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Diabetes: Part 1. R eview Part 2. Assessment

Pierce College Summer Boot Camp. Diabetes: Part 1. R eview Part 2. Assessment. Review . Normal glucose metabolism. Diabetes is a disorder of carbohydrate metabolism. Liver produces too much glucose Pancreas secretes insufficient insulin Peripheral tissues resistant to insulin.

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Diabetes: Part 1. R eview Part 2. Assessment

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  1. Pierce College Summer Boot Camp Diabetes:Part 1. ReviewPart 2. Assessment

  2. Review

  3. Normal glucose metabolism

  4. Diabetes is a disorder of carbohydrate metabolism

  5. Liver produces too much glucose • Pancreas secretes insufficient insulin • Peripheral tissues resistant to insulin Problems can occur at 3 sites in diabetes

  6. Plasma glucose levels reach higher levels after eating in older adults • Plasma glucose levels take longer to return to normal • Significantly due to: • Accumulated abdominal/visceral fat • Decreased muscle mass Type 2 becomes more common with age

  7. Categories of diabetes mellitus

  8. Comparison type 1 and type 2 diabetes

  9. Childhood obesity is epidemic • Prevalent in specific ethnic groups • No genets responsible for type 2 DM have been identified Type 2 diabetes becoming increasingly common

  10. Onset is NOT sudden • Fatigue • Frequent urination • Increased thirst • Increased hunger • Weight loss • Slow healing wounds or sores Type 2 symptoms develop gradually

  11. Common symptoms & signs 1

  12. Severe dehydration causes: • Weakness • Fatigue • Mental status changes • Weight loss • Nausea and vomiting • Blurred vision • Predisposition to bacterial and fungal infections Common symptoms & signs 2

  13. Complications are primarily VASCULAR • GLYCOSYLATION—carbohydrate attached to a group of another molecule • Produces protein kinase C • Kinase C increases vascular permeability • Leads to endothelial dysfunction Complications of diabetes

  14. Microvascular changes

  15. Diabetic retinopathy Manifestations of microvascular disease in diabetes 1

  16. Vision with diabetic retinopathy

  17. Diabetic nephropathy Manifestations of microvascular disease in diabetes 2

  18. Diabetic neuropathy Manifestations of microvascular disease in diabetes 3

  19. Paresthesias • Loss of sense of touch, vibration, proprioception, temperature • Blunted perception of foot trauma • Carpal tunnel • Cranial neuropathies: • Diplopia • Ptosis • Anisocoria Effects of diabetic neuropathy

  20. Complications develop due to atherosclerotic changes Macrovascular changes

  21. Angina pectoris • Myocardial infarction • TIAs and strokes • Peripheral arterial disease • Unlike with microvascular disease, control of glucose alone is not effective! Diabetic macrovascular disease

  22. Plasma glucose 80-120 mg/dl (100-140 at HS) • HbgA1c <7% • May be adjusted in elderly, short life expectancy, brittle diabetics, those who cannot communicate hypoglycemic symptoms (e.g., children) Diabetes treatment goals

  23. Key elements for all patients

  24. Causes • Roles of diet and exercise • Self monitoring • Symptoms of hypo, hyperglycemia • Diabetic complications • Type 1—how to titrate medication Education

  25. Low in saturated fat and cholesterol • Moderate amounts of carbohydrate • Type 1: 1 unit rapid acting insulin per each 15 grams of carbohydrate in a meal • Exercise should be increased to whatever level the patient can tolerate • All forms of exercise are beneficial • Lower insulin dose may be required before exercise Diet and exercise counseling

  26. Medications based on site of defect

  27. Sulfonylureas Glipizide Glyburide Glimeperide Meglitinides Prandin Starlix Cause pancreas to release more insulin

  28. Biguanides Metformin Should not be used in patients with kidney damage Improve ability to move glucose into the cell (esp. muscle cells)

  29. Pioglitazone (Actose) Rosiglitazone (Avandia) Lower amount of sugar released by liver

  30. Assessment of the diabetic patient

  31. What is the patient’s age? Why: Diabetes becomes more common with age. Over 90% of adults with DM have type 2 diabetes. Older adults are less tolerant of fluctuations in blood glucose levels. Medical history

  32. What is the patient’s eating pattern? Nutritional status? Weight history? Why: Is there polyphagia? Polydipsia? Poor eating habits? History of insidious weight gain? A more recent weight loss? Medical history

  33. Is there a history of visual disturbance? History of kidney problems? History of numbness? Tingling? Pain? Why: Microvascular complications will predispose to diabetic retinopathy , nephropathy, and neuropathy. Medical history

  34. Is there a history of chest pain? Palpitation? DOE? History of intermittent claudication? Why: Macrovascular complications produce large vessel atherosclerosis resulting from hyperinsulinemia, dyslipidemias, and hyperglycemia. Medical history

  35. Is there a history of smoking? Hypertension? Why: Smoking 1 pack of cigarettes a day increases one’s risk of developing type 2 diabetes by 61% over that of the nonsmoker. A diabetic smoker is 3 times more likely to die of cardiovascular disease than the diabetic nonsmoker. HTN is a major risk factor for diabetes. Medical history

  36. Is there a family history of diabetes? Other endocrine disorders? Why: Family history of diabetes increases one’s risk for developing diabetes. Many studies have shown a connection through obesity, hypertension, and metabolic syndrome. NO study has shown there is NO increased risk with a positive family history. Medical history

  37. What is the patient’s educational and economic background? Why: Patients with diabetes with lower educational and economic levels have been shown to have less utilization of services and monitor their glucose status less frequently that patients with higher educational and economic levels. Medical history

  38. Height and weight Why: Obesity contributes to type 2 diabetes BMI of <25 should be maintained to lower the risk of diabetes. Risk increases with weight circumference: All women > 31.5”, White and Black men > 37”, Asian men > 35” Physical examination

  39. Blood pressure, including orthostatic Why: Having diabetes makes having hypertension and other heart conditions more likely. Diabetes damages arteries and makes them susceptible to hardening. Orthostatic hypotension can be due to diabetic neuropathy. Physical examination

  40. Fundoscopic examination Why: Evaluate for diabetic retinopathy as a result of nerve ischemia from microvascular disease. Physical examination

  41. Diabetic retinopathy

  42. Thyroid palpation Why: Patients with diabetes have a higher risk of thyroid disease. Both are endocrine disorders and may have common autoimmune origins. Physical examination

  43. Thyroid palpation

  44. Skin assessment Why: One-third of diabetic patients will develop a skin condition. Increased glucose in the blood predisposes to skin infections. Physical examination

  45. Scleredermadiabeticorum

  46. Vitiligo

  47. Acanthosisnigricans

  48. Foot exam: Inspection every 3-6 months Palpation DP and PT pulses Monofilament exam Why: Diabetic neuropathy leads to decreased awareness of foot trauma and foot ulceration. Physical examination

  49. Monofilament exam

  50. Patellar and Achilles reflexes annually Why: Diabetic neuropathy is a late finding in type 1 diabetes but can be an early finding in type 2. Physical examination

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