creased operative interventions. The fetus can have increased weight and size (macrosomia) or congenital anomalies. Even after birth, such infants may have respiratory distress syndrome and subsequent childhood and adolescent obesity. Older age, obesity, excessive gestational weight gain, history of congenital anomalies in previous children, or stillbirth, or a family history of diabetes are risk factors for GDM.
A single genetic mutation in an autosomal dominant gene causes this type of diabetes. Examples of monogenic diabetes include conditions like neonatal diabetes mellitus and maturity-onset diabetes of the young (MODY). Around 1 to 5% of all diabetes cases are due to monogenic diabetes. MODY is a familial disorder and usually presents under the age of 25 years.
Secondary diabetes is caused due to the complication of other diseases affecting the pancreas (for example, pancreatitis), hormone disturbances (for example, Cushing disease), or drugs (for example, corticosteroids).
Diabetes is a worldwide epidemic. With changing lifestyles and increasing obesity, the prevalence of DM has increased worldwide. The global prevalence of DM was 425 million in 2017. According to the International Diabetes Federation (IDF), in 2015, about 10% of the American population had diabetes. Of these, 7 million were undiagnosed. With an increase in age, the prevalence of DM also increases. About 25% of the population above 65 years of age has diabetes.
In T1DM, there is cellular-mediated, autoimmune destruction of pancreatic beta cells. T1DM has a strong genetic predisposition. The major histocompatibility complex (MHC), also known as human leukocyte antigens (HLA), is reported to account for approximately 40 to 50% of the familial aggregation of T1DM. The significant determinants are polymorphisms of class II HLA genes encoding DQ and DR4-DQ8, with DR3-DQ2, found in 90% of T1DM patients.
Another form of T1DM is latent autoimmune diabetes of adults (LADA). It occurs in adulthood, often with a slower course of onset.
The rate of destruction is generally rapid in children and faster in adults. Autoantibodies against islet cells, insulin, glutamic acid decarboxylase-65 (GAD-65), and zinc transporter 8 (Zn T8) may be detected in the serum of such patients. These antibodies wane over time and do not have sufficient diagnostic accuracy to be used routinely for diagnosis, especially after the first year. With the progressive destruction of beta cells, there is little or no secretion of insulin. These patients are generally not obese. They are more prone to develop other autoimmune disorders such as Addison disease, Graves disease, Hashimoto thyroiditis, and celiac disease. A subset of T1DM not associated with insulin autoimmunity and not associated with the above HLA is termed idiopathic T1DM. It is more common in African and Asians and presents with episodic diabetic ketoacidosis (DKA).
T2DM is an insulin-resistance condition with associated beta-cell dysfunction. Initially, there is a compensatory increase in insulin secretion, which maintains glucose levels in the normal range. As the disease progresses, beta cells change, and insulin secretion is unable to maintain glucose homeostasis, producing hyperglycemia. Most of the patients with T2DM are obese or have a higher body fat percentage, distributed predominantly in the abdominal region. This adipose tissue itself promotes insulin resistance through various inflammatory mechanisms, including increased FFA release and adipokine dysregulation. Lack of physical activity, prior GDM in those with hypertension or dyslipidemia also increases the risk of developing T2DM. Evolving data suggest a role for adipokine dysregulation, inflammation, abnormal incretin biology with decreased incretins such as glucagon-like peptide-1 (GLP-I) or incretin resistance, hyperglucagonemia, increased renal glucose reabsorption, and abnormalities in gut microbiota.
History and Physical
Patients with diabetes mellitus most commonly present with increased thirst, increased urination, lack of energy and fatigue, bacteria