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Nurse Licensure Examination Review Diabetes Mellitus pinoynursing.webkotoh.com

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Diabetes Mellitus <ul><li>A group of metabolic diseases characterized by elevated levels of glucose in the blood resulting from defects in insulin secretion, insulin action, insulin receptors or any combination of conditions. </li></ul>

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Diabetes Mellitus <ul><li>A chronic disorder of impaired glucose metabolism, protein and fat metabolism </li></ul>

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Diabetes Mellitus <ul><li>BASIC PATHOLOGY : Insulin problem (deficiency or impaired action) </li></ul>

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Diabetes Mellitus <ul><li>Insulin is a hormone secreted by the BETA cells of the pancreas </li></ul><ul><li>Stimulus of insulin- HYPERGLYCEMIA </li></ul>

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Diabetes Mellitus <ul><li>Action of insulin: it promotes entry of Glucose into the body cells by binding to the insulin receptor in the cell membrane </li></ul>

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INSULIN : Physiology <ul><li>Insulin Metabolic Functions: </li></ul><ul><li>1. Transports and metabolizes GLUCOSE </li></ul><ul><li>2. Promotes GLYCOGENESIS </li></ul><ul><li>3. Promotes GLYCOLYSIS </li></ul><ul><li>4. Enhances LIPOGENESIS </li></ul><ul><li>5. Accelerates PROTEIN SYNTHESIS </li></ul>

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Diabetes Mellitus <ul><li>RISK FACTORS for Diabetes Mellitus </li></ul><ul><li>1. Family History of diabetes </li></ul><ul><li>2. Obesity </li></ul><ul><li>3. Race/Ethnicity </li></ul>

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Diabetes Mellitus <ul><li>RISK FACTORS for Diabetes Mellitus </li></ul><ul><li>4. Age of more than 45 </li></ul><ul><li>5. Previously unidentified IFG/IGT </li></ul><ul><li>6. Hypertension </li></ul>

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Diabetes Mellitus <ul><li>RISK FACTORS for Diabetes Mellitus </li></ul><ul><li>7. Hyperlipidemia </li></ul><ul><li>8. History of Gestational Diabetes Mellitus </li></ul>

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Diabetes Mellitus <ul><li>CLASSIFICATION OF DM </li></ul><ul><li>1. Type 1 DM </li></ul><ul><ul><li>Insulin dependent Diabetes Mellitus </li></ul></ul><ul><li>2. Type 2 DM </li></ul><ul><ul><li>Non-insulin dependent Diabetes Mellitus </li></ul></ul><ul><li>3. Gestational DM </li></ul><ul><ul><li>Diabetes Mellitus diagnosed during pregnancy </li></ul></ul><ul><li>4. DM associated with other conditions or syndromes </li></ul>

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Diabetes Mellitus <ul><li>CLASSIFICATION OF DM </li></ul><ul><li>1. Type 1 DM </li></ul><ul><ul><li>Insulin dependent Diabetes Mellitus </li></ul></ul>

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Diabetes Mellitus <ul><li>CLASSIFICATION OF DM </li></ul><ul><li>2. Type 2 DM </li></ul><ul><ul><li>Non-insulin dependent Diabetes Mellitus </li></ul></ul>

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Diabetes Mellitus <ul><li>CLASSIFICATION OF DM </li></ul><ul><li>3. Gestational DM </li></ul><ul><ul><li>Diabetes Mellitus diagnosed during pregnancy </li></ul></ul>

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Diabetes Mellitus <ul><li>CLASSIFICATION OF DM </li></ul><ul><li>4. DM associated with other conditions or syndromes </li></ul>

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Diabetes Mellitus <ul><li>Other types of DM </li></ul><ul><li>1. Impaired Glucose Tolerance </li></ul><ul><li>2. Impaired Fasting Glucose </li></ul><ul><li>3. Pre-diabetes </li></ul>

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TYPE 1- Diabetes Mellitus <ul><li>This type of DM is characterized by the destruction of the pancreatic beta cells </li></ul>

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TYPE 1- Diabetes Mellitus <ul><li>Etiology: </li></ul><ul><li>1. Genetic susceptibility- HLA DR3 and DR4 </li></ul><ul><li>2. Autoimmune response </li></ul><ul><li>3. Toxins, unidentified viruses and environmental factors </li></ul>

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TYPE 1- Diabetes Mellitus <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>Destruction of BETA cells  decreased insulin production  uncontrolled glucose production by the liver  hyperglycemia  signs and symptoms </li></ul>

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TYPE 1- Diabetes Mellitus <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>CLASSIC P’s </li></ul><ul><li>Polyuria </li></ul><ul><li>Polydipsia </li></ul><ul><li>Polyphagia </li></ul>

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TYPE 2- Diabetes Mellitus <ul><li>A type of DM characterized by insulin resistance and impaired insulin production </li></ul>

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TYPE 2- Diabetes Mellitus <ul><li>Etiology: </li></ul><ul><li>1. Unknown </li></ul><ul><li>2. Probably genetic and obesity </li></ul>

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TYPE 2- Diabetes Mellitus <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>Decreased sensitivity of insulin receptor to insulin  less uptake of glucose  HYPERGLYCEMIA </li></ul>

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TYPE 2- Diabetes Mellitus <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>Decreased insulin production  diminished insulin action  hyperglycemia  signs and symptoms </li></ul>

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TYPE 2- Diabetes Mellitus <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>BUT (+) insulin in small amount  prevent breakdown of fats  DKA is unusual </li></ul>

