HYPEROSMOLAR HYPERGLYCAEMIC STATES
Initially
called hyperosmolar non-ketotic (HONK) hyperglycaemia. The dominant clinical
feature is dehydration. It mainly occurs in older subjects with type 2 diabetes
mellitus. The cycle of hyperglycaemia, dehydration (occurring due to vomiting,
polyuria, glycosuria osmotically takes more water in urine) and increased
counter regulatory hormones (induced by acidosis and dehydration and
hyperglycemia) is same in ketoacidosis but is more severe. There is
hypernatremia caused by renal sodium resorption in response to hypovolaemia, together
with osmotic diuresis causing persistent free water loss.
Non-ketotic
hyperosmolar state usually occurs during marginal insulin deficiency, and their
insulinaemia has sufficient antilipolytic effect to prevent the lipolytic and
ketotic problems seen in ketoacidosis. There is decrease in anion gap <20
mmol/L and bicarbonate is normal and pH >7.30. There is hypernatraemia and
more severe water loss 18 L in typical adult.
ALCOHOLIC KETOACIDOSIS
During
alcoholism and resulting poor diet is association with vomiting, this cause
ketoacidosis and low, normal or elevated blood glucose. Ketosis is caused by
lack of insulin action which results in mobilization of NEFAs and their
conversion to ketone bodies as alternative fuel. This is potentiated by
counter-regulatory hormones like glucagon, cortisol and catecholamines secreted
in response both to hypoglycaemia and extracellular fluid volume contraction.
In addition, alcohol metabolism depletes cellular NAD+ which by
restricting pyruvate formation from lactate, causes accumulation of lactate and
depletion of pyruvate, a gluconeogenic substrate. As is the case in DKA,
alteration in mitochondrial redox state favors beta hydroxybutyrate over
acetoacetate production. A complex acid-base disorder ensues from the combined
effects of ketosis causing metabolic acidosis, and a combination of
extracellular fluid contraction and vomiting causing metabolic alkalosis.
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