Diabetic Ketoacidosis
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Just letting you know you are AWESOME and helped soooo much with understanding biochemistry xoxox
I cannot thank you enough for how much your videos have helped me clearly understand biochem. My professors always leave out the details, leaving the students trying to fill in the blanks by themselves. You, however, cover everything! and your videos are the most helpful resource!!
Excellent – THE BEST explanation I’ve heard. Thank you so much.
Best lecture ever! Thanks a lot.
How do you know all this stuff? And you explain it so well..
You’re an amazing teacher.
Awesome, the best ever…..really helped me with biochemistry nd still enjoying ?
Thank you so much your lectures very useful
thx for video. extra glucose in the blood also damages proteins by sticking to them irreversbly.
Prefect ♥️??
amazing explanation?keep on
Really I am bad at Biochem but when i watch ur lectures it’s just easy. i would love u to cover every point of Biochem.
Thanks! 🙂
0:50 I thought the liver had Insulin independant (GLUT-2) transporters. Is it not able to take up glucose even if the Insulin level is low?
@Jehanzaib Zafar oh okay thanks a lot now I got it!
@Ema Z ketone bodies are produced in fasting state when glycogen reserves are depleted. Reasons for ketone production is that during fasting state there is breakdown of FAs which result in lots of production of Acetyl CoA. Now at the same time, Oxaloacetate of krebs cycle is depleted bcz it is being used in glucogeonesis, so the only pathway Acetyl CoA has is the production of Ketone Bodies.
@Jehanzaib Zafar so if the liver takes up the glucose even in the absence of insulin, what is the actual reason for the production of ketone bodies then?
yeah you are right. Liver is able to uptake glucose through GLUT 2 receptors which are insulin independent glucose uptakers
You are right, Insulin stimulates the GLUT 4 transporters located in the heart muscle, skeletal muscle and adipose tissue. Glucose gets into the liver by the GLUT 2 transporter that has low affinity (high Km) to glucose thus it is active (aka transports glucose) when the concentration of glucose is high in the portal vein = after eating. Hope this helps 🙂
Your videos are very helpful!!!!Thank you!!!!!
My sister had diabetic ketoacidosis and it is a life-threatening condition.thank you ak lecture to teach such a important and complex topic so easily…..
the legend has back
+ליאל אדרי 🙂
thank you Sir.
I’d like to ask you about the real cause of abdominal pain in people with DKA.
I’ve been searching a lot and didn’t get any information
why there is gastritis, pancreatitis…
what happens to them
I want to know the exact pathology of that
The pathogenesis of abdominal pain in DKA is unclear, though it’s believed to be related to gastritis, pancreatitis, and liver engorgement.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2589676/pdf/yjbm00105-0009.pdf
Excelent lecture, but you did forgot to mention that advanced tipe 2 diabetics can also develop ketoacidosis, if almost all of their pancreas beta-cells are down. You are also not telling us how is it that muscle cells are not able to use ketone bodies quickly enough, what`s going on there?
El Vegano Cordobes &
very nice sir
very analytical explanations
Thankyou. your explaination is very clear