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GO! Diabetes Program. Goals For Today Review evidence based guidelines and equip you to deliver state of the art care to your diabetic patients Understand.

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Presentation on theme: "GO! Diabetes Program. Goals For Today Review evidence based guidelines and equip you to deliver state of the art care to your diabetic patients Understand."— Presentation transcript:

1 GO! Diabetes Program

2 Goals For Today Review evidence based guidelines and equip you to deliver state of the art care to your diabetic patients Understand tools that support practice performance and improvement Review oral and injectable medicines hypoglycemics Review multifaceted approach to cardiovascular disease protection

3 Effect of Tighter Glycemic Control on Progression of Retinopathy DCCT

4 Effect of Intense Glycemic Control on Nephropathy from DCCT

5 United Kingdom Prospective Diabetes Study Study summary – 10 years –Type 2 diabetics – convention vs. intense control Glycemic control – 7.0 vs. 7.9 Hypertension control – 144/82 vs. 154/87 –Glycemic control metformin, sulfonylureas, and insulin –Hypertension captopril, atenolol

6 UKPDS Blood Pressure Study: Tight vs. Less Tight Control 1148 type 2 patients BP lowered to avg. 144/82 (controls-154/87); 9 yr follow-up EndpointRisk Reduction(%)P Value______ Any diabetes related endpoint Diabetes related deaths Heart failure Stroke Myocardial infarction21 NS Microvascular disease UKPDS. BMJ. 317:

7 Glycemic Control Reduces Complications DCCTUKPDS HbA1C 9 7.2%8 7% Retinopathy63%17% to 21 % Nephropathy54%24% to 33% Neuropathy60%- Cardiovascular Disease 41%16% Diabetes Control and Complications Trial (DCCT) Research Group. N Engl J Med 1893:329: UK Prospective Diabetes Study (UKPDS) Group. Lancet 1993; 352:

8 ABCs Of Diabetes Management Glycemic control A1C<7.0% Preprandial plasma glucose mg/dL Postprandial plasma glucose<180 mg/dL Blood pressure<130/80 mmHg Lipids LDL-cholesterol<100 mm/dL Triglycerides<150 mm/dL HDL>40 mm/dL Antiplatelet therapyEveryone over 40 Smoking cessationUniversal Diabetes Care 2009;32:S6-12

9 Control of CV Risk Factors in Diabetic Hypertensive Patients in Academic Medical Centers McFarlane SI. Diabetes Care 2002;25:718 2%BP, Lipids, A1C + ASA 3%BP, Lipids and A1C 46%Daily Aspirin (ASA) Use 27%BP <130/85 mmHg 36%LDL <100 27%A1C <7%

10 Type 1 Vs Type 2: How To Tell Them Apart Type 1Type 2 TreatmentAlways insulin; 4+ shots Pills  Insulin Age at Onset10% of adults w/ new dx50% of children w/ new dx Weight~20% obese~10% thin Family History10% w/ a close relative>50% w/ a close relative DKACan happen Blood GlucoseMore variable; big hypo’sMore stable; milder hypo’s Thyroid DiseaseOftenSometimes AntibodiesUsually (Anti-GAD)Not usually C-peptideEarly: low nl; Late: ~0Early: high nl; Late: low nl

11 Diabetes: Early Detection and Lifestyle Monitoring

12 Metabolic Syndrome Requires 3 or more: –Triglycerides > 150 –HDL < 40 –Waist size >40” men, >35” women –BP > 130/85 –Fasting glucose > 100 Caveat: Treatment counts for requirements… (Grundy, Circulation, 2005)

13 Pre-Diabetes Definition FastingGTT or If FBG >100 there is a 10-15% risk of DM within 7 years…

14 Who and When to Screen? Family history Overweight (BMI 25) Dyslipidemia HTN High risk ethnicity Vascular disease Prior glucose elevation Hx or exam findings Starting at age 45, a fasting blood glucose every three years More frequent screening if:

15 Role of Obesity in Diabetes Obesity (specifically abdominal) has one of the highest associations with insulin resistance and glucose intolerance Numerous studies have tied weight loss to diabetes prevention A 5-10% weight loss yields a 58% reduction in the incidence of diabetes! –At the end of four years Diet and exercise regimens average a 4kg loss after two years Advice alone results in a 1kg gain (Franz, Journal Amer. Diabetes Assoc, 2007)

