1. Diabetes mellitus Is a group of metabolic diseases characterized by increased blood glucose level resulting from defect in insulin secretion, action or both Major source of glucose is GI and formation of glucose by liver

2. DM introduction Insulin is a hormone that controls glucose by regulating production and storage of glucose; cells may stop responding to insulin or pancreas may stop producing insulin, leading to hyperglycemia. DM has devastating consequences: leading cause of non- traumatic amputation, blindness, and end-stage renal diseases; leading cause of death because of cardiovascular complications; high hospitalization rate. Costs continue to increase primary goals of treatment: control glucose level; prevent acute and long-term complications, develop self-care management skills

3. Classification  Type 1 DM, Beta cells are destroyed by autoimmune process, so little or no insulin is produced, insulin injections are required to control blood glucose;  Type 2 DM, decreased sensitivity of cells and impaired beta cells;  occurs in older, 30 or greater and obese, treated with diet and exercise if high glucose persists antidiabetic agents are added, in some cases insulin may be required  Complications occur in both

4. DM PATHOPHYSIOLOGY  Insulin is an anabolic hormone that  Transports and metabolizes glucose for energy  Stimulates storage of glucose in the liver, glycogen  Signals liver to stop release of glucose  Enhances storage of fat in adipose tissue  Accelerates transport of amino acids into cells  Inhibits the break dawn of stored glucose, protein and fat  Glucagon is secreted by alpha cells when blood glucose level decreases and stimulate liver to release stored glucose

5.  Both insulin and glucagon maintain a constant blood glucose level  The liver produces glucose through glycogenolysis, break dawn of glycogen;  gluconeogenesis, break dawn of non-CHO substances including amino acids

6. DM pathophysiology type 1  Combined genetic, immunologic and environmental (viral) may contribute to beta cells destruction; people do not inherit type 1 but rather a genetic predisposition or tendency  Autoimmune response, in which antibodies are directed against normal tissues;  Plus, viral or toxins may contribute; as a result there is decreased in insulin production and unchecked glucose production by the liver, and hyperglycemia  Glucose can not be stored in liver and contribute to postprandial (after meal) hyperglycemia  If concentration of blood glucose exceeds renal threshold 180- 200 mg, glycosuria, this is associated by excessive loss of fluid and electrolytes, osmotic diuresis

7. DM pathophysiology type 1  Because of no insulin, glycogenolysis and gluconeogenesis occur; break dawn of fats results in increased production of ketone bodies  Type II: The 2 main problems are insulin resistance and impaired insulin production  However there is enough insulin to prevent break dawn of fat and formation of ketone bodies  It may discovered incidentally; Primary treatment: diet, exercise, if not successful antidiabetic agents, in some cases insulin may be required; type 2 can be prevented or delayed by diet and exercise.

8. DM pathophysiolog type 2  Gestational DM  Hyperglycemia during pregnancy; because of placental hormones that cause insulin resistance check up for women at high risk  Primary treatment dietary modification and blood glucose monitoring, if persists insulin therapy; the goal is 105 mg/dL before meal or 130 mg/L or less 2 hrs after meals  Usually women with GDM return to normal, however, those with high GDM may develop type 2 later; diet modification and exercise are essentials for prevention

9. DM / assessment  Three Ps: polyuria, polydipsia, polyphagia (increased appetite resulting from catabolic state  Other symptoms\; fatigue, weakness, sudden vision changes, tingling or numbness, dry skin, wounds that slow to heal; wt loss in type 2 DM  Criteria for diagnosis:  causal plasma, at any time, of > than 200 mg /dL (11.1 mmol/L)  Fasting no caloric intake for at least 2 hrs, equal or greater than 126 mg /dL  2-hr post load glucose of 200 mg /dL using WHO guidelines containing 75 gram of anhydrous glucose dissolved in water  Assess for complications

10. Management  The main goal is to achieve normal glucose level (euglycemia) without hypoglycemia, to control complications, while maintaining a high quality of life  Nutritional therapy  Exercise  Monitoring  Pharmacologic therapy  Education  Diabetes management involve constant assessment and modification of treatment plan  Patient and family education is essential because the patient is responsible and must manage the therapeutic regimen

11. Nutritional therapy Foundation of DM management is nutrition, meal planning, wt control Objectives are control total caloric intake, maintain a reasonable body wt, control blood glucose, and normalization of lipids and BP, to prevent cardiovascular diseases To achieve these objectives the following goals must be met: 1. Providing all essential food components (vitamins and minerals) 2. Achieving and maintaining a normal body wt 3. Prevent daily fluctuations in blood glucose with normal glucose level 4. Decreasing lipids level; address individual nutritional needs; maintain pleasure of eating

