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Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
Diabetes Mellitus   Ppt May 2006 Revised
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Diabetes Mellitus Ppt May 2006 Revised

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overview of diabetes

overview of diabetes

Published in: Health & Medicine
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  • 1. Diabetes Mellitus
  • 2. Diabetes Mellitus <ul><li>A multisystem disease related to: </li></ul><ul><li>Abnormal insulin production </li></ul><ul><li>Impaired insulin utilization </li></ul><ul><li>Both abnormal production & impaired utilization </li></ul>
  • 3. Diabetes Mellitus <ul><li>Maori & Pacific Islanders are twice as likely to be diagnosed as European/Pakeha </li></ul><ul><li>Leading cause of heart disease, stroke, adult blindness, & non-traumatic lower limb amputations </li></ul>
  • 4. Normal Insulin Metabolism <ul><li>Insulin produced by β cells in the islets of Langerhans of pancreas </li></ul><ul><li>Normally insulin is released in small increments continuously into bloodstream (basal rate) </li></ul><ul><li>Increase in release (bolus) when food ingested </li></ul>
  • 5. Normal Insulin Metabolism <ul><li>Insulin facilitates normal glucose range of 3-8mmol/L </li></ul><ul><li>Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell </li></ul>
  • 6. Counter-Regulatory Hormones <ul><li>Glucagon, adrenaline, growth hormone & cortisol work to oppose the effects of insulin </li></ul><ul><li>Hormones work to increase blood glucose levels by stimulating glucose production and decreased movement of glucose into cells </li></ul>
  • 7. Insulin Secretion
  • 8. ↑ Insulin after Meals <ul><li>Stimulates storage of glucose as glycogen in liver & muscles </li></ul><ul><li>Inhibits gluconeogenesis (formation of glycogen from fatty acids & proteins rather than carbohydrates) </li></ul><ul><li>Enhances fat deposition in adipose tissue </li></ul><ul><li>Increases protein synthesis </li></ul>
  • 9. Type 1 Diabetes Mellitus <ul><li>Formerly known as “juvenile onset” or “insulin dependent” diabetes </li></ul><ul><li>Most often occurs in people under 30yrs of age </li></ul><ul><li>Peak onset between ages 11 and 13 </li></ul><ul><li>Represents 10-20% of all persons with diabetes </li></ul>
  • 10. Type 1 DM <ul><li>Results from: </li></ul><ul><li>Progressive destruction of pancreatic β cells due to an autoimmune process in susceptible people </li></ul><ul><li>Auto-antibodies cause a reduction of 80-90% of normal β cell function before hyperglycaemia and other manifestations occur </li></ul>
  • 11. Causes of Type 1 DM <ul><li>Genetic predisposition & exposure to a virus </li></ul><ul><li>Related to human leucocyte antigens (HLAs) </li></ul><ul><li>When individual with certain HLA type is exposed to viral infection, the β cells of pancreas are destroyed </li></ul>
  • 12. Onset of Type 1 DM <ul><li>Manifestations develop when pancreas can no longer produce insulin </li></ul><ul><li>Rapid onset of symptoms </li></ul><ul><li>Present at ED with ketoacidosis </li></ul>
  • 13. Onset of Type 1 DM <ul><li>Polydipsia (excessive thirst) </li></ul><ul><li>Polyuria (excessive urinary output) </li></ul><ul><li>Polyphagia (excessive eating) </li></ul><ul><li>Recent & sudden weight loss </li></ul>
  • 14. Type 2 DM <ul><li>Accounts for 90% of patients with DM </li></ul><ul><li>Incidence ↑ with age – 50% are over 55 yrs </li></ul><ul><li>Can occur in children & adolescents </li></ul><ul><li>80-90% of patients are overweight </li></ul><ul><li>↑ incidence in Maori & Pacific Islanders </li></ul>
  • 15. Type 2 DM <ul><li>Pancreas continues to produce some endogenous (self-made) insulin </li></ul><ul><li>Insulin produced is either insufficient or poorly utilized by the tissues </li></ul>
  • 16. 3 Major Metabolic Abnormalities in DM Type 2 <ul><li>Insulin Resistance </li></ul><ul><li>Body tissues do not respond to action of insulin </li></ul><ul><li>Results in hyperglycaemia </li></ul>
