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Type 1 diabetes and insulin therapy.

Much attention is given to the global epidemic of type 2 diabetes mellitus (T2DM), while less is paid to the increasing incidence of type 1 diabetes (T1DM). Incidence of T1DM is increasing by three to five per cent a year, most rapidly in the under-fives. T1DM has more severe consequences, at an earlier age, than T2DH. Absolute loss of beta cell function ensures those with T1DM require insulin therapy from very early on in the disease process. By contrast, many people with T2DM will not require insulin therapy until their disease has progressed significantly.

This article looks at the causes and consequences of T1DM and discusses insulin therapy, which is used to treat both T1DM and advanced T2DM.

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INTRODUCTION

According to Diabetes New Zealand (1) there are about 15,000 people in New Zealand diagnosed with type 1 diabetes (T1DM), 3500 of them under the age of 25. The incidence of T1DM is increasing by about five per cent per annum. Internationally, this increase in incidence is more evident in the under-five age group, but recent data shows the upsurge in New Zealand is more marked in the 10-14 age group. (2)

T1DM used to be called juvenile-onset diabetes--renaming the disease reflects that, while the peak incidence of onset is 11-13 years of age, 50 per cent of new cases occur in those over 20. (3)

T1DM decreases life expectancy and increases morbidity. Later onset brings a particularly increased risk of premature death, especially for women. (4) The complications associated with diabetes--both acute and chronic--place a disproportionate burden on the health budget. Most recent cost projections estimate the cost of treating type 2 diabetes (T2DM) could consume up to 15 per cent of the total health budget by 2021. (5) There are no cost projections available for T1DM.

T1DM involves loss of insulin secretion from the beta cells in the pancreas. Generally, signs of diabetes are not seen until more than 80 per cent of beta-cell function is lost, when the lack of circulating insulin affects glucose handling sufficiently that normal body metabolism is disrupted. The rate of cell loss can be rapid in children, leading to the development of ketoacidosis--where the body can't use glucose due to lack of insulin, and starts to break down body fats, producing a dangerously acidic metabolic state--which becomes the presenting feature of the disease. In adults, destruction may be slower, with residual beta-cell function allowing avoidance of ketoacidosis until infection or other metabolic stress tips the balance. (6)

MECHANISMS IN DEVELOPMENT OF T1DM

T1DM is an auto-immune disorder occurring in genetically susceptible individuals where there has been an environmental insult that damages pancreatic beta cells.

Genetic susceptibility

Close relatives of a person with T1DM have a higher risk of developing the disease, providing evidence that T1DM has a genetic component. Risk of T1DM is about 0.4 per cent in the general population. This increases to two per cent if the mother has T1DM, six per cent if the father or a sibling has T1DM, and 50 per cent for an identical twin. (7)

Numerous genes have been identified as playing a role in T1DM, but the most significant appears to be a genetic variation in three of the genes that code for human Leukocyte antigen (HLA). HLA is a protein that presents molecules to the body's T-cells for identification as "self" or "non-self." The presentation of "non-self molecules triggers immune attack and destruction. About 90 per cent of people with T1DM have mutations in these genes, which are believed to present damaged beta cell molecules as "non-self'. (7)

Autoimmune aspects

The involvement of HLA and T-cells triggers an autoimmune inflammatory attack against the pancreatic beta cells. People with T1DM have a higher risk of developing other autoimmune disorders such as Graves' disease and Addison's disease. (3) Antibodies to beta-cell proteins, insulin, glutamic acid decarboxylase (GAD) and tyrosine phosphatase 1A-2 are found in elevated concentrations in up to 90 per cent of newly diagnosed T1DM patients. (6)

GAD is an enzyme used in the synthesis of gamma-aminobutyric acid (GABA), an essential chemical in the regulation of insulin secretion. Tyrosine phosphatase is required for the secretion of insulin from the beta cells.

Drug therapy that interferes with autoimmune responses has long been hoped for, in the prevention or cure of T1DM. Unfortunately, toxicity associated with immunosuppression has limited the use of these therapies. New therapies targeting T-cell function are in development, eg the drug otelixizumab. (8,9)

Environmental factors

Research has found that identical twins do not always have the same T1DM status, and that incidence of the disease in genetically similar populations varies with living conditions. This supports the existence of precipitating environmental factors for the development of the disease.

New Zealand Europeans have a higher rate of T1DM than non-Europeans, but the incidence of T1DM in Polynesians is much higher for immigrants than those remaining in the islands. (2) Potential environmental triggers include diet, viruses and toxins.