16 Quantifying Obesity Easiest is by waist circumferences. 40” males, 35” females Some variation by ethnicity (35” and 31” for Asians) Measured across iliac crest in the back and the umbilicus in the front

17 Healthcare Maintenance Latest ADA guidelines (2009) Lab surveillance Diabetic education Vaccinations/routine healthcare Smoking cessation Foot exams Eye exams

18 Reasons to Look at Feet Up to 70% of diabetics eventually develop a neuropathy Up to 25% develop foot ulcers Diabetes doubles your risk of LE disease (vascular, neuro, skin) More than half of the foot ulcers become infected at some point

19 Foot Surveillance Examine the feet at every visit Annual comprehensive evaluation –Sensation –Pulses –Skin condition (ulcers, hair, nails) –Anatomic deformities –Shoe evaluation

20 Sensory Exam 10-gram monofilament –Patient should not watch –Five sites per foot –Apply filament perpendicular to skin –Allow slight buckle of filament in one motion –Each site should take 1-2 sec –Do not apply to ulcers or calluses

21 Eye Care Diabetic retinopathy is the leading preventable cause of blindness Prevalence of DR increases with duration of diabetes (100% Type 1, 60% Type 2 after 20 years) Of all recommendations, eye screening is the least likely to get done

22 Pathogenesis Increased circulating glucose leads to weakness of capillary walls Microaneurysms and leakage occurs causing eventual infarction of the nerve fiber layers (cotton wool spots) The localized hypoxia then leads to vasoproliferation Extension into the vitrea (+/- hemorrhage) leads to fibrosis and vision loss

23 Diabetic Retinopathy Normal Retina (left) contrasted with Proliferative Diabetic Retinopathy (right) Refer patients for ophthalmologist evaluation

24 Glycemic Control – Oral Agents

25 General Rules Hypoglycemic Therapy Normalize fasting glucose levels first ( mg/dl) –Many patients will achieve A1C < 7% When to target postprandial glucose levels? –Fasting and preprandial values are at goal –A1C levels are not met Measure 1-2 hours after beginning of the meal –Glucose are generally at their peak

26 Diabetes Care 2009;32:S6-12 Goal Premeal plasma glucose (mg/dL) 2-h postprandial plasma glucose A1C ADA <180* <7%** Glycemic Goals of Therapy * Evaluation and treatment of postprandial glucose may be useful in the setting of suspected postprandial hyperglycemia, with the use of agents targeting postprandial hyperglycemia and for suspected hypoglycemia ** More stringent glycemic goals (i.e. a normal A1C, <6%) may further reduce complications at the cost of increased risk of hypoglycemia Verbal Target ~100 <<200 As low as possible w/o unacceptable adverse effects

27 Biguanides: Metformin Mechanism of action –Reduces hepatic glucose production –Depends upon presence of insulin Safety and efficacy –Decreases A1C 1-2% –Adverse effects: diarrhea and nausea; main risk: lactic acidosis –Discontinuation rate 5% –Contraindications: renal, cardiac, hepatic insufficiency; IV contrast –No direct effect on kidney Dosing –Initial dose: 500 mg once a day; dosing: usually BID –Maximum effective dose: 2,000 mg per day –Titration frequency: week(s) to months –Alternate formulations: “XR” and combinations

28 Metformin Outperformed Other Meds in Obese Patients (UKPDS) Lancet 1998 Sep 12;352(9131):

29 Insulin Secretagogues: Sulfonylureas (SFU) and “Glinides” Mechanism of action –Stimulate basal and postprandial insulin secretion –Require functioning beta cells (no effect on beta cell dysfunction) –Work quickly Safety and efficacy –Decrease A1C approximately 1-2% –Lower fasting glucose 20% –Adverse events: weight gain, allergy (rare); main risk, hypoglycemia Dosing –Initial dose: 1/8 to 1/4 maximum dose; dosing: 1-2 times/day (SFU), 3 times/day (glinides) –Maximum effective dose: 1/2 maximum (full dose with nateglinide) –Titration frequency: day(s) to weeks