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GESTATIONAL Diabetes Mellitus <ul><li>Any degree of glucose intolerance with its onset during pregnancy </li></ul><ul><li>Usually detected between 24-28 th week gestation </li></ul>

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GESTATIONAL Diabetes Mellitus <ul><li>Blood glucose returns to normal after delivery of the infant </li></ul><ul><li>NEVER administer ORAL HYPOGLYCEMIC AGENTS to PREGNANT MOTHERS! </li></ul>

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Diabetes Mellitus <ul><li>ASSESSMENT FINDINGS </li></ul><ul><li>1. Classic 3 P’s </li></ul><ul><li>2. Fatigue </li></ul><ul><li>3. Body weakness </li></ul>

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Diabetes Mellitus <ul><li>ASSESSMENT FINDINGS </li></ul><ul><li>4. Visual changes </li></ul><ul><li>5. Slow wound healing </li></ul><ul><li>6. Recurrent skin and mucus membrane infections </li></ul>

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Diabetes Mellitus <ul><li>DIAGNOSTIC TESTS </li></ul><ul><li>1. FBS- > 126 </li></ul><ul><li>2. RBS- >200 </li></ul><ul><li>3. OGTT- > 200 </li></ul>

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Diabetes Mellitus <ul><li>DIAGNOSTIC TESTS </li></ul><ul><li>4. HgbA1- for monitoring!! </li></ul><ul><li>5. Urine glucose </li></ul><ul><li>6. Urine ketones </li></ul>

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Diabetes Mellitus <ul><li>DIAGNOSTIC CRITERIA </li></ul><ul><li>1. FBS equal to or greater than 126 mg/dL (7.0mmol/L) </li></ul><ul><ul><li>(Normal 8 hour FBS- 80-109 mg/dL) </li></ul></ul>

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Diabetes Mellitus <ul><li>DIAGNOSTIC CRITERIA </li></ul><ul><li>2. OGTT value 1 and 2 hours post-prandial equal to or greater than 200 mg/dL </li></ul><ul><li>Normal OGTT 1 and 2 hours post-prandial- is </li></ul><ul><ul><li>140 mg/dL </li></ul></ul>

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Diabetes Mellitus <ul><li>DIAGNOSTIC CRITERIA </li></ul><ul><li>3. RBS of equal to or greater than 200 mg/dL PLUS the 3 P’s </li></ul>

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Diabetes Mellitus <ul><li>NURSING MANAGEMENT OF DM </li></ul><ul><li>The main goal is to NORMALIZE insulin activity and blood glucose level by: </li></ul>

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Diabetes Mellitus <ul><li>NURSING MANAGEMENT OF DM </li></ul><ul><li>1. Nutritional modification </li></ul><ul><li>2. Regular Exercise </li></ul><ul><li>3. Regular Glucose Monitoring </li></ul><ul><li>4. Drug therapy </li></ul><ul><li>5. Client Education </li></ul>

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Diabetes Mellitus <ul><li> The Patient with DM </li></ul><ul><li>HISTORY </li></ul><ul><ul><li>Symptoms and characteristics </li></ul></ul><ul><li>PHYSICAL EXAMINATION </li></ul><ul><ul><li>VS, BMI, Fundoscopy, Neuro </li></ul></ul><ul><li>LABORATORY EXAMINATION </li></ul><ul><ul><li>FBS, RBS, HgbA1c, lipid profile, ECG, UA </li></ul></ul><ul><li>REFERRALS </li></ul><ul><ul><li>Ophthalmologist, Podiatrist, Dietician, etc.. </li></ul></ul>

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Diabetes Mellitus <ul><li>The Patient with DM </li></ul><ul><li>HISTORY </li></ul><ul><ul><li>Symptoms and characteristics </li></ul></ul><ul><li>PHYSICAL EXAMINATION </li></ul><ul><ul><li>VS, BMI, Fundoscopy, and Neuro assessment </li></ul></ul>

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Diabetes Mellitus <ul><li> The Patient with DM </li></ul><ul><li>LABORATORY EXAMINATION </li></ul><ul><ul><li>FBS, RBS, HgbA1c, lipid profile, ECG, and Urinalysis </li></ul></ul><ul><li>REFERRALS </li></ul><ul><ul><li>Ophthalmologist, Podiatrist, Dietician, etc.. </li></ul></ul>

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DM Nutritional management

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Diabetes Mellitus <ul><li>NUTRITIONAL MANAGEMENT </li></ul><ul><li>1.Review the patient’s diet history to identify eating habits and lifestyle </li></ul><ul><li>2. Coordinate with the dietician in meal planning for weight loss </li></ul>

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Diabetes Mellitus <ul><li>NUTRITIONAL MANAGEMENT </li></ul><ul><li>3. Plan for the caloric intake distributed as follows- CHO 50-60%; Fats 20-30%; and Proteins 10-20% </li></ul><ul><li>4. Advise moderation in alcohol intake </li></ul><ul><li>5. Using artificial sweeteners is acceptable </li></ul>

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DM Exercise management

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Diabetes Mellitus <ul><li>EXERCISE Management </li></ul><ul><li>1. Teach that exercise can lower the blood glucose level </li></ul><ul><li>2. Diabetics must first control the glucose level before initiating exercise programs. </li></ul>

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Diabetes Mellitus <ul><li>EXERCISE Management </li></ul><ul><li>3. Offer extra food /calories before engaging in exercise </li></ul><ul><li>4. Offer snacks at the end of the exercise period if patient is on insulin treatment. </li></ul>

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Diabetes Mellitus <ul><li>EXERCISE Management </li></ul><ul><li>5. Advise that exercise should be done at the same time every day, preferably when blood glucose levels are at their peak </li></ul>

