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An introduction to diabetes
- 3. share our experiences of management of diabetes in local perspective. early identify the diabetic pts and complications of DIABETES motivate patients to achieve targets understand the advantages of treatment and disadvantages of not achieving targets attain Hb A1c less than 7%
- 5. Principal Aims in Diabetes Care Medical/Diabetes Care Team-orientated ( A)Promote overall well-being and a normal life expectancy (B) Prevent/delay the onset of cardiovascular disease (C)Manage diabetes-related complications early and aggressively as appropriate (D) Minimize hypo glycaemia and adverse drug event rate (E) Provide specialist care at optimal time points Patient/Care-orientated (1)To acquire the education and skills to self-manage (2) Maintain an optimal level of physical and cognitive function (3) To be confident of access to services and support where necessary to manage their DIABETES
- 6. Definition Diabetes mellitus is a complex metabolic disorder characterised by persistent hyperglycaemia due to relative or absolute deficiency of insulin or insulin resistance
- 7. IS Diagnostic Criteria???? FPG (Fasting Plasma Glucose) >126mg/dl RPG (Random Plasma Glucose) >200mg/dl OGTT (Oral Glucose Tolerance Test)2hr pp >200mg/dl(75GM GLUCOSE)
- 8. AACE ADA GOAL GOAL Pre- <110 90-13 meal mg/dl 0 Mg/dl 2 hour <140 <180 PP Mg/dl Mg/dl
- 9. TYPES of DIABETES Type 1 Diabetes: 5 to 10% patients have type 1 diabetes. Type 2 Diabetes: 90 to 95% patient have type 2 diabetes. Other Types. GDM IGT IFG
- 10. Characteristic Type 1 ( 10% ) Type 2 Onset (Age) Usually < 30 Usually > 40 Type of onset Abrupt Gradual Nutritional status Usually thin Usually obese Clinical symptoms Polydipsia, polyphagia, Often asymptomatic polyurea, Wt loss Ketosis Frequent Usually absent Endogenous insulin Absent Present, but relatively ineffective (in. resistance) Related lipid Hypercholesterolemia Cholesterol & triglycerides abnormalities frequent, all lipid fractions often elevated; carb elevated in ketosis induced hyper TG common Insulin therapy Required FOR WHOLE Required in only 20 - 30% LIFE(DEPENDS ON INSULIN) of patients FOR CONTROL Hypoglycemic drugs Should not be used Clinically indicated Diet Mandatory with insulin Mandatory with or without drug COMPLICATIONS AFTER 5 40-50% AT DIAGNOSIS YEARS(MAJORITY)
- 11. DIFFERENCE TYPE 2 (TYPE II, TYPE 1(TYPE I, IDDM) NIDDM) YOUNGER AGE OVER 35 , ANY AGE ABRUPT ONSET INSIDOUS ONSET NO FAMILY HIST. SIGNIFICANT FAMILY HIST. VIRUS,TOXINS, OVEREATING ATTITUDE AUTOIMMUNITY OVERWEIGHT MINIMAL OR ABSENT INSULIN DELAYED OR REDUCED INSULIN THIN OR CATABOLIC STATE OBESE OR NORMAL STATE CLASSICAL SYMPTOMS NONE OR MILD SYMPTOMS KETOSIS PRONE KETOSIS RESISTANT DIET ESSENTIAL DIET ESSENTIAL INSULIN ESSENTIAL(FOR INSULIN MAY BE REQUIRED SURVIVAL) (20 – 30%) FOR CONTROL. SU S NOT EFFICACIOUS SU S EFFICACIOUS Complications .AFTER 5 YRS IN FREQUENT(35-50%) INITIALLY / MAJORITY. at diagnosis/PC
- 12. Table 4—Criteria for testing for diabetes in asymptomatic adult individuals 1. Testing should be considered in all adults who are overweight (BMI 25 kg/m2*) and have additional risk factors: ● physical inactivity ● first-degree relative with diabetes ● members of a high-risk ethnic population (e.g., African American, Latino, Native American, Asian American, Pacific Islander) ● women who delivered a baby weighing 9 lb or were diagnosed with GDM ● hypertension (140/90 mmHg or on therapy for hypertension) ● HDL cholesterol level 35 mg/dl (0.90 mmol/l) and/or a triglyceride level 250mg/dl (2.82 mmol/l)
- 13. ● women with polycystic ovary syndrome ● A1C 5.7%--6.4%, IGT, or IFG on previous testing ● other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans) ● history of CVD 2. In the absence of the above criteria, testing diabetes should begin at age 45 years 3. If results are normal, testing should be repeated at least at 3-year intervals, with consideration of more frequent testing depending on initial results and risk status. *At-risk BMI may be lower in some ethnic groups
- 14. The foundation of our current practices in diabetes stems from large prospective studies, such as the UK Prospective Diabetes Study (UKPDS) and the Diabetes Control and Complications Trial (DCCT), which suggested that better control of blood glucose reduces complications
- 15. Diabetes Mellitus: Health Impact of the Disease 6th leading cause of death Renal Life expectancy failure 5 to 10 yr ↑ ↑ Blindness Diabetes Cardiovascular disease ↑ 2 to 4X Nerve damage in Amputation 60 to 70% of patients e most common cause of renal failure, blindness, and nontraumatic amputations
- 16. UKPDS: decreased risk of diabetes-related complications associated with a 1% decrease in A1C Observational analysis from UKPDS study data corresponding to a 1% decrease in HbA1C Any Percentage decrease in relative risk diabetes- Diabetes- All Peripheral Micro- related related cause Myocardial vascular vascular Cataract endpoint death mortality infarction Stroke disease† disease extraction 12% 14% 14% * 19% 21% 21% ** ** ** ** ** 37% † Lower extremity amputation or fatal peripheral vascular disease 43% *P = 0.035; **P < 0.0001 ** ** Adapted from Stratton IM, et al. UKPDS 35. BMJ 2000; 321:405–412.