30 Preferred Sulfonylureas All available as generic agents Glipizide ER 5-20 mg once per day Once daily, flat profile, low plasma levels resulting in a low risk of weight gain and hypoglycemia Glipizide 2.5 to 20 mg twice a day Twice daily. Half-life 2-4 hours, peaks in 2-3 hours. By taking it once a day at low dose it stimulates insulin secretion for 6-12 hours Glimepiride 1-8 mg per day Once daily. Half-life 9 hours, peak action for 4 hours. Special utility like with glipizide but with longer half-life Buse J. Personal Opinion Melander A. Diabetes 2004;53 Suppl 3:S151

31 Thiazolidinediones (TZD’s or Glitazones): Pioglitazone and Rosiglitazone Mechanism of action –Enhance insulin sensitivity in muscle, adipose tissue –Inhibit hepatic gluconeogenesis –Reduced rate of beta cell dysfunction Safety and efficacy –Decrease A1C 1-2% –Adverse events: edema, weight gain, anemia; rare serious risk: liver failure Dosing –Initial dose (monotherapy): 1/2 to 2/3 maximum; dosing,1-2 x/day –Maximum effective dose: maximum dose –Titration frequency: weeks to month(s)

32 Oral Hypoglycemics TZD Lipid Effects Rosiglitazone (Avandia) –+LDL –+HDL –+Triglycerides Rosiglitazone – Black box warning for CHF and ischemic heart disease; warnings about increased fracture risk in women Pioglitzaone – Black box warning for CHF and warning about increase fracture risk. No evidence to suggest increased ischemic heart disease. Pioglitazone (Actos) –+LDL –+HDL –-Triglycerides

33 AHA/ADA Consensus Statement for TZDs Not recommended for patients with NY Heart Association class III or IV heart failure TZDs alone, or particularly in combination with insulin, may cause fluid retention which can lead to heart failure –Incidence of CHF <1% with TZD monotherapy –Increased to 2%-3% in combination with insulin Patients should be observed for signs and symptoms of heart failure TZDs should be discontinued if any deterioration in cardiac status occurs Nesto RW et al. Diabetes Care 2004;27:256

34 Alpha-Glucosidase Inhibitors: Acarbose And Miglitol Mechanism of action –Delay absorption of carbohydrates –Depend upon postprandial hyperglycemia Safety and efficacy –Decrease A1C 0.5-1% –Adverse events: flatulence; main risk: rare liver enzyme elevation Dosing –Initial dose: 1/4 maximum once daily; dosing: 3 times daily –Maximum effective dose: 1/2 maximum dose –Titration frequency: week(s) to months –Used infrequently by most clinicians

35 INCRETINS Role of Glucagon Like Peptide (GLP-1) in Glucose Homeostasis DeficiencyType 2 DM/+/-type 1 Site of synthesisSmall intestine Glucose dependent stimulation of insulin secretion Yes Slow gastric emptyingYes Reduce inappropriate glucagon secretion Yes Weight lossYes (exenatide) Beta cell proliferation/regenerationYes Therapies Exenatide (Byetta) Sitagliptin (Januvia) Target populationType 2 on oral agents

36 Incretin Drugs Exenatide (Byetta) – GLP-1 analog –Injection twice daily 5mcg bid AC x 1 month, then 10mcg bid AC –Beneficial effects described previously –Expensive –Weight loss –Reduction in HgBA1C Sitagliptin (Januvia)– DPP4 inhibitor –Technically not an incretin but similar effects –Oral administration 100mg daily –Weight neutral

37 Key Points to Consider for Therapy Maximal benefits of metformin are observed at the recommended daily dose of 2000 mg (1 g BID) 1 Thiazolidinediones should be started at low doses and slowly increased to minimize side effects 2 Glucose-lowering effects of a sulfonylurea plateau at half the maximum recommended dose 3 1.Garber AJ et al. Am J Med 1997;103:491 2.Nesto RW et al. Diabetes Care 2004;27:256 3.Stenman S et al. Ann Intern Med 1993;118:169

38 Glycemic Control - Injected Therapies

39 63% Of Patients with Diabetes Are Not at ADA A1C Goal <7% 37.2% >8% 63%  7% 7.8% 25.8% 37.0% 17.0% 12.4% % of Subjects n=404 A1C Adults aged years with previously diagnosed diabetes who participated in the interview and examination components of the National Health And Nutrition Examination Survey (NHANES), Saydah SH et al. JAMA 2004;291:335

