Secretion of glucagon is via a negative feedback system (Fig. 9.3); if the blood glucose level falls below normal, chemical sensors stimulate the alpha cells to secrete glucagon. When blood glucose level rises, the cells are no longer stimulated and production ceases. Exercise and protein-heavy meals also stimulate glucagon secretion. Somatostatin inhibits glucagon secretion.

Figure 9.3 Control of blood glucose.

Emotional stress commonly raises blood glucose levels. Cortisol is a corticosteroid hormone produced by the adrenal cortex and is involved in the response to stress. It increases blood pressure and blood glucose levels. Cortisol has widespread actions which help to restore homeostasis after stress. Cortisol acts as a physiological antagonist to insulin by promoting gluconeogenesis, the breakdown of fats and proteins and the mobilization of amino acids and ketone bodies. This leads to an increase in blood glucose levels and the storage of glycogen in the liver (Marieb & Hoehn 2007).

Insulin is produced by beta cells. Its physiological action is the reverse of glucagon. Insulin accelerates the transport of glucose from the blood into the cells, especially skeletal muscle cells, and thereby decreases the blood glucose level. Insulin also accelerates the conversion of glucose to glycogen. This is known as glycogenesis. It decreases glycogenolysis and gluconeogenesis and stimulates the conversion of glucose and other nutrients into fatty acids (lipogenesis). Insulin also stimulates protein synthesis.

Regulation of insulin is determined by the glucose level in the blood. Increased blood glucose levels stimulate insulin secretion, while decreased blood glucose levels inhibit it (Fig. 9.3). Increased levels of certain amino acids also stimulate insulin release. Human growth hormone (hGH) and adrenocorticotrophic hormone (ACTH) both raise blood glucose levels, and the rise in blood glucose level stimulates insulin secretion. Somatostatin inhibits the secretion of insulin.

Metabolism

The word ‘metabolism’ is translated from ‘metabolismos’, the Greek word for ‘change’, or ‘overthrow’. Metabolism is the biochemical modification of chemical compounds in living organisms and cells. This includes the biosynthesis of complex organic molecules and their breakdown. Nutrients are digested and broken down into chemical compounds; some of these chemical compounds recombine to form other compounds or building blocks (anabolism) and some chemicals break down to provide energy (catabolism).

Metabolism usually consists of sequences of enzymatic steps, or metabolic pathways which are a series of chemical reactions occurring within a cell, catalyzed by enzymes. Many of these pathways are elaborate, and involve a step by step modification of the initial substance to shape it into the product with the exact chemical structure desired. Catabolic pathways break down complex molecules into simple compounds, while anabolic pathways create building blocks and compounds from simple precursors.

TYPES OF DIABETES MELLITUS

There are two main types of diabetes mellitus. Type 1, which was formerly known as insulin dependent diabetes mellitus (IDDM), occurs mainly in the young. Type 2, which was known as non-insulin dependent diabetes mellitus (NIDDM) was said to occur in the middle-aged, overweight adult. These are rather simplistic generalizations and not entirely accurate, as insulin may be required in individuals with type 2 diabetes mellitus and also type 2 diabetes is now occurring in younger age groups. Other forms of diabetes include impaired glucose regulation, which refers to a metabolic state between normal glucose homeostasis and diabetes. This condition may be a risk factor for the development of diabetes in the future. Maturity onset diabetes of the young (MODY) is a rare type of diabetes associated with genetic defects. For the midwife, this discussion will focus on the two main types of diabetes mellitus and the form of diabetes which occurs in pregnancy – gestational diabetes mellitus.

Type 1 diabetes mellitus

Aetiology

The aetiology of type 1 diabetes mellitus is thought to be multifactorial and far from being completely understood. It is considered to have an autoimmune basis and a number of risk factors have been identified, which may be divided into genetic and environmental. These risk factors include links to chromosomes and several chromosomal regions have been implicated. The most significant gene loci defining the risk of type 1 diabetes are to be found within leucocyte antigen (HLA) gene region (BMA 2004).

There has been a rapidly rising incidence in migrant populations suggesting environmental links, for example viral infections. It has been observed that IgM antibodies to Coxsackie B virus are found in 25–35% of newly diagnosed diabetics (Kanno et al 2006). An increased incidence of type 1 diabetes has been noted in individuals with congenital rubella, and cytomegalovirus DNA has also been found in 22% of newly diagnosed diabetics (Jaeckel et al 2002).

It has also been suggested that those with diabetes were breast-fed for a significantly shorter time than non-diabetic infants, and that the incidence of diabetes can be modified by the exclusion of cow’s milk, suggesting that early exposure to cow’s milk may be an important factor in the aetiology of type 1 diabetes (BMA 2004). The condition varies considerably in incidence between cultures with the 10 countries with the highest proportion of sufferers being India, China, USA, Indonesia, Japan, Pakistan, Russia, Brazil, Italy and Bangladesh (WHO 2006).

Incidence

The incidence of diabetes mellitus appears to be on the increase, and a likely factor related to this increase is obesity and lifestyle in western culture. The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% in 2000 and is estimated to rise to 4.4% by 2030 (Wild et al 2004). The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030.

The costs to people’s quality of life, the economy, society and the NHS, are already evident. Diabetes can lead to serious complications, such as heart disease, blindness, kidney failure and stroke and nerve damage, leading to amputation (Diabetes UK 2006).

