What do we know about diabetes as far as the evidence goes ……

1. What do we know about diabetes as far as the evidence goes…… REVIEW PRESENTATION RAQUEL GAROFANO R4 MFYC AXARQUÍA

2. The word ‘diabetes’ refers to a group of disorders with a number of common features, of which raised blood glucose is the most evident. ● Type 1 diabetes ● Type 2 diabetes ● Gestational diabetes (diabetes of pregnancy).

3. DIABETES TYPE 1

4. A condition of deficiency of insulin secretion from the pancreas, usually due to auto-immune damage of the insulin producing cells. • The clinical condition is generally recognized on the basis of : -----diabetes (high blood glucose levels) occurring in mainly younger and thinner people. -----in the absence of other precipitating causes. DEFINITION WORLD HEALTH ORGANIZATION

5. DIABETES TYPE 2 • A degree of high plasma glucose levels sufficient to put the individual at risk of the specific (microvascular) complications of diabetes. • If they do not have Type 1 diabetes or other medical conditions or treatment suggestive of secondary diabetes. WORLD HEALTH ORGANIZATION

6. DRAFTING RECOMMENDATIONS • Ia Evidence from meta-analysis of randomised controlled trials. • Ib Evidence from at least one randomised controlled trial. • IIa Evidence from at least one controlled study without randomisation. • IIb Evidence from at least one other type of quasi-experimental study. A B

7. DRAFTING RECOMMENDATIONS • III Evidence from non-experimental descriptive studies, such as comparative studies, correlation studies and case control studies. • IV Evidence from expert committee reports or opinions and/or clinical experience of respected authorities. • DS Evidence from diagnostic studies. • NICE Evidence from NICE guidelines or health technology appraisal programme. C D DS NICE

8. DIAGNOSIS- D • Single diagnosticlaboratoryglucosemeasurementover 200 mg / dl + SYMPTOMS. ( Weightlost, increase in urinaryfrequency , polydipsia) • Twodiagnosticlaboratoryglucosemeasurements of: -Fastingglucose>126 mg /dl -Glucosetwohoursafter 75 mg of glucoseintake > 200 mg / dl -HbA1 > 6.5% TYPE 1: • Specific auto-antibodies. • Measure of C-peptidedeficiency

9. CARE PROCESS-D INDIVIDUAL CARE PLAN: • Diabetes education. (Nutritional advice) • Insulin therapy. • Self-monitoring of glucose. • Arterial risk factor assestmment and management. • Means and frequency of communication with the professional care team. • Follow-up consultations including next annual review

10. DIABETES EDUCATION • Programme of structured diabetes education covering all major aspects of diabetes self-care: A • Flexible so that they can be adapted to specific educational, social and cultural needs D • Designed and delivered by members of the multidisciplinary diabetes team. D

11. SELF MONITORING OF GLUCOSE- D • Self-monitoring skills should be taught close to the time of diagnosis. • Self-monitoring results should be interpreted in the light of clinically significant life events. • It should be performed using meters and strips chosen by adults with diabetes to suit their needs. (Low blood requirements, fast analysis times and integral memories.) • Structured assessment of self-monitoring skills should be made annually.

12. OPTIMAL SELF MONITORING FREQUENCY- D • Characteristics of an individual’s blood glucose control. • The insulin treatment regimen. • Personal preference in using the results to achieve the desired lifestyle.

13. OPTIMAL TARGETS- D pre-prandial blood glucose level of 70-130 mg/dl post-prandial blood glucose level of less than 180 mg/dl.

14. DIETARY MANAGEMENT • Nutritional information sensitive to personal needs and culture. D • Nutritional information should be offered individually. D • It should include advice from professionals with specific and approved training. D • The hyperglycaemic effects of different foods a person wishes to eat should be discussed in the context of the insulin preparations chosen to match those food choices. A

15. DIETARY MANAGEMENT-D • The choice of content, timing and amount of snacks between meals or at bedtime should be agreed on the basis of informed discussion. • Information should also be made available on: • Effects of different alcohol-containing drinks on blood glucose and calorie intake. • Use of high-calorie and high-sugar ‘treats’. • Use of foods of high glycaemic index.

16. DIETARY MANAGEMENT-D Modificationsaccordingto: • Excessweight and obesity. • Underweight. • Eatingdisorders. • Raisedbloodpressure. • Renal failure.

17. DIETARY RECOMMENDATIONS • High-fibre, low glycaemic index sources of carbohydrate in the diet, such as fruit, vegetables, wholegrains; include low-fat dairy products and oily fish; and control the intake of foods containing saturated and trans fatty acids. • Target, for people who are overweight, an initial body weight loss of 1–5 %. • Discourage the use of foods marketed specifically for people with diabetes.

18. PSHYSICAL ACTIVITY • It can reduce their enhanced arterial risk in the medium and longer term. C • They should be offered information about: D • Appropriate intensity and frequency of physical activity. • Role of self-monitoring of changed insulin and/or nutritional needs. • Effect of activity on blood glucose levels when insulin levels are adequate. ( Likely fall ).