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Diabetes Mellitus <ul><li>EXERCISE Management </li></ul><ul><li>6. Regular exercise, not sporadic exercise, should be encouraged. </li></ul><ul><li>7. For most patient, WALKING is the safe and beneficial form of exercise </li></ul>

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Glucose Self Monitoring

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Diabetes Mellitus <ul><li>GLUCOSE MONITORING </li></ul><ul><li>Self-monitoring of blood glucose (SMBG) enables the patient to adjust the treatment regimen to obtain optimal glucose control </li></ul>

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Diabetes Mellitus <ul><li>GLUCOSE MONITORING </li></ul><ul><li>Most common method involves obtaining a drop of capillary blood applied to a test strip. </li></ul><ul><li>The usual recommended frequency is TWO-FOUR times a day. </li></ul>

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Diabetes Mellitus <ul><li>When is it done? </li></ul><ul><li>At the peak action time of the medication to evaluate the need for adjustments. </li></ul><ul><li>To evaluate BASAL insulin  test before meals </li></ul>

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Diabetes Mellitus <ul><li>When is it done? </li></ul><ul><li>To titrate bolus or regular and lispro  test 2 hours after meals. </li></ul><ul><li>To evaluate the glucose level of those taking ORAL hypoglycemics  test before and two hours after meals. </li></ul>

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Diabetes Mellitus Monitoring therapy <ul><li>Testing the glycosylated hemoglobin (HbA1c) </li></ul><ul><li>This glycosylated hemoglobin refers to the blood test that reflects the average blood glucose over a period of TWO to THREE months. </li></ul>

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Diabetes Mellitus Monitoring therapy <ul><li>Normal value is 4 to 6 % </li></ul><ul><li>No patient preparation is needed for this testing </li></ul><ul><li>Done to monitor therapy </li></ul>

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Diabetes Mellitus <ul><li>Urine testing for glucose </li></ul><ul><ul><li>Benedict’s test </li></ul></ul>

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Diabetes Mellitus <ul><li>Urine testing for ketones </li></ul><ul><ul><li>Ketones are by-products of fat breakdown </li></ul></ul>

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Diabetes Mellitus <ul><li>Urine testing for ketones </li></ul><ul><ul><li>This is performed whenever TYPE 1 DM have glucosuria or persistent elevation of blood glucose, during illness, and in gestational diabetes </li></ul></ul>

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DM Drug therapy

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Diabetes Mellitus <ul><li>DRUG THERAPY and MANAGEMENT </li></ul><ul><li>Usually, this type of management is employed if diet modification and exercise cannot control the blood glucose level. </li></ul>

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Diabetes Mellitus <ul><li>DRUG THERAPY and MANAGEMENT </li></ul><ul><li>Because the patient with TYPE 1 DM cannot produce insulin, exogenous insulin must be administered for life. </li></ul>

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Diabetes Mellitus <ul><li>DRUG THERAPY and MANAGEMENT </li></ul><ul><li>TYPE 2 DM may have decreased insulin production, ORAL agents that stimulate insulin production are usually employed. </li></ul>

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Diabetes Mellitus <ul><li>PHARMACOLOGIC INSULIN </li></ul><ul><li>This may be grouped into several categories according to: </li></ul><ul><li>1. Source- Human, pig, or cow </li></ul><ul><li>2. Onset of action- Rapid-acting, short-acting, intermediate-acting, long-acting and very long acting </li></ul>

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Diabetes Mellitus <ul><li>PHARMACOLOGIC INSULIN </li></ul><ul><li>This may be grouped into several categories according to: </li></ul><ul><li>3. Pure or mixed concentration </li></ul><ul><li>4. Manufacturer of drug </li></ul>

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Diabetes Mellitus <ul><li>GENERALITIES </li></ul><ul><li>1. Human insulin preparations have a shorter duration of action than animal source </li></ul>

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Diabetes Mellitus <ul><li>GENERALITIES </li></ul><ul><li>2. Animal sources of insulin have animal proteins that may trigger allergic reaction and they may stimulate antibody production that may bind the insulin, slowing the action </li></ul>

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Diabetes Mellitus <ul><li>3. ONLY Regular insulin can be used INTRAVENOUSLY! </li></ul>

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Diabetes Mellitus <ul><li>4. Insulin are measured in INTERNATIONAL UNITS or “iu” </li></ul><ul><li>5. There is a specified insulin injection calibrated in units </li></ul>

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Diabetes Mellitus <ul><li>RAPID ACTING INSULIN </li></ul><ul><li>Lispro (Humalog) and Insulin Aspart (Novolog) </li></ul><ul><li>Produces a more rapid effect and with a shorter duration than any other insulin preparation </li></ul>

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Diabetes Mellitus <ul><li>RAPID ACTING INSULIN </li></ul><ul><li>ONSET- 5-15 minutes </li></ul><ul><li>PEAK- 1 hour </li></ul><ul><li>DURATION- 3 hours </li></ul><ul><li>Instruct patient to eat within 5 to 15 minutes after injection </li></ul>

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Diabetes Mellitus <ul><li>REGULAR INSULIN </li></ul><ul><li>Also called Short-acting insulin </li></ul><ul><li>“ R” </li></ul><ul><li>Usually Clear solution administered 30 minutes before a meal </li></ul>

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Diabetes Mellitus <ul><li>REGULAR INSULIN </li></ul><ul><li>ONSET- 30 minutes to 1 hour </li></ul><ul><li>PEAK- 2 to 3 hours </li></ul><ul><li>DURATION- 4 to 6 hours </li></ul>

