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MS WordPerinatologist Corner - C.E.U/C.M.E. Modules
Diabetes In Pregnancy Series
Sponsored by The Indian Health Service Clinical Support Center
PART 1: Screening and Diagnosis
7. Pathophysiology
By any criteria, it would appear that Mrs. Kanulie has GDM. Might she be a pre-gestational diabetic?
Her having an elevated fasting blood sugar makes this more likely, as does her clinical picture, and, if we had obtained these values in the first trimester, we probably could have diagnosed her. Now however, we will have to see how she responds to medical nutrition therapy, and, to definitively make the diagnosis, will need to test her postpartum. More on that later. At present her working diagnosis is, "GDM, class A-1", gestational diabetes, hopefully able to be diet-controlled.
What are the physiologic mechanisms that occur during pregnancy that allow women with a diabetic diathesis to manifest themselves? Thinking of the changes as fostering "survival of the species" is helpful in understanding what we consider a "disorder". The high quantities of estriol, progesterone, cortisol, and human placental lactogen (also known as chorionic somatomammotropin) produced by the placenta in late pregnancy result in a state of "facilitated anabolism".
That is to say, when feeding occurs, glucose excursions rise to values considerably above those seen in non-pregnant individuals. Glucose crosses the placenta by facilitated diffusion once its threshold is met. A large amount of substrate (glucose) is therefore enabled to siphon across to the fetus so it will have a "surfeit of substrate" to be used for growth. This mechanism is so efficient that subsequently, relative hypoglycemia will ensue in the mother if she does not eat well.
Thus, according to the hypothesis, "accelerated starvation" actually occurs during fasting. In order to keep glucose levels high so that this substrate can be utilized for fetal aims, the hormonal milieu of late pregnancy produces a state of relative insulin resistance in the maternal tissues. This is thought to be a post-receptor "defect", which has implications for therapy. We'll discuss this again later as well.
Insulin levels are actually significantly higher postprandially in pregnant women compared to non-pregnant subjects. In keeping with the "accelerated starvation" hypothesis, the hyperinsulinemia and insulin resistance results in lipolyis, which produces free fatty acids and ketones for fetal consumption, and enhances hepatic gluconeogenesis.
These mechanisms allow fetal survival from whatever maternal intake is available, even at her nutritional expense. When a genetic diabetic diathesis exists in the mother however, all these mechanisms are exaggerated and the fetus itself may experience hyperglycemia. In response, this will then result in fetal hyperinsulinemia. Since insulin is a growth factor, the fetus will develop increased muscle mass, increased adipose deposition, increased hepatic glycogen storage, and so the theory goes... macrosomia.
The increased osmotic load presented to the fetal kidney by the high glucose will result in fetal polyuria, and possibly, the development of polyhydramnios.