19. PHISICAL ACTIVITY- D • Effect of exercise on blood glucose levels when hyperglycaemic and hypoinsulinaemic appropriate adjustments of insulin dosage and/or nutritional intake for exercise and post-exercise periods, and the next 24 hours • Interactions of exercise and alcohol

20. CLINICAL MONITORING OF GLUCOSE-D • Clinical monitoring of blood glucose levels by high-precision DCCT*-aligned methods of haemoglobin A1c (HbA1c) should be performed every 2–6 months, depending on: • Achieved level of blood glucose control. • Stability of blood glucose control. • Change in insulin dose or regimen.

21. GLUCOSE CONTROL ASSESSMENT LEVELS • Maintaining a HbA1c below 7.5% is likely to minimize their risk of developing diabetic eye, kidney or nerve damage in the longer term. B • If there is evidence of increased arterial risk (raised albumin excretion rate, features of the metabolic syndrome, or other arterial risk factors), approaching lower HbA1c levels (for example, 6.5% or lower) may be of benefit to them. NICE • When the target HbA1c levels are not reached in the individual- Any improvement is beneficial in the medium and long term.B

22. TREATMENT

23. ORAL GLUCOSE LOWERING DRUGS should generally not be usedin the management of adults with type 1 diabetes D

24. ORAL GLUCOSE CONTROL THERAPIES Metormine secretagogues acarbose

25. METFORMINE-Ia • Greater benefit than chlorpropamide, glibenclamide, or insulin for any diabetes-related outcomes, and for all-cause mortality. • Overweight participants assigned to intensive blood glucose control with metformin showed a greater benefit than overweight patients on conventional treatment. • Monotherapy with metformin produced significantly greater improvements in glycaemic control (i.e. HbA1c and FPG/fasting blood glucose (FBG)) when it was compared with placebo, diet and sulfonylureas.

26. METFORMINE-Ia • Significant difference in terms of body weight/BMI reduction favouring metformin monotherapy when compared with sulfonylureas, glitazones and insulin therapies. • Non-significant differences in terms of lipid profile were found when metformin was compared with placebo or metiglinides. • When compared to diet, metformin significantly reduced total cholesterol (TC).

27. METFORMINE • When compared to an α-glucosidase inhibitor, metformin significantly increased TC.Ia • In a comparison of metformin against insulin, significant benefits for metformin were found in terms of total and LDL-C levels but not high-density lipoprotein cholesterol (HDL-C). Ia

28. INSULINE SECRETAGOGUES-Ia • Metiglinides (repaglinide and nateglinide) vs placebo: • Produced a significantly greater glycaemic control and a higher incidence of hypoglycaemic events when compared with placebo. • No differences were found in terms of body weight and lipid profile.

29. INSULINE SECRETAGOGUES-Ia • Repaglinide vs nateglinide: • Repaglinide was more effective than nateglinide in reducing HbA1c and FPG values. • A greater weight gain was seen in repaglinide-treated patients. • Hypoglycaemic events were more frequently reported by patients receiving repaglinide.

30. INSULINE SECRETAGOGUES-Ia Metiglinides vs sulfonylureas • Metiglinides failed to demonstrate better glucose control and led to a similar number of hypoglycaemic events. • No significant differences were observed in terms of lipid profile and body weight reduction.

31. INSULINE SECRETAGOGUES-Ia Gliclazide modified release version vs glimepiride: • Both interventions were equally effective in terms of glycaemic control (alone or in combination with metformin or alpha-glucosidase inhibitors). • Gliclazide MR had a better safety profile than glimepiride.

32. INSULINE SECRETAGOGUES-Ia Nateglinide + metformin vs gliclazide + metformin • No significant difference was seen between the groups in terms of HbA1c Glimepiride + metformin vs glimepiride vs metformin • Combination treatment was more effective than either drug alone in terms of glycaemiccontrol. • Combination therapy was more effective than either drug in reducing TC levels.

33. ACARBOSE-Ia • Failed to demonstrate better glycaemic control when compared with other oral agents. • It did not demonstrate superiority over other oral agents when lipid profile and body weight were evaluated. • Reports of adverse effects were higher with acarbose. (GI complaints: Flatulence).

34. GLITAZONES: pioglitazone and rosiglitazone-Ia • Alternative to treatment with a combination of metformin and a sulfonylurea – is not recommended except for those who are unable to take metformin and a sulfonylurea in combination because of intolerance or a contraindication to one of the drugs.

35. Exenatide: GLP-1 mimeticsIb • Indicated for treatment of Type 2 diabetes mellitus in combination with metformin and/or sulphonylureas in patients who have not achieved adequate glycaemic control on maximally tolerated doses of these oral therapies. • SC. 5 mcgtwicedailyforonemonth; thenit can beincreasedto 10 mcgtwicedaily. • 1 h beforemeals.

36. ADVERSE EFFECTS- Ia The main differences across all the different treatment groups were: • The high frequency of gastrointestinal (GI) complaints reported by metformin-treated patients. • The high frequency of hypoglycaemic events reported by sulfonylurea-treated patients. • The high number of episodes of oedema reported by glitazone-treated patients. • The high number of cases of upper respiratory infection in patients treated with metiglinides.