12. Nutritional therapy  In insulin case, consistency in time interval between meals is important  For obese patients, wt loss is the key of treatment  Over weight is a BMI of 25 – 29; obesity is defined as 20% above ideal  or a BMI of 30 or greater; obesity increases resistance to insulin  Nutritional Therapy  Meal planning and related teaching:  Consider patients’ food preferences, usual eating times and cultural background  Advances in insulin therapy permits greater flexibility in timing and content of meals; intensive insulin therapy

13. Nutritional therapy  First step, assessment of diet history and eating habits; assessment of the need for wt loss, gain or maintenance  Clinical dietitians do teaching about;  Consistent eating habit  Relationship of food and insulin  Provision of individualized meal plan  In-depth follow up education focuses on:  Skills required for eating at restaurant, reading food labels, and adjusting a meal according to exercise, illness and special occasions

14. NT caloric requirements  Caloric-controlled diet: calculate energy needs based on age, gender, ht, wt, and physical activity; e.g. 1-2 pound loss / week require a 500-1000 calories cut daily; then a meal plan is developed; caloric distribution  The meal plan focuses on % of calories that come from CHO, protein and fats; CHOs have the greatest effect because a) they are digested more quickly and diverted to glucose rapidly  50-60% of calories should come from CHOs, 20-30% from fat and 10-20% from protein; the CHOs should come from whole grains; all CHOs food should be eaten but moderately, that contain glucose (sucrose) or starch  Food high in sucrose should reflect 10% of total CHOs because they rich in fat And lacks vitamins minerals, and fiber

15. NT caloric requirement  Carbohydrate counting is a nutritional approach for glucose management; in which all food sources should be considered; 100% of CHOs are converted to glucose, but 50% of protein converted to glucose  Methods of CHOs counting: counting grams of CHOs; another method is measuring servings; one serving = 15 grams of CHOs; reading labels is important in counting  FATs: reducing total calories from fat to 30% from the total caloric intake; and from saturated fat to 10%;  limit cholesterol to less than 300 mg / day; this approach may reduce risk of CADs;  use non-animal sources of proteins, legumes, whole grain  Limit protein intake in patients with renal diseases

16. FIBER  may lower cholesterol and low-density lipoprotein; may also improve blood glucose level;  soluble fiber play more role than insoluble fiber in lowering blood glucose and lipid ; it slows stomach emptying and food movement—slowing absorption of glucose from food containing soluble fiber;  soluble is found in oat, legumes, some fruit;  insoluble in whole grains and vegetables, increases stool bulk and preventing constipation, reduces wt,  ideally 25 gm of fiber should be ingested daily;  there may be a need to adjust insulin dose to prevent hypoglycemia if fiber taken suddenly  Abdominal fullness, cramps, nausea, constipation if fluid intake is low; Introduced gradually

17. Food classification systems  Are systems in which foods are grouped according to certain characteristics of calories, composition of foods, and effect on glucose level Exchange lists for meal planning: There are 6 main exchange lists: bread/starch, vegetable, milk, meat, fruit and fat Foods included on one list contain equal number of calories; and equals of grams of fat protein and CHOs Meal plans are based of patients’ preferences and recommended number of calories; see Table 41-2 P. 1204. Nutritional labels: reading food labels is an important skills; patients can adjust their insulin; e.g. 1 unit of insulin for 15 gram of CHOs

18. Food guide pyramid  Is commonly used for patients with type 2 DM  Food pyramid consists of grains, vegetables, fruits, milk and dairy products, meats and beans  Food lowest in calories and fat and high in fiber make the basis of the diet  50-60% of caloric intake should be from the first 3 groups  May cause fluctuations in blood glucose  Used as a first step teaching  Glycemic index: is used to describe how much a given food increases blood glucose level; under studies; patients can develop their glycemic index.

