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  2. Session Overview This session covers brief information about the pancreas and its major functions. A major disorder of the pancreas, diabetes mellitus is also discussed. 2
  3. Outline of Presentation • Brief information about the pancreas • Definition of diabetes • Types of diabetes –type 1, causes, clinical manifestations, Diabetic Ketoacidosis (DKA) • Type 2 diabetes mellitus – causes • Hyperglycaemic Hyper-Osmolar Non-Ketotic State (HONK) • Gestational Diabetes Mellitus 3
  4. Outline of Presentation contd. • Other types of diabetes • Clinical Manifestations of diabetes mellitus • Diagnosis of Diabetes Mellitus • Medical Management of diabetes mellitus • Nursing management of diabetes mellitus • Complications • Diabetes screening • UK model of diabetes prevention • Somogyi Effect and Dawn Phenomenon • Insulin Therapy and Kinetics with examples. 4
  5. Session Objectives At the end of the session, the student should be able to: • Indicate the role of the pancreas in the regulation of blood sugar. • Describe the three major types of diabetes. • Identify patients with clinical manifestations of diabetes mellitus. • Describe treatment protocols available for the treatment of patients living with diabetes mellitus • Identify ways to empower individuals living with diabetes mellitus. 5
  6. Brief information about the pancreas Functions of the Pancreas • The pancreas is involved in blood sugar control and metabolism within the body, and also in the secretion of substances which help digestion. 6
  7. Brief information about the pancreas contd. • Basically, the roles are divided into (1) endocrine role, associated with the secretion of insulin and other hormones within pancreatic islets and helping control blood sugar levels and metabolism within the body, and (2) an exocrine role, about the secretion of enzymes involved in digestion of substances such as trypson and chymotrypson to digest protein, amylase for digestion of carbohydrates, and lipase to break down fats 7
  8. Picture of the Pancreas 8
  9. Picture of the Pancreas 9
  10. Picture of the Pancreas 10
  11. Brief information about the pancreas contd. Primary hormones secreted by the pancreas include: • Glucagon (secreted by alpha cells): Glucagon helps maintain normal blood glucose by working in the opposite way of insulin. It stimulates the cells to release glucose, and this raises the blood glucose level (Young, 2006). In simple terms alpha cells produce the hormone glucagon, which raises blood glucose. 11
  12. Brief information about the pancreas contd. • Insulin (secreted by beta cells): This hormone regulates blood glucose level by allowing many of the body’s cells to absorb and use glucose. It implies that beta cells produce the hormone insulin, which lowers blood glucose levels. • In turn, this maintains blood glucose levels (Hall, 2011). 12
  13. Brief information about the pancreas contd. • Somatostatin (secreted by delta cells): When levels of other pancreatic hormones, such as insulin and glucagon, get too high, somatostatin is secreted to maintain a balance of glucose and/or salt in the blood (Young, 2006). • In other words, somatostatin inhibits the secretion of pancreatic hormones, including glucagon and insulin. 13
  14. 14 Diabetes Mellitus (DM) Diabetes Mellitus (DM) is a long-lasting and incapacitating illness associated with raised blood sugar levels in affected individuals. Hyperglycaemia results from disturbances related to carbohydrate, protein and fat metabolism due to malfunctioning of the pancreas in terms of insulin secretion, insulin action or the two together (Melmed et al., 2011).
  15. Diabetes Mellitus (DM) contd. • It causes variations/changes in metabolism of carbohydrates, proteins as well as fats. When insulin is discharged by the pancreas, the body is able to regulate how and when fats, proteins and carbohydrates are metabolized. 15
  16. 16 Diabetes Mellitus (DM) contd. The subsequent deficiency of insulin leads to increased blood and urine glucose. The body’s central source of energy are carbohydrates. Carbohydrates are transformed/changed into glucose and provide the required nutrients for the body when they are processed or digested.
  17. 17 Diabetes Mellitus (DM) contd. • Insulin is discharged uninterruptedly by the pancreas according to the body’s requirements (Melmed et al., 2011).
  18. 18 Diabetes Mellitus (DM) contd. Grouping of Diabetes Mellitus: • Diabetes mellitus type 1 (T1D or type 1 diabetes) is a form of diabetes mellitus that results from the autoimmune destruction of the insulin-producing beta cells in the pancreas (Longo et al., 2012). • Formerly it was known as Insulin-Dependent Diabetes Mellitus (IDDM) or Juvenile Diabetes (JD).
  19. Type 1 Diabetes contd. • A number of explanatory theories have been put forward, and the cause may be one or more of the following: genetics or viruses or autoimmune response (single-handedly or blend of these factors). • Another theory also postulates that the cause of type 1 diabetes is unknown. • Other causative factors include chemicals and drugs (Longo et al., 2012). 19
  20. Type 1 Diabetes contd. • Globally, about 5-10% of people with diabetes have type 1 DM. It was projected/estimated that about 80,000 children develop the disease each year (Chiang, Kirkman, Laffel and Peters, 2014). 20
  21. Type 1 Diabetes contd. • Most people with this type are diagnosed before the age 30 (Chiang, Kirkman, Laffel and Peters, 2014). In the affected individuals there is inadequate supply of insulin in this type, so patients require exogenous/external source of insulin. 21
  22. 22
  23. 23 Type 1 Diabetes contd. Causes of type 1 diabetes mellitus • Autoimmune destruction of the insulin- producing beta cells: • The disease process in diabetes type 1 is a destruction of beta cells in the pancreas, regardless of which risk factors or causative entities have been present, in which the immune system attacks the insulin-secreting cells of the pancreas (Longo et al., 2012) .
  24. Type 1 Diabetes contd. • Type 1 diabetes results from the destruction of the beta cells in the islets of Langerhans in the pancreas. This destruction usually results from immunological defect that produces antibodies against the beta cells (Chiang, Kirkman, Laffel and Peters, 2014) . • These antibodies may be present for months or years before clinical symptoms of diabetes develop in the affected person. 24
  25. 25 Type 1 Diabetes contd. • Genetic predisposition/causes of diabetes mellitus type 1: • Type 1 diabetes is a disease that implicates many genes. Over 50 genes are linked to type 1 diabetes (Bluestone, Herold and Eisenbarth, 2010). • For example, research with the Human Leukocyte Antigen (HLA) System that is used in tissue typing has demonstrated a relationship with some HLA antigens and diabetes.
  26. Type 1 Diabetes contd. ***A tissue type test (may also be called HLA typing) is a blood test that identifies substances called antigens on the surface of body cells and tissues. Examining the antigens helps to find if donor tissue is safe (compactible) for transplant to another person. Based on the antigens, the immune system can tell the difference between normal body tissue and foreign tissue (for example, tissue from another person's body). 26
  27. Type 1 Diabetes contd. • Some of these antigens are reliably found in patients with insulin-dependent diabetes mellitus (type 1 diabetics). Typical examples are D,A,Q & B genes (Bluestone, Herold and Eisenbarth, 2010). 27
  28. 28 Type 1 Diabetes contd. • Similarly, selected researchers have also observed a relationship between various HLA antigens and persons with long term complications of diabetes (Bluestone, Herold and Eisenbarth, 2010). • However, not all persons with these antigens develop diabetes mellitus type 1. • This limitation renders this theory futile or pointless.
