Neonatal Diabetes

Type 1 diabetes is well known disease, some of us or someone we know are the victim of this chronic illness. There are controversial explanation such as, genetic susceptibility and in contrary, environmental factors that are viral infection, prenatal and neonatal influence, nitrate in drinking water, (Norris et al, 2003) early exposure to cow’s milk towards why the immune system destroy the insulin producing beta cell. In this essay, I will be discussing about the pathophysiology of type 1 diabetes and how it affect the homeostasis of our normal functioning body. In subject to Carol, I will be explaining the signs and symptoms of the illness and also the possible effects to her developing foetus and herself.

Gestational diabetes is a disorder characterized by impaired ability to metabolize carbohydrates, usually caused by a deficiency of insulin resistance, occurring in

Shannon’s glucose levels are still high (above 6.1 mmol/L) thus still needs the insulin drip (Robbins et al., 2010). Administration of insulin and efforts made to correct metabolic acidosis forces potassium into the cells causing hypokalemia (Bopp, 2010). Thus, even though the potassium is within therapeutic levels (3.5-5 mmol/L) there is a high chance that Shannon may experience hypokalemia and the administration of NS with potassium is necessary (Bopp, 2010).

It is estimated that 387 million people, globally live with diabetes (Phillips & Mehl, 2015). According to Medical News Today [MNT], diabetes is a metabolic disorder; which causes patients to be extremely thirsty and produce a lot of urine. Diabetes arises due to high blood pressure, due to the body not being able to produce enough insulin or because the body does not respond well to high insulin levels (MNT, 2016). There are four types of diabetes; there is the pre-diabetic stage, type 1 diabetes, type 2 diabetes and gestational diabetes. In 2014, 29 million people died due to diabetes. This equates to 1 diabetic patient dying every seven seconds due to preventable complications (including complications affecting lower limbs) caused by diabetes. It is said that 20-40% of health care costs are spent on the treatment of lower limb complications due to diabetes. The risk of a diabetic patient developing a foot ulcer is 25% and foot ulcers account approximately 85% of lower limb amputations. Diabetic complications that affect lower limbs are caused by both type 1 and type 2 diabetes (Phillips & Mehl, 2015). It is said that the World Health Organization described diabetic foot syndrome as including all possible complications in relation to the feet of a diabetic patient. Diabetic foot syndrome is defined as the ulceration of the foot, from the ankle downwards. Causes of foot ulceration include peripheral sensory neuropathy, vascular disease (ischaemia) and infection

In 2014, diabetes was responsible for 4.9 million deaths, approximately one death every seven seconds (Bone, 2015). For some women, pregnancy can precipitate diabetes causing numerous subsequent lifelong complications for both the mother and her fetus/newborn. The previous shocking statistic is just one of the many reasons why implementing evidence-based practice (EBP) protocols is an essential aspect in providing great patient care. In addition, EBP is crucial in improving patient outcomes while decreasing negative outcomes that can result in lifelong complications due to gestational diabetes. The process of establishing an EBP requires research to be critically appraised before it could be used

Diabetic Ketoacidosis (DKA) is a disease state, most often seen in individuals with Type I Diabetes. While it most often results from uncontrolled insulin levels, young children can often present in diabetic ketoacidosis as the initial presentation of undiagnosed type I Diabetes. The major symptoms of Type I Diabetes, polydipsia, polyphagia, and polyuria, are often subtle and can be normal in growing children (Urden, Stacy & Lough, 2014; Wilson, 2012). Unless alert to the symptoms of Diabetes they can often be overlooked until severe enough to warrant immediate medical attention.

- Neonatal hypoglycemia is a global health problem and a preventable cause of neurological injury in newborn period. Approximately 1/5th of neonates have a risk of being hypoglycemic. Some of these infants fail to normalize their blood glucose by feeds alone and require intravenous (IV) dextrose therapy. In our institution, IV dextrose therapy is offered in the neonatal intensive care unit (NICU). This leads to separation of mother from baby and undue anxiety affecting bonding and breastfeeding.

