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Diabetes mellitus

Diabetes mellitus. Zeenat ayaz. Diabetes mellitus. D iabetes mellitus is a group of metabolic diseases characterized by elevated levels of glucose in the blood ( hyperglycemia ) resulting from defects in insulin secretion, insulin action, or both.

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Diabetes mellitus

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  1. Diabetes mellitus Zeenat ayaz

  2. Diabetes mellitus Diabetes mellitus is a group of metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both

  3. Insulin, a hormone produced by the pancreas, controls the level of glucose in the blood by regulating the production and storage of glucose. • Transports and metabolizes glucose for energy • Stimulates storage of glucose in the liver and muscle (in the form of glycogen)

  4. Signals the liver to stop the release of glucose Enhances storage of dietary fat in adipose tissue Accelerates transport of amino acids (derived from dietary protein) into cells Also inhibits the breakdown of stored glucose, protein, and fat.

  5. Insulin • Insulin and glucagon are hormones secreted by islet cells within the pancreas • Insulin is normally secreted by the beta cells (a type of islet cells) of the pancreas • Stimulus for insulin is high blood glucose levels

  6. Classification Type 1 diabetes (insulin-dependent diabetes mellitus) Type 2 diabetes (non-insulindependentdiabetes mellitus) Gestational diabetes mellitus

  7. Type 1 Diabetes Mellitus • Most often occurs in people under 30 years of age • Peak onset between ages 11 and 13 • Formerly known as “juvenile onset” or “insulin dependent” diabetes

  8. Type 1 Diabetes MellitusEtiology and Pathophysiology • Progressive destruction of pancreatic  cells • Autoantibodies cause a reduction of 80% to 90% of normal  cell function before manifestations occur

  9. Type 1 Diabetes MellitusEtiology and Pathophysiology • Causes: • Genetic predisposition • Related to human leukocyte antigens (HLAs) • Exposure to a virus

  10. Type 1 Diabetes MellitusOnset of Disease • Manifestations develop when the pancreas can no longer produce insulin • Rapid onset of symptoms • Present at ER with ketoacidosis

  11. Type 1 Diabetes MellitusOnset of Disease • Weight loss • Polydipsia • Polyuria • Polyphagia

  12. Type 1 Diabetes MellitusOnset of Disease • Diabetic ketoacidosis (DKA) • Occurs in the absence of exogenous insulin • Life-threatening condition • Results in metabolic acidosis

  13. Type 2 Diabetes Mellitus • Accounts for 90% of patients with diabetes • Usually occurs in people over 40 years of age • 80-90% of patients are overweight

  14. Type 2 Diabetes MellitusEtiology and Pathophysiology • Pancreas continues to produce some insulin • Insulin produced is either insufficient or poorly utilized by the tissues

  15. Type 2 Diabetes MellitusEtiology and Pathophysiology • Insulin resistance • Body tissues do not respond to insulin • Results in hyperglycemia

  16. Type 2 Diabetes MellitusEtiology and Pathophysiology • Inappropriate glucose production by the liver • Not considered a primary factor in the development of type 2 diabetes

  17. Type 2 Diabetes MellitusEtiology and Pathophysiology

  18. Type 2 Diabetes MellitusOnset of Disease • Gradual onset • Person may go many years with undetected hyperglycemia • 75% of type 2 diabetes is detected incidentally

  19. Gestational Diabetes • Develops during pregnancy • Detected at 24 to 28 weeks of gestation •  Risk for cesarean delivery, perinatal death, and neonatal complications

  20. Secondary Diabetes • Results from another medical condition or due to the treatment of a medical condition that causes abnormal blood glucose levels • Cushing syndrome • Hyperthyroidism • Parenteral nutrition

  21. Clinical ManifestationsDiabetes Mellitus • Polyuria • Polydipsia (excessive thirst) • Polyphagia • In Type I • Weight loss • Ketoacidosis

  22. Clinical ManifestationsNon-specific symptoms • Fatigue and weakness • Sudden vision changes • Tingling or numbness in hands or feet • Skin lesions or recurrent infections • Prolonged wound healing • Visual changes

  23. Clinical Manifestations

  24. Risk Factors for Diabetes Mellitus Family history of diabetes (i.e., parents or siblings with diabetes) Obesity (i.e., ≥20% over desired body weight or BMI ≥27 kg/m2) Race/ethnicity (e.g., African Americans, Hispanic Americans, Native Americans, Asian Americans, Pacific Islanders) Age ≥45 years Previously identified impaired fasting glucose or impaired glucose tolerance

  25. Risk factors (cont.) Hypertension (≥140/90 mm Hg) HDL cholesterol level ≤35 mg/dL (0.90 mmol/L) and/or tri- glyceride level ≥250 mg/dL (2.8 mmol/L) History of gestational diabetes or delivery of babies over 9 lbs

  26. ASSESSMENT AND DIAGNOSTIC FINDINGS high blood glucose level Fasting plasma glucose (FPG) levels of 126 mg/dL (7.0 mmol/L) or more random plasma glucose levels exceeding 200 mg/dL (11.1 mmol/L) on more than one occasion Plasma glucose values may be 10% to 15% higher than whole

  27. goal The main goal of diabetes treatment is to normalize insulin activity and blood glucose levels to reduce the development of vascular and neuropathic complications.