  29. 29 Type 1 Diabetes contd. • The viral theory: • One theory proposes that type 1 diabetes is a virus-triggered autoimmune response in which the immune system attacks virus- infected cells along with the beta cells in the pancreas (National Institute of Health, 2013).
  30. Type 1 Diabetes contd. • The virus (environmental factor) is believed to act to trigger the autoimmune response. It is also believed that the genetic make up of cells in an individual probably determines whether the virus can attach itself to the cell surface, enter the cell, and change its metabolism. • This certainty/belief has been traced to HLA genotypes, though the connection between them and the triggering of an autoimmune reaction remains poorly understood (National Institute of Health, 2013). 30
  31. 31 Type 1 Diabetes contd. • The characteristically abrupt appearance of insulin-dependent diabetes (type 1) could be the result of an infection with a diabetogenic virus in a person already genetically predisposed. And that the infection might cause an autoimmune reaction (antigen- antibody reaction).
  32. 32 Type 1 Diabetes contd. • In order for type 1 to develop, at least 90% of the individual’s beta cells must stop producing insulin. This could result from one very potent viral attack or it could be the result of a series of viral infections that eventually destroy the beta cells (National Institute of Health, 2013).
  33. 33 Type 1 Diabetes contd. • Antibodies against one of the suspected viruses (Coxsackie B4) have been found in the blood of patients newly diagnosed with insulin-dependent diabetes and not in Non- Insulin Dependent Diabetics. • Similarly, rubella is also implicated, even though the evidence is inconclusive/questionable.
  34. 34 Type 1 Diabetes contd. Evidence/Proof: Evidence that suggests a viral cause for Insulin-Dependent Diabetes (type 1) include the following: 1. It usually occurs in young people whose systems are more prone to viral infections. 2. It occurs suddenly, like viral infection 3. It usually occurs when viral infections are prevalent.
  35. 35 Type 1 Diabetes contd. 4. Beta cells are inflamed early in the viral infection. 5. A viral infection may develop before the diabetes develops (from health history of the patient). 6. It may develop in a child with no family history of diabetes mellitus. (National Institute of Health, 2013)
  36. Type 1 Diabetes contd. • As noted already the Coxsackie virus, family or rubella is implicated, although the evidence is inconclusive. • This vulnerability/susceptibility is not shared by everyone, because it is not every person infected by the suspected virus who develops type 1 diabetes. 36
  37. Diabetes Mellitus (DM) contd. • Chemicals and drugs • Some chemicals and drugs destroy pancreatic cells. • For example, Pyrinuron (Vacor), a rodenticide (for rodent control [pale yellow crystalline solid, odourless]) made known in the United States in 1976, particularly destroys pancreatic beta cells, resulting in type 1 following its ingestion by humans. 37
  38. Diabetes Mellitus (DM) contd. • If it is ingested by humans in high doses, it may selectively destroy insulin-producing beta cells in the pancreas and cause type 1 diabetes (Vogel, 1982). • May also cause death resulting from cardiovascular and respiratory failures and central nervous system dysfunction. Human survivors gradually develop an insulin-deficient, ketosis- prone form of diabetes millitus (EPA, 1998). 38
  39. Diabetes Mellitus (DM) contd. • It was withdrawn from the U.S. market in 1979 but is still used in some countries. • Similarly, Streptozotocin (Zanosar), an antibiotic and antineoplastic agent employed in chemotherapy for the treatment and management of pancreatic cancer, destroys beta cells, resulting in loss of insulin production (EPA, 1998). 39
  40. 40 Type 1 Diabetes contd. Family History of T1DM • Although the exact mechanism of how other people get the condition in families is not well understood, blood relatives of known patients with diabetes need to maintain life-long vigilance for this condition. Obese persons and mothers who have delivered large babies are also susceptible. These high risk individuals should be examined regularly for signs of diabetes.
  41. Type 1 Diabetes contd. • Reading Assignment: Some books also employ lay perspectives to explain causes of chronic conditions such as DM I & II by using (1) naturalistic, (2) personalistic, and (3) emotionalistic disease causal theories. So far we have focused our attention on naturalistic model of disease causation, nevertheless you should consider reading the other 2 models of illness causality by Kottak (2014) in order to offer appropriate care to people with varied cultural and ethnic backgrounds who get diabetes. 41
  42. 42 Type 1 Diabetes Mellitus (DM) contd. Clinical Manifestations: When diagnosed individuals have four cardinal clinical manifestations: 1. Weight loss and muscular wasting due to breakdown of protein and lipids (catabolism).
  43. 43 Type 1 Diabetes Mellitus (DM) contd. 2. Frequent urination (polyuria) because glucose attracts water and an osmotic diuresis occurs. This polyuria results in the loss of water and electrolytes, particularly Na, Cl, K and Phosphate.
  44. 44 Type 1 Diabetes Mellitus (DM) contd. 3. Excessive thirst (polydpsia). The loss of water and sodium results in thirst and increases fluid intake. 4. Eat excessively (polyphagia). Extreme hunger and increased food intake are triggered as the cells become starved of their fuel.
  45. 45 Clinical Manifestations of type 1 DM contd. In addition: 1. It usually begins in childhood but may also occur at any age. 2. Measurable circulating insulin may still be present early in the course of the disease, but it soon disappears 3. As insulin production decreases, hyperglycemia develops as a result of the body’s inability to use glucose
  46. 46 Clinical Manifestations of type 1 DM contd. 4. If the concentration of glucose in the blood is sufficiently high, the kidney may not reabsorb all of the filtered glucose; the glucose then may appear in urine (Glucosuria). Fluid loss through the kidneys result as the kidneys work to excrete the increased load of glucose, producing loss of water, Na, magnesium, calcium, potassium chloride, and phosphate. (Longo et al., 2012)
  47. 47 Summary (type 1 DM) It may develop through: 1. Active autoimmunity 2. Genetic Predisposition 3. Viral factor/Environmental trigger 4. Chemical or drug factor 5. There is progressive beta dysfunction 6. Overt diabetes mellitus
  48. 48 Diabetic Ketoacidosis (DKA) When there is deficiency of insulin, muscles cannot utilize glucose. Free fatty acids are then mobilized from the adipose tissue cells and broken down by the liver into ketone bodies for energy (Melmed et al., 2011). In other words, there is a severe lack of insulin. For this reason the blood glucose, although very high, can not be utilized for energy production. Fat is broken down instead, producing toxic chemicals called ketones.
  49. Diabetic Ketoacidosis (DKA) contd. (Ketones are end-products of fat metabolism in the body. That is, they are formed when fat is burned for energy by the muscles. Chemically, they are strong acids known as ketone bodies which are very dangerous to organs of the body (Melmed et al., 2011). For example, the brain. 49
  50. 50 Diabetic Ketoacidosis (DKA) contd. Ketoacidosis is therefore characterized by excessive ketone bodies in the blood. Patients with ketoacidosis exhibit loss of Na, kcl, and water from the body. The net metabolic result of acute, uncontrolled diabetes mellitus is loss of fat stores, cellular protein, electrolytes and water. There is severe dehydration and electrolyte imbalance (Longo et al., 2012).
