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Doctors of Optometry | Course Notes

OD10 – 1CE Diabetes Mellitus On Overview for Health Practitioners

Saturday, February 17, 2018 12:00 pm – 12:55 pm Plaza A – 2nd Fl

Presenter: Dr. Leo Mok In 1997, Dr. Mok began his career as an optometrist, before going on to medical school in 1998. He graduated from UBC medical school in 2008, followed by an internship at Royal Columbian Hospital. He went on to complete residency training in ophthalmology at UBC, graduating in 2013. Dr. Mok’s practice encompasses comprehensive ophthalmology, including chronic medical conditions, glaucoma, lid lesions and cataracts. He is now a Comprehensive Ophthalmologist working in Maple Ridge and Port Moody.

Course Description

Have you ever wondered what it means when a patient tells you their sugar levels are in the 8-9 range that morning, or that their A1C is 7.3%, or what all these new diabetes medications are? With such a high prevalence of our patient population afflicted with diabetes and the new antihyperglycemic agents available, it is important to understand this disease beyond screening for diabetic retinopathy. A comprehensive review of diabetes, with an emphasis on the Canadian Diabetes Practice Guidelines, will provide a framework for learning with the goal of being able to better understand our patients diabetes status and to more effectively communicate with the general medical community regarding diabetes.

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Doctors of Optometry | Course Notes

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Diabetes MellitusOn Overview for Health

PractictionersA Canadian Perspective

Leo Mok, O.D., M.D.

Goals

To get acquainted with the Clinical PracticeGuidelines from the Canadian DiabetesAssociationTo review the “lingo” of diabetesTo be able to better communicate with otherhealth care professionalTo better serve our patients

GoalsClinical practice guidelines are becoming moreprevalent in medicineThe language of diabetes

Patients often tell us they are well controlled “I’m notdiabetic, I’m on meds.”

There is a discrepancy in knowledge between differentspecialties

There tends to be an assumption of knowledge andsometimes insecurity between different fields of medicine

To help us take care of our patientsAt the end of the day, we should have the properbackground and knowledge to assess our patients

Definition

A syndrome of disordered metabolism andinappropriate hyperglycemia secondary to anabsolute/relative deficiency of insulin, or areduction in biological effectiveness of insulin,or both

Classification

Type 1: primarily a result of pancreatic celldestructionType 2: characterized by insulin resistanceGDM: glucose intolerance with onset or firstrecognition during pregnancy

Epidemiology

Major health concern, affecting up to 10% ofCanadiansIncidence of type 2 DM is rising due to increasingobesity, sedentary lifestyle, and age of thepopulationLeading cause of new onset blindness and renaldysfunctionCanadian adults with DM are twice as likely to dieprematurely, compared to persons without DM

Diagnostic Criteria (CDA)Any one of the following is diagnosticFBG 7.0 mmol/L (fasting = no caloric intake for at least 8 h) OR2h 75 g OGTT 11.1 mmol/L ORRandom BG 11.1 mmol/L ORHbA1c 6.5% (not for diagnosis of suspected Type 1 DM, children,adolescents, or pregnant women)In the presence of hyperglycemia symptoms (polyuria, polydipsia,polyphagia, weight loss, blurry vision), a confirmatory test is notrequiredIn the absence of hyperglycemic symptoms, a repeat confirmatorytest is required to make the diagnosisof diabetes

Treatment of DiabetesHbA1c reflects glycemic control over 3 months and is a measure ofpatient’s long term glycemic controlTherapy in most individuals with type 1 or type 2 DM (especially youngerpatients) should be targeted to achieve a HbA1c 7.0% in order to reducethe risk of microvascular and if implemented early in the course ofdisease, macrovascular complicationsMore intensive glucose control, HbA1c <6.5%, may be targeted in type 2DM in patients with a shorter duration of DM with no evidence ofsignificant CVD and longer life expectancy, to further reduce risk ofnephropathy and retinopathy, provided this does not result in a significantincrease in hypoglycemiaLess stringent HbA1c targets (7.1 8.5%) may be more appropriate in type 1and type 2 patients with limited life expectancy, higher level of functionaldependency, a history of recurrent severe hypoglycemia, multiplecomorbidities, extensive CAD, or a failure to attain HbA1c <7.0% despiteintensified basal and bolus insulin therapyThere may be harm associated with strategy to target HbA1c <6.0%