19. General recommendations  Combine starch food with fat and protein-containing foods  Eat raw and whole foods than chopped, pureed and cooked  Eat Whole fruits than juice  Eat food with sugars with slowly absorbed food  These lower glycemic response

20. Other dietary concerns  Alcohol is absorbed before nutrients; can be converted to fat / DKA  May lead to hypoglycemia/ decreasing the physiologic response: gluconeogenesis  May negatively affects patients ability to recognize and treat hypoglycemia  Consumed food with alcohol  Be aware of sweeteners: nutritive sweeteners, have fructose / fruit sugar has calories; nonnutritive are sugar free no calories – approved by FDA  Be aware of food labels: sugar free not calories free; dietetic includes calories

21. Exercise  Benefits:  decreases glucose by increasing glucose uptake and improving insulin utilization  Resistance training increase lean muscle mass thus increasing resting metabolic rate  Decreases wt and eases stress and improves feeling of well- being  Protect heart by increasing HDL, decreasing total cholesterol and triglycerides

22. Exercise / precaution  In patients with glucose level of 250 mg/dl and have ketones in urine start exercise after negative urine test and blood glucose near normal; Exercising with high glucose level increases glucagon, GHs and catecholamines, increase BG  Exercise decreases physiologic insulin but not in those receiving insulin, 15grams of CHOs before exercise; adjust insulin dose;  if do exercise 1-2 hrs after a meal no need for a snack;  to prevent post exercise hypoglycemia provide snack; monitor BG more frequently  Patients with type 2 DM exercise with dietary modification improves glucose level, however those who are taking medications may need snack

23. Exercise / recommendation  Exercise at the same day when glucose at peak level, everyday, same amount  Altered exercise training in patients with DM complications, hemorrhage in retinopathy because of increased BP; angina, neuropathy  Avoiding trauma to lower extremities is important  Recommend exercise stress test for patients aged greater than 30 years with 2 or more risk factors for hear disease

24. Monitoring glucose level Self monitoring of BG, SMBG  Is a cornerstone of DM management  Doing SMBG and knowledge how to respond and adjust their treatment may achieve optimal BG level this,  Allows prevention of hypo and hyperglycemia; normalizing BG; reduces risks of long term complication  Various methods are available  Must match patients skills and condition  May be subjected to erroneous readings because Blood too small; outdated or damaged strips; improper cleaning and maintenance  Role of nurse to provide teaching  Every 6-12 months compare with lab measured BG

25. SMBG candidates  Is useful for every one with DM for self-care  A key component for intensive insulin therapy, 2-4 per day and during pregnancy  A motive for patients managed by diet and exercise; also for  Patients with unstable diabetes; hypoglycemia without warning signs; a tendency to develop sever ketosis or hypoglycemia  Frequency: for patients on insulin 3 times before meals; for not receiving insulin 2-3 times per week; for all whenever hyper or hypoglycemia is suspected

26. SMBG  Keep records or logs for patterns  IN Type 2: do testing before and 2 hrs after largest meal;  If insulin by pump or at bed time; test at 3.00 am  Compliance issue  Continuous glucose monitoring system to determine that the treatment is adequate over 24 hours  Glycatd hemoglobin; glycosylated hemoglobin, HgA1c  Urine glucose testing; testing for ketones

27. Pharmacologic therapy insulin therapies and insulin preparation  In type 1 for life; In type 2 either for a long period or temporarily during infection, illness, pregnancy  An accurate monitoring is essential to determine the dose and frequency  Insulin preparation vary according to time course of action, source, manufacturer  Human insulin preparations have a shorter duration of action than insulin from animal sources Rapid acting insulin, lispro-humalog, and aspart-novolog; onset 10-15; peak, 60-90 minutes; duration 2-4 hours producing rapid effect; instruct patients to eat 5-15 minutes after injection, patients may require long acting insulin

28. Insulin continues  Short-acting insulin, regular insulin: marked R on the bottle; onset 30 minutes – 1 hr; peak, 2-3 hrs; duration 4-6 hrs; is a clear solution administered 20-30 minutes before meal e. g. humlin R, novolin R  Intermediate acting insulin, NPH insulin (neutral protamine hagedorn, lente insulin); white and cloudy, onset 2-4 hrs; peak, 4-12 hrs; duration, 16-20 hrs; taken 30 minutes before meal;  Long acting insulin, humulin ultrlente, has a long slow sustained action; onset, 6-8 hrs; peak 12-16 hrs; duration 20-30 hrs  Peakless, basal or very long acting insulin, glargine (lantus); absorbed very slowly over 24 hrs; given once a day, can not be mixed with other insulin; should be given at the same time every day

29. Insulin regimens  Conventional regimen: simplified 1-2 injections per day; a mixture of short and intermediate acting insulin; should not vary meal pattern; for patients with limited self-care  Intensive regimen: a complex regimen to achieve much control; change doses according to changes in eating and activity; 3-4 doses a day; reduces risk of DM complications; but hypoglycemia is a complication; not all are candidates