  51. 51 Diabetic Ketoacidosis (DKA) contd. Often the diagnosis of DM is first made when the patient is brought to the hospital in coma state due to Ketoacidosis. Diabetic ketoacidosis is the commonest cause of death among patients with diabetes in Ghana. It is common in newly diagnosed diabetics, example children, young adults and other Type 1 diabetes patients. What factors may contribute to DKA among these patients?
  52. Diabetic Ketoacidosis (DKA) contd. Causes: 1. Previously undiagnosed diabetes 2. Interruption of insulin therapy (usually for financial reasons or for alternative treatment) 3. Stress of intercurrent illness (e.g. infection, myocardial infarction, stroke etc.) 4. Other factors including “Healer Shopping”
  53. Diabetic Ketoacidosis (DKA) contd. Clinical Manifestations: • Passing excess urine • Dehydration with dry skin, reduced skin turgor or sunken eyes • Drinking excess amounts of water • Relatives may report changes in sensorium • etc.
  54. Diabetic Ketoacidosis (DKA) contd. Investigations: • Blood glucose is usually greater than 18mmol/L. • Urine glucose is usually more than 3+ • Urine ketones (usually higher than 2+). • Blood urea and electrolytes (usually low, however if in renal failure urea and potassium are high) • Other test may be ordered.
  55. Management of Diabetic Ketoacidosis (DKA) • Bed rest/Admission of patient • Administration of IVF with fast acting insulin (soluble regular insulin) Normal Saline/Dextrose Saline/5%Dextrose Water?? etc. • Liberal oral fluids (water if patient can drink) • Intake and Output Monitoring • Monitoring of blood glucose levels (sliding scale) • Monitoring of urine ketones • General observation of the patient • Etc. 55
  56. 56 Complications Over a period of years, blood glucose levels that are consistently above normal appear to cause complications that affect the large vessels in the brain, heart, kidneys and extremities and small vessels in the eyes, kidneys and nerves (Beare and Myers, 2003).
  57. Diabetes Mellitus (DM) contd. Read on: Pancreas transplantation: In some persons, pancreas transplant may restore proper glucose regulation. Nevertheless, the surgery involved may be more costly and risky than continued insulin replacement therapy (Lakey et al., 2003). 57
  58. Diabetes Mellitus (DM) contd. Read on: Islet cell transplantation: Islet cell transplantation may be a choice for some people with type 1 diabetes that are not well controlled with insulin. Difficulties include finding donors that are a compactible, getting the new islets to survive, and the side effects from the medications used to prevent rejection (Lakey et al., 2003). 58
  59. 59 Diabetes Mellitus (DM) contd. 2. Type 2 Diabetes (Non-Insulin-Dependent Diabetes Mellitus). Diabetes mellitus type 2 is a long term metabolic disorder that is characterized by high blood sugar, insulin resistance, and relative lack of insulin (Beare and Myers, 2003).
  60. Diabetes Mellitus (DM) contd. • The development of type 2 diabetes is caused by a combination of lifestyle and genetic factors (Beare and Myers, 2003). • Some of these factors are under personal control, such as diet and obesity, other factors are not, such as increasing age and genetics. 60
  61. Diabetes Mellitus (DM) contd. • In type 2 DM, genetics and obesity play a more significant role. The exact role that heredity and obesity play is not yet completely understood, though they contribute. There is apparently no relationship between viruses and the etiology of NIDDM. 61
  62. Diabetes Mellitus (DM) contd. Lifestyle causes of diabetes mellitus type 2: A number of lifestyle factors are known to be important to the development of type 2 diabetes, including: • obesity and being overweight • lack of physical activity • poor diet • Urbanization (Beare and Myers, 2003). 62
  63. Diabetes Mellitus (DM) contd. • Dietary factors influence the risk of developing type 2 diabetes. • Consumption of sugar-sweetened drinks in excess is associated with an increased risk. • The type of fats in the diet are also important, with saturated fats increasing the risk. 63
  64. Diabetes Mellitus (DM) contd. • Eating lots of white rice appear to also play a role in increasing risk. • A lack of exercise is believed to cause 7% of cases. 64
  65. Diabetes Mellitus (DM) contd. Genetic causes of diabetes mellitus type 2: • Most cases of diabetes involve many genes, with each being a small contributor to an increased probability of becoming a type 2 diabetic. • For example, if one identical twin has diabetes, the chance of the other developing diabetes within his lifetime is greater than 90%, while the rate for non- identical siblings is 25–50% (Merck’s Medical Manual, 2002). 65
  66. Diabetes Mellitus (DM) contd. Medical conditions and drugs that can predispose persons to T2DM. • There are a number of medications and other health problems that can predispose to diabetes. Some of the medications include: glucocorticoids, cortisol, prednisolone, etc. Those who have previously had gestational diabetes are at a higher risk of developing type 2 diabetes (Merck’s Medical Manual, 2002. 66
  67. Diabetes Mellitus (DM) contd. • Other health problems that are associated include: Cushing's syndrome etc (Beare and Myers, 2003). 67
  68. 68 Type 2 Diabetes contd. Basically, type 2 DM results from a decrease in the amount of insulin produced or an insensitivity of the cell to insulin. About 90- 95% of people with diabetes have type 2. Individuals have onset after age 40 years. Classic symptoms are not present when first diagnosed (Beare and Myers, 2003).
  69. 69 Type 2 Diabetes contd. In some Non-Insulin Dependent Diabetes persons, insulin secretion is increased, resulting in higher circulating insulin levels. Although excessive insulin is present, it is not utilized because of an inadequate number of insulin receptors present in cells.
  70. 70
  71. 71 Type 2 Diabetes contd. This mechanism has been observed in obese non-insulin dependent patients. With weight loss the number of insulin receptors on the cells increase, thereby allowing glucose to enter the cell. This may result in return of a normal glucose utilization (Merck’s Medical Manual, 2002).
  72. 72 Diabetes Mellitus type 2 contd. Although the symptomatology of type 2 diabetes is less obvious than that of type 1, this classification of diabetes is accompanied by vascular and neuropathic complications.
  73. 73 DM type 2 contd. Typically, they are not absolutely dependent on exogenous insulin for survival, although insulin therapy is often employed to lower their blood glucose levels. **Note that being treated with insulin supplements does not change the classification of Type 2 to Type 1 (NIDDM to IDDM)** (Standard Treatment Guideline for Ghana, 2010).
  74. DM type 2 contd. • Insulin therapy may be required temporarily in Type 2 patients during severe stress e.g. severe infections, acute myocardial infarction, surgical operations, trauma, hyperosmolar state. 74
  75. 75 DM type 2 contd. In practice: 1. These patients may not require insulin and are usually managed adequately with exercises and diet alone. 2. The majority (about 80%) of patients with NIDDM are overweight when the condition is first diagnosed unless due to one or two reasons the diagnosis is delayed.
  76. 76 DM type 2 contd. 3. Symptoms may be so minor that the disease is undetected for many years (Develops slowly/Insidious). 4. Diagnosis may be suspected as a result of a routine urinalysis or during presentation of another condition like HPT/screening.