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Diabetes Mellitus <ul><li>INTERMEDIATE ACTING INSULIN </li></ul><ul><li>Called “NPH” or “LENTE” </li></ul><ul><li>Appears white and cloudy </li></ul>

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Diabetes Mellitus <ul><li>INTERMEDIATE ACTING INSULIN </li></ul><ul><li>ONSET- 2-4 hours </li></ul><ul><li>PEAK- 4 to 6-12 hours </li></ul><ul><li>DURATION- 16-20 hours </li></ul>

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Diabetes Mellitus <ul><li>LONG- ACTING INSULIN </li></ul><ul><li>“ UltraLENTE” </li></ul><ul><li>Referred to as “peakless” insulin </li></ul>

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Diabetes Mellitus <ul><li>LONG- ACTING INSULIN </li></ul><ul><li>ONSET- 6-8 hours </li></ul><ul><li>PEAK- 12-16 hours </li></ul><ul><li>DURATION- 20-30 hours </li></ul>

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Diabetes Mellitus <ul><li>HEALTH TEACHING </li></ul><ul><li>Regarding Insulin SELF- Administration </li></ul><ul><li>1. Insulin is administered at home subcutaneously </li></ul>

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Diabetes Mellitus <ul><li>HEALTH TEACHING Regarding Insulin SELF- Administration </li></ul><ul><li>2. Cloudy insulin should be thoroughly mixed by gently inverting the vial or ROLLING between the hands </li></ul>

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Diabetes Mellitus <ul><li>HEALTH TEACHING Regarding Insulin SELF- Administration </li></ul><ul><li>3. Insulin NOT IN USE should be stored in the refrigerator, BUT avoid freezing/extreme temperature </li></ul>

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Diabetes Mellitus <ul><li>4. Insulin IN USE should be kept at room temperature to reduce local irritation at the injection site </li></ul>

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Diabetes Mellitus <ul><li>5. INSULIN may be kept at room temperature up to 1 month </li></ul>

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Diabetes Mellitus <ul><li>6. Select syringes that match the insulin concentration. </li></ul><ul><ul><li>U-100 means 100 units per mL </li></ul></ul>

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Diabetes Mellitus <ul><li>7. Instruct the client to draw up the REGULAR (clear) Insulin FIRST before drawing the intermediate acting (cloudy) insulin </li></ul>

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Diabetes Mellitus <ul><li>8. Pre-filled syringes can be prepared and should be kept in the refrigerator with the needle in the UPRIGHT position to avoid clogging the needle </li></ul>

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Diabetes Mellitus <ul><li>9. The four main areas for insulin injection are- ABDOMEN, UPPER ARMS, THIGHS and HIPS </li></ul>

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Diabetes Mellitus <ul><li>Insulin is absorbed fastest in the abdomen and slowest in the hips </li></ul><ul><li>Instruct the client to rotate the areas of injection, but exhaust all available sites in one area first before moving into another area. </li></ul>

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Diabetes Mellitus <ul><li>10. Alcohol may not be used to cleanse the skin </li></ul><ul><li>11. Utilize the subcutaneous injection technique- commonly, a 45-90 degree angle. </li></ul>

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Diabetes Mellitus <ul><li>12. No need to instruct for aspirating the needle </li></ul><ul><li>13. Properly discard the syringe after use. </li></ul>

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Diabetes Mellitus <ul><li>T-I-E </li></ul><ul><li>T est blood  I nject insulin  E at food </li></ul>

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Diabetes Mellitus <ul><li>COMPLICATIONS OF INSULIN THERAPY </li></ul><ul><li>1. Local allergic reactions </li></ul><ul><li>Redness, swelling, tenderness and induration appearing 1-2 hours after injection </li></ul><ul><li>Usually occurs in the beginning stage of therapy </li></ul>

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Diabetes Mellitus <ul><li>COMPLICATIONS OF INSULIN THERAPY </li></ul><ul><li>1. Local allergic reactions </li></ul><ul><li>Disappears with continued use </li></ul><ul><li>Antihistamine can be given 1 hour before injection time </li></ul><ul><li>Porcine and bovine insulin preparations have a higher tendency to produce this reaction. </li></ul>

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<ul><li>2. SYSTEMIC ALLERGIC REACTIONS </li></ul><ul><li>Very rare </li></ul><ul><li>Generalized urticaria is the manifestation </li></ul><ul><li>Treatment is desensitization </li></ul>Diabetes Mellitus

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<ul><li>COMPLICATIONS OF INSULIN THERAPY </li></ul><ul><li>3. INSULIN DYSTROPHY </li></ul><ul><li>A localized reaction in the form of lipo atrophy or lipo hypertrophy </li></ul>Diabetes Mellitus

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<ul><li>Lipoatrophy- loss of subcutaneous fat usually caused by the utilization of animal insulin </li></ul>Diabetes Mellitus

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<ul><li>Lipohypertrophy- development of fibrofatty masses, usually caused by repeated use of injection site </li></ul>Diabetes Mellitus

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<ul><li>4. INSULIN RESISTANCE </li></ul><ul><li>Most commonly caused by OBESITY </li></ul><ul><li>Defined as daily insulin requirement of more than 200 units </li></ul><ul><li>Management- Steroids and use of more concentrated insulin </li></ul>Diabetes Mellitus

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<ul><li>5. MORNING HYPERGLYCEMIA </li></ul><ul><li>Elevated blood sugar upon arising in the morning </li></ul><ul><li>Caused by insufficient level of insulin </li></ul><ul><ul><li>DAWN phenomenon </li></ul></ul><ul><ul><li>SOMOGYI effect </li></ul></ul><ul><ul><li>INSULIN WANING </li></ul></ul>Diabetes Mellitus

