Hyper/hypoglycaemia

It is usually easier to differentiate hypoglycaemia from severe diabetic ketosis than from other causes of coma, which are as likely in a diabetic as in anyone else. It is unsound to advocate blind administration of i.v. glucose to comatose diabetics on the basis that it will revive them if they are hypoglycaemic and do no harm if they are hyper-glycaemic. A minority of comatose insulin-dependent diabetics have hyperkalaemia and added glucose can cause a brisk and potentially hazardous rise in serum potassium (mechanism uncertain), in contrast to nondiabetics in whom glucose causes a fall in serum potassium. 

Maternal hyperglycaemia leads to fetal hyper-glycaemia with consequent fetal islet cell hyperplasia, high birthweight babies, and postnatal hypoglycaemia. 

It is important to realize that some medical conditions can mimic the symptoms of generalized anxiety disorder, for example hyper- or hypothyroidism, hypoglycaemia, drug or alcohol withdrawal and cardiac arrhythmias. 

Babies of diabetic mothers. A fetus that is exposed to maternal hyper-glycaemia will have pancreatic islet cell hyperplasia and elevated insulin levels. After delivery the neonate is unable to suppress its inappropriately high insulin levels and will develop hypoglycaemia. 

Propionyl-CoA is the key intermediate in the formation of the majority of the abnormal urinary metabolites observed in propionic acidaemia and is also responsible for the accumulation of odd-carbon-number fatty acids and abnormal triglycerides and lipids in the disease by competition with acetyl-CoA in fatty acid biosynthesis. The metabolite may also inhibit other enzyme systems, particularly in mitochondria, giving rise to other symptoms. Inhibition of A -acetylglutamate synthetase has been used to explain the hyper-ammonaemia that is frequently observed in patients with propionic acidaemia (Coude et al., 1979), sometimes occurring as the major presenting biochemical abnormality (Harris et ai, 1980). Inhibition of other enzyme systems and of mitochondrial function by propionyl-CoA may well also be responsible for the occasional occurrence of hypoglycaemia in the diseases. Propionyl-CoA accumulation is also Important in the biochemical and clinical presentation of patients with methylmalonic aciduria, the disease described in the next section (11.2). 

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