  77. Diabetes Mellitus (DM) contd. • 5. Frequently the disease is discovered when the patient seeks health care treatment of complications such as deteriorating vision, pain in legs or impotence or reduction in feeling for sex. • 6. Often blood glucose tests are normal, with hyperglycemia being seen only in postprandial (following a meal). (Standard Treatment Guideline for Ghana, 2010) 77
  78. 78 DM type 2 contd. 7. Onset is insidious/sneaky and may take years to develop. Other warning symptoms of type 2 DM are: Fatigue, itching of the skin (of the vulva in females), skin wounds that heal poorly, cramps in the muscle, blurring of vision etc.
  79. Diabetes Mellitus (DM) contd. • Individuals with type 2 diabetes mellitus may present with hyperosmolar hyperglycemic state (a condition of very high blood sugar level associated with/without decreased level of consciousness and low blood pressure). • The blood pressure may however be high in an already a hypertensive patient. (Longo et al., 2012). 79
  80. DM type 2 contd. Hyperglycaemic Hyper-Osmolar Non-Ketotic State (HONK)/Hyperosmolar Hyperglycaemic State. • Hyperglycaemic Hyper-Osmolar Non-Ketotic Coma (HONK) is a dangerous condition brought on by very high blood glucose levels in type 2 diabetes (e.g. above 33 mmol/L). • The condition of very high blood glucose without signs of ketosis may also be called Hyperosmolar Hyperglycaemic State. 80
  81. DM type 2 contd. • Hyperglycaemic Hyper-Osmolar Non-Ketotic Coma is a short term complication requiring immediate treatment by a healthcare professional (Standard Treatment Guideline for Ghana, 2010). 81
  82. DM type 2 contd. Clinical manifestations of HONK • Before loss of consciousness and coma takes place, patients may show signs of very high blood sugar levels with associated manifestations which may include: • Extreme thirst • Frequent need to urinate • Disorientation • Nausea 82
  83. DM type 2 contd. Causes of HONK • May be due to undiagnosed type 2 diabetes that has been developing over a number of years. • On the other hand, HONK may be brought about by not taking diabetic medication or • Due to very high blood glucose levels resulting from long period of illness. 83
  84. DM type 2 contd. Treatment for HONK • Treatment for hyperglycaemic hyperosmolar non- ketotic coma will include fluids being given to the patient and insulin administered intravenously (Standard Treatment Guideline for Ghana, 2010; Beare and Mters, 2003).Similar to the management of DKA Differentiate between Hyper-Osmolar Non-Ketotic State and Diabetic Ketoacidosis. 84
  85. DM type 2 contd. • Hyperglycaemic hyperosmolar non-ketotic state results from very high blood glucose levels in a patient with normal ketone levels. • If very high blood glucose levels are combined with high ketone levels, the state is likely to be ketoacidosis. 85
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  87. 87
  88. Gestational Diabetes Mellitus 3. Gestational Diabetes Mellitus (GDM) also called Pregnancy Induced Diabetes. GDM applies only to women in whom glucose intolerance develops or discovered during pregnancy. After pregnancy diagnostic classification may be changed to IDDM or NIDDM. Women who had the disease before the pregnancy are not included in this classification. Women with GDM have an increased future risk for progression to NIDDM or rarely IDDM (Beare and Myers, 2003). 88
  89. Gestational Diabetes Mellitus contd. What are the possible causes of GDM? • Women without previously diagnosed diabetes exhibit high blood glucose (blood sugar) levels during pregnancy (especially during their third trimester). Gestational diabetes is caused by improper insulin responses. 89
  90. Gestational Diabetes Mellitus contd. Pregnancy and Diabetes Development Pregnancy is diabetogenic due to increased production of insulin antagonists such as human placental lactogen, placental insulinase, cortisol, oestrogens and progesterone. Insulin requirements increases during pregnancy due to increased production of insulin antagonists while it decreases postpartum (Beare and Myers, 2003). 90
  91. 91
  92. Gestational Diabetes Mellitus contd. Risk factors of GDM • Classic risk factors for developing gestational diabetes are: • A previous diagnosis of gestational diabetes/Pregnancy Induced Diabetes or pre- diabetes • A family history showing a first-degree relative with type 2 diabetes. 92
  93. Gestational Diabetes Mellitus contd. • Maternal age – a woman's risk factor increases as she gets older (especially for women over 35 years of age). • Ethnicity (those with higher risk factors include African-Americans, Afro-Caribbeans, and people originating from South Asia region • Being overweight, obese or severely obese increases the risk T2DM. 93
  94. Gestational Diabetes Mellitus contd. • Management of GDM (Lifestyle) • Assessment and Counseling before pregnancy and multidisciplinary management are important for good pregnancy outcomes. • Since insulin resistance is highest in mornings, breakfast carbohydrates need to be restricted more. Intake of more fiber in foods with whole grains, or fruit and vegetables can also reduce the risk of gestational diabetes. 94
  95. Gestational Diabetes Mellitus contd. • Regular moderately intense physical exercise is advised, although there is no consensus on the specific structure of exercise programs for GDM. • However, this should be done with caution/care. (Chiang, Kirkman, Laffel and Peters, 2014). 95
  96. Other types of Diabetes Other types of Diabetes include: 1. Impaired Glucose Tolerance (IGT) is the term used to describe fasting glucose levels between 120 and 200 mg/dl. The term IGT replaces borderline diabetes. (Beare and Myers, 2003) 96
  97. Other types of Diabetes contd. 2. Secondary DM as a result of other disorders. Causes include pancreatic disorders like pancreatitis and pancreatectomy etc. Therapy is similar to that of treating diabetes using modalities of meal planning, exercises and medication and also looking at the underlying cause. Read on other types such as drug induced DM etc. 97
  98. General Clinical Manifestations As already noted in type 1 DM: When diagnosed individuals have four cardinal clinical manifestations: 1. Weight loss and muscular wasting due to breakdown of protein and lipids (catabolism). 98
  99. Clinical manifestations contd. 2. Frequent urination (polyuria) because glucose attracts water and an osmotic diuresis occurs. This polyuria results in the loss of water and electrolytes, particularly Na, Cl, K and Phosphate. 99
  100. Clinical manifestations contd. 3. Excessive thirst (polydpsia). The loss of water and sodium results in thirst and increases fluid intake. 4. Eat excessively (polyphagia). Extreme hunger and increased food intake are triggered as the cells become starved of their fuel. 100
  101. If the concentration of glucose in the blood is sufficiently high, the kidney may not reabsorb all of the filtered glucose; the glucose then may appear in urine (Glucosuria). Fluid loss through the kidneys results as the kidneys work to excrete the increased load of glucose, producing loss of water, Na, magnesium, calcium, potassium chloride, and phosphate. (Longo et al., 2012) 101
  102. 102 Diagnosis of Diabetes 1. Based on classic clinical manifestations which are: Polyuria, polydipsia, polyphagia, rapid weight loss. (Beare and Myers, 2003). 2. Elevated Fasting Blood Glucose on more than one occasion (above 5.5mmol/L). The presence of abnormally high blood glucose levels is the criterion on which the diagnosis of diabetes should be based. Blood glucose levels elevated above (5.5mmol/L or more, more than one occasion suggest a diagnosis of diabetes.