  • 17. 3 Major Metabolic Abnormalities in DM Type 2 <ul><li>2. Impaired glucose tolerance (IGT) (prediabetes </li></ul><ul><li>- Occurs when the alteration in β cell function is mild </li></ul><ul><li>Blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes </li></ul>
  • 18. 3 Major Metabolic Abnormalities in DM Type 2 <ul><li>3. Inappropriate glucose production by liver </li></ul><ul><li>Instead of liver regulating the release of glucose in response to blood levels, it does so in a haphazard way </li></ul><ul><li>Only a minor factor in Type 2 </li></ul>
  • 19. Gestational Diabetes <ul><li>Develops during pregnancy </li></ul><ul><li>Detected at 24-28 weeks of gestation </li></ul><ul><li>↑ risk for caesarian delivery, peri-natal death, & neonatal complications </li></ul><ul><li>Most have normal glucose levels at 6 weeks postpartum </li></ul>
  • 20. Secondary Diabetes <ul><li>Results from another medical condition or due to the treatment of a medical condition that causes abnormal blood glucose levels </li></ul><ul><li>Cushing syndrome </li></ul><ul><li>Hyperthyroidism </li></ul><ul><li>Parental nutrition </li></ul><ul><li>Usaully resolves when underlying condition is treated </li></ul>
  • 21. Clinical Manifestations Type 1 DM <ul><li>Onset rapid & manifestations are usually acute </li></ul><ul><li>Polyuria </li></ul><ul><li>- When blood glucose ↑, the amt of glucose filtered by glomeruli of kidneys exceeds amt reabsorbed by renal tubules. This results in glycosuria & large losses of water in urine </li></ul>
  • 22. Clinical Manifestations Type 1 DM <ul><li>Polydipsia </li></ul><ul><li>Results from the intracellular dehydration that occurs as blood glucose levels rise and water is pulled out of body cells </li></ul><ul><li>Polyphagia </li></ul><ul><li>Result of cellular malnourishment when insulin deficiency prevents using glucose for energy </li></ul>
  • 23. Clinical Manifestations Type 1 <ul><li>Weight loss </li></ul><ul><li>Body cannot utilize glucose & turns to other energy sources such as fat & protein </li></ul><ul><li>Weakness & fatigue </li></ul><ul><li>Body cells lack needed energy from glucose </li></ul>
  • 24. Clinical Manifestaions Type 2 DM <ul><li>Non-specific symptoms </li></ul><ul><li>Fatigue </li></ul><ul><li>Recurrent infections </li></ul><ul><li>Prolonged wound healing </li></ul><ul><li>Visual changes </li></ul>
  • 25. Acute Complications of DM Diabetic Ketoacidosis <ul><li>Caused by profound deficiency of insulin </li></ul><ul><li>Most likely to occur with Type 1 </li></ul><ul><li>Caused by illness, infection, inadequate insulin dosage, undiagnosed Type 1 DM, poor self-management & neglect </li></ul>
  • 26. Diabetic Ketoacidosis <ul><li>When circulating supply of insulin is insufficient, glucose cannot be used properly for energy </li></ul><ul><li>Body breaks down fat stores as secondary source of fuel </li></ul><ul><li>Ketones are by-products of fat metabolism that can cause serious problems when they are excessive in the blood </li></ul><ul><li>Ketones alter pH balance causing metabolic acidosis </li></ul>
  • 27. Clinical Manifestaions of Ketoacidosis <ul><li>Dehydration – poor skin turgor, dry mucous membranes, tachycardia and orthostatic hypotension </li></ul><ul><li>Lethargy & weakness </li></ul><ul><li>Flushed, dry skin </li></ul><ul><li>Abdominal pain, nausea & vomiting </li></ul><ul><li>Rapid deep breathing </li></ul><ul><li>Acetone on breath (sweet, fruity odour) </li></ul><ul><li>Elevated blood sugar </li></ul><ul><li>Ketones in blood & urine </li></ul>
  • 28. Hypoglycaemia <ul><li>Low blood sugar levels </li></ul><ul><li>Occurs when there is too much insulin in proportion to available glucose in the blood </li></ul><ul><li>Causes blood glucose level to drop to less than 3.5mmol/L </li></ul>