37. Oral agents and Insulintherapy • Patients receiving a combination treatment with insulin (NPH or pre-mixes) and metformin or a sulfonylurea showed significantly lower HbA1c levels when compared to those treated with insulin monotherapy. • Insulin–OHA combination therapy was associated with a significantly lower insulin dose compared to insulin monotherapy. • There is no difference in Well-being, quality of life or treatment satisfaction.

38. INSULIN THERAPY • Access to the types of insulin they find allow them optimal well-being. A • Cultural preferences need to be discussed and respected. D • Multiple insulin injection regimens, in adults who prefer them, should be used as part of an integrated package of which education, food and skills training should be integral parts. A

39. INSULIN THERAPY • Meal-time insulin injections should be provided by injection of unmodified (‘soluble’) insulin or rapid-acting insulin analogues before main meals. D • Rapid-acting insulin analogues should be used as an alternative to meal-time unmodified insulin: A • Where nocturnal or late inter-prandial hypoglycaemia is a problem. • In those in whom they allow equivalent blood glucose control without use of snacks between meals and this is needed or desired.

40. INSULIN THERAPY -D • Basal insulin supply should be provided by the use of isophane (NPH) insulin or long-acting insulin analogues (insulin glargine). • Isophane(NPH) insulin should be given at bedtime. • If rapid-acting insulin analogues are given at meal times, the need to give isophane (NPH) insulin twice daily (or more often) should be considered.

41. INSULIN THERAPY-D • Long-acting insulin analogues (insulin glargine) should be used when: • Nocturnal hypoglycaemia is a problem on isophane (NPH) insulin. • Morning hyperglycaemia on isophane (NPH) insulin results in difficult daytime blood glucose control. • Rapid-acting insulin analogues are used for meal-time blood glucose control.

42. INSULIN THERAPY-D Twice-daily insulin regimens should be used by those adults who consider number of daily injections an important issue in quality of life. • Biphasic insulin preparations (pre-mixes). • Advantage to those prone to hypoglycaemia at night. Such twice daily regimens may also help: • Those who find adherence to their agreed lunch-time insulin injection difficult. • Adults with learning difficulties who may require assistance from others.

43. INSULIN THERAPY-D • Adults with erratic and unpredictable blood glucose control rather than a change in a previously optimised insulin regimen, the following should be considered: • Resuspension of insulin and injection technique. • Injection sites • Self-monitoring skills. • Knowledge and self-management skills • Nature of lifestyle • Psychological and psychosocial difficulties • Possible organic causes such as gastroparesis.

44. INSULIN THERAPY-NICE • Continuous subcutaneous insulin infusion (or insulin pump therapy) is recommended WHEN: •Multiple-dose insulin therapy (including, where appropriate, the use of insulin glargine) has failed. • Those receiving the treatment have the commitment and competence to use the therapy effectively.

45. INSULIN DELIVERY-D • Access to the insulin injection delivery device they find allows them optimal well-being, often using one or more types of insulin injection pen. • Insulin injection should be made into the deep subcutaneous fat. To achieve this, needles of a length appropriate to the individual should be made available.

46. INSULIN DELIVERY-D • Abdominal wall is the therapeutic choice for meal-time insulin injections. • Isophane (NPH) insulin, may give a longer profile of action when injected into the subcutaneous tissue of the thigh rather than the arm or abdominal wall. • Use one anatomical area for the injections given at the same time of day, but to move the precise injection site around in the whole of the available skin within that area.

47. HYPOGLYCAEMIA • Specific education on the detection and management of hypoglycaemia in adults with problems of hypoglycaemia awareness should be offered. D • Adults should be informed that late post-prandial hypoglycaemia may be managed by appropriate inter-prandial snacks or the use of rapid-acting insulin analogues before meals. D • Any available glucose/sucrose-containing fluid is suitable for the management of hypoglycaemic symptoms or signs in people who are able to swallow. A

48. HYPOGLYCAEMIA • Adults with decreased level of consciousness due to hypoglycaemia who are unable to take oral treatment safely should be:D • Given intramuscular glucagon by a trained user (intravenous glucose may be used by professionals skilled in obtaining intravenous access). • Monitored for response at 10 minutes, and then given intravenous glucose if the level of consciousness is not improving significantly. • Then given oral carbohydrate when it is safe to administer it, and placed under continued supervision.

49. HYPOGLYCAEMIA • Review should be made of the following possibly contributory causes: D •Inappropriate insulin regimens (incorrect dose distributions and insulin types). • Meal and activity patterns, including alcohol. • Injection technique and skills. • Injection site problems. • Possible organic causes including gastroparesis. • Changes in insulin sensitivity (the latter including drugs affecting the renin-angiotensin system and renal failure). • Psychological problems. • Previous physical activity. • Lack of appropriate knowledge and skills for self management.

50. ARTERIAL RISK- C Should be assessed annually: • Albumin excretion rate. • Smoking. • Blood glucose control. • Blood pressure. • Full lipid profile (including HDL and LDL cholesterol and triglycerides). • Age. • Family history of arterial disease. • Abdominal adiposity.