30. Complications  :  A local allergic reaction 1-2 hrs after injection; appeared in the beginning stage  Systemic allergic reaction local skin reaction spread to generalized urticaria; treatment by desensitization, gradually increase doses  Lipodystrophy: lipohypretrophy at sites of injection; as pitting due to loss of fat; or fibrofatty mass  Insulin resistance because of obesity—managed by giving a more concentrated insulin, U500 or by prednisone to block the production of antibodies  Morning hypoglycemia—insulin waning; dawan phenomenon; somogyi effect

31. Methods of insulin delivery  Insulin pump: Continuous subcutaneous insulin infusion ;  3-ml syringe; with needle or catheter; should be changed every 3 days; rate of delivery, 0.5 – 2 units / hr;  PTs calculate unit necessary for CHOs needed;  side effects, sudden disruption, inconvenience; need to assess BG several times / daily  Insulin pens; for injecting only one type of insulin  Traditional methods

32. Oral antidiabetic agent  For type 2 DM, not responding to nutrition and exercise  Effectiveness may be enhanced by multi-dose multiple medications  Sulfonylureas: stimulating pancreas to secrete insulin, improves insulin action, decreases glucose production by liver; side effects GI and skin reaction; diabinese, tolinase, orinase (first generation); seconf generation include glucatrol, amyral  Non-sulfonylurea: action the same, has fast action and fast duration; contraindicated in type 1; prandin  Biguanides; metformin (glucophage); facilitates action of insulin, can be used with others, prandin

33. Oral Hypoglycemic agents  Alpha-glucosidase inhibitors, acarbose (precose) and miglitol (glyset); act by delaying absorption of glucose  Thiazolidiones, rosiglitazone (avandia), pioglitazone (actos) stimulate insulin receptor; used alone or in combination.  Read Table 41-6; P. 1216

34. Nursing management patient education DM a disease that requires life time self-management; must learn daily self-care to control BG and preventive measures Teach the seven tips for managing DM HEALTHY EATING; BEING ACTIVE; MONITORING; TAKING MEDICATIONS; PROBLEM SOLVING; REDUCINGS RISKS HEALTHY COPING TEACHING SURVIVAL SKILL Ps. 1217-1222 Plus; foot care, eye care, general hygiene; risk factor management, BP, lipid levels, normalizing BG; methods of insulin delivery

35. Patient education  Assessing readiness to learn; assess coping methods  Determining teaching methods; practice skills booklets and video tapes; teaching/educational material according to learning needs, and patients condition  Implementing phase; teaching content pp 1217-1222

36. Acute complications Hypoglycemia  BG level less than 50-60 mg / dl (2.7-3.3 mmol / L); gerontologic consideration  Can be adrenergic symptoms; stimulation of SNS in mild hypoglycemia; sweating, tremor, tachycardia, palpitation, Or CNS symptoms in moderate hypoglycemia; decreased concentration, confusion, headache slurred speech memory lapses  MANAGEMENT; 15 grams of fast acting CHOs; (3-4 glucose tablet, fruit juice, 6-10 hard candies, 2-3 teaspoon sugar or honey) reassess after 15 minutes if not near normal; repeat treatment; teach to carry simple sugar, not to eat high CHO with high fat, this slows absorption of glucose; In coma give 1 mg of glucagon (subcutaneous or IM) onset with 8-10 minutes lasting 27 minutes; or 25-50 ml of dextrose IV; irritating to veins

37. Diabetic ketoacidosis  A disorder in metabolism of CHO, protein, fat  Main clinical features are: hyperglycemia, dehydration and electrolyte loss, acidosis  Osmotic diuresis lead to dehydration ay loose 6.5 liter and electrolytes; Lipolysis in fatty acids glycerol; fatty acids convert to ketones; metabolic acidosis  Manifestations: GI symptoms and fruity odor breath with hyperventilation, Kussmaul respiration; mental changes;  BG 300-800; low sodium bicarbonate; low Na and K, low pH  Prevention: teach sick day rules, Chart 41-9; P. 1226  Management: rehydration, restoring electrolytes; reversing acidosis, with continuous IV insulin read the details Ps. 1226- 1227.