There is a significant association between the enteroviruses (EV) and T1DM. EVs are a large group of RNA-viruses that are responsible for, among other illnesses, hand, foot and mouth disease (Coxsackie virus and EV-71), the common cold (rhinovirus), nonspecific febrile illnesses and poliomyelitis. A large proportion of people with T1DM have persistent EV present in the blood, pancreas and intestinal mucosa. (10)

Mumps and congenital rubella have also been implicated in development of T1DM. However, there is also a hygiene hypothesis about T1DM (similar to the one accounting for increasing rates of asthma): lack of early exposure to infectious organisms results in an immune system that cannot distinguish between legitimate threats and minor triggers such as allergens or the body's own molecules, reacting to them all in a similar manner. (11) In T1DM, this is thought to trigger the autoimmune destruction of beta cells.

Dietary factors may play a role in the development of T1DM but the accelerator hypothesis --whereby increasing childhood obesity was postulated to be causing earlier onset of T1DM--has not been supported by a recent New Zealand-based study. (2,11)

Other dietary suspects include gluten, cow's milk, and nitrosamines (found in some smoked foods), although there is insufficient data to support any of these with confidence. (11) Lack of Vitamin D in childhood has been implicated to some extent, although research results conflict. (3)

SIGNS AND SYMPTOMS OF T1DM

A cluster of symptoms is classically associated with T1DM: polyuria, polydipsia and polyphagia, accompanied by fatigue, nausea and blurred vision. Symptoms may appear over several weeks, but the disease can present with rapid onset of ketoacidosis.

Glucose in the plasma is filtered by the glomeruli in the kidneys and enters the urinary filtrate. As it travels along the proximal renal tubule, almost all the filtered glucose will be reabsorbed. This is a carrier-mediated transport process. If the amount of glucose exceeds the maximum capacity of the carriers (the renal threshold), glucose will enter the loop of Henle and disrupt the osmotically dependent removal of water from the filtrate. Thus hyperglycaemia causes loss of water from the body and the production of copious volumes of dilute urine (polyuria).

Hyperglycaemia, and the loss of body water due to polyuria, increase the osmolality of the extracellular fluid (ECF) and this triggers the movement of water from the cells into the ECF. Ensuing intracellular dehydration triggers hypothalamic centres and the sensation of thirst arises. (12) In diabetic ketoacidosis (see below), typical water loss is 80-100ml per kilogram of body weight, or about six litres of water from a 70kg adult. (13)

Dehydration causes weight loss, which is compounded by the need for alternative fuel sources (lipids and proteins), triggering a catabolic state in the body. The person may become hungry because she or he needs more energy and nutrients to replace those being used instead of glucose.

Fatigue arises due to dehydration and hypovolaemia (low blood volume), loss of sleep due to polyuria, muscle wasting as proteins are mobilised for energy, and electrolyte imbalances, particularly potassium. Serum potassium levels may appear to be near normal on testing, due to dehydration and shifts from intracellular to extracellular compartments. Polyuria causes loss of total body potassium (and sodium), impairing the function of excitable cells, eg skeletal muscle, and also causing muscle cramps.

Blurred vision occurs when the osmotic effects of high glucose cause dilation of the lens, altering focal length.

COMPLICATIONS 0F T1DM

Dysregulation of glucose metabolism causes abnormal secretion and control of other hormones. Glucagon secretion is unregulated in the absence of insulin and the secretion of other hormones is also affected. This leads to short-term complications for people with T1DM, and prolonged hyperglycaemia contributes to long-term complications.

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) occurs when there is no insulin present, as in newly-diagnosed T1DM, or where the amount of insulin present is insufficient to overcome counter-regulatory hormones. Infection, metabolic stress, trauma or myocardial infarction dramatically increase the concentration of catabolic hormones--adrenaline, noradrenaline, Cortisol, growth hormone and glucagon. These hormones oppose the effects of insulin, reducing cellular uptake of glucose, increasing glucose production by the liver, and promoting mobilisation of fatty acids from fat stores.

Catabolic hormones also inhibit secretion of insulin from the beta cells, which is why people with T2DM may be at risk of DKA if they experience metabolic stress. (14) The enzymes that release free fatty acids into the plasma are normally inhibited by even relatively small amounts of insulin in T2DM, preventing DKA. This is the reason that hyperglycaemia in T2DM leads to hyperosmolar hyperglycaemic nonketotic syndrome (HHNS), rather than DKA (see figure 1, this page).