40 Difficulties In Achieving Target A1C Values Challenges –Late diagnosis and initiation of therapy –Therapeutic inertia –Lack of effective lifestyle intervention –Secondary failure –Adverse events associated with antihyperglycemic therapies –Complexity of care –Role of postprandial glucose in failure

41 Common Concerns When Transitioning To Insulin Fear of needles or pain from injections Fear of hypoglycemia Weight gain Funnel M. Self-management Support for Insulin Therapy in Type 2 Diabetes. The Diabetes Educator 2004;30:274

42 Adverse impact on lifestyle; inconvenient; loss of personal freedom and independence Belief that insulin means diabetes is worse or more serious disease Insulin as a personal failure Insulin causes complications Treated differently by family members Funnel M. Self-management support for insulin therapy in type 2 diabetes. The Diabetes Educator 2004;30:274 Common Concerns When Transitioning To Insulin

43 Potential Insulin Regimens Insulin pump Physiologic/COMPLEX/Flexible Multiple daily injections Free mixing - twice daily Pre-mixed - twice daily Basal only SIMPLE/Inflexible How do we balance simplicity and flexibility to achieve glycemic control?

44 Indications for Insulin Not contraindicated at anytime Consider as initial therapy –HgbA1C > 10% –Fasting glucose > 250mg/dl –Random glucose > 300 Recommended as initial therapy –Polyuria, polydipsia, weight loss, ketones

45 Insulin Initiation Answers to Provider Concerns Normalize the fasting glucose –Fasting FSBS –Once Daily Options Start 10 units or 0.2 u/kg –Basal Insulin (glargine or detemir) –NPH (bedtime) –Premixed before dinner Increase 2-3 units every 3 days prn to reach target of fasting Decrease 3 units for fasting < 70

46 Once Daily Insulin Options Basals vs. NPH vs. Premixed INSULIN TYPEADVANTAGESDISADVANTAGES GlarginePeakless, less hypoglycemia, less wt gain; simple Cost; can’t mix; no meal time coverage DetemirLess wt gain, less hypoglycemia; simple Cost, shorter duration than glargine; can’t mix, basal only Pre Mixed 70/30 or 75/25 Covers meal time and basal; easy transition to bid More hypoglycemia and weight gain than basals NPHLess expensiveMore hypoglycemia than basals

47 Insulin Action Effect Of Various Formulations Short (Regular) Rapid (Glulisine, Lispro, Aspart,) Insulin Level (  U/ml) Hours Intermediate (NPH) Long (Glargine) Detimir

48 Fasting Glucose at Target HgbA1C Not at Goal Must Normalize Post Prandial Glucose Options –Change HS NPH to BID NPH –Change Pre-mixed Insulin from QD to BID –Add Mealtime Insulin to Basal Insulins

49 Monomeric Insulin Analogs How to switch or start –Insulin immediately before the meal (or after) –Review signs, symptoms and management of hypoglycemia Safety –Arguably, glulisine, aspart, lispro and are safer than regular human insulin Patient preference –Significant patient preference for monomeric analog versus regular human insulin Duration of action –Covers postprandial glucose surge well –In type 1 diabetes, will need an additional injection of basal or NPH

50 Carbohydrate Counting Technique based on the concept that most meal-related glucose increase is due to the carbohydrate content Patients count either – Carbohydrate choices (milk, fruit, breads, sweets, starchy vegetables) – Grams of “total carbohydrates” on food label Providers prescribe insulin-to-carbohydrate ratio – Start with 1 unit per choice or 1 unit per 15 grams – Typical dose is 2-4 units per choice in type 2 diabetes Titrate based on postprandial glucose monitoring Generally, start with glulisine/lispro/aspart administered just after meals

51 Mixed-Analog Insulin BID Starting dose in most –Pre-breakfast 10 units –Pre-supper 10 units Titration, once or twice a week (self-adjusted or with supervision) Alternatively, could just increase at both breakfast and supper in parallel If most values over the last 3 days fall in the range Adjust dose by ≤80 mg/dL-2 units mg/dLno change mg/dL+2 units mg/dL+4 units ≥180 mg/dL+6 units Buse JB et al. Clinical Diabetes 2005;23:78

52 Pre-Mixed Insulin BID Compared to Basal Alone – INITIATE Study Aspart 70/30 bid Glargine qhs –Minor hypoglycemia 43% 16% –Median rate per pt per mo –Severe hypoglycemiaNone 1 episode –Weight gain (Kg)5.4   4.5 –Total daily insulin (u/Kg)0.82   0.27 Raskin P et al. Diabetes Care 2005;28:260