  28. management There are five components of diabetes management • Nutritional management • Exercise • Monitoring • Pharmacologic therapy • Education

  29. Treatment varies because of changes in lifestyle and physical and emotional status as well as advances in treatment methods. Therefore, diabetes management involves constant assessment and modification of the treatment plan by health professionals and daily adjustments in therapy by the patient.

  30. Diabetes MellitusAcute Complications • Hypoglycemia • Diabetic ketoacidosis (DKK) • Hyperosmolar hyperglycemic nonketotic syndrome (HHNS)

  31. hypoglycemia • Type 1 or type 2 diabetes • Blood glucose < 50-60 mg/dL • Causes • Too much insulin • Overdose of oral antidiabetic agents • Too little food • Excess physical activity • May experience S & S of hypoglycemia if there is sudden decrease in BS

  32. hypoglycemia • Treatment • Mild • Immediate treatment • 15 g rapid-acting sugar • Severe • Hospitalized • Intravenous glucose • Teach patients to carry simple sugar with them

  33. Life-threatening illness in type 1 • Hyperglycemia • Dehydration and electrolyte loss • Acidosis • Causes of DKA • Decreased or missed dose of insulin, • Illness or infection, • Undiagnosed and untreated diabetes

  34. Without insulin, the amount of glucose entering the cells is reduced, and production and release of glucose by the liver is increased (lead to hyperglycemia). • Excess glucose leads to polyuria (6.5 L/day) dehydration, sodium and potassium loss • Burning of fat leads to ketosis • Kidneys unable to excrete ketones, leads to ketoacidosis

  35. Diagnosis: Blood glucose (300 and 800 mg/dL) • Treatment • Rehydration (0.9-0.45% saline) • Restoring Electrolytes (K+) • loss of potassium from body stores and an intracellular-to-extracellular shift of potassium • Reversing Acidosis (reversed with insulin) • Regular insulin infusion (5 units/hr) • Hourly blood glucose monitoring

  36. Hyperosmolar hyperglycemic nonketotic syndrome (HHNS) • Is a serious condition most frequently seen in older persons. • HHNS is usually brought on by something else, such as an illness or infection, dialysis, drugs that increase BS. • Blood sugar levels rise resulting into glycosuria, polyuria, thirst. • Severe dehydration will lead to seizures, coma and eventually death. • HHNS may take days or even weeks to develop. Know the warning signs of HHNS.

  37. HHNS/ clinical manifestations Hypotension, profound dehydration (dry mucous membranes, poor skin turgor), tachycardia, and variable neurologic signs (eg, alteration of sensorium, seizures, hemiparesis). Blood glucose level (600 to 1200 mg/dL) Treatment: fluid replacement, correction of electrolyte imbalances, and insulin.

  38. Diabetes MellitusChronic Complications • Macrovascular (atherosclerotic plaque) • Coronary arteries → (MI’s) • Cerebral arteries → (strokes) • Peripheral vessels → (ulcers, amputations, infection) • Microvascular (capillary damage) • Retinopathy • Neuropathy • Nephropathy

  39. Macrovascular Complications • Macrocirculation • Blood vessel walls thicken, sclerose, and become occluded by plaque that adheres to the vessel walls. finally, blood flow is blocked. • Complications • Coronary artery disease • Stroke • Peripheral vascular disease

  40. Complication: CAD CAD account for 50% to 60% of all deaths among patients with diabetes. High cholesterol and high triglycerides MI is twice as common in men and three times in women with diabetes, compared to people without diabetes. Silent MI Higher risk for a second infarction

  41. Complication: Stroke People with diabetes have twice the risk of developing cerebrovascular disease. There is a greater likelihood of death from cerebrovascular disease. Recovery is slower with high BS. Hypertension plays a role

  42. Complication: Peripheral Vascular Disease • Diabetes-induced arteriosclerosis • 2-3 times higher than in nondiabetic people • S & S: diminished peripheral pulses and intermittent claudication (pain in the buttock, thigh, or calf during walking) • Can lead to leg ulcers and gangrene and amputation.

  43. Management of Macrovascualr changes • Prevention and treatment of risk factors for atherosclerosis. • obesity, hypertension, and hyperlipidemia (exercise, stop smoking). • Control of blood glucose levels may reduce triglyceride concentrations and can significantly reduce the incidence of complications.

  44. Microvascular Complications • Microcirculation • Eyes • Kidneys • Nerves

  45. Complication: Diabetic Retinopathy Leading cause of blindness in people ages 20 to 74 in US Almost all patients with type 1 diabetes and more than 60% of patients with type 2 diabetes have some degree of retinopathy after 20 years

  46. Diabetic Retinopathy Changes in the retinal capillaries; lead to retinal ischemia. Changes include microaneurysms, intraretinal hemorrhage, hard exudates, and focal capillary closure. Yearly eye exams are recommended

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