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Diabetes mellitus Lecturer: Dr.Zainab Sajid Al-Shimmari

Diabetes mellitus Lecturer: Dr.Zainab Sajid Al-Shimmari. Diabetes Mellitus 1-The term diabetes is derived from a Greek word meaning“going through” and mellitus from the Latin word for“honey ” or “sweet.”

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Diabetes mellitus Lecturer: Dr.Zainab Sajid Al-Shimmari

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  1. Diabetes mellitus Lecturer: Dr.Zainab Sajid Al-Shimmari

  2. Diabetes Mellitus 1-The term diabetes is derived from a Greek word meaning“going through” and mellitus from the Latin word for“honey” or “sweet.” 2-Diabetes is a disorder of carbohydrate, protein, and fat metabolism resulting from an imbalance between insulin availability and insulin need.

  3. 3-It can represent an absolute insulin deficiency, impaired release of insulin by the pancreatic beta cells, inadequate or defective insulin receptors, or the production of inactive insulin or insulin that is destroyed before it can carry out its action. 4-A person with uncontrolled diabetes is unable to transport glucose into fat and muscle cells; as a result, the body cells are starved, and the breakdown of fat and protein is increased.

  4. CLASSIFICATION AND ETIOLOGY. 1-The revised system for the classification of diabetes was continues to include type 1 and type 2 diabetes, but uses Arabic rather than Roman numerals and eliminates the use of “insulin dependent”and “non–insulin-dependent” diabetes mellitus. Type 2 diabetes currently accounts for about90% to 95% of the cases of diabetes.

  5. 2-Included in the classification system are the categories of gestational diabetes mellitus and other specific types of diabetes, many of which occur secondary to other conditions (e.g., Cushing’s syndrome, hematochromatosis, pancreatitis, a cromegaly). 3-also includes a system for diagnosing diabetes according to stages of glucose in tolerance.The revised criteria have retained the former category of impaired glucose tolerance (IGT) and have added a new category of impaired fasting plasma glucose(IFG).

  6. Type 1 Diabetes Mellitus. 1-Type 1 diabetes mellitus is characterized by destruction of the pancreatic beta cells. Type 1 diabetes is subdivided into two types: type 1A, immune-mediated diabetes, and type 1B, idiopathic diabetes. In the United States and Europe, approximately 10% of people with diabetes mellitus have type 1 diabetes, with 95% of them having type 1A,immune-mediated diabetes.

  7. 2-Type 1A diabetesis characterized by autoimmune destruction of beta cells. This type of diabetes, formerly calledjuvenile diabetes, occurs more commonly in young persons but can occur at any age.3- Type 1 diabetes is a catabolic disorder characterized by an absolute lack of insulin, an elevation in blood glucose, and a breakdown of body fats and proteins. The absolute lack of insulin in people with type 1diabetes mellitus means that they are particularly prone to the development of ketoacidosis.

  8. 4- One of the actions of insulin is the inhibition of lipolysis (i.e., fat breakdown) and release of free fatty acids (FFAs) from fat cells. In the absence of insulin, ketosis develops when these fatty acids are released from fat cells and converted to ketones in the liver. 5-Because of the loss of the first-phase insulin (preformed insulin) response, all people with type 1A diabetes require exogenous insulin replacement to reverse the catabolic state, control blood glucose levels, and prevent ketosis.

  9. 6-The rate of beta cell destruction is quite variable, being rapid in some individuals and slow in others. A-The rapidly progressive form commonly is observed in children, but also may occur in adults. B-The slowly progressive form usually occurs in adults and is sometimes referred to as latent autoimmune diabetes in adults (LADA). 7-LADA may constitute up to 10% of adults who are currently classified as having type 2 diabetes.

  10. A- It has been suggested that type 1A, immune-mediated diabetes results from a genetic predisposition. B-A hypothetical triggering event that involves an environmental agent that incites an immune response ,and immunologically mediated beta cell destruction. C- The inherited major histocompatibility complex (MHC) genes that encode three human leukocyte antigens found on the surface of body cells

  11. 8-Type 1 diabetes–associated auto antibodies may exist for years before the onset of hyperglycemia. There are two major types of auto antibodies: (i)insulin auto antibodies (IAAs), and (ii)islet cell auto antibodies and antibodies directed at other islet autoantigens, including glutamic acid decarboxylase (GAD) and the protein tyrosine phosphatase . These people also may have other autoimmune disorders such as Graves’ disease, rheumatoid arthritis, and Addison’s disease.

  12. 9-The term idiopathictype 1B diabetesis used to describe those cases of beta cell destruction in which no evidence of autoimmunity is present. Only a small number of people with type 1 diabetes fall into this category; most are of African or Asian descent. Type 1B diabetes is strongly inherited. People with the disorder have episodic ketoacidosis due to varying degrees of insulin deficiency with periods of absolute insulin deficiency that may come and go.