Once released from fat stores, free fatty acids travel to the liver where again, due to lack of insulin and increased catabolic hormones, the oxidation pathway is switched to generate ketone bodies: beta-hydroxybutyric acid and acetoacetic acid. (15) Acetoacetic acid spontaneously forms into acetone which, being volatile, is excreted via the lungs and gives the distinctive "nail polish remover" odour to the breath of those with DKA.

Ketones are weak acids and must be buffered by the body, using bicarbonate. As this compensatory mechanism is overwhelmed, plasma bicarbonate and pH decline and a metabolic acidosis develops. The person will develop Kussmaul respiration (rapid, deep sighing breaths) as the respiratory system tries to compensate for loss of renal buffering mechanisms. As the body becomes increasingly dehydrated, lactic acidosis may also occur, further decreasing plasma pH.

Potassium levels in DKA: Serum potassium levels may be elevated in DKA, but this is misleading because total body potassium will be depleted. Intracellular potassium is invariably depleted, due to a number of mechanisms:

* Lack of insulin decreases potassium uptake into cells.

* Acidosis triggers exchange of H+ ions from the plasma for K+ ions from the cell.

* Loss of water from the cell due to dehydration causes loss of potassium due to alterations in cellular tonicity.

At the same time, potassium is being lost via the kidneys, due to:

* Action of aldosterone, which is released in response to dehydration and attempts to conserve water and sodium in the kidney, but this is at the expense of potassium.

* High volume of urine due to hyperglycaemia promotes secretion of potassium in the distal tubules.

Insulin therapy used to reverse DKA may trigger abrupt, severe and life-threatening hypokalaemia as potassium is taken back up into the cells. For this reason, even where plasma potassium levels may be recorded as normal or elevated, potassium is always monitored closely during treatment. Sodium and phosphate are also disordered in DKA and should be monitored during treatment. (15)

Cerebral effects of DKA: Hyperosmolarity of the extracellular fluids causes loss of water from the brain cells. However, the brain is able to compensate for this by increasing the uptake of electrolytes and, over several days, larger organic molecules, balancing osmotic pressure with the extracellular fluid. Thus brain function may be relatively normal, until hyperglycaemia, acidosis and dehydration are severe, or if onset of DKA was abrupt. Fewer than 20 per cent of patients present in a comatose state. (16) If there is rapid replacement of body fluids during treatment, brain cells cannot correct for the excess fluid, leading to life-threatening cerebral oedema. (15)

Other signs and symptoms of DKA include abdominal pain, nausea and vomiting. The mechanisms underlying these are not well understood, but may be due to the accumulation of ketones, especially beta-hydroxybutyrate. Nausea and vomiting may complicate the detection of underlying causes of DKA, and contribute to fluid and electrolyte loss. (13) Other signs and symptoms are related to dehydration, although initial water loss is intracellular so that typical signs of dehydration do not appear until after extra-cellular fluid (ECF) is depleted.

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Long-term complications of T1DM

T1DM predisposes people to various long-term conditions that can have a significant impact on quality of life and life span. People with T1DM have a mortality rate five to six times higher than non-diabetics, (17) despite considerable improvements in therapy over the last two decades.

Increased risk of infection: High blood-glucose levels and acidosis both impair immune function by interfering with the actions of immune cells, including their ability to phagocytose and destroy foreign micro-organisms. In turn, infections lead to increased risk of hyperglycaemia and acidosis, depressing immune responses.

Risk of infection is also increased by the microvascular and macrovas-cular changes that occur in diabetes, which lead to impaired nutrient and oxygen delivery to tissues. Poor tissue perfusion leads to increased risk and delayed healing of infections. Poor nutrient delivery and the presence of peripheral neuropathies compromise the ability of the skin to act as a primary barrier to micro-organisms. (12)

Most common sites of infection for diabetes are the skin (staphylococcal, superficial fungal, oral and genital candidal infection and cellulitis) and urinary tract. Skin infections have a higher risk of developing into osteomyelitis, sepsis and necrotising infections. Frequent urinary tract infections increase the risk of acute pyelonephritis that, if recurrent, can cause or contribute to the development of renal failure. (3)

Diabetic nephropathy: Up to 30 per cent of people with T1DM will develop nephropathy, with a significantly increased risk of end-stage renal failure and death. (18) Microvascular disease, macrovascular disease and hyperglycaemia all play a role in the development of nephropathy.