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Diabetes Mellitus <ul><li>DAWN PHENOMENON </li></ul><ul><li>Relatively normal blood glucose until about 3 am, when the glucose level begins to RISE </li></ul><ul><li>Results from the nightly surges of GROWTH HORMONE secretion </li></ul><ul><li>Management: Bedtime injection of NPH </li></ul>

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Diabetes Mellitus <ul><li>SOMOGYI EFFECT </li></ul><ul><li>Normal or elevated blood glucose at bedtime, decrease blood glucose at 2-3 am due to hypoglycemic levels and a subsequent increase in blood glucose (rebound hypergycemia) </li></ul>

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Diabetes Mellitus <ul><li>SOMOGYI EFFECT </li></ul><ul><li>Nocturnal hypoglycemia followed by rebound hyperglycemia </li></ul>

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Diabetes Mellitus <ul><li>SOMOGYI EFFECT </li></ul><ul><li>Due to the production of counter regulatory hormones- glucagon. cortisol and epinephrine </li></ul><ul><li>Management- decrease evening dose of NPH or increase bedtime snack </li></ul>

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Diabetes Mellitus <ul><li>INSULIN WANING </li></ul><ul><li>Progressive rise in blood glucose from bedtime to morning </li></ul><ul><li>Seen when the NPH evening dose is administered before dinner </li></ul><ul><li>Management: Move the insulin injection to bedtime </li></ul>

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Diabetes Mellitus <ul><li>ORAL HYPOGLYCEMIC AGENTS </li></ul><ul><li>These may be effective when used in TYPE 2 DM that cannot be treated with diet and exercise </li></ul><ul><li>These are NEVER used in pregnancy! </li></ul>

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Diabetes Mellitus <ul><li>ORAL HYPOGLYCEMIC AGENTS </li></ul><ul><li>There are several agents: </li></ul><ul><ul><li>Sulfonylureas </li></ul></ul><ul><ul><li>Biguanides </li></ul></ul><ul><ul><li>Alpha-glucosidase inhibitors </li></ul></ul><ul><ul><li>Thiazolidinediones </li></ul></ul><ul><ul><li>Meglitinides </li></ul></ul>

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Diabetes Mellitus <ul><li>SULFONYLUREAS </li></ul><ul><li>MOA- stimulates the beta cells of the pancreas to secrete insulin </li></ul><ul><li>Classified as to generations- first and second generations </li></ul>

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Diabetes Mellitus <ul><li>SULFONYLUREAS </li></ul><ul><li>FIRST GENERATION- Acetoheximide, Chlorpropamide, Tolazamide and Tolbutamide </li></ul><ul><li>SECOND GENERATION- Glipizide, Glyburide, Glibenclamide, Glimepiride </li></ul>

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Diabetes Mellitus: Sulfonylureas <ul><li>The most common side –effects of these medications are Gastro-intestinal upset and dermatologic reactions. </li></ul><ul><li>HYPOGLYCEMIA is also a very important side-effect </li></ul>

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Diabetes Mellitus: Sulfonylureas <ul><li>Chlorpropamide has a very long duration of action. This also produces a disulfiram-like reaction when taken with alcohol </li></ul><ul><li>Second generation drugs have shorter duration with metabolism in the kidney and liver and are the choice for elderly patients </li></ul>

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Diabetes Mellitus <ul><li>BIGUANIDES </li></ul><ul><li>MOA- Facilitate the action of insulin on the peripheral receptors </li></ul><ul><li>These can only be used in the presence of insulin </li></ul>

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Diabetes Mellitus <ul><li>BIGUANIDES= “ formin” </li></ul><ul><li>They have no effect on the beta cells of the pancreas </li></ul><ul><li>Metformin (Glucophage) and Phenformin are examples </li></ul>

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Diabetes Mellitus: Biguanides <ul><li>The most important side effect is LACTIC ACIDOSIS! </li></ul><ul><li>These are not given to patient with renal impairment </li></ul>

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Diabetes Mellitus: Biguanides <ul><li>These drugs are usually given with a sulfonylurea to enhance the glucose-lowering effect more than the use of each drug individually </li></ul>

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Diabetes Mellitus <ul><li>ALPHA-GLUCOSIDASE INHIBITORS </li></ul><ul><li>MOA- Delay the absorption of glucose in the GIT </li></ul><ul><li>Result is a lower post-prandial blood glucose level </li></ul><ul><li>They do not affect insulin secretion or action! </li></ul><ul><li>Side-effect: DIARRHEA and FLATULENCE </li></ul>

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Diabetes Mellitus <ul><li>Examples of AGI are Acarbose and Miglitol </li></ul><ul><li>They are not absorbed systemically and are very safe </li></ul><ul><li>They can be used alone or in combination with other OHA </li></ul>

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Diabetes Mellitus <ul><li>Side-effect if used with other drug is HYPOGLYCEMIA </li></ul><ul><li>Note that sucrose absorption is impaired and IV glucose is the therapy for the hypoglycemia </li></ul>

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Diabetes Mellitus <ul><li>THIAZOLIDINEDIONES </li></ul><ul><li>MOA- Enhance insulin action at the receptor site </li></ul><ul><li>They do not stimulate insulin secretion </li></ul>

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Diabetes Mellitus <ul><li>THIAZOLIDINEDIONES </li></ul><ul><li>Examples- Rosiglitazone, Pioglitazone </li></ul><ul><li>These drugs affect LIVER FUNCTION </li></ul><ul><li>Can cause resumption of OVULATION in peri-menopausal anovulatory women </li></ul>

