PHYSICAL EXAMINATION

LABORATORY STUDIES

DIAGNOSIS

Gestational diabetes

PATHOPHYSIOLOGY OF KEY SYMPTOMS

Pregnancy dramatically alters maternal steroids and peptide hormone production. For the steroids, this includes marked increases in the production of the estrogens, progesterone, aldosterone, and deoxycorticosterone. For the peptides, this includes insulin, plasma renin, angiotensinogen, and human chorionic gonadotropin. Placental secretions include thyrotropin, adrenocorticotropic hormone (ACTH), and somatostatin. The endocrine “overproduction” is necessary to support the growth and development of the fetus and to allow maternal changes necessary to provide a nurturing environment for the fetus.

Insulin is produced by the pancreas in response to an elevation in blood glucose. Insulin acts to decrease plasma glucose by stimulating cellular glucose uptake in a variety of tissues, especially the liver and skeletal muscle (Fig. 84-1). One consequence of the changing endocrine environment is that the maternal tissues lose their sensitivity to insulin. As tissues become less responsive to glucose, fasting plasma glucose levels rise, plasma insulin levels rise, and the body is unable to efficiently store ingested glucose. Gestational diabetes results from a loss of tissue insulin sensitivity during the third trimester of pregnancy and resembles type 2 diabetes mellitus. Gestational diabetes develops in around 4% of pregnancies in the United States.

FIGURE 84–1 Plasma glucose levels represent the balance between gastrointestinal glucose absorption, movement into and out of storage pools, and metabolism by mitochondria. Insulin stimulates adipose synthesis and glycogen synthesis, and enhances glucose uptake in skeletal muscle.