Another important electrolyte shift in ketoacidosis is the change in plasma potassium levels which can result in a whole body potassium depletion. Insulin regulates potassium entry into the intracellular space compartment, during inadequate production of insulin. potassium is confined to

Gestational diabetes mellitus (GDM) is an intolerance of glucose documented for the first time during pregnancy. It is usually a short-term type of diabetes and the most common health problem with pregnant women. GBM is caused by the way the hormones in pregnancy affect the mother. GDM accounts for 5-7% of all pregnancies (American Diabetes Association, 2010). During pregnancy the placenta develops and becomes the main bond between the mother and the baby. It is used to make sure the baby has and gets enough nutrients. The placenta makes several hormones which make it hard for insulin to control blood glucose and block the action of the mother’s insulin in her body (American Diabetes Association, 2010). Hormonal changes during the

Research concerning the functional role of potassium ions in the cardiovascular system with respect to hypertension and diabetes mellitus has boomed in the past decade. Through a series of experiments, data has been gathered which shows the diverse response of K+ channels in the cardiovascular system when exposed to these diseases.

The main stimulus for insulin release is a high glucose concentration (hyperglycemia), however insulin release is also stimulated by other factors, such as high amino acid and fatty acid levels in the blood, hormones released from the stomach and intestine as well as neurotransmitters (Lang, 1999). Glucose entrance into pancreatic beta cell and its further metabolism in mitochondria alters the adenosine triphosphate (ATP)/ adenosine diphosphate (ADP) ratio that leads to closure of ATP-sensitive K+ channels. It results in membrane depolarisation and opening of voltage-dependent calcium channels. The subsequent increase in cytosolic free Ca+2 coupled with the multiple phosphorylation events modulated by protein kinase C and protein kinase A (PKA) induce exocytosis and insulin secretion [(Ashcroft et al., 1994 and Lang, 1999), see Fig.

It is a disabling disorder because its progression starts from the earliest years and possible complications get worse with age. If not diagnosed in time, it leads to a serious condition called ketoacidosis. In case of some mutations, the patient experiences learning problems. It can be explained by reduced intake of glucose by brain cells. Diagnosis of neonatal diabetes is based on blood glucose and urine glucose tests, and symptoms, including frequent urination and intrauterine growth restriction. After diabetes is confirmed, the genetic diagnosis is performed for the patient. Unlike other forms of diabetes, which are caused by environmental factors and viruses, in case of type I diabetes, the neonatal one is primarily a genetic condition. The suggested treatment consists of insulin injections to provide the organism with lacking hormone. Because of insulin injections, the blood glucose returns to normal and the main complications are relieved (Støy et al.,

The neonatal hypoglycemia mechanism occurs when maternal diabetics’ mother gives birth to newborns. Glucose is the main nutrient source for newborns received in the maternal placenta. The symptoms of hypoglycemia are difficult to treat in newborns. If untreated, the hypoglycemia can lead to brain damage or seizures. The most common symptoms are coma, apathy, jitteriness, and inadequate feedings. Infants born with small gestational age (SGA) or large gestational age (LGA) can be susceptible to hypoglycemia. Maternal diabetics secrete extra insulin which causes neonates to have low blood glucose levels. Zhou et al conducted a study of 668 neonates who were admitted to the Pediatrics Center Hospital at Shanghai for hypoglycemia (Zhou et al, 2015). After being admitted, maternal diabetics were separated from neonates and inhibited from breastfeeding. Neonates with hypoglycemia were monitored on a regular basis on their blood glucose levels. Results show that 113 out of

One of the most common medical disorders of pregnancy is gestational diabetes mellitus (GDM). Diagnosing, treating, and managing health outcomes for the mother and baby can be challenging. The impact of GDM can be far reaching past the postpartum period, and can affect both mom and baby for years to come. The purpose of this paper is to review the pathophysiology of GDM, explore the available treatments and discuss the impact and how education is essential in the management of GDM.

Glucose is transported into the pancreatic β-cell by type 2 glucose transporters (GLUT2). Once inside, the first step in glucose metabolism is the phosphorylation of glucose to produce glucose-6-phosphate. This step is catalyzed by glucokinase; and its further metabolism in mitochondria alters the adenosine triphosphate (ATP)/ adenosine diphosphate (ADP) ratio that leads to closure of ATP-sensitive K+ channels. It results in membrane depolarisation and opening of voltage-gated calcium channels. The subsequent increase in cytosolic free calcium ion (Ca2+) cause phosphorylation of protein kinase which induce insulin secretion via exocytosis [(Ashcroft et al., 1994; Lang, 1999 and Henquin, 2000) as shown in fig.