Treatment TargetsHbA1c <7.0%

Fasting plasma glucose 4 7 mmol/L (72 126 mg/dL)

2h post prandial glucose 5 10 mmol/L (90 180 mg/dL)5 8 mmol/L (90 144 md/dL)if not meeting target A1c andcan be safely achieved

Lipids As per high risk group if age40 or age >30 if DM duration>15 yr

Blood pressure <130/80

General Treatment Goals

Avoid complications (e.g. ketoacidosis,hyperglycemia, infection)Prevent long term complications(microvascular and macrovascular)Minimize negative sequelae associated withtherapies (e.g. hypoglycemia, weight gain)

Treatment Targets for A1C

<7% or <6.5% in some type 2 DM patients atrisk for nephropathySuboptimal: 7 8.4%Inadequate: >8.4%Frail elderly, advanced co morbidities,recurrent severe hypoglycemia orhypoglycemia unawareness: target is 7.1 8.5%

Treatment Targets for Fasting orPreprandial Blood Glucose

Ideal: 4 7 mmol/L (72 126 mg/dL)Suboptimal: 7.1 10 mmol/L (128 180 mg/dL);action may be requiredInadequate: >10.0 mmol/L (180 mg/dL);action requiredFrail Elderly: target is 5 12 mmol/L

Treatment Targets for2H Postprandial Blood Glucose

5 10 mmol/L (90 180 mg/dL) if HbA1c targetmet5 8 mmol/L (90 144 mg/dL) if HbA1c targetnot metFrail elderly: use clinical judgment

Treatment Targets

Blood Pressure <130/80 in adults (DMand HTN guidelines)

Lipids LDL <2.0 mmol/L (36 mg/dL)

Prediabetes

Impaired fasting glucose (IFG): fasting plasmaglucose (FPG) 6.1 6.9 mmol/LImpaired glucose tolerance (IGT): 2h 75 g oralglucose tolerance test (OGTT) 7.8 11.0mmol/LHbA1c: 6.0 6.4%

Prediabetes

1 5% per yr go on to develop DM50 80% revert to normal glucose toleranceWeight loss may improve glucose toleranceIncreased risk of developing macrovascularcomplications (IGT >IFG)Lifestyle modifications decrease progressionto DM by 58%

Nonpharmacological Treatment

DietAll diabetics should see a registered dietician fornutrition counsellingCan reduce HbA1c by 1 2%Moderate weight loss (5%) improves glycemic controland CVD risk factorsDecrease combined saturated fats and trans fattyacids to <10% of caloriesAvoid simple sugars, choose low glycemic index foods,ensure regularity in timing and spacing of meals

Nonpharmacological Treatments

Physical activity and exerciseAt least 150 min of aerobic exercise per wk, plus 2sessions per wk of resistance exercise isrecommendedEncourage 30 45 min of moderate exercise 4 7 d/wkPromote cardiovascular fitness: increases insulinsensitivity, lowers BP, and improves lipid profileIf insulin treated, may require alterations of diet,insulin regimen, injection sites, and self monitoring

Self Monitoring of GlucoseType 1 DM: 3 or more self tests is associated with a 1%reduction in HbA1cType 2 DM: recommendations vary based on treatmentregimen (e.g. insulin dependent requires more)Frequent monitoring – refer to 2013 Canadian PracticeGuidelines)If FBG >14 mmol/L, perform ketone testing to rule out DKAIf bedtime level is <7 mmol/L, have bedtime snack to reducerisk of nocturnal hypoglycemia

Hypoglycemic Agents for T2DMOral

Biguanide: metformin (Glucophage®)Thiazolidinedione: troglitazone (Rezulin®), rosiglitazone(Avandia®)glucosidase inhibitor: acarbose (Precose®)

Nonsulfonylureas: nateglinide (Starlix®), repaglinide(Gluconorm®)Sulfonylureas: glyburide (DiaBeta®), glimepiride (Amaryl®),gliclazide (Diamicron®)DPP 4 inhibitor: sitagliptin (Januvia®)