  • 29. Hypoglycaemia Clinical Manifestations <ul><li>Confusion, irritability </li></ul><ul><li>Diaphoresis </li></ul><ul><li>Tremors </li></ul><ul><li>Hunger </li></ul><ul><li>Weakness </li></ul><ul><li>Headaches </li></ul><ul><li>Visual disturbances </li></ul><ul><li>Can progress to loss of consciousness, seizures, coma & death </li></ul>
  • 30. Causes of Hyper & Hypoglycaemia <ul><li>Hyperglycaemia </li></ul><ul><li>Too much food </li></ul><ul><li>Too little or no diabetes medication </li></ul><ul><li>Inactivity </li></ul><ul><li>Emotional, physical stress </li></ul><ul><li>Poor absorption of insulin </li></ul><ul><li>Hypoglycaemia </li></ul><ul><li>Alcohol intake with food </li></ul><ul><li>Too little food </li></ul><ul><li>Too much diabetic medication </li></ul><ul><li>Diabetes medication or food taken at wrong time </li></ul>
  • 31. Clinical Manifestations <ul><li>Hyperglycaemia </li></ul><ul><li>↑ blood glucose </li></ul><ul><li>↑ in urination </li></ul><ul><li>↑ appetite </li></ul><ul><li>Weakness, fatigue </li></ul><ul><li>Blurred vision </li></ul><ul><li>Glycosuria </li></ul><ul><li>Nausea & vomiting </li></ul><ul><li>Abdominal cramps </li></ul><ul><li>Progression to DKA </li></ul><ul><li>Hypoglycaemia </li></ul><ul><li>Blood glucose < 2.8mmol/L </li></ul><ul><li>Numbness of fingers, toes, mouth </li></ul><ul><li>Tachycardia </li></ul><ul><li>Emotional changes </li></ul><ul><li>Headache </li></ul><ul><li>Nervousness, tremors </li></ul><ul><li>Unsteady gait, slurred speech </li></ul><ul><li>Hunger </li></ul><ul><li>Changes in vision </li></ul><ul><li>Seizures, coma </li></ul>
  • 32. Chronic Complications Angiopathy <ul><li>Blood vessel disease </li></ul><ul><li>Accounts for majority of deaths among patients with DM </li></ul><ul><li>Macrovascular or microvascular complications </li></ul>
  • 33. Macroangiopathy Cerebrovascular Disease <ul><li>-TIAs & strokes </li></ul><ul><li>Incidence twice as frequent in diabetics </li></ul><ul><li>Hypertension major risk factor </li></ul><ul><li>Risk highest for females </li></ul><ul><li>Strokes more serious & higher mortality rates </li></ul>
  • 34. Macroangiopathy Heart Disease <ul><li>CAD, atheroscleotic changes -> ↓ O 2 & nutrient supply to myocardium </li></ul><ul><li>More severe and more affected vessels </li></ul><ul><li>MIs have higher mortality rate & experience CHF, shock & arrhythmias </li></ul>
  • 35. Macroangiopathy Peripheral Vascular Disease <ul><li>Intermittent claudication, absent pedal pulses & ischaemic gangrene - ↑ incidence in diabetics </li></ul><ul><li>Diabetes cause of more than 50% of non-traumatic amputations </li></ul><ul><li>Trauma to lower limb with resultant ulceration, infection & poor wound healing </li></ul>
  • 36. Microvascular Complications <ul><li>Result for thickening of the vessel membranes in the capillaries & arterioles in response to conditions of chronic hyperglycaemia </li></ul><ul><li>Complications are specific to diabetes </li></ul><ul><li>Mainly affect eyes (retinopathy), the kidneys (nephropathy) and the nervous system (neuropathy) </li></ul><ul><li>Clinical manifestations occur 10-20 years after onset of diabetes </li></ul>
  • 37. Diabetic Retinopathy <ul><li>Process of microvascular damage to retina as a result of chronic hyperglycaemia </li></ul><ul><li>Most common cause of new cases of blindness </li></ul><ul><li>Cataracts are also common </li></ul>
  • 38. Diabetic Nephropathy <ul><li>Microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidneys </li></ul>
  • 39. Diabetic Neuropathy <ul><li>Nerve damage that occurs because of metabolic derangements associated with DM </li></ul><ul><li>Approx 60-70% of pts with diabetes have some degree of neuropathy </li></ul><ul><li>Most common type is sensory neuropathy which leads to loss of protective sensation in lower extremities and increases risk of complications that result in limb amputation </li></ul>
  • 40. Neuropathic Ulcers
  • 41. Useful Website <ul><li>http://www.diabetes.org.nz/about/ </li></ul>

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