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Diabetes Mellitus <ul><li>MEGLITINIDES </li></ul><ul><li>MOA- Stimulate the secretion of insulin by the beta cells </li></ul><ul><li>Examples- Repaglinide and Nateglinide </li></ul>

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Diabetes Mellitus <ul><li>MEGLITINIDES </li></ul><ul><li>They have a shorter duration and fast action </li></ul><ul><li>Should be taken BEFORE meals to stimulate the release of insulin from the pancreas </li></ul>

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Diabetes Mellitus <ul><li>MEGLITINIDES </li></ul><ul><li>Principal side-effect of meglitinides- hypoglycemia </li></ul><ul><li>Can be used alone or in combination </li></ul>

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Diabetes Mellitus <ul><li>ACUTE COMPLICATIONS OF DM </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Diabetic ketoacidosis </li></ul><ul><li>Hyperglycemic hyperosmolar non-ketotic syndrome (HHNS) </li></ul>

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Diabetes Mellitus <ul><li>CHRONIC COMPLICATIONS OF DM </li></ul><ul><li>Macrovascular complications- MI, Stroke, Atherosclerosis, CAD, and Peripheral vascular disease </li></ul><ul><li>Microvascular complications- micro-angiopathy, retinopathy, nephropathy </li></ul><ul><li>Peripheral neuropathy </li></ul>

124.
Diabetes Mellitus <ul><li>HYPOGLYCEMIA </li></ul><ul><li>Blood glucose level less than 50 to 60 mg/dL </li></ul><ul><li>Causes: Too much insulin/OHA, too little food and excessive physical activity </li></ul><ul><li>Mild- 40-60 </li></ul><ul><li>Moderate- 20-40 </li></ul><ul><li>Severe- less than 20 </li></ul>

125.
HYPOGLYCEMIA <ul><li>ASSESSMENT FINDINGS </li></ul><ul><li>1. Sympathetic manifestations- sweating, tremors, palpitations, nervousness, tachycardia and hunger </li></ul>

126.
HYPOGLYCEMIA <ul><li>ASSESSMENT FINDINGS </li></ul><ul><li>2. CNS manifestations- inability to concentrate, headache, lightheadedness, confusion, memory lapses, slurred speech, impaired coordination, behavioral changes, double vision and drowsiness </li></ul>

127.
HYPOGLYCEMIA

128.
HYPERGLYCEMIA

129.
HYPOGLYCEMIA <ul><li>DIAGNOSTIC FINDINGS </li></ul><ul><li>RBS- less than 50-60 mg/dL level </li></ul>

130.
HYPOGLYCEMIA <ul><li>Nursing Interventions </li></ul><ul><li>1. Immediate treatment with the use of foods with simple sugar- glucose tablets, fruit juice, table sugar, honey or hard candies </li></ul>

131.
HYPOGLYCEMIA <ul><li>Nursing Interventions </li></ul><ul><li>2. For unconscious patients- glucagon injection 1 mg IM/SQ; or IV 25 to 50 mL of D50/50 </li></ul>

132.
HYPOGLYCEMIA <ul><li>Nursing Interventions </li></ul><ul><li>3. re-test glucose level in 15 minutes and re-treat if less than 75 mg/dL </li></ul><ul><li>4. Teach patient to refrain from eating high-calorie, high-fat desserts </li></ul>

133.
HYPOGLYCEMIA <ul><li>Nursing Interventions </li></ul><ul><li>5. Advise in-between snacks, especially when physical activity is increased </li></ul><ul><li>6. Teach the importance of compliance to medications </li></ul>

134.
Diabetic Ketoacidosis <ul><li>This is cause by the absence of insulin leading to fat breakdown and production of ketone bodies </li></ul><ul><li>Three main clinical features: </li></ul><ul><ul><li>1. HYPERGLYCEMIA </li></ul></ul><ul><ul><li>2. DEHYDRATION & electrolyte loss </li></ul></ul><ul><ul><li>3. ACIDOSIS </li></ul></ul>

135.
DKA <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>No insulin  reduced glucose breakdown and increased liver glucose production  Hyperglycemia </li></ul>

136.
DKA <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>Hyperglycemia  kidney attempts to excrete glucose  increased osmotic load  diuresis  Dehydration </li></ul>

137.
DKA <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>No glucose in the cell  fat is broken down for energy  ketone bodies are produced  Ketoacidosis </li></ul>

138.
DKA <ul><li>Risk factors </li></ul><ul><li>1. infection or illness- common </li></ul><ul><li>2. stress </li></ul><ul><li>3. undiagnosed DM </li></ul><ul><li>4. inadequate insulin, missed dose of insulin </li></ul>

139.
DKA <ul><li>ASSESSMENT FINDINGS </li></ul><ul><li>1. 3 P’s </li></ul><ul><li>2. Headache, blurred vision and weakness </li></ul><ul><li>3. Orthostatic hypotension </li></ul>

140.
DKA <ul><li>ASSESSMENT FINDINGS </li></ul><ul><li>4. Nausea, vomiting and abdominal pain </li></ul><ul><li>5. Acetone (fruity) breath </li></ul><ul><li>6. Hyperventilation or KUSSMAUL’s breathing </li></ul>

141.
HYPERGLYCEMIA

142.
Hyperglycemia

143.
DKA <ul><li>LABORATORY FINDINGS </li></ul><ul><li>1. Blood glucose level of 300-800 mg/dL </li></ul><ul><li>2. Urinary ketones </li></ul>