  103. Diagnosis of Diabetes contd. • Normal value ranges may differ slightly among different laboratories due to different test devices. The normal blood glucose level (tested while fasting) should be between 3.9 and 5.5 mmol/L (70 to 100 mg/dL). The mean normal blood glucose level in humans is about 5.5 mmol/L (100 mg/dL). 103
  104. 104 Diagnosis of Diabetes contd. 3. If fasting glucose levels are normal or nearly normal, the diagnosis must be based on Glucose Tolerance Test (Gold Standard Method). Glucose Tolerance Test: Oral Glucose Tolerance Test (Standard Treatment Guideline for Ghana, 2010).
  105. Diagnosis of Diabetes contd. Eg. Two hour glucose tolerance test after ingesting the standardized 75 Gm glucose solution, the blood sugar level is then checked again. 1. Blood glucose is checked before the test. 2. Glucose is administered and blood sugar level rechecked exactly after two hours. (Beare and Myers, 2003). 105
  106. Diagnosis of Diabetes contd. 4. Glycosylated Hemoglobin or Glycated Hemoglobin - HbA1c or A1c test is used as a guide to know what is the average blood glucose level during the past 2 or 3 months/usually 3 months. Glucose tends to stick to red blood cells and more the glucose in the blood, the more the number of red cells that have glucose on its surface. 106
  107. Diagnosis of Diabetes contd. Normally 4 to 6 red cells in 100 have glucose attached to its surface; hence the range of HbA1c in a normal person is 4 to 6%. Better control of glucose means lesser the complications of diabetes to the heart, blood vessels, kidneys, brain, nerves, eyes and feet etc. (Chiang, Kirkman, Laffel and Peters, 2014). 107
  108. Diabetes Mellitus (DM) contd. • HbA1c has the advantages that fasting is not required and results are more stable but the disadvantage is that the test is more costly and takes some time before the result is available. • HbA1c may be useful to diagnose individuals in whom the clinical manifestations are not clear and straight forward to support decision making for diagnosis. 108
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  110. 110 Diagnosis of Diabetes contd. 5. Urine Tests: Urine tests should not be used because both false-negative and false-positive results occur. Renal glucosuria occurs when the renal threshold for glucose is decreased (LeMone and Burke, 1996).
  111. 111 Diagnosis of Diabetes contd. In this instance, glucose appears in the urine despite normal blood glucose values. In the elderly, renal threshold levels are higher than normal, so no glucose is found in the urine despite elevated blood glucose values/levels.
  112. SOME BASIC INVESTIGATIONS UPON DIAGNOSIS The following investigations are important for each patient upon diagnosis to serve as a reference point. • ECG/Chest X-Ray/Scan of the Heart • Renal Function Test (Kidney Function Test) • Liver Function Tests (LFTs) • Eye Tests including Scan of the Eye • Others
  113. Management of DM Therapeutic objectives: The objectives of long-term diabetes treatment are to: 1. Relieve symptoms and maintain fasting (4 – 6mmol/L) and 2-hourly post meal (4 – 8mmol/L) blood glucose levels within the normal limits.
  114. Management of DM contd. 2. Prevent acute diabetes complications such as hypoglycaemia, ketoacidosis state, HONK etc. 3. Prevent the chronic complications of diabetes, namely; blindness, limb amputation, kidney disease, nerve damage, hypertensive heart disease etc. (Standard Treatment Guideline for Ghana, 2010).
  115. Management of DM contd. Other therapeutic objectives are: • To achieve a Glycated haemoglobin 6.5 % or less • To ensure weight reduction in overweight and obese individuals • To maintain blood pressure less than 130/80 mmHg in patients with diabetes and • To maintain cholesterol level at less than 2.5 mmol/L (Beare and Myers, 2003). 115
  116. Management of DM contd. These objectives may be achieved by strict blood glucose control and regular screening for diabetes complications. Regular follow-up of all individuals with diabetes is therefore important to assess their metabolic control.
  117. Practically, these objectives may be achieved based on the following components of management: 1. Diet 2. Exercise 3. Medication 4. Monitoring 5. Education 6. Other factors 117
  118. 118 Management of DM contd. Achievement and maintenance of metabolic control requires the judicious use of: 1. Medication A. Insulin and Oral medications: B. Biguanides e.g. Metformin Hydrochloride 500mg-1g 12 hourly with, or soon after meals. Metformin decreases insulin resistance and increases insulin sensitization. (Standard Treatment Guideline for Ghana, 2010).
  119. Management of DM contd. C. Sulphonylureas: All sulphonylureas are of equal potency and efficacy. The recommended total daily doses for the commonly available ones are – 1. Tolbutamide, oral, 250mg-1g, 8-12 hourly. 2. Gliclazide, oral, 40-160mg 12 hourly 3. Glibenclamide, 2.5-10mg as a single dose in the morning (if required, not more than 5mg could additionally be given in the evening, maximum total dose 15mg per day.
  120. Management of DM contd. • Sulphonylureas are best taken with meals. Tolbutamide and Gliclazide are short-acting and are preferred in the elderly and those with mild kidney disease. • In general sulphonylureas should be avoided in all patients with liver disease and used with care in kidney disease.
  121. Management of DM contd. D. Thiazolidinediones are additional oral medications which may be used either alone or in combination with metformin or a sulphonylurea in type 2 diabetics.
  122. Management of DM contd. • Examples of Available Thiazolidinediones are: • Pioglitazone, oral, 15-45 mg, as single daily dose • Or • Rosiglitazone, oral, 4-8 mg, as single daily dose (Standard Treatment Guideline for Ghana, 2010). 122
  123. Management of DM contd. • E. Combined Oral Therapy: Individuals with Type 2 diabetes not responding to maximum tolerable doses of a sulphonylurea, metformin or a thiazolidinedione alone, could be given combined oral therapy with two or three oral anti-diabetic medications. However, two different products from the same group (e.g. Two sulphonylureas) should never be used together. 123
  124. Management of DM contd. For Oral Hypoglycaemic Medications: Note • Patients, who usually have Type 2 diabetes, exercise and diet alone should be tried first. When diet and exercise fail to achieve satisfactory control within 3 months, non- obese patients are preferably, but not compulsorily or exclusively, be treated with a sulphonylurea, and obese patients with metformin. 124
  125. Management of DM contd. • Avoid metformin and long-acting oral anti- diabetic drugs, such as Glibenclamide in the individuals with poor kidney and liver functions. • Oral anti-diabetic drugs should be avoided in Type 1 patients and should not be used during pregnancy and breast-feeding.
  126. Management of DM contd. • Insulin is always indicated in a patient who has been in ketoacidosis, and in most young patients who usually have type 1 diabetes. • Insulin is also indicated in older or Type 2 patients when oral anti-diabetic drugs cease to be effective and in all pregnant and breast- feeding women.
  127. Management of DM contd. • The starting dose of any long-term treatment for diabetes must initially be low, with increments in the dose over several days or weeks according to results of blood glucose testing. • Hypoglycaemia is a potential side-effect with most of the anti-diabetic drugs, so patient should be observed closely. (Read on Hypoglycaemia).