InjectableGLP 1 analogue: liraglutide (Victoza®)

Other Medications Used in DMACEI or ARB in those with any of

Clinical macrovascular diseaseage 55 yearsage <55 and microvascular complications

Statin in those with any ofClinical macrovascular diseaseage 40 yearsage <40 and any of the following:diabetes duration >15 years and age >30 yearsMicrovascular complicationsOther cardiovascular risk factors

Low dose ASA (81 325 mg)for secondary prevention in people with established CVD (NOT to beused routinely for primary prevention)

Non insulin Antihyperglycemic Agents(Type 2 DM)

Initiate non insulin antihyperglycemic therapywithin 2 3 mo if lifestyle management does notresult in glycemic controlIf initial HbA1c >8.5% at the time of diagnosis,initiate pharmacologic therapy with metforminimmediately and consider combination oftherapies or insulin immediatelyContinue to add additional pharmacologictherapy in a timely fashion to achieve targetHbA1C within 3 6 months of diagnosis

InsulinUsed for type 1 DM at onset, may be used in type 2 DM atany point in treatmentRoutes of administration: subcutaneous injections,continuous subcutaneous insulin infusion pump, IV infusion(regular insulin only)Bolus insulins: short acting (Insulin regular), rapid actinganalogue (Insulin aspart, Insulin glulisine, Insulin lispro)Basal insulins: intermediate acting (Insulin NPH), longacting analogue (Insulin detemir, glargine)Premixed insulins (combination of basal and bolus insulins)available but not used regularlyEstimated total daily insulin requirement: 0.5 0.7 units/kg(often start with 0.3 0.5 units/kg/d)

Variable Insulin Dose Schedule(“Supplemental/Correction Scale”)For patients on Basal Bolus regimen: patient takes usual doses of basalinsulin but varies doses of bolus insulin based on BG reading at time ofdoseUse baseline bolus insulin dose when within BG target range; add orsubtract units when above or below targetWhen used in hospital (including perioperative management of DM),patient should also receive basal insulin to prevent fluctuations in bloodsugar levels or long periods of hyperglycemiaConstruction of a supplemental sliding scale for a patient on antihyperglycemicsCorrection Factor (CF) = 100/Total Daily Dose of insulin (TDD)

BG <4: call MD and give 15 g carbohydratesBG between 4 to 8: no additional insulinBG between 8 to (8 + CF): give one additional unitBG between (8 + CF) to (8 + 2CF): give two additional unitsBG between (8 + 2CF) to (8 + 3CF): give three additional units

Insulin Pump Therapy: ContinuousSubcutaneous Insulin Infusion (CSII)External battery operated device providescontinuous basal dose of rapid acting insulinanalogue (aspart, glulisine, or lispro) throughsmall subcutaneous catheterAt meals, patient programs pump to deliverinsulin bolusProvides improved quality of life and flexibilityRisk of DKA if pump is inadvertently disconnectedCoverage available for insulin pumps forindividuals with Type 1 DM varies by province

Macrovascular Complications

increased risk of CAD, ischemic stroke, andperipheral arterial disease secondary toaccelerated atherosclerosis

Coronary Artery Disease

Risk of MI is 3 5x higher in those with DMcompared to age matched controlsCAD is the leading cause of death in type 2DMMost patients with DM are considered “highrisk” under the risk stratification for CAD

Risk of Stroke

Risk of stroke is approximately 2.5x higher inthose with DMLevel of glycemia is both a risk factor forstroke and a predictor of a poorer outcome inpatients who suffer a strokeHbA1c level is a significant and independentpredictor of the risk of stroke

Peripheral Arterial Disease

Manifested by intermittent claudication inlower extremities, intestinal angina, footulcerationRisk of foot gangrene is 30x higher in thosewith DM compared to age matched controlsRisk of lower extremity amputation is 15xhigher in those with DM

Treatment for MacrovacularComplications

Tight blood pressure control (<130/80 mmHg);especially for stroke preventionTight glycemic control in early DM withoutestablished CVD (refer to ACCORD, VADT,ADVANCE, DCCT, EDIC, UKPDS extension studies)Tight low density lipoprotein (LDL) cholesterolcontrol (LDL 2.0 mmol/L)ACEI or angiotensin receptor blocker in high riskpatientsSmoking cessation