144.
DKA <ul><li>LABORATORY FINDINGS </li></ul><ul><li>3. ABG result of metabolic acidosis- LOW pH, LOW pCO2 as a compensation, LOW bicarbonate </li></ul><ul><li>4. Electrolyte imbalances- potassium levels may be HIGH due to acidosis and dehydration </li></ul>

145.
DKA <ul><li>NURSING INTERVENTIONS </li></ul><ul><li>1. Assist in the correction of dehydration </li></ul><ul><ul><li>Up to 6 liters of fluid may be ordered for infusion, initially NSS then D5W </li></ul></ul><ul><ul><li>Monitor hydration status </li></ul></ul><ul><ul><li>Monitor I and O </li></ul></ul><ul><ul><li>Monitor for volume overload </li></ul></ul>

146.
DKA <ul><li>NURSING INTERVENTIONS </li></ul><ul><li>2. Assist in restoring Electrolytes </li></ul><ul><ul><li>Kidney function is FIRST determined before giving potassium supplements! </li></ul></ul>

147.
DKA <ul><li>NURSING INTERVENTIONS </li></ul><ul><li>3. Reverse the Acidosis </li></ul><ul><ul><li>REGULAR insulin injection is ordered IV bolus 5-10 units </li></ul></ul><ul><ul><li>The insulin is followed by drip infusion in units per hour </li></ul></ul><ul><ul><li>BICARBONATE is not used! </li></ul></ul>

148.
HHNS <ul><li>A serious condition in which hyperosmolarity and extreme hyperglycemia predominate </li></ul><ul><li>Ketosis is minimal </li></ul><ul><li>Onset is slow and takes hours to days to develop </li></ul>

149.
HHNS <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>Lack of insulin action or Insulin resistance  hyperglycemia </li></ul><ul><li>Hyperglycemia  osmotic diuresis  loss of water and electrolytes </li></ul>

150.
HHNS <ul><li>PATHOPHYSIOLOGY </li></ul><ul><li>Insulin is too low to prevent hyperglycemia but enough to prevent fat breakdown </li></ul><ul><li>Occurs most commonly in type 2 DM, ages 50-70 </li></ul>

151.
HHNS <ul><li>Precipitating factors </li></ul><ul><li>1. Infection </li></ul><ul><li>2. Stress </li></ul><ul><li>3. Surgery </li></ul><ul><li>4. Medication like thiazides </li></ul><ul><li>5. Treatment like dialysis </li></ul>

152.
HHNS <ul><li>ASSESSMENT FINDINGS </li></ul><ul><li>1. Profound dehydration </li></ul><ul><li>2. Hypotension </li></ul><ul><li>3. Tachycardia </li></ul><ul><li>4. Altered sensorium </li></ul><ul><li>5. Seizures and hemiparesis </li></ul>

153.
HHNS <ul><li>DIAGNOSTIC TESTS </li></ul><ul><li>1. Blood glucose- 600 to 1,200 mg/dL </li></ul><ul><li>2. Blood osmolality- 350 mOsm/L </li></ul><ul><li>3. Electrolyte abnormalities </li></ul>

154.
HHNS <ul><li>NURSING INTERVENTIONS </li></ul><ul><li>Approach is similar to the DKA </li></ul><ul><li>1. Correction of Dehydration by IVF </li></ul><ul><li>2. Correction of electrolyte imbalance by replacement therapy </li></ul>

155.
HHNS <ul><li>NURSING INTERVENTIONS </li></ul><ul><li>3. Administration of insulin injection and drips </li></ul><ul><li>4. Continuous monitoring of urine output </li></ul>

156.
MACROVASCULAR CX <ul><li>Nursing management </li></ul><ul><li>1. Diet modification </li></ul><ul><li>2. Exercise </li></ul>

157.
MACROVASCULAR CX <ul><li>Nursing management </li></ul><ul><li>3. Prevention and treatment of underlying conditions such as MI, CAD and stroke </li></ul><ul><li>4. Administration of prescribed medications for hypertension, hyperlipidemia and obesity </li></ul>

158.
MICROVASCULAR CX <ul><li>Retinopathy- a painless deterioration of the small blood vessels in the retina, may be classified as to background retinopathy, pre-proliferative and proliferative retinopathy </li></ul><ul><li>Permanent vision changes and blindness can occur </li></ul>

159.
MICROVASCULAR CX <ul><li>Retinopathy-ASSESSMENT FINDINGS </li></ul><ul><li>Blurry vision </li></ul><ul><li>Spotty vision </li></ul><ul><li>Asymptomatic </li></ul>

160.
MICROVASCULAR CX <ul><li>Retinopathy: Diagnostic findings </li></ul><ul><li>1. Fundoscopy </li></ul><ul><li>2. Fluorescein angiography </li></ul><ul><ul><li>Painless procedure </li></ul></ul><ul><ul><li>Side-effects- discoloration of the skin and urine for 12 hours, some allergic reactions, nausea </li></ul></ul><ul><ul><li>Flash of camera may be slightly uncomfortable </li></ul></ul>

161.
MICROVASCULAR CX <ul><li>NURSING INTERVENTIONS </li></ul><ul><li>1. Assist in diagnostic procedure </li></ul><ul><li>2. Assist in the preparation for surgery- laser photocoagulation </li></ul>

162.
MICROVASCULAR CX <ul><li>NURSING INTERVENTIONS </li></ul><ul><li>3. Health teaching regarding prevention of retinopathy by regular ophthalmic examinations, good glucose control and self-management of eye care regimens </li></ul><ul><li>4. Maintain client safety </li></ul>