  128. Some newer medications: Tab Galvus Met: This is a combination of Metformin and Vildagliptin Metformin belongs to Biguanide and Vildagliptin belongs to class of medicines known as islet enhancers. E.g 50 mg Vildagliptin and 500 mg of Metformin. Forxiga (Dapaglifloxin) is also used as daily dosage to manage type 2 DM- belongs to sodium-glucose cotransporter 2 inhibitor
  129. Management of DM contd. 2. Non-pharmacological treatment (Standard Treatment Guideline for Ghana, 2010). All patients with diabetes require diet therapy. Diet (Meal Plan)-Breakfast, Lunch, (**Afternoon Snack**), Supper, Bed time. All patients with diabetes require diet therapy. All patients and close relations who cook or control their meals must be referred to a dietician or diet nurse for individualized meal plans.
  130. Management of DM contd. • In practice, patients must avoid ‘free’ or refined sugars, such as soft drinks, or adding sugar to their beverages. ‘Diet’ soft drinks, which contain a sweetener and not glucose, may however be used but care must always be taken as we may have false nutritional information these days. • Diet must be selected.
  131. Management of DM contd. They should not eat plenty at one point in time. We should encourage enough fibre intake. Some healthcare professionals advice patients to eat only one diet etc. This practice is improper and must be discouraged.
  132. Management of DM contd. • Carbohydrates (60%), protein (15%) and fat (25%) mostly of plant-origin and low in animal fat. (Moderate consumption of……) • Increase in the amount of fibre e.g. vegetables, fruits and cereals. (Beare and Myers, 2003) 132
  133. GLYCAEMIC INDEX (GI) AND GLYCAEMIC LOAD (GL): (read on these, get examples) • A food with a high GI raises blood sugar more than a food with a medium to low GI. But the glycemic index does not take into account the amount of carbohydrate in a food. So glycemic load is a better indicator of how a carbohydrate food will affect blood sugar. (read on these, get examples) 133
  134. 134 Management of DM contd. 3. Exercise (Activity): • Is good for both type 1&2 DM. • Diet and exercise may be used to control blood glucose levels in individuals with type 2 DM but when the response to these measures is inadequate, oral agents are tried.
  135. Management of DM contd. • Regular, simple exercise (e.g. walking 1 hour daily) is helpful in ensuring good glucose control. All advice on exercise must give consideration to the patient’s age and the presence of complications and co-morbid conditions. • Regular, simple exercise e.g. 30 minutes brisk walking at least 3 days a week in ambulant patients.
  136. 136 Activity contd. Exercise is an important part of the medical management and deserves careful and thorough explanation before implementation. Activity is a wonderful insulin sensitizer, enhancing glucose uptake into skeletal muscle. The exact mechanism is unknown but it occurs in both type 1 and type 2 DM.
  137. 137 Activity contd. Benefits of Exercises 1. Improve insulin sensitivity 2. Lowers blood glucose 3. Assists with weight loss 4. Preserve with cardiovascular fitness 5. Improves sense of wellbeing and leads to. 6. High Quality of Life (HQoL) (LeMone and Burke, 1996)
  138. 138 Activity contd. For effective activity/exercise in the management of Diabetes Mellitus consider: • Frequency (F) • Intensity (I) • Time (T) Risk of exercise is hypoglycemia which is a diabetes emergency. (Read on this please)
  139. 139 Monitoring 4. Monitoring: For example monitoring blood glucose levels using sliding scale: (Beare and Myers, 2003)
  140. 140 Sliding Scale contd. Blood Glucose less than 6mmol/L= Urine Glucose Negative= Blue colour = No insulin ( in adults)= No insulin (in children) 6.1-9.0mmol/L=1+= Green = 4units= 0.06 units/kg 9.1-12mmo/L=2+= Yellow = 6units=0.09units/kg 12.1-15mmol/L= 3+= Brown = 8units=0.12units/kg 15.1-18mmol/L=4+= Brick Red =10Units=0.15/kg In this instance monitor blood or (**urine**) glucose 4 hourly and give the corresponding amount of insulin as ordered by the doctor. Insulin therapy and kinetics is fully discussed at the end with examples.
  141. 141 Monitoring contd. i. Self monitoring (Use of symptoms as a guide for self monitoring. ii. Use of diary to record date, time and monitoring results by the use of glucometers and test strips.
  142. 142 Monitoring contd. iii. Other diary notations may include medications, food intake, activity levels, and illness so that the person can begin to see the relationship between blood glucose or urine ketones and treatment regimen. As patients gain flexibility and self determination, they may manipulate insulin, diet, and exercise independently on the basis of monitoring results.
  143. 143 Monitoring contd. iv. Tell patient the importance of performing a home blood glucose test to correlate a subjective symptom.
  144. 144 Management of DM contd. 5. Education – meal plan to control weight, glucose, and lipids composition of diet, reading nutritional labels, monitoring and use of results, performing test accurately, interpreting test results, behavioral change strategies, risk factor reduction (Beare and Myers, 2003).
  145. 145 Management of DM contd. Exercises and activity- benefits and risk, preparing for exercises, medication- goal of treatment, injection techniques, complications of treatment: hypoglycemia etc. So by its nature, diabetes can be significantly influenced by each of these management components.
  146. Questions • Achievement and maintenance of metabolic control in DM requires the judicious use of Medication, Diet, Monitoring, Exercise and Education. Discuss • Effective use of standardized protocol for the management of DM is a predictor of a better Glycated Haemoglobin level (HbA1c or A1c). Discuss 146
  147. • Part of the Answer Q. 2 For people without diabetes, the normal range for the haemoglobin A1c test is between 4% and 6%. Because studies have repeatedly shown that out-of-control of diabetes results in complications from the disease, the goal for people with diabetes is an hemoglobin A1c less than 7%. The higher the hemoglobin A1c, the higher the risks of developing complications related to diabetes. 147
  148. 148 Nursing Management of DM 1. Myths about the disease must be dispelled through education: This determines direction of education that must be given. 2. Health History- Psychosocial/emotional status (perception of the meaning of the diagnosis, how it affects the patient’s life and future plans, day to day activities, coping mechanisms that are employed by the person: How do they affect glycemic control?
  149. 149 Nursing Management of DM contd. 3. Physical Examination 4. Patient Education- Insulin self administration, family involvement and social support, diabetes as a family challenge, stress and psychological adjustment, adaptation to living with a chronic disease, foot, skin, and dental care: daily self care measures: the need for regular evaluation of feet and teeth
  150. 150 Nursing Management of DM contd. Use of health care systems and community resources: planned follow ups, emergency care: patient tag, planning for travel, patient’s responsibility: name and telephone numbers of her/his nurse, avoid group eating etc. 5. Promoting Adequate Nutrition 6. Managing Medications 7. Decreasing fear
  151. 151 Complications of DM Complications of diabetes are associated with the development of microvascular and macrovascular diseases. Microvascular disease is a disease of small blood vessels, capillaries and precapillaries arterioles. Macrovascular disease is a large vessel disease. (Beare and Myers, 2003).