Thickening in the walls of the kidney's arterioles and capillaries causes ischaemia of the renal tissue and reduces function. Dilation of the afferent arterioles (due to ischaemic injury) causes glomerular hypertension, hyperfiltration and damage to the glomerulus and its basement membrane.

Hyperglycaemia leads to the accumulation of reactive oxygen species that cause disruption and thickening of the extracellular matrix and basement membrane of the glomerulus.

Finally, macrovascular disease, such as atherosclerosis and hypertension, causes increased stress on afferent arterioles. (18)

This damage to the kidneys causes abnormal loss of proteins in the urine, especially albumin, which is the most abundant of the plasma proteins. Persistent loss of proteins in the urinary filtrate may trigger immune responses within the renal tubules and further damage the kidneys. (12) The end result is chronic renal failure.

Early detection and treatment of diabetic nephropathy is essential to prevent progression of the condition. Reducing dietary salt intake, strict glycaemic control and management of hypertension are the main forms of therapy. Use of ACE-inhibitors protects the kidneys, even in the absence of hypertension. (18)

Diabetic retinopathy: Acute blurring of the vision can occur with hyperglycaemia or rapid reduction of plasma glucose concentrations. This is due to osmotic shifts of water in and out of the lens, causing it to change shape. But the main ophthalmological condition related to T1DM is diabetic retinopathy.

In New Zealand it is estimated that 10 per cent of people with diabetes (types 1 and 2) have sight-threatening retinopathy and a further 20 per cent have some degree of retinopathy. (19) There is evidence to suggest a higher rate in Maori and Pacific groups, accompanied by lower use of screening services. (200 All people with diabetes require regular screening for retinopathy: early detection and treatment can reverse the progress of this condition and preserve sight.

Risk of diabetic retinopathy is increased with duration of diabetes, poor glycaemic control, hypertension, nephropathy, dyslipidaemia and pregnancy. (19) Genetic factors may dictate susceptibility, and whether retinopathy progresses despite good management of risk factors. (20)

Nonproliferative or background retinopathy arises due to microvascular changes occurring in diabetes. Microaneurysms, haemorrhages and protein exudate from the retinal capillaries may not cause any change in vision initially, unless they occur in the centre of the macula. As the condition progresses, oedema is the commonest reason for vision loss. Leakage of plasma and blood components causes hypoxia, thickening of the retina, inflammation and necrosis.

Proliferative retinopathy is induced by ischaemia that triggers the growth of new blood vessels in the eye. These new vessels grow on to the surface of the retina and other abnormal locations. They are prone to haemorrhage and can cause retinal detachment as they force the separation of the retina from its fibrous attachments. Both of these can cause sudden blindness. (3)

Diabetic neuropathy: Abnormal peripheral nerve function occurs in up to 50 per cent of people with diabetes. Risk is increased with poor glycaemic control, duration of T1DM, heavy alcohol use and cardiovascular risk factors. (21) The underlying pathophysiology in the development of neuropathies is not well understood, but it is known that oxidative stress and structural damage to neurones affect function and repair processes.

Neuropathy can be sensory, motor, autonomic or a combination of these. Symptoms and outcomes vary with the type of nerve damaged. Sensorimotor neuropathy increases the risk of foot ulcers and subsequent lower limb amputation. Autonomic neuropathy can affect many body functions, including cardiac regulation (postural hypotension, exercise intolerance); GI function (gastroparesis, constipation or diarrhoea); and genitourinary function (neurogenic bladder, impotence). (12)

Macrovascular complications: This is the leading cause of death in diabetes: 65-75 per cent of people with diabetes will die from macrovascular disease (compared with about 35 per cent of the general population). (3)

Accelerated rates of atherosclerosis affect the vessels of the heart, kidneys, lower limbs, carotid arteries and brain, increasing the incidence of myocardial infarction, renal disease, peripheral vascular disease and stroke well above that of the general population.

In the last 20 years, the treatment of T1DM has undergone a revolution. Before 1993, treatment was aimed at reducing episodes of hyperglycaemia, but following publication of the Diabetes Control and Complication Trial results that year, the goal shifted to tight glycaemic control, implemented as early as possible in the course of the disease. (22)

This research showed maintenance of normal plasma glucose concentrations and HbAlc levels of less than 53mmol/mol (seven per cent) decreased the risk of microvascular and macrovascular complications and reduced overall mortality. More tailored insulin regimes, accounting for basal and prandial insulin requirements, were developed. Tighter glycaemic control has, however, increased the risk of episodes of hypoglycaemia.