163.
MICROVASCULAR CX <ul><li>DIABETIC NEPHROPATHY </li></ul><ul><li>Progressive deterioration of kidney function </li></ul>

164.
MICROVASCULAR CX <ul><li>DIABETIC NEPHROPATHY </li></ul><ul><li>HYPERGLYCEMIA  causes the kidney filtration mechanism to be stressed  blood proteins leak into the urine </li></ul><ul><li>Pressure in the kidney blood vessels increases  stimulate the development of nephropathy </li></ul>

165.
MICROVASCULAR CX <ul><li>ASSESSMENT findings for diabetic nephropathy </li></ul><ul><li>1. Albuminuria </li></ul><ul><li>2. Anemia </li></ul><ul><li>3. Acidosis </li></ul>

166.
MICROVASCULAR CX <ul><li>ASSESSMENT findings for diabetic nephropathy </li></ul><ul><li>4. Fluid volume overload </li></ul><ul><li>5. Oliguria </li></ul><ul><li>6. Hypertension </li></ul><ul><li>7. UTI </li></ul>

167.
MICROVASCULAR CX <ul><li>NURSING MANAGEMENT 1. Assist in the control of hypertension- use of ACE inhibitor </li></ul><ul><li>2. Provide a low sodium and low protein diet </li></ul><ul><li>3. Administer prescribed medication for UTI </li></ul>

168.
MICROVASCULAR CX <ul><li>NURSING MANAGEMENT </li></ul><ul><li>4. Assist in dialysis </li></ul><ul><li>5. Prepare patient for renal transplantation, if indicated </li></ul>

169.
MICROVASCULAR CX <ul><li>Diabetic Neuropathy </li></ul><ul><li>A group of disorders that affect all type of nerves including the peripheral, autonomic and spinal nerves </li></ul>

170.
MICROVASCULAR CX <ul><li>Diabetic Neuropathy </li></ul><ul><li>Two most common types of Diabetic Neuropathy are sensori-motor polyneuropathy and autonomic neuropathy </li></ul>

171.
MICROVASCULAR CX <ul><li>Peripheral neuropathy- ASSESSMENT findings </li></ul><ul><li>1. paresthesias- prickling, tingling or heightened sensation </li></ul><ul><li>2. decreased proprioception </li></ul><ul><li>3. decreased sensation of light touch </li></ul><ul><li>4. unsteady gait </li></ul><ul><li>5. decreased tendon reflexes </li></ul>

172.
MICROVASCULAR CX <ul><li>Peripheral neuropathy- Nursing Management </li></ul><ul><li>1. Provide teaching that good glucose control is very important to prevent its development </li></ul><ul><li>2. Manage the pain by analgesics, antidepressants and nerve stimulation </li></ul>

173.
MICROVASCULAR CX <ul><li>Autonomic Neuropathy- ASSESSMENT findings </li></ul><ul><li>1. Silent, painless ischemia </li></ul><ul><li>2. delayed gastric emptying </li></ul><ul><li>3. orthostatic hypotension </li></ul><ul><li>4. N/V and bloating sensation </li></ul><ul><li>5. urinary retention </li></ul><ul><li>6. sexual dysfunction </li></ul>

174.
MICROVASCULAR CX <ul><li>Autonomic Neuropathy-Nursing management </li></ul><ul><li>1. Educate about the avoidance of strenuous physical activity </li></ul><ul><li>2. Stress the importance of good glucose control to delay the development </li></ul>

175.
MICROVASCULAR CX <ul><li>Autonomic Neuropathy-Nursing management </li></ul><ul><li>3. Provide LOW-fat, small frequent feedings </li></ul><ul><li>4. Administer bulk-forming laxatives for diabetic diarrhea </li></ul><ul><li>5. Provide HIGH-fiber diet for diabetic constipation </li></ul>

176.
MICROVASCULAR CX <ul><li>MANAGEMENT OF FOOT AND LEG PROBLEMS </li></ul><ul><li>Soft tissue injury in the foot/leg  formation of fissures and callus  poor wound healing  foot/leg ulcer </li></ul>

177.
MICROVASCULAR CX <ul><li>RISK FACTORS for the development of foot and leg ulcers </li></ul><ul><li>1. More than 10 years diabetic </li></ul><ul><li>2. Age of more than 40 </li></ul><ul><li>3. Smoking </li></ul><ul><li>4. Anatomic deformities </li></ul><ul><li>5. History of previous leg ulcers or amputation </li></ul>

178.
MICROVASCULAR CX <ul><li>MANAGEMENT of Foot Ulcers </li></ul><ul><li>Teach patient proper care of the foot </li></ul><ul><li>Daily assessment of the foot </li></ul><ul><li>Use of mirror to inspect the bottom </li></ul>

179.
MICROVASCULAR CX <ul><li>MANAGEMENT of Foot Ulcers </li></ul><ul><li>Inspect the surface of shoes for any rough spots or foreign objects </li></ul><ul><li>Properly dry the feet </li></ul><ul><li>Instruct to wear closed-toe shoes that fit well, recommend use of low-heeled shoes </li></ul>

180.
MICROVASCULAR CX <ul><li>MANAGEMENT </li></ul><ul><li>Instruct patient NEVER to walk barefoot, never to use heating pads, open-toed shoes and soaking feet </li></ul><ul><li>Trim toenails STRAIGHT ACROSS and file sharp corners </li></ul><ul><li>Instruct to avoid smoking and over-the counter medications and home remedies for foot problems </li></ul>

181.
End of DM