  152. 152 Complications of DM contd. Generally, microvascular diseases predominate in patients diagnosed early in life i.e. IDDM where as macrovascular diseases are common in those later diagnosed i.e. NIDDM.
  153. 153 Complications of DM contd. Microvascular Disease The most common chronic complications of DM include: 1. Retinopathy (Eye) 2. Nephropathy (Kidneys) 3. Neuropathy (Nerves) The main degenerative changes in diabetes occur because of a thickening of the capillary basement membrane. Read on these.
  154. 154
  155. 155 Complications of DM contd. Macrovascular Diseases 1. Coronary Heart Disease (CHD)- Usually these individuals who suffer from CHD tend to be overweight and often have hypertension and hyperlipidemia. These risk factors are particularly evident in persons with type 2 DM (Beare and Myers, 2003).
  156. 156 Complications of DM contd. 2. Hypertension 3. Hyperlipidemia
  157. 157 Complications of DM contd. 4. Diabetic foot-persons with DM are prone to foot problems for a number of reasons. E.g. Microvascular and Macrovascular diseases may result in ischemia and delayed healing. Problems associated with neuropathy, including absence of sensation resulting in lack of pain awareness contribute to the development of foot lesions. Necrosis and ulcerations may develop later.
  158. 158 Complications of DM contd. Manifestation of autonomic neuropathy can result in excessive dryness and cracking of the skin, which also contribute to infection. Microvascular and macrovascular alterations produce tissue ischemia and may lead to sepsis.
  159. 159 Complications of DM contd. The triad of Neuropathy, Ischemia and Sepsis results in gangrene and possible amputation (Merck’ Medical Manual, 2002; Beare and Myers, 2003). Other Complications 1. Skin disorders, frequent infections, reduced blood circulation in vessels of the skin.
  160. 160
  161. 161 Complications of DM contd. 1. Oral complications: commonly associated with Type 1 DM is periodontitis manifested by eventual tooth loss. The reduced vascular perfusion may reduced oxygen consumption. This provides optimal consideration for anaerobic microorganism growth. Thus dental education, care and follow up are critical to the overall health of the diabetic patient.
  162. 162 Complications of DM contd. Infections due to alterations in host defenses, vascular insufficiency that limits infection fighting factors. Read on Prevention of DM Prevention of type 1 DM is under active research. It focuses on arresting the autoimmune process. Primary Prevention of type 2 DM:
  163. 163 Read on Prevention of DM contd It involves identification and modification of risk factors. It should be directed toward lifestyle changes which include 1. Exercises 2. Weight control 3. Knowledge of risk factors. Be made aware of familial tendencies and risk for siblings of the individuals with either type of diabetes etc. 4. Choice of diet and preparation
  164. 164 Read on Prevention of DM contd. Secondary Prevention of types 1 and 2: Treatment at the hospital or clinic based on: 3Rs • Reporting early • Right diagnosis and • Right treatment
  165. 165 Read on Prevention of DM contd. Tertiary Prevention of DM: The aim is to prevent complications based on early detection of sign and symptoms of complications. The major emphasis of tertiary preventive education will be on the ability of the nurse to counsel the patient about the early detection of and interventions for complications (Patient Empowerment)
  166. Diabetes Screening • Fasting blood glucose screening should begin at age 30-45 and be repeated at least every three years (Melmed et al, 2011). • Earlier and more frequent screening should be conducted in at-risk individuals. The risk factors for which screening is important are listed below: 166
  167. Diabetes Screening contd. • Family history(parent or sibling) • Overweight or obese • History of gestational diabetes or infant born with birth weight greater than 4 kg • High cholesterol level 167
  168. Diabetes Screening contd. • High risk ethnic group • Hypertension • High fasting blood glucose value at a particular point in time • Etc. (Melmed et al., 2011) 168
  169. UK MODEL FOR PREVENTION OF DM AND CHRONIC CONDITIONS • UK introduced sugar tax on soft drinks • The tax was introduced to improve children's health due to increasing obesity and other problems among children (BBC News Report, 2015). 169
  170. UK MODEL FOR PREVENTION OF DM AND CHRONIC CONDITIONS CONTD. • Drinks with more than 8 grams of sugar per 100 millilitres was taxed at a higher rate than drinks with less than 5 grams of sugar per 100 millilitres. 170
  171. UK MODEL FOR PREVENTION OF DM AND CHRONIC CONDITIONS CONTD. • Companies were to pay the tax but the government expected some manufacturers to pass on the costs to customers making soft- drinks more expensive, and consumed less. • The UK government spends the revenue on fitness programs and extend school hours for children so they can take part in more sports. • 171
  172. UK MODEL FOR PREVENTION OF DM AND CHRONIC CONDITIONS CONTD. • Scandinavian countries, Hungary, Mexico and France, Chile and Dominica also have similar sugar tax. • Denmark also introduced a soft drink tax and fat tax and then repealed/cancelled them because it was not successful. 172
  173. 173 Somogyi Effect and Dawn Phenomenon Somogyi Effect: Somogyi effect results from excessive insulin administration which results in blood glucose fluctuations.
  174. 174 Somogyi Effect and Dawn Phenomenon contd. The hypoglycemia provokes secretion of insulin antagonists (glucagon) or hypoglycemia in persons with diabetes stimulates the production of counter regulatory hormones (glucocorticoids, growth hormone, epinephrine) (Beare and Myers, 2003).
  175. 175 Somogyi Effect and Dawn Phenomenon contd. Usually, this situation coupled with intake of carbohydrate to combat symptoms of low blood sugar results in hyperglycemia. Many hypoglycemic episodes occur during sleep, and an early morning hyperglycemia results.
  176. 176 Somogyi Effect and Dawn Phenomenon contd. The person then chases elevated morning blood glucose levels with increased insulin doses, which can lead to increased hypoglycemia episodes.
  177. 177 Somogyi Effect and Dawn Phenomenon contd. The signs and symptoms of Somogyi effect can be any of those associated with hypoglycemia but consist mainly of: Night time sweats Night mares Restless sleep Early Morning Headache (EMH)
  178. 178 Somogyi Effect and Dawn Phenomenon contd. Dawn Phenomenon: An elevation in blood glucose between 5am and 9am with no recorded episodes of nocturnal hypoglycemia is referred to as the dawn phenomenon (Beare and Myers, 2003).
  179. 179 Somogyi Effect and Dawn Phenomenon contd. Persons with type 1 DM may find that they require more insulin in the morning to cover their breakfast. Likewise, persons with type 2 DM may find that their fasting blood glucose is always higher when they wake up in the morning as opposed to their late blood glucose.
  180. 180 Somogyi Effect and Dawn Phenomenon contd. Both situations can be the result of the dawn phenomenon. As dawn approaches, the level of certain hormones in the blood naturally increase. These hormones probably, growth hormone and cortisol, cause blood sugar levels to rise (Beare and Myers, 2003, Longo et al., 2012).
  181. 181 Difference Between Somogyi Effect and Dawn Phenomenon 1. In the Somogyi effect hypoglycemia will be identified and then followed by hyperglycemia. 2. In dawn phenomenon there is no overnight hypoglycemia, rather there is consistent rise in blood glucose levels overnight. Decreasing the dose of insulin precipitating the hypoglycemia treats the Somogyi effect.