53 Oral Meds – What to Do When Insulin Started (General Rules) Metformin –Continue unless contraindicated Sulfonylureas –Continue with basals generally –Stop if using large doses of insulin –Stop if using premixed insulin TZDs –Proceed with caution –Exacerbates weight gain and edema

54 Non Insulin Injectables

55 Initiation  1 Mo 5 mcg BID Stable Dose 10 mcg BID Stable Dose Indicated for use in patients failing metformin or sulfonylurea Generally reduce SFU dose to smallest tablet to minimize risk of hypoglycemia No dosage adjustments based on meal size or physical activity No additional glucose monitoring required Exenatide Prescribing Information General Prescribing Considerations Dosing

56 Glargine Vs Exenatide in Patients Failing Oral Therapies ITT patient sample Mean ± SE shown * p<0.0001, exenatide vs insulin glargine at same time point  Body Weight (lbs) * * * * * *  A1C (%) Heine RJ et al. Ann Intern Med 2005;143(8):559

57 Diagnosis by screening or with symptoms Treatment Algorithm - Glucose Yes Quarterly to semi-annual follow-up Lifestyle intervention MNT, physical activity, education Are A1C/FPG targets achieved? Monthly to quarterly follow-up Target PPG Target Insulin Deficiency FPG >200 mg/dL FPG <130 mg/dL Metformin, glitazone Exenatide, nateglinide, α-glucosidase inhibitors, rapid-acting insulin, pramlintide SFUs/glinide, insulin, exenatide * * Keep adding agents until target reached. Self-titration at home when possible Target Insulin Resistance No

58 Causes of Hypoglycemia Incorrect amount of insulin/oral agents Skipped or delayed meal/snack Carbohydrate intake less than normal Alcohol intake without food Exercise without insulin/food adjustment Not re-testing 1 to 2 hours after hypoglycemia treatment if meal or snack is not eaten

59 Treatment of Hypoglycemia Definition of hypoglycemia: Plasma glucose <70 mg/dL Symptoms may or may not be present –Sweaty, cold, unable to concentrate, dizzy Treatment –Treat with 15 g carbohydrate; wait 15 minutes; test BG, if BG not >70 mg/dL, treat again –All carbohydrates raise blood glucose –On average, 15 g of glucose can increase BG from 60 to ~110 mg/dL (50mg/dL) over ~40 minutes –BG starts to fall at 60 minutes and reaches previous treatment level at 2 hours Cryer et al. Diabetes Care 2003;26:1902

60 Treatment of Severe Hypoglycemia Definition: Requires assistance to treat Inject glucagon with loss of consciousness or seizure Administered by another person –May be given intramuscular or subcutaneous Standard dose –1.0 mg for adults; 0.5 mg for children under 5 yrs Prescription is required Precautions –May cause nausea/vomiting/headache Call 911

61 Cardiovascular Disease Prevention Blood Pressure, Dyslipidemia, Antiplatelet Therapy

62 Diabetes and Hypertension Key Questions Why should we pay so much attention? What parameters? Non Drug Recommendations Which drugs and how many? What do others besides the ADA say? What about resistant cases?

63 Diabetes and Hypertension Why? Volume Expansion –Increased insulin levels Higher sympathetic activity –Increased glucose level Increased sodium resorption with hyperglycemia Decreased arterial compliance Obesity

64 UKPDS Blood Pressure Study: Tight vs. Less Tight Control 1148 type 2 patients BP lowered to avg. 144/82 (controls-154/87); 9 yr follow-up EndpointRisk Reduction(%) P Value Any diabetes related endpoint Diabetes related deaths Heart failure Stroke Myocardial infarction21 NS Microvascular disease UKPDS. BMJ. 317:

65 Diabetes Treatment Goals for Blood Pressure Control blood pressure –130/80 mmHg for most patients –125/75 mmHg for patients who have proteinuria >1 g/day and renal insufficiency Reduce the risk of end-organ failure Reduce the risk of cardiovascular events –Myocardial infarction –Cardiovascular death Delay or prevent the progression to heart failure JNC 7 Report. JAMA 2003;289:2560; Bakris GL et al. Am J Kidney Dis 2000;36:646 ADA. Diabetes Care 2007;30(suppl 1):S15