INSULIN THERAPY IN DIABETES

Insulin is a peptide hormone, synthesised in the beta cells in the pancreas. Before its discovery, T1DM was invariably fatal, and some of the treatments extreme. Originally, all commercial insulin was extracted from pig or cow pancreases and purified. Now most is recombinant human insulin synthesised by genetically programmed micro-organisms.

Roles of insulin

The most obvious role of insulin is transporting glucose into cells, but not all body cells are dependent on insulin for glucose uptake. The brain and liver can access glucose independent of insulin. In adipose tissue, and skeletal and cardiac muscle, binding of insulin to its receptor triggers the insertion of GLUT4 glucose transporters into the cell membrane, allowing the uptake of glucose. Insulin also: (12,23)

* acts as a counter-regulator to the secretion of glucagon and other hormones that increase plasma glucose concentration.

* stimulates lipogenesis and decreases lipolysis, promoting fat storage and inhibiting its mobilisation.

* is a powerful inhibitor of ketogenesis.

* increases uptake of amino acids into cells, making these available for protein synthesis.

* modulates DNA transcription and protein synthesis.

* increases DNA synthesis and cell replication.

* promotes cell growth.

* increases synthesis of GLUT4 receptors. (Low insulin levels, or insulin resistance, leads to a decrease in the numbers of GLUT4 receptors, reducing glucose uptake.)

* regulates endothelial cell function via nitrous oxide pathways, reducing inflammation and recruitment of leukocytes.

* in the liver, stimulates storage of glucose (glycogenesis) and inhibits glycogenosis and gluconeogenesis.

During insulin synthesis in the pancreas's beta cells, the prohormone is folded and split, leaving a surplus strand of peptide that gets secreted along with the insulin. This C peptide can be measured in the serum of people with diabetes, to indicate the amount of insulin still being synthesised in the pancreas.

When the pancreas is working normally, there is a continuous basal release of insulin, with peaks following ingestion of food. The aim of modern insulin therapy is to mimic this physiological action as closely as possible, by using a tailored combination of rapid and slower-acting insulin.

Types of exogenous insulin Insulin comes in a variety of types: rapid, short, intermediate or Long-acting; single or biphasic mixtures; and animal, human or analogue forms. Most insulin today is recombinant human insulin, which was first marketed in the early 1980s. There are no significant differences between the actions or adverse effects of animal and recombinant insulin, despite a belief that more allergies develop in response to bovine or porcine-sourced drug. Insulin is sensitive to heat and oxygen: vials must be discarded after 28 days as the contents lose effectiveness.

Rapid and short-acting insulin: Insulin lispro (Humalog), asparte (Novorapid), and glulisine (Apidra) are all analogue insulin--they have an altered molecular structure that allows rapid absorption following subcutaneous injection. It starts to act within five to 10 minutes. Peak plasma concentrations occur at about 30 minutes after administration, in contrast to short-acting insulins where the peak concentration occurs between one to two hours. The half-life of rapid-acting insulin is also shorter than short-acting insulin (one hour compared to 1.5). Rapid insulin more closely mimics the post-prandial burst of secretion from beta cells.

Neutral insulin (Actrapid and Humulin R) is a short-acting recombinant human insulin. It starts to act within 30-60 minutes after subcutaneous injection.

Intermediate and long-acting insulin: Insulin isophane (Protophane and Humulin NPH) is a recombinant form, classed as an intermediate-duration insulin. Onset of action is about 90 minutes following injection, with peak concentration between four and 12 hours and duration of action up to 24 hours. Newer analogue insulins are marketed as being more effective for basal administration, with fewer hypoglycaemic episodes. Analogue, long-acting insulin includes insulin glargine (Lantus) and insulin detemir (not available in New Zealand). Analogue insulin is modified to provide a slow, steady absorption over 24 hours.

