Gestational Diabetes diabetes diagnosed during pregnancy It is a disorder of late pregnancy (typically) caused by the increased pancreatic stimulation

on associated with pregnancy. babies born to mothers with gestational diabetes are at increased risk of problems typically such as being large for gestational age (which may lead to delivery complications), low blood sugar, and jaundice 2 Subtypes of Gestational Diabetes (diabetes which began during pregnancy): Type A1: abnormal oral glucose tolerance test (OGTT) but normal blood glucose levels during fasting and 2 hours after meals; diet modification is sufficient to control glucose levels Type A2: abnormal OGTT compounded by abnormal glucose levels during fasting and/or after meals; additional therapy with insulin or other medications is required Predisposing Factors of Gestational Diabetes: 1. A previous diagnosis of gestational diabetes or prediabetes, impaired glucose tolerance, or impaired fasting glycaemia 2. A family history revealing a first degree relative with type 2 diabetes 3. Maternal age a womans risk factor

increases as she gets older (especially for women over 35 years of age) 4. Ethnic background (those with higher risk factors include African-Americans, Afro-Caribbeans, Native Americans, Hispanics, Pacific Islanders, and people originating from the Indian subcontinent) 5. Being overweight, obese or severely obese increases the risk by a factor 2.1, 3.6 and 8.6, respectively.[7] 6. A previous pregnancy which resulted in a child with a high birth weight (>90th centile, or >4000 g (8 lbs 12.8 oz)) 7. Previous poor obstetric history Placenta secretes anti-insulin substances; such as human placental lactogen (HPL), hCG, estriol, cortisol and progesterone

Glucose intolerance develops in the mother; mainly if maternal cells are unable to produce additional insulin which is required to counteract this antagonism Maternal Gestational Diabetes Mellitus Maternal nutrients mainly glucose can readily crosses placenta but not maternal insulin As the mother develops hyperglycemia due to Gestational Diabetes Mellitus hence fetal pancreas will secrete additional insulin to cope with the fetal hyperglycemia

Fetal cells hyperplasia Fetal hyperinsulinemia

PATHOPHYSIOLOGY Pancreas is composed of cells scattered throughout called the islets of Langerhans Two types of cells are important to glucose control Alpha cells- produce glucagon Hormone that acts opposite of insulin Causes release of glucose from cell storage Beta cells- produce insulin Allows body cells to use and store carbohydrate, fat, and protien

Risk Category and Clinical Characteristics High risk Marked obesity Diabetes in first-degree relative Current glycosuria Previous history of GDM or glucose intolerance Previous infant with macrosomia Average risk Neither high or low risk Low risk Age < 25 years No previous poor obstetrical out-comes Belongs to a low-risk ethnic group* No diabetes in first-degree relatives

Normal prepregnancy weight and weight gain during pregnancy No history of abnormal glucose tolerance *Low-risk ethnic groups are those other than Hispanic,African American, Native American, South Asian, EastAsian, Pacific Islander, or Indigenous Australian. Pathophysiology Pregnancy is a condition characterized by progressive insulin resistance that begins near midpregnancy and progresses through the third rimester. In late pregnancy, insulin sensitivity falls by 50%.17 Two main contributors to insulin resistance include increased maternal adiposity and the insulin desensitizing effects of hormones produced by the placenta. The fact that insulin resistance rapidly decreases post-delivery suggests that the major contributors are placental hormones. The placentas produces human chorionic somatomammotropin (HCS, for merely called human placental lactogen), bound and free cortisol, estrogen, and progesterone. HCS stimulates pancreatic secretion of insulin in the fetus and inhibits peripheral uptake of glucose in the mother.18As the pregnancy progresses and the size of the placenta increases, so does the production of the aforementioned hormones, leading to a more insulinresistant state. In no diabetic pregnant women, the firstand second-phase insulin responses compensate for this reduction in insulin sensitivity, and this is associated withcell hypertrophy and hyperplasia.18 However, women who have a deficit in this additional insulin secretory capacity develop GDM.-Cell dysfunction in women diagnosed with GDM may fall into one of three major categories:1) autoimmune,2) mono-genic, or3) occurring on a background

of insulin resistance (as is most common).19The loss of the first-phase insulin response leads to postprandial hyperglycemia, whereas impaired suppression of hepatic glucose production is responsible for fasting hyperglycemia when present. Because insulin does not cross the placenta, the fetus is exposed to the maternal hyperglycemia. At the 11th or 12th week of gestation, the fetal pancreas is capable of esponding to this hyperglycemia.20The fetus thus becomes hyperinsulinemic, which in turn promotes growth and subsequent macrosomia.

Pathophysiology Pregnancy is a state of relative insulin insensitivity. During the early part of pregnancy there is increase in insulin secretion and beta cell hyperplasia. This leads to an increase in insulin sensitivity with low fasting blood sugar levels, increased glucose uptake by peripheral tissue and glycogen storage as well as decreased hepatic gluconeogenesis. This process is crucial for the build-up of maternal adipose tissue, to be used in the later part of pregnancy. During the late phase, there is an increase in hormones such as cortisol, prolactin, progesterone and human placental lactogen which leads to a state of relative insulin resistance, possibly via a post receptor defect in the cells. This is a critical step which ensures adequate delivery of nutrients to the fetus. The pancreas responds to this increased resistance by doubling the release of insulin. It has been found that women diagnosed with gestational diabetes already have insulin resistance at baseline with a higher level of plasma insulin levels. This state gets further aggravated by the metabolic changes associated with pregnancy. The pancreas however, is unable to cope with this additional stress of elevated level of insulin resistance. This results in an inadequate release of insulin and elevated blood sugar levels.