- 20. Stages of Type 2 Diabetes— UKPDS 100 75 β-Cell Function (%) 50 IGT Postprandial Type 2 Type 2 Diabetes 25 Hyperglycemia Diabetes Type 2 Phase III Phase I Diabetes Phase II 0 -12 -10 -6 -2 0 2 6 10 14 Years From Diagnosis Lebovitz H. Diabetes Review. 1999;7:139.
- 22. TABLE OF OHAS / OADS SECRETOGOGUES INSULIN INHIBITORS OF SENSITIZERS CHO ABSORPTION SULFONYLUREAS BIGUANIDES ALPHA GLUCOSIDASE INHIBITORS GLICLAZIDE METFORMIN ACARBOSE TZDS OTHERS- GLIBENCLAMIDE NEW GLIMEPIRIDE PIOGLITAZONE DI -PEPTIDYL PEPTIDASE-4 INHIBITORS NON ROSIGLITAZONE GLIPTINS Black box warning -SULFONYLUREAS REPAGLINIDE
- 23. Sulfonylureas Meglitinides Biguanides α-glucosidase Thiazolidin inhibitor e-diones Hypoglycemia + ± BW gain + ± + GI upset + + Lactic acidosis + Hepatotoxicity + Increased plasma + volume Contraindication Significant Significant Cr (M) >1.5, Gastroparesis Active liver liver/kidney liver (F) >1.4 m/dl IBD disease or dysfunction∗ dysfunction∗ Acidosis GPT >2.5 UNL CHF CHF Hypoxia Radiocontrast ∗ relative Short & rapid onset ∗ relative
- 25. Stepped management of type 2 diabetes
- 26. The Moral of the Tale Aslong as we reach the objective (TARGETS), it doesn’t matter how we get there
- 27. Tools to manage Diabetes Whether it is pills, insulin shots or both GOAL IS CONTROL HbA1c <7%
- 29. The August 2006 guidelines from the ADA and the European Association for the Study of Diabetes recommends the inclusion of METFORMIN in initial diabetes treatment, AS PART OF TLC
- 30. An Algorithm to Guide …..
- 31. Clinical implications Algorithm encourages flexibility and clinical judgement in Type 2 diabetes treatment Algorithm is cautious in use of newer treatments Lack of head-to-head trials continues to impede informed comparisons of strategies In severely uncontrolled diabetes, lifestyle + insulin is preferred regimen Long-term ability to control diabetes or reduce cardiovascular complications still a concern
- 33. An Algorithm to Guide …..
- 35. Advantages of Insulin Therapy Most clinical experience Most effective (lowering glycemia) Can decrease any level of elevated HbA1c No maximum dose of insulin beyond which a therapeutic effect will not occur Beneficial effects on triglyceride and HDL cholesterol levels Nathan DM et al. Diabetes Care 2006;29(8):1963-72.
- 38. Why Aren’t Patients Achieving Blood Glucose Goals? Physicians not setting appropriate glycemic targets Type 2 diabetes is progressive - what works now may not work in the future Type of medications used are not appropriate Insulin therapy only used as a “threat”
- 39. Yikes! I have 5 minutes to tell this patient everything about diabetes!!