The newer analogue insulin is significantly more expensive than the older isophane: $94.50 for five vials of 3ml of 100u/ml, compared to $29.86. (24) Analogue insulin now comprises 83 per cent of the global market in basal insulins, up from 60 per cent in 2005. (25) Data does not, however, support benefits of newer analogue basal insulins over isophane. A Cochrane review in 2006 found little support for the more expensive insulin, showing both to be equally effective at controlling HbAlc. While there were fewer hypoglycaemic episodes when using the glargine or detemir, the incidence of severe hypoglycaemic episodes was similar to those for isophane. (26)

Adverse effects of insulin therapy

The main risk of insulin therapy, which is increased with tight glycaemic control, is hypoglycaemia. Recurrent episodes of hypoglycaemia are suggested to cause permanent cognitive impairment, but recent data does not support this link. (3)

Dawn versus Somogyi phenomena: There is a normal rise in plasma glucose concentrations in the early morning. This is believed to be due to increased growth hormone secretion overnight that leads to mild insulin resistance, combined with increased nocturnal Cortisol secretion, triggering gluconeogenesis.3 People with T1DM may record elevated capillary glucose before breakfast due to these effects.

However, there is also the rarely occurring Somogyi phenomenon, where an overnight hypoglycaemic episode triggers a rebound hyperglycaemia, with an increase in plasma ketones. Pre-breakfast hyperglycaemia may require adjustments to an insulin regime.

Signs and symptoms of hypoglycaemia: While people with T1DM must regularly monitor capillary glucose (CG) levels, an awareness of impending hypoglycaemia is also essential to safety and well-being. The actual plasma glucose concentration at which an individual experiences hypoglycaemic effects is highly variable, but generally will occur where CG falls below 2.8mmol/l. The threshold below which a person experiences effects may become lower with repeated episodes. (27) This is a problem under tighter glycaemic control, as repeated mild hypoglyacaemic episodes may contribute to hypoglycaemia unawareness. (30)

Hypoglycaemia may occur as a result of medication errors or deliberate overdose, failure to co-ordinate dosing with meals and/or exercise, and where there is a change to the medication regime. Ethanol and other drugs have been associated with hypoglycaemia. Oral hypoglycaemic agents used in the treatment of T2DM can also trigger hypoglycaemia. Sometimes there is no apparent cause for episodes. (27)

Once plasma glucose concentration falls below an individual's threshold, the sympathetic nervous system is stimulated. This triggers sweating, palpitations and shaking, hunger and anxiety. The brain cannot function without glucose, so further falls in plasma glucose concentration will trigger cerebral effects: headache, difficulty concentrating, confusion, irritability and aggression, motor impairments and eventually coma and death.

Hypoglycaemia unawareness: For some, hypoglycaemia can occur without sympathetic effects. This can occur where there is an autonomic neuropathy, desensitisation due to repeated episodes, or with the use of drugs that inhibit sympathetic action.

Beta-blockers--beta-adrenergic antagonists--may have some effect in masking hypoglycaemic symptoms. This is particularly so for nonspecific beta-blockers. This risk is not well-demonstrated and remains largely theoretical so beta-blockers are not contraindicated with T1DM but should be used with caution. (30) Selective serotonin reuptake inhibitors have been reported to increase hypoglycaemic episodes and decrease awareness in three adolescents with T1DM, but, conversely, fluoxetine is used to increase awareness of episodes. (29,30) Additional risk factors include increasing age, duration of diabetes, alcohol and sleep.

CONCLUSION

Incidence of T1DM is increasing, but this form of diabetes has been somewhat overlooked in the publicity about the global epidemic of T2DM. While people with T1DM face some similar complications as those with T2DM, morbidity is often greater and occurs at a younger age. All T1DM is treated with exogenous insulin and, as the incidence of type 2 increases, more of this group will also be using insulin therapy. Knowledge of types of insulin and the risks and benefits of tight glycaemic control can help nurses support people with diabetes to manage their condition.

LEARNING OUTCOMES

After reading this article and completing the accompanying online learning activities, you should be able to:

* Outline the basic mechanisms underlying the development of type 1 diabetes (T1DM).

* Discuss current theories about the factors which cause T1DM.

* Describe acute and chronic complications of T1DM.

* Describe differences between the various types of exogenous insulin available for therapy.

* Discuss adverse effects of insulin therapy.

* For this article's references, go to CPD4nurses.co.nz and click under the 'News' link.

Georgina Casey, RN, BSc, PGDipSci, MPhil (nursing), is the director of CPD4nurses.co.nz. She has an extensive background in nursing education and clinical experience in a wide variety of practice settings.
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Title Annotation:CONTINUING PROFESSIONAL DEVELOPMENT: CPD +nurses
Author:Casey, Georgina
Publication:Kai Tiaki: Nursing New Zealand
Geographic Code:8NEWZ
Date:Apr 1, 2012
Words:4533
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