There are several reasons why the prevalence of diabetes is increasing: the greater life expectancy means that there is an increasingly ageing population. Also, the UK has a rapidly growing obesity problem, and the risk of developing type 2 diabetes increases by up to 10 times in people with a body mass index (BMI) >30. In people with an African-Caribbean or Asian background, the prevalence is approximately five times higher than that of the indigenous population (BMA 2004).

Pathophysiology

Type 1 diabetes mellitus occurs as the result of rapid and progressive loss of beta cells, resulting in an absolute deficiency of insulin, and is thought to be precipitated by a response to physical or psychological stress.

Lack of insulin has a domino effect, as cells cannot therefore obtain glucose for metabolism and this illustrates how the clinical features arise. Ingested glucose which is unable to enter cells accumulates in the blood leading to hyperglycaemia; this high blood glucose level circulates throughout the body including the renal system, which cannot cope with the increasing amounts of glucose. As a consequence, the renal threshold is exceeded, and glucose appears in the urine, resulting in glycosuria. Glucose is highly osmotic (it attracts and holds water to itself), therefore, as glucose is lost in the urine, large volumes of water are lost with it. This is known as polyuria. Furthermore, nocturia may occur resulting in disturbed sleep patterns. As fluid loss continues, symptoms of dehydration occur, resulting in copious drinking in response to severe thirst – polydipsia.

As the cell requirements for glucose are not being met, the response is for increased secretion of glucagon. Glycogen is converted back into glucose and released by the liver – glycogenolysis. However, glycogen storage is quickly depleted and in an attempt to supply the cells there is a breakdown of body fat and protein to produce glucose – gluconeogenesis.

Body cells are not being supplied with glucose, so may stimulate appetite – polyphagia, although this may be tempered somewhat because of nausea and/or vomiting. Weight loss occurs due to depletion of body fat and insulin stores, which together with cell deprivation of glucose, fluids and electrolyte imbalance results in muscle weakness and exhaustion. This exhaustion may be so overwhelming as to mask the presence of the other clinical features in the affected individual.

Because there is no insulin, fat metabolism results in ketone bodies being produced. These accumulate in the blood and urine, causing ketonaemia and ketonuria. Ketone bodies are weak acids, which release free hydrogen ions causing metabolic acidosis. Excess acidity in the blood causes hyperventilation – the body’s response to removing excessive hydrogen ions.

Uncontrolled and untreated, these features will lead to a life-threatening condition known as diabetic ketoacidosis (McIntyre & Strachan 2000).

Diagnosis

Onset of type 1 diabetes mellitus is often sudden, but can vary in severity, with some patients acutely ill at the time of diagnosis. Sudden weight loss, thirst and passing frequent and large amounts of urine, particularly at night, with increasing tiredness is noted by the patient or their parents, causing them to visit their family doctor. The GP may perform urinalysis to test for glucose and ketones, although urinalysis is not an accurate or precise measure of high or low blood glucose levels. Blood glucose will also be measured, a normal blood glucose level is 4–7 mmol/L, and a result of 11.1 mmol/L or more in the symptomatic patient is indicative of diabetes mellitus.

Where symptoms are suggestive, but not conclusive of diabetes, a fasting blood glucose analysis will be carried out on 2 separate days, and a result of >8 mmol/L is indicative of diabetes mellitus.

Patients who are acutely ill at the time of diagnosis because of the rapid onset of the condition may be drowsy or semi-conscious due to diabetic ketoacidosis. These individuals will require urgent hospital admission to treat the acidosis and to stabilize their diabetes.

Hospital admission is not automatic. Currently, patients less acutely ill may be referred to diabetic day centres where full assessment may be carried out by a multidisciplinary diabetic team, including a diabetic consultant, specialist diabetic nurse practitioners, dieticians, ophthalmologist and podiatrists.

Management

The mainstay of care is dietary advice, insulin, blood glucose monitoring, education and psychological care. At the time of diagnosis, intensive educational and psychological support is provided and as the patient learns and becomes more familiar with the condition, she will be encouraged to manage her own condition. Newly diagnosed individuals may experience a wide range of emotions including shock, anger and fear. Because of this, education should be given in small bites and verbal information should be backed up with written reinforcement. Information on how to contact the diabetic liaison nurse by telephone or a local diabetic self-help group is also helpful.

Giving insulin injections is usually a concern, and must be demonstrated and practised carefully by the individual until they feel confident. Alcohol swabbing is contraindicated, as it causes the skin to toughen, making injections more difficult. Needle length, angle of injection, as well as suitable sites for injection must also be addressed (Box 9.1, Fig. 9.4). Various devices are available to deliver insulin to the individual, including insulin pens, which are loaded with a single use cartridge containing the required dose.

Box 9.1 Administration of insulin

Insulin is available in different presentations depending on the device used. Insulin vials are used with insulin syringes. Insulin cartridges are used with reusable pens and disposable pre-filled pens are also available.

Insulin is administered by subcutaneous injection. There are three main areas for injection – abdomen, buttocks and thighs (Fig. 9.4). The upper arm is the least preferred site as it has little subcutaneous tissue. Overuse of one site can lead to fat hypertrophy and loss of sensitivity. If insulin is injected into fatty tissue, this will result in slower and more erratic absorption of insulin, resulting in variable and unstable blood glucose readings. It is advisable to use a different site each day and by rotating sites, this ensures the insulin will act quickly and effectively.

To reduce the discomfort of an injection, some newly diagnosed diabetics hold an ice cube against the skin for a few seconds, just prior to injection. This can help numb the area to any pain.