€οΈβ€οΈπŸ“•β€οΈπŸ“˜πŸ’™β€οΈπŸ’™πŸ“˜πŸ“•πŸ“˜πŸ’™β€οΈπŸ’™β€οΈπŸ“•β€οΈβ€οΈπŸ’™πŸ“•β€οΈπŸ“•πŸ“˜πŸ’™πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰πŸ’‰

  3. Thank you very much,Dr. Campbell. You are very helpful. Your concept maps are amazing.

  4. absolutely loved the way you explained this, thank you so much!

  5. 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 ?

  6. you are the BEST , Thank you 😍❀

  7. Hi Mr. Campbell. I love your videos but can you please use white board instead of paper.
    Please excuse me for this.
    I cannot stand screaching sounds on paper while listening your videos.

  8. 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.

  9. thank you for explaining so clearly!

  10. Does DKA occur in type 2 dm?

  11. 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.

  12. 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.

  13. 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.

  14. 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. ..

  15. 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?

  16. 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!

  17. 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.

  18. Thanks.Β  Well done and helpful.

  19. 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.

  20. What is the cause for the vasodilation?

  21. 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?

  22. in 7:58 you say hypoglycaemia, but you write down Β hyperglycaemic, Β  Β  Β low insulin levels cause hyperglycaemic as in diabetes

  23. so very low insulin levels (almost none) causes hypoglyceamia and very high levels causes hypoglyceamia, Β the 2nd one called hyperglycaemic hypoglyceamia

  24. 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?

  25. Thank you, Dr. Campbell. What a wonderful explanation!

  26. 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

  27. thank you Dr. John. this video is very nice!

  28. Beautiful talk. Loved this. Thanks for educating us dr campbell

  29. 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.

  30. 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.

  31. Thank you Dr. John. It will help me a lot for my research assignment.

  32. i need to do alot more work but you made it so simple thank youΒ 

  33. 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 asΒ  well????

  34. Thanks a lot… helped me to understand

  35. 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%

  36. Thank you, it helped me a lot.

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