الفهرس 
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Abstract
Diabetic ketoacidosis (DKA) is the commonest endocrinal emergency encountered in clinical practice. It is a frequent cause of morbidity and occasionally mortality whether associated with coma or not (Alberti & Hockaday, 1977 and Kreisberg, 1978).
tWA is the state of metabolic acidosis caused by a complex interplay among insulin deficiency, increased stress hormones levels and intravascular depletion (Porte & Halter, 1981).
Insulin (a pancreatic B—cell hormone) deficiency is the primary cause of tWA (Bergenstal, 1985). This, not only results in continued hyperglycaemia, but also leads to catabolism of fat and protein. Protein breakdown yields aminoacids, which enhance giuconeogenesis. Lipolysis results in the production of glycerol and free fatty acids (FFA) which are converted in the liver to glucose and ketone bodies, respectively (Bergenstal, 1985).
A small amount of insulin secreted into the portal vein and not detected peripherally may be enough to inhibit ketogenesis by direct action on liver or may act intraislet on alpha cells (McGarry & Foster, 1977
Introduction (2)
and Madsbad at al, 1979). Also absence of kotosis in. non—insulin dependent diabetic (NIDD) patients may be related to the relatively higher intraportal insulin concentrtion due to maintained endogenous insulin secretion ( Keller, 1986).
Linked to the insulin deficiency is marked increase in counter—regulatory hormones (cRa) levels (glucagon, growth hormone, cortisol, and catecholamines) (Schade & Eaton,1977 and Waldhausl et al, 1979). Both events combines to acidosis hyperglycasnia, hyperlipidae— mia and ketonaemia with acidosis (Keller, 1986).
Maichoff et al (1984) demonstrated in a clinical study in patients with OKA, that hyperketOnaemia correlated with the degree of c—peptide deficiency and with plasma ETA concentrtionS whereas the severity of hyper— glycaemia on admission was significantly associated with plasma glucagon.
Somatostatin (SS), secreted by pancreatic 13 cells, having marked inhibitory effect on alpha cell (Koerker et al, 1974) and beta cell (Alberti et al, 1973), plays indirect important role in controlling carbohydrate metabolism in addition to its direct action on glucose absorption and metabolism (Porte & Halter, 1981).