66 Number of Medications to Achieve Goal BP In 5 Trials of DM and/or Renal Disease AASK (<92 mmHg MAP) HOT (<80 mmHg DBP) MDRD (<92 mmHg MAP) ABCD (<75 mmHg DBP) UKPDS (<150/85 mmHg) Number Of BP Meds Bakris. J Clin Hypertens 1999;1:141

67 NKF Recommendations On Treatment Of Hypertension And Diabetes Blood pressure goal: ≤130/80 mmHg BP-lowering medications should reduce both BP + proteinuria Lower goal has been recommended to reduce renal disease progression and incidence of ischemic heart disease Antihypertensive drug classes shown to reduce proteinuria and cardiovascular events – ACE inhibitors –  -  -blocker (carvedilol) –  -blockers – CCBs – Diuretics Bakris GL et al. Am J Kidney Dis 2000;36:646

68 UKPDS: ACE Inhibitor Vs  -Blocker Aggregate Clinical Endpoints Relative Risk & 95% CI Any diabetes-related endpoint PRR UKPDS Group. BMJ 1998;317:713 Favors ACE Inhibitor Favors  -Blocker Diabetes-related deaths All-cause mortality Myocardial infarction Stroke Microvascular disease

69 Which Class Of Agents Should Be Added Second-Line? Thiazide diuretics –Complementary mechanism to ACEs or ARBs –ALLHAT showed benefit –Particularly effective in African American patients –BUT slightly higher deterioration of glucose metabolism Beta blockers –Good evidence of benefit particularly for those with coronary heart disease or congestive heart failure –BUT mechanism of action may not complement ACEs or ARBs

70 Additional BP Recommendations Lower blood pressure gradually in the elderly If unable to achieve goal, don’t hesitate to discuss with peers Check for orthostasis in some patients when clinically indicated If angiotensin modifying drugs or diuretics are used, monitor renal function and potassium Use as many medicines as necessary to achieve blood pressure target –130/80 mmHg –125/75 mmHg if proteinuria is found Begin with an angiotensin modifying drug Add a thiazide in African American patients Add a Beta blocker in patients with heart disease ADA. Diabetes Care 2007;30(Suppl1):16

71 Causes Of Resistant Hypertension  Improper blood pressure measurement  Excess sodium intake  Inadequate diuretic therapy  Medication –Inadequate doses –Drug actions and interactions (e.g. nonsteroidal anti-inflammatory drugs (NSAIDs), illicit drugs, sympathomimetics, oral contraceptives) –Over-the-counter (OTC) drugs and herbal supplements  Excess alcohol intake  Identifiable causes of hypertension

72 Statins: Primary And Secondary Prevention Adapted from Illingworth. Med Clin North Am 2000;84:23 and LaRosa. N Engl J Med 2005;352 (e-pub) and Colhoun. Lancet 2004;364: % With CVD Event LDL-C (mg/dL) WOSCOPS AFCAPS HPS (estimated) CARDS CARE 4S LIPID HPS (estimated) TNT PROVE-IT

73 ADA Standards 2009 Dyslipidemia Fasting lipid profile annually Without overt CVD –LDL<100 –At age 40 start on statin regardless of LDL to reduce LDL 30-40% With overt CVD –Start statin to reduce LDL 30-40% –LDL<70 is an option –Normalizing triglycerides and raising HDL with fibrates reduces CV events

74 ADA Standards 2009 Dyslipidemia High LDL, High triglycerides, Low HDL –Consider statin + fibric acid Remember the increased risk of rhabdomyolysis –Consider statin + niacin Remember niacin can increase glucose levels moderate doses = mild changes in glycemia

75 Anti-platelet Therapy ADA Standards Recommendations for Aspirin –ASA mg/day for 2 o prevention –ASA mg/day for 1 o prevention Age > 40 Any age with CV risk factors (htn, hyperlipidemia, renal disease, family history, smoking) –Not recommended ages < 21 (Reye’s syndrome) Clopidogrel –Very high risk diabetics; intolerance to ASA

76 Practice Performance and Improvement

77 METRIC Metric stands for Measuring, Evaluating, and Translating Research Into Care. It is an innovative online practice improvement program where you will input records of 10 diabetic patients prior to today and again within 90 days.

78 Questions?

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