[haji]

We had a pt. in our unit recently with HHNk and he had recently had an MI. I heard from someone that an MI can precipitate HHNK. Does anyone have an explanation for how this process happens? Also, the same patient had a triglyceride level of >17,000 (his blood was apparently thick like milk b/c the hyperlipidemia). I have no idea how his lipids got this high. Still reading about it. thanks for any explanations

[phiposurde]

For your first question about the MI. Any process that increase the metabolism demand increase the demand on sugar.In that case patient with diabetes since they have difficulty producing the right amount of insulin won't be able to cope correctly. The body is a great machine but don't make a difference between an infection, a MI, a laceration, atrauma. The only info it receive:" dammage cells please activate repair system" It always use the same system. That's why anaphylactic shock and sepsis are in a way the same process but with different causes!!

As for the sesond question,I found that possible explanation on the net. Taking that this patient was propably alreay with high level. Probably why he Had an MI:
"In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase II to form fatty acyl coenzyme A, which enters the ß-oxidative pathway to produce acetyl coenzyme A. Most of the acetyl coenzyme A is used in the synthesis of ß-hydroxybutyric acid and acetoacetic acid, 2 relatively strong acids responsible for the acidosis in DKA. "http://www.cmaj.ca/cgi/content/full/168/7/859

Hope I help.

[Burnt2]

Hmm; I don't know if that would explain a triglyceride level of 17,000; thats talking about ketogenesis and the release of amino acids that are then converted (and as far as I know triglycerides are 3 fatty acids and a carb, so that lab value does not reflect free fatty acids)


thats insanely high - talk about emboli risk; I am completely clueless as to why he would have that high of a level; definitely some kind of endocrine disorder is involved?

I did a little search, and all I found was that sometimes new onset diabetes can elevate them, along with alot of alcohol consumption (as well as the normal factors for elevated levels).

A level of 17,000 is too high for that though.


Did they redraw? What did his blood look like when they drew labs?