Figure 622

Role of insulin deficiency and the counter-regulatory hormones, and their respective sites of action, in the pathogenesis of hyper-glycemia and ketosis in diabetic ketoacido-sis (DKA).A, Metabolic processes affected by insulin deficiency, on the one hand, and excess of glucagon, cortisol, epinephrine, norepinephrine, and growth hormone, on the other. B, The roles of the adipose tissue, liver, skeletal muscle, and kidney in the pathogenesis of hyperglycemia and ketone-mia. Impairment of glucose oxidation in most tissues and excessive hepatic production of glucose are the main determinants of hyperglycemia. Excessive counterregula-tion and the prevailing hypertonicity, metabolic acidosis, and electrolyte imbalance superimpose a state of insulin resistance. Prerenal azotemia caused by volume depletion can contribute significantly to severe hyperglycemia. Increased hepatic production of ketones and their reduced utilization by peripheral tissues account for the ketonemia typically observed in DKA.


Pure DKA Mixed forms

Pure NKH


5-10 times higher <=>

5-10 times lower


5-10% <=>



Rapid (<2 days) <=>

Slow (> 5 days)

Age of patient

Usually < 40 years <=>

Usually > 40 years

Type I diabetes



Type II diabetes

Rare <==>


First indication of diabetes

Often <==>


Volume depletion

Mild/moderate <=>


Renal failure (most com-

Mild, inconstant <=>

Always present

monly of prerenal nature)

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