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Discussion Starter · #1 ·
Infection, trauma, surgery are some conditions that trigger DKA.

Why is it so?

I read some where anything that increase need of insulin can trigger DKA in a patient with severe insulin impairment.
but as far as i know infection, surgery, trauma,,,all are stress conditions and stress hormones should go up NOT insulin.
please help me figure out this
thanks
 

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stress --> increase stress hormones --> counter regulate insulin ---> need more insulin

hana, you need to get some sleep :rolleyes:
 

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Discussion Starter · #3 ·
stress --> increase stress hormones --> counter regulate insulin ---> need more insulin

hana, you need to get some sleep :rolleyes:
:))
i am not sleepy now but have a question that might sound coming from a very sleeeeepy:rolleyes: person,

why we develop ketoacidosis and keton building up in insulin deficiency situation such as DM1, but we do not have this issue when we simply have just hypoglycemia for any reason?
i need some one tell me please what is exact roll of insulin when cells need to use glucose?? my confusion is since i know insulin has no effect on glucose uptake by cells-except skeletal resting muscles and adipose tissue - i can not find other reason for insulin, maybe it is because cells can not do glycolysis without insulin??
 

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DKA pathogenesis

DKA PATHOGENESIS
Mechanisms for hyperglycemia
(1) Increased gluconeogenesis
(a) Due to increase in glucagon and epinephrine
(b) Most imp mechanism of hyperglycemia
(2) Increased glycogenolysis in the liver
Mechanism for ketone bodies
(1) Increased lipolysis with release of fatty acids
•​
No inhibition of hormone-sensitive lipase
(2) increased (beta-oxidation of fatty acids increases production of acetyl CoA.
• No malonyl Co-A to inhibit carnitine acyltransferase, the rate-limiting enzyme of beta-oxidation
(3) Acetyl CoA is converted by the liver to ketone bodies.

• Acetone (fruity odor), acetoacetic and (3-hydroxybutyric acid

hope this helps :)
 

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I think that Dr Z is making the point that insulin is also important as a counterregulatory hormone opposing glucagon. DKA is not so much from hyperglycemia or lack of insulin; rather, from the body being too long under the influence of glucagon: release of FFA's, beta-oxidation & production of ketone bodies -> eventual ketoacidosis.
 
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