- 42. (ABC )–ALPHABET STRETEGY) JOINT BRITISH SOCIETIES GUIDELINES- 2005 A ADVICE EDUCATION, COMPLIANCE, SMOKING CESSATION, DIET, PHYSICAL ACTIVITY,WEIGHT REDUCTION. B BLOOD PRESSURE < 130/80, ACE/ARB, DIURETICS, CCB C CHOLESTREROL < 160 MG/DL, LDL<100MG/DL, TG<160, HDL>40 IN MALES >50 IN FEMALES D DIABETES CONTROL HBA1C < 6.5% METFORMIN 1ST CHOICE E EYE CARE ANNUAL OPHTHALMOLOGICAL EXAM F FOOT CARE ANNUAL EXAM G GUARDIAN DRUGS ASPIRIN > 50 YRS, > 10 YRS DM, HTN / PROTEINUREA( NEPHROPATHY) ACE/ARB STATINS(EVEN IF LIPID PROFILE IS WITHIN NORMAL LIMITS)
- 44. TAKE HOME MESSAGE “Insulin should not be the treatment of last resort for many of our patients, but should be the treatment of best resort. Starting insulin is always resisted. A lot depends on the clinician to handle the different situations in a tactful way”
- 45. TAKE HOME MESSAGE DIABETES”S therapy should be individualized and adjusted according to the changing needs of the patients
- 50. •THANK YOU
Hinweis der Redaktion
- UKPDS 35 was a prospective observational study to determine the relationship between exposure to hyperglycemia over time and the risk of macrovascular or microvascular complications in patients with type 2 diabetes who were participants in the UKPDS. 3,642 white, Asian Indian and Afro-Caribbean UKPDS patients who had HbA 1c measured 3 months after their diabetes diagnosis and with complete data for potential confounders were included in the sub-analysis of relative risk. Reductions in the risk of microvascular and macrovascular complications that might be achieved by lowering HbA 1c by 1% were estimated. The incidence of clinical complications was found to be significantly associated with hyperglycemia. While any reduction in HbA 1c is likely to reduce the risk of complications, the lowest risk was observed in those with HbA 1c values in the normal range (< 6.0%). A 1% decrease in HbA 1c was estimated to correspond with significant reductions in any diabetes-related endpoint, diabetes-related death, all cause mortality, myocardial infarction, stroke, peripheral vascular disease, microvascular disease and cataract extraction. Stratton IM, et al. UKPDS 35. BMJ 2000; 321 :405–412.
- This is Mr. M.C.’s left heel ulcer. Note the maggots infesting – but perhaps also debriding – this wound.
- Slide 1-24 Stages of Type 2 Diabetes Epidemiological studies suggest that the onset of diabetes occurs 10 to 12 years before a clinical diagnosis is made. (Harris 1997) In the UKPDS study of type 2 diabetics, at least 50% of the patients had evidence of diabetic tissue damage when diabetes was first diagnosed. (UKPDS Study 16, 1995) In the earliest phase, when beta-cell function is not impaired, the ability of the beta-cells to hypersecrete insulin masks the impaired glucose tolerance, often for years. During the IGT phase, the FPG will be higher than the normal 110 mg/dL but lower than the 126 mg/dL that is indicative of diabetes. As beta-cell function continues to decline, mild postprandial hyperglycemia develops, reflecting the inability of the beta-cell to hypersecrete enough insulin to overcome insulin resistance. At the end of this prediabetic phase, the first phase of type 2 diabetes typically produces symptoms that lead to a diagnosis. During phase I, in the first 2 years after diagnosis of diabetes, beta-cell function decreases to between 70% and 40% of normal function. CORE
- The classical approach to treating type 2 diabetes can be described as stepped management. The first step is to encourage the patient to reduce hyperglycemia through a combination of diet and exercise followed by support with an oral antidiabetic agent in monotherapy. If glycemic control continues to deteriorate, additional oral agents are added in a step-wise fashion followed by insulin where necessary. Slide 17
- Published simultaneously in the August 2006 issues of Diabetes Care and Diabetologia , the new consensus statement takes into account the characteristics of individual interventions, their synergies, and expenses (Figure 1) to facilitate the management of hyperglycemia. “We have developed a step-by-step algorithm that simplifies how and when treatments should be administered [Figure 2],” says Dr. Nathan. “We want to achieve and maintain glycemic levels as close to the non-diabetic range as possible and to change interventions at as rapid a pace as titration of medications allows.”
- Key Points Insulin is the oldest of the currently available medications for the management of hyperglycemia in type 2 diabetes and has the most clinical experience. It is the most effective of diabetes medications in lowering glycemia: when used in adequate doses it can decrease any level of elevated HbA 1c to, or close to, the therapeutic goal, and there appears to be no maximum dose beyond which a therapeutic effect will not occur. Insulin has also been shown to beneficially affect triglyceride and HDL cholesterol levels. Reference: Nathan DM et al. Management of hyperglycemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy. Diabetes Care 2006;29(8):1963-72 .
- We as health care providers need to know blood glucose goals and develop strategies for our patients to reach these goals. However, it must be made clear that regardless of appropriate control, changes in blood glucose is part of the disease’s progressions. This may have a psychological impact on the patient. Insulin is used as a punishment, therefore, it is often used too late. Insulin must be presented as a wonderful tool to control blood glucose levels.
- According to Dr. Nathan, there are several key points for physicians to remember when using the newly created algorithm. “First, physicians need to quickly and aggressively move onto the next step if A1C improvements do not occur. The earlier these new interventions are initiated, the better chance we have at preventing complications. Second, we must recognize that lifestyle interventions [eg, a healthy diet and regular exercise] and early administration of metformin are essential throughout treatment. Patients should receive these interventions as soon as a diabetes diagnosis is made and continue them. Third, physicians should not hesitate to initiate early and aggressive insulin therapy because it can further prevent diabetes-related complications. Lastly, each treatment goal will need to be individualized based on the patient’s characteristics. What may work for some patients will not work for all.”