  182. 182 Difference Between Somogyi Effect and Dawn Phenomenon contd. Treatment of the dawn phenomenon consists of increasing the dose of the insulin, which is affecting nocturnal glucose levels.
  183. 183 Difference Between Somogyi Effect and Dawn Phenomenon contd. A primary nursing role is to document reports of hypoglycemia, glucose intake, and laboratory results and to assess for the presence of night sweats, night mares, and early morning headaches. The nurse should also correlate these complaints and laboratory results with mealtimes. Such data help identify the phenomenon.
  184. 184 Insulin Therapy Regime This is based on the needs of the patient. Intensive multiple daily insulin injections has become the gold standard. Convectional therapies, which uses once and twice daily insulin injection programmes, has been shown to be less effective in the management and control of diabetes. Note that Once or Twice daily insulin therapy is still used with good effect in Ghana (Standard Treatment Guideline for Ghana, 2010).
  185. Insulin Therapy Regime contd. • Insulin therapy should usually begin with teaching the patient the correct technique for subcutaneous injections, as self-injections are to be strongly encouraged. • Patients should be made aware of the different appearance of different kinds of insulin (soluble/regular which is fast-acting = gin clear; Neutral Protamine Hagedorn (NPH) or Lente which are intermediate-acting = cloudy; pre-mixed insulin preparations containing both soluble and NPH insulin = cloudy) (Beare and Myers, 2003).
  186. Insulin Therapy Regime contd. • Cloudy Insulin (intermediate-acting or pre- mixed) can only be given subcutaneously and SHOULD NOT be injected IM or IV. Only soluble/regular insulin may be given by the IM or IV route during emergency treatment.
  187. Insulin Therapy Regime contd. • Most Insulins currently available in Ghana are preferably injected 15-30 minutes before a meal. Two injections daily (before breakfast and dinner) of an intermediate-acting or pre-mixed insulin give better blood glucose control than once daily injections. • Older patients and those with kidney disease may sometimes be managed adequately on a single daily injection (Beare and Myers, 2003).
  188. Insulin Therapy Regime contd. • Two-thirds of the total daily insulin requirement is given before breakfast, and the remainder before the evening meal. • Insulin requirements vary from patient to patient irrespective of age and body weight.
  189. 189 Types of Insulin (Kinetics) 1. Quick-Acting Insulin e.g. Regular (onset 30min, duration 6-8 hrs) Lispro (onset 12min, duration 3hrs), Aspart (onset 12min, duration 3hrs) 2. Intermediate Insulin e.g. Lente (onset 2½hrs, duration 22hrs), Neutral Protamine Hagedorn (NPH) onset 1½hrs, duration 22hrs
  190. 190 Types of Insulin (Kinetics) contd. 3. Long-Acting Insulin eg. Ultralente (onset 4hrs, duration 28hrs), Glargine (onset 1-2 hours, duration 24+hrs) 4. Combination Insulin (combined preparations) e.g. Humulin (regular+neutral protamine hagedorn(NPH), Novolin (regular+NPH, Humalog Mix (NPH+Lispro): (onset 12-30 mins, duration 22 hours
  191. 191 Intensive Insulin Therapy Regime Examples: Three injections per day: The three injections per day method uses rapid and intermediate-acting insulin for the pre- breakfast dose, regular as a pre-supper dose, and a small dose of intermediate-acting at bedtime. (Beare and Myers, 2003).
  192. 192 Intensive Insulin Therapy Regime contd. Multidose Insulin: This therapy involves three or four injections of short acting insulin before meals coupled with long-acting preparations. This regimen may also consist of three pre- prandial doses of rapid-acting insulin coupled with a dose of bed time lente. (Longo et al., 2012; Beare and Myers, 2003).
  193. 193 Intensive Insulin Therapy Regime contd. Another option involves injecting long-acting insulin once a day or divided into 2 equal doses given before breakfast and supper. Injection Sites: Read on sites for insulin injection for practical demonstration at the skills laboratory at a later date. Right and Left buttocks Right and Left abdomen Right and Left thigh Right and Left arm
  194. 194 Intensive Insulin Therapy Regime contd. Try to rotate these sites to avoid problems with abscesses Routes of Administration: Read on these. Subcutaneous IV is preferred during Ketoacidosis Intra peritoneal for implantable insulin devices IM may also be given
  195. 195 Hypoglycemia and Hyperglycemia Read on signs and symptoms of hypoglycemia and its management.
  196. Sample Question • Effective use of standardized protocol for the management of DM is a predictor of a better Glycated Haemoglobin level (HbA1c or A1c). Discuss • Plan Medication Diet Monitoring Exercise Education Then link with the concept of A1c results (normal values in individuals with DM) 196
  197. Sample Question • What is the link between coping strategies utilized by patients newly diagnosed with type 2 diabetes mellitus and their levels of HbA1c. • Plan Positive coping methods Negative coping methods Link these with anticipated A1c results for the two extremes. 197
  198. Sample Question Achievement and maintenance of metabolic control in DM requires the judicious use of Medication, Diet, Monitoring, Exercise and Education. Discuss 198
  199. References Beare, P. G. & Myers, J. L. (2003). Adult Health Nursing, Medical-Surgical Nursing, Health and Illness Perspectives. 7th Edition, Mosby 2003. Chiang, J. L., Kirkman, M. S., Laffel, L. M. and Peters, A. L. (2014). Type 1 diabetes through the life span: a position statement paper of American Diabetes Association (ADA) . Diabetes Care, 2014, 141140. 199
  200. References • Lakey, JR; Burridge, PW; Shapiro, AM (September 2003). "Technical aspects of islet preparation and transplantation.". Transplant international : official journal of the European Society for Organ Transplantation. 16 (9): 613–32. doi:10.1111/j.1432- 2277.2003.tb00361.x. PMID 12928769 • LeMone, P. & Burke, M. K. (1996). Medical Surgical Nursing: Critical Thinking in Client Care. Addison Wesley – California, USA. 200
  201. References Longo, D; Fauci, A; Kasper, D; Hauser, S; Jameson, J; Loscalzo, J (2012). Harrison's Principles of Internal Medicine (18th ed.). NewYork: McGraw-Hill. pp. 2995–3000. ISBN 978-0071748896. Hall, J. (2011). Guyton and Hall textbook of medical physiology (12th ed.). Philadelphia, Pa.: Saunders/Elsevier. p. 781. ISBN 978-1-4160-4574-8. 201
  202. References Melmed, S; Polonsky, KS; Larsen, PR; Kronenberg, HM (2011). Williams Textbook of Endocrinology (12th ed.). Saunders. ISBN 978-1437703245 Merck’s Medical Manual 2002 Kottak, C. P. (2014). Windows on Humanity, New York: McGraw-Hill 202
  203. Reference • Young, B., ed. (2006). Wheater's functional histology : a text and colour atlas (5th ed.). Churchill Livingstone/Elsevier. pp. 299–301. ISBN 978-0-443-06850- 8. 203
  204. THANK YOU!!!!! 204