  13. Type 2 Diabetes Mellitus and the Metabolic Syndrome. I-Type 2 diabetes mellitus is a heterogeneous condition that describes the presence of hyperglycemia in association with relative insulin deficiency. In contrast to type 1. A-diabetes in which absolute insulin deficiency is present, type 2 diabetes can be associated with high, normal, or low insulin levels. However, in the presence of insulin resistance, the insulin cannot function effectively, and hyperglycemia can result.

  14. B-Type 2 diabetes is therefore a disorder of both insulin levels (beta cell dysfunction) and insulin function (insulin resistance). C- Type 2 diabetes(unlike type 1) is not associated with auto antibodies. D-Most people with type 2 diabetes are older and over weight;however, type 2 diabetes is becoming a more common occurrence in obese adolescents.

  15. II-The metabolic bnormalities that contribute to hyperglycemia in people with type 2 diabetes include.(i)impaired beta cell function and insulin secretion. (ii)peripheral insulin resistance. (iii)increased hepatic glucose production. Insulin resistance initially produces an increase in beta cell secretion of insulin (resulting in hyperinsulinemia)as the body attempts to maintain a normoglycemic state.

  16. III-the insulin response declines because of increasing beta cell dysfunction. (i)This results initially in elevated postprandial blood glucose levels. Eventually, fasting blood glucose levels also rise until frank type 2 diabetes occurs. (ii)During the evolutionary phase, an individual with type 2 diabetes may eventually develop absolute insulin deficiency because of progressive beta cell failure.

  17. IV- As with persons with type 1 diabetes, these persons require insulin therapy to survive. Because most persons with type 2 diabetes do not have an absolute insulin deficiency,they are less prone to develop ketoacidosis as compared with people with type 1 diabetes (the presence of circulating insulin in most type 2 diabetics suppresses ketone body formation).

  18. V-Beta Cell Dysfunction. Specific causes of beta cell dysfunctionin patients with prediabetes and type 2 diabetes may include: (1)an initial decrease in the beta cell mass (this may be related to genetic factors responsible for beta cell differentiation and function, and environmental factors such as the presence of maternal diabetes during pregnancy or in utero factors such as the presence of intrauterine growth retardation),

  19. (2)increased beta cell apoptosis/decreased regeneration, (3)long-standing insulin resistance leading to beta cell exhaustion,(4)chronic hyperglycemia can induce beta cell desensitization termed glucotoxicity, (5)chronic elevation of free fatty acids can cause toxicity to beta cells termed lipotoxicity. (6)Amyloid deposition in the beta cell can cause dysfunction.

  20. VI-Insulin Resistance and the Metabolic Syndrome. 1-There is increasing evidence to suggest that insulin resistance not only contributes to the hyperglycemia in persons with type 2 diabetes, but may also play a role in other metabolic abnormalities. These include high levels of plasma triglycerides and low levels of high-density lipoproteins(HDLs), hypertension, systemic, abnormal fibrinolysis, abnormal function of the vascular endothelium.

  21. 2-A major factor in persons with the metabolic syndrome that leads to type 2 diabetes is central obesity. Approximately80% of persons with type 2 diabetes are over weight. a-Obese people have increased resistance to the action of insulin and impaired suppression of glucose production by the liver, resulting in both hyperglycemia and hyperinsulinemia.

  22. b-The type of obesity is an important consideration in the development of type 2 diabetes. It has been found that people with upper body obesity (central obesity)are at greater risk for developing type 2 diabetes and metabolic disturbances than persons with lower body obesity.c-The increased insulin resistance has been attributed to increased visceral (intraabdominal) obesity detected on computed tomography scan. d- The new terminology that is emerging for persons with obesity and type 2 diabetes is diabesity.

  23. e-insulin resistance may improve with weight loss, to the extent that many people with type 2 diabetes can be managed with a weight-reduction program and exercise. It has been theorized that the insulin resistance and increased glucose production in obese people with type 2 diabetes may stem from an increased concentration of free fatty acids (FFAs).f- Visceral obesity is especially important because it is accompanied by increases in fasting and postprandial FFA concentrations.

  24. This has several consequences: (i)acutely, FFAs act at the level of the beta cell to stimulate insulin secretion, which, with excessive and chronic stimulation, causes beta cell failure (lipotoxicity). (ii)they act at the level of the peripheral tissues to cause insulin resistance and glucose underutilization by inhibiting glucose uptake and glycogen storage through a reduction in muscle glycogen synthetase activity.

