Diabetic Ketoacidosis and Hypoglycemia

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I have read my book regarding Ketoacidosis and I understand why it is caused by diabetes type 1. However, one question that I still have unanswered is whether hypoglycemia and cause DKA or not. I know that hyperglycemia can cause it, but why can't hypoglycemia cause it too? If we have low blood sugar (hypoglycemic) and cannot use carbohydrates for fuel, the second option would be to break down triglycerides, which would produce ketones that are acidic. So why can't hypoglycemia cause ketoacidosis?????

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Some1 please clarify this for me, I have a test coming up soon

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Specializes in Emergency.

https://allnurses.com/nursing-student-assistance/dka-in-hypoglycemia-761095.html

edit: ****, above poster posted said thing as me. LOL. :D Google ftw.

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I had read this before and it doesn't clarify anything, so I posted this instead -.-

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Think of what is going on in the body with hyperglycemia, and think about what is going on with the body in hypoglycemia. You usually see DKA in type 1 diabetics, and their body is not making any insulin at all.

For hypoglycemia, what is the inevitable outcome if the person does not treat the low blood sugar? Your brain needs glucose to function. So a hypoglycemic patient will be in trouble a little bit faster than the patient with hyperglycemia.

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Hmm ok seems to make sense now, I was just confusing starvation ketoacidosis and hypoglycemic ketoacidosis. Thanks for the clarification.

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Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

Hypoglycemia is not a "ketoacidosis" while they may spill ketones from starvation of protein and breakdown of muscle mass....they are acidic from lactic acidosis.

The mechanisms of acidosis are different.....

Causes metabolic acidosis. http://emedicine.medscape.com/article/242975-overview#aw2aab6b2b2aa

  • Lactic acidosis – L-Lactate, D-lactate

  • Ketoacidosis - Beta-hydroxybutyrate, acetoacetate

  • Renal failure - Sulfate, phosphate, urate, and hippurate

  • Ingestions - Salicylate, methanol or formaldehyde (formate), ethylene glycol (glycolate, oxalate), paraldehyde (organic anions), phenformin/metformin

  • Infusions - Propylene glycol (D-lactate, L-lactate)

  • Pyroglutamic acidemia (5-oxoprolinemia)

  • Massive rhabdomyolysis (release of H+ and organic anions from damaged muscle)

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This is a really good question and now I'm left wondering as well!

Why does our not use fat when in a hypoglycemic state but yet uses it in a situation such as DKA - it's because with DKA you are given sufficient time to use those fats? Whereas hypoglycemia is "faster" - so what is the lactic acid a byproduct of?

I thought lactic acid was a product of anarobic metabolism --- WHICH requires A LOT more glucose than aerobic.

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It doesn't use your fat, I believe, in a hypoglycemic state because your liver is producing glucagon. With ketoacidosis, your body breaks down fat for energy because it can't use the glucose, producing ketones, which also need insulin to be broken down. Since there's a build up in your blood, your body will push it out in urine, breath, etc. Ketones are acid, I believe, and the buildup makes your blood acidic.

Of course, I don't know the whole mechanism. I just know some of it, because I've been hospitalized for DKA more than once. (Ugh.)

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