Microvascular Complications

Diabetic RetinopathyDiabetic NephropathyDiabetic Neuropathy

Diabetic RetinopathyEpidemiology

type 1 DM: 25% affected at 5 yr, 100% at 20 yrtype 2 DM: 25% affected at diagnosis, 60% at 20 yrleading cause of blindness in North America between the ages of 2074most important factor is disease duration

Treatment and Preventiontight glycemic control (delays onset, decreases progression), tight lipidcontrol, manage HTN, smoking cessationophthalmological treatments availableannual follow up visits with an optometrist or ophthalmologistexamination through dilated pupils whether symptomatic or not(immediate referral after diagnosis of type 2 DM; 5 yr after diagnosisof type 1 DM)interval for follow up should be tailored to severity of retinopathy

Diabetic NephropathyEpidemiology

DM induced renal failure is the most common cause of renal failure inNorth America20 40% of persons with type 1 DM (after 5 10 yr) and 4 20% with type2 DM have progressive nephropathy

Screeningserum creatininerandom urine test for albumin to creatinine ratio (ACR) plus urinedipstick test for all type 2 DM patients at diagnosis, then annually, andfor postpubertal type 1 DM patients with 5yr duration of DM

Treatment and Preventionappropriate glycemic controlappropriate blood pressure control (<130/80 mmHg)use either ACEI or ARB (often used first line for their CVD protection)limit use of nephrotoxic drugs and dyes

Diabetic NeuropathyEpidemiology

approximately 50% of patients within 10 yr of onset of type 1 DM and type 2DM

Pathophysiologycan have peripheral sensory neuropathy, motor neuropathy, or autonomicneuropathymechanism poorly understoodacute cranial nerve palsies and diabetic amyotrophy are thought to be due toischemic infarction of peripheral nervethe more common motor and sensory neuropathies are thought to be relatedto metabolic or osmotic toxicity secondary to increased sorbitol and/ordecreased myoinositol (possible mechanisms include accumulation ofadvanced glycation endproducts [AGE], oxidative stress, protein kinase C,nerve growth factor deficiency)

Screening• 128 Hz tuning fork or 10 g monofilament

Treatment and Management forDiabetic Neuropathy

Tight glycemic controlFor neuropathic pain syndromes: tricyclic antidepressants(e.g. amitriptyline), pregabalin, duloxetine, anti epileptics(e.g. carbamazepine, gabapentin), and capsaicinFoot care educationJobst® fitted stocking and tilting of head of bed maydecrease symptoms of orthostatic hypotensionTreat gastroparesis with domperidone and/ormetoclopramide (dopamine antagonists), erythromycin(stimulates motilin receptors)Medical, mechanical, and surgical treatment for erectiledysfunction

Other ComplicationsDermatologic

Diabetic dermopathy: atrophic brown spots commonly in pretibial region known as “shinspots”, secondary to increased glycosylation of tissue proteins or vasculopathyEruptive xanthomas secondary to increased triglyceridesNecrobiosis lipoidica diabeticorum: rare complication characterized by thinning skin over theshins allowing visualization of subcutaneous vessels

Bone and Joint DiseaseJuvenile cheiroarthropathy: chronic stiffness of hand caused by contracture of skin over jointssecondary to glycosylated collagen and other connective tissue proteinsDupuytren’s contractureBone demineralization: bone density 10 20% below normalAdhesive capsulitis (“frozen shoulder”)

CataractsSubcapsular and senile cataracts secondary to glycosylated lens protein or increased sorbitolcausing osmotic change and fibrosis

Infections

Clinical Presentations of DiabeticNeuropathies

Titrating Insulin Doses Insulin Regimen for T2DM and T1DM

Duration of Activity for DifferentInsulins

Available Insulin Formulations Available Insulin Formulations

Antiphyperglycemic Agents Comparison of T1DM and T2DM

Comparison of T1DM and T2DM Comparison of T1DM and T2DM

Etiological Classification of DM

Diagnosis of Prediabetes and Diabetes Goals of Therapy in Diabetes

Assessment and Monitoring

Management of Hyperglycemia inT2DM