  25. (iii) the accumulation of FFAs and triglycerides reduce hepatic insulin sensitivity, leading to increased hepatic glucose production and hyperglycemia, especially fasting plasma glucose levels. Thus, an increase in FFA that occurs in obese individuals (especially visceral obesity) with a genetic predisposition to type 2 diabetes may eventually lead to beta cell dysfunction/failure, increased insulin resistance, and hepatic glucose production.

  26. 3-The diversion of excess FFAs to non adipose tissues, including liver, skeletal muscle, heart, and pancreatic beta cells. The uptake of FFAs from the portal blood can lead to hepatic triglyceride accumulation and nonalcoholic fatty liver disease. 4-A proposed link to the insulin resistance associated with obesity is an adipose cell secretion (a dipocytokine)called adiponectin. Adiponectin is secreted by adipose tissue and circulates in the blood. It has been shown that decreased levels of adiponectin coincide with insulin resistance in animal models and patients with obesity and type 2 diabetes.

  27. Other Specific Types. 1-diabetes can occur with pancreatic disease or the removal of pancreatic tissue and with endocrine diseases, such as acromegaly, Cushing’s syndrome, or pheochromocytoma. 2-Endocrine disorders that produce hyperglycemia do so by increasing the hepatic production of glucose or decreasing the cellular use of glucose. 3-Several specific types of diabetes are associated with monogenetic defects in beta cell function.

  28. Gestational Diabetes. 1-Gestational diabetes mellitus (GDM) refers to any degree of glucose intolerance that is detected first during pregnancy. 2-It occurs to various degrees in 1% to 14% of all pregnancies, depending on the population and diagnostic tests used. It most frequently affects women with a family history of diabetes; with glycos uria; with a history of stillbirth or spontaneous abortion, fetal anomalies in a previous pregnancy, and who are obese, of advanced maternal age, or have had five or more pregnancies.

  29. 3-All pregnant women should undergo risk assessment for diabetes during their first prenatal visit. Those with significant risk should undergo plasma glucose testing as soon as feasible. women with GDM are at higher risk for complications of pregnancy, mortality, and fetal abnormalities. 4-Fetal abnormalities include macrosomia (i.e., large body size), hypoglycemia, hypocalcemia, polycythemia,and hyperbilirubinemia.

  30. CLINICAL MANIFESTATIONS. 1- In type 1 diabetes, signs and symptoms often arise suddenly. Type 2 diabetes usually develops more insidiously its presence may be detected during a routine medical examination or when a patient seeks medical care for other reasons. 2-The most commonly identified signs and symptoms of diabetes are referred to as the three polys: (i) polyuria(i.e., excessive urination), (ii) polydipsia (i.e., excessive thirst), and (iii) polyphagia (i.e., excessive hunger). These three symptoms are closely related to the hyperglycemia and glycos uria of diabetes.

  31. 3-When blood glucose levels are sufficiently elevated, the amount of glucose filtered by the glomeruli of the kidney exceeds the amount that can be reabsorbed by the renal tubules; this results in glycosuria accompanied by large losses of water in the urine. Thirst results from the intracellular dehydration that occurs as blood glucose levels rise and water is pulled out of body cells, including those in the thirst center.

  32. 4-Cellular dehydration also causes dryness of the mouth. This early symptom maybe easily overlooked in people with type 2 diabetes, particularly in those who have had a gradual increase in blood glucose levels. 5-Polyphagia usually is not present in people with type 2 diabetes. In type 1 diabetes, it probably results from cellular starvation and the depletion of cellular stores of carbohydrates, fats, and proteins.

  33. 6-Weight loss despite normal or increased appetite is a common occurrence in people with uncontrolled type 1diabetes. The cause of weight loss is twofold. First,loss of body fluids results from osmotic diuresis. Vomiting may exaggerate the fluid loss in ketoacidosis. Second, body tissue is lost because the lack of insulin forces the body to use its fat stores and cellular proteins as sources of energy.

  34. 7-Interms of weight loss, there often is a marked difference between type 2 diabetes and type 1 diabetes. Weight loss is a frequent phenomenon in people with uncontrolled type 1diabetes, whereas many people with uncomplicated type 2diabetes have problems with obesity. Other signs and symptoms of hyperglycemia include recurrent blurred vision, fatigue, paresthesias, and skin infections.

  35. 8-In type 2 diabetes, these often are the symptoms that prompt a person to seek medical treatment. Blurred vision develops as the lens and retina are exposed to hyperosmolar fluids. Lowered plasma volume produces weakness and fatigue. Paresthesias reflect a temporary dysfunction of the peripheral sensory nerves. Chronic skin infections are common in people with type 2 diabetes. Hyperglycemia and glycosuria favor the growth of yeast organisms.

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