38. Hyperglycemic hyperosmolar nonketotic syndrome  A serious condition: hyperosmolarity and hyperglycemia  Alteration in sensorium; no acidosis or ketosis  The defect is insulin resistance; mainly in type 2  Causes osmotic diuresis-loss of fluid and electrolyte; fluid from intracellular to extracellular; glycosuria, dehydration, hypernatremia  Signs of hypotension, decreased sense of awareness, mortality 10-40  Management: Fluid replacement, correction of electrolytes, and insulin therapy,  Glucose administered after glucose level becomes 250-300  Treat underlying cause; Nursing; monitoring, prevention of injury, cardiopulmonary assessment

39. Nursing diagnoses  Risk for fluid volume deficit  Imbalanced nutrition  Potential self-care deficit  Knowledge deficit  Anxiety related to fear and misconception  Potential complications: -fluid overload, pulmonary edema, heart failure; -Hypokalemia; -Hyperglycemia and ketoacidosis; - Hypoglycemia;  -Cerebral edema

40. Complications of DM  Macrovascular complications Accelerated Atherosclerosis occurs in medium to large vessels resulting in CAD, cerebrovascular, and peripheral vascular diseases Aggressive management of risk factors

41. Microvascular complications are characterized by thickening of capillary membrane basement that surrounds endothelial cells  Diabetic retinopathy: caused by changes in small blood vessels in retina, retina receives images and sends information to brain  Has 3 stages nonproliferative, preproliferative, proliferative  Changes appear after 20 years; changes in the microvasculature include microaneurysms intra- retinal hemorrhage hard exudates, and focal capillary closure  The greatest threat to vision is proliferative; proliferation of blood vessels into vitreous; visual loss is caused by vitreous hemorrhage and retinal detachment floaters or cobwebs in the visual fields indicate hemorrhage  Prevention / slow of retinopathy: control glucose, BP, and smoking cessation

42. RETINOPATHY  Management: Laser photocoagulation; a major hemorrhage may be treated by vitrectomy Nursing frequent check on BG, eye and vision, early detection is essential; patient teaching and assistance in coping

43. Nephropathy  Consistent elevation of BG for a significant period affects kidney’s filtration mechanism; lead to leak of protein, increased pressure in blood vessels  Earliest sign is albumin in urine, microalbuminuria  Creatinine BUN  Management: control BG, hypertension, prevent or rigorous treatment of UTI; avoid toxic substances, medications, low salt and protein diet  If microalbuminuria exceeds 30 mg/24 hrs on 2 consecutive tests, use ACE inhibitor  If end-stage renal disease, dialysis and transplantation

44. Neuropathy  Is a group of diseases that affect all type of nerves, autonomic, peripheral, spinal  Capillary basement membrane thickening and capillary closure may be present; Demyelinization affects nerve conduction  Peripheral neuropathy: paresthesias, burning sensation, decrease in proprioception, decrease pain and temp sensation; control BG and pain medication  Autonomic neuropathy affects a wide range of systems, orthostatic hypotension, GI constipation and nocturnal diarrhea, painless MI, sexual dysfunction  Management: manage risk factors; and underlying condition

45. Foot and leg problem  Complications of DM that increase risk for foot problem: neuropathy-loss of pain sensation and fissuring; peripheral vascular disease-poor circulation; immunocompromise-DM impairs leukocytes to destroy bacteria  Management: teach foot care skins chart 41-10, P. 1237  Daily inspection  Properly bathing, drying and lubricating  Wearing closed toe shoes  Trimming toe nails  Reduce risk factors that contribute to peripheral vascular diseases  Avoiding home remedies

46. DM and Surgery  BG level increases during period of stress because of increased level of stress hormones  Preoperative and postoperative period: frequent monitoring of BG  Assess for cardiovascular complication, adequate nutrition and BG control is essential for wound healing; Involve patients in the plan of care, self-care  Hyperglycemia may occur during hospitalization because of:  -change in treatment plan  -medication; prednisolone  -IV glucose to administer antibiotics; -Vigorous treatment of hypoglycemia; -Inappropriate withholding of insulin  -Mismatched timing of meals and insulin

47. Management  BE sure to correct all of these factors  Approximate home plan of management  BG monitoring, vital sign  Short acting insulin may be needed to prevent post prandial hyperglycemia  Antibiotics with N/S  Treatment of hypoglycemia; 15 gm of CHO, or.5 – 1 ampule of 50% dextrose IV repeat after 15 minutes  read chart 41-12, P. 1240.  Hypoglycemia may occur because of overuse of insulin and delayed meals

48. Alterations in diet / surgery  In NPO change doses of insulin, administration of insulin is an important nursing action  For extended NPO 24 hrs glucose testing and insulin should be performed at regular intervals 4 times a day  Monitor enteral feeding, contains simple CHO, also parenteral feeding; adjust insulin doses  Skin and dental care  Foot care  Teach patients about diet, skin and foot care  Avoid emotional stress  Gerontologic considerations