Your FREE CDCES Flashcards 2026 – 250+ Cards

Certified Diabetes Care and Education Specialist (formerly CDE, renamed 2020).

The Certification Board for Diabetes Care and Education (CBDCE), formerly the NCBDE.

Autoimmune destruction of pancreatic beta cells → absolute insulin deficiency; requires exogenous insulin.

Insulin resistance plus progressive beta-cell dysfunction (relative insulin deficiency).

Latent Autoimmune Diabetes in Adults — a slow-onset autoimmune (type 1) diabetes in adults, often misdiagnosed as type 2.

Maturity-Onset Diabetes of the Young — a monogenic (single-gene), inherited diabetes; often non-insulin-dependent.

Polyuria, polydipsia, polyphagia (plus weight loss and fatigue).

Cells respond poorly to insulin, so the pancreas compensates with higher insulin output until beta cells fail.

Central obesity, high triglycerides, low HDL, hypertension, and elevated fasting glucose (>= 3 of 5).

Secreted by pancreatic alpha cells; raises blood glucose by stimulating hepatic glycogenolysis and gluconeogenesis.

Secreted by beta cells; lowers glucose by promoting cellular uptake and storage (glycogenesis), and inhibiting hepatic glucose output.

Gut hormones released after eating that stimulate glucose-dependent insulin secretion and suppress glucagon.

Glucagon, epinephrine, cortisol, growth hormone — raise glucose and oppose insulin (e.g., during stress/illness).

A temporary period after diagnosis when residual beta-cell function lowers insulin needs; not a cure.

High glucose pulls water osmotically and causes osmotic diuresis, leading to thirst.

Without insulin, cells cannot use glucose, so the body breaks down fat and muscle for energy.

Blurred vision, fatigue, slow-healing wounds, recurrent infections, and weight loss.

Pancreatitis/pancreatectomy, Cushing syndrome, acromegaly, glucocorticoids, and certain medications.

Declines progressively, so therapy is intensified over time (often adding insulin eventually).

LADA progresses slowly to insulin dependence; classic type 1 in youth presents abruptly with DKA risk.

Chronic hyperglycemia further impairs beta-cell function and insulin sensitivity, worsening control.

< 7% (individualize; ADA Standards of Care).

80-130 mg/dL for most nonpregnant adults.

< 180 mg/dL (1-2 hours after the start of a meal).

>= 6.5% (confirmed with a repeat test unless clearly symptomatic with marked hyperglycemia).

5.7-6.4% (also FPG 100-125 mg/dL or 2-hr OGTT 140-199 mg/dL).

>= 126 mg/dL (fasting = no caloric intake for >= 8 hours).

>= 200 mg/dL 2 hours after a 75 g oral glucose load.

>= 200 mg/dL WITH classic symptoms of hyperglycemia (polyuria, polydipsia, weight loss).

Glucose attached (glycated) to hemoglobin in red blood cells — reflects average glucose over ~2-3 months.

~154 mg/dL (each 1% A1C change ≈ 28-29 mg/dL).

Hemoglobinopathies, recent transfusion, hemolysis, pregnancy, anemia, or shortened RBC lifespan.

GAD65, IA-2, ZnT8, and islet cell autoantibodies confirm autoimmune (type 1) diabetes.

A marker of endogenous insulin production; low/absent in type 1, normal/high in early type 2.

At least twice a year if at goal/stable; quarterly if therapy changed or not meeting goals.

Adults with overweight/obesity plus a risk factor, and all adults beginning at age 35 (ADA).

Without symptoms it lacks specificity, so fasting glucose or A1C is preferred for diagnosis.

Repeat the same test (or two different tests) above threshold, unless clearly symptomatic with marked hyperglycemia.

75 g oral glucose; diagnostic sample at 2 hours.

Medical history, medications, psychosocial/behavioral factors, readiness to learn, literacy, culture, and support systems.

Identify the stage of change, learning preferences, barriers, and what matters most to the person before teaching.

Positive islet autoantibodies (GAD65, etc.) and low C-peptide point to type 1/LADA.

If A1C is unreliable, use fructosamine, glycated albumin, or CGM/SMBG data for assessment.

No caloric intake for at least 8 hours before the fasting plasma glucose draw.

A single abnormal value can be transient; confirmation (unless clearly symptomatic) avoids misdiagnosis.

< 180 mg/dL, measured 1-2 hours after the start of the meal.

Metformin (a biguanide) — unless contraindicated.

Decreases hepatic glucose production and improves insulin sensitivity; does NOT cause hypoglycemia alone.

GI upset (nausea, diarrhea); take with meals and titrate slowly. Hold around iodinated contrast/renal impairment (lactic-acidosis risk).

Stimulate pancreatic insulin secretion; main risks are hypoglycemia and weight gain (e.g., glipizide, glimepiride).

'Gliptins' (sitagliptin) increase incretin levels; weight-neutral, low hypoglycemia risk, modest A1C lowering.

'Flozins' (empagliflozin) block renal glucose reabsorption → glucosuria; benefit heart failure and CKD; cardiorenal protection.

Genital mycotic infections, volume depletion, and euglycemic DKA (DKA with near-normal glucose).

'-tides' (semaglutide, liraglutide) enhance glucose-dependent insulin, slow gastric emptying, promote weight loss & cardiovascular benefit.

Nausea (often improves with gradual dose escalation); also delayed gastric emptying.

Dual GIP/GLP-1 receptor agonist — strong A1C lowering and weight loss.

Pioglitazone improves insulin sensitivity; risks: weight gain, edema, heart-failure exacerbation, fracture.

Lispro, aspart, glulisine: onset ~15 min, peak ~1-2 hr, duration ~3-5 hr; dose at the meal.

Onset ~30 min, peak ~2-3 hr, duration ~5-8 hr; give ~30 min before meals.

Onset ~1-2 hr, peak ~4-12 hr, duration ~12-18 hr; the cloudy insulin — roll to mix.

Glargine, detemir, degludec: relatively peakless, duration ~24 hr (degludec > 42 hr); covers background needs.

Long-acting insulin for background needs PLUS rapid-acting insulin at each meal — mimics physiologic secretion.

Clear before cloudy — draw up regular (clear) first, then NPH (cloudy), to avoid contaminating the regular vial.

Units of rapid insulin per grams of carb (e.g., 1 unit per 10 g); covers the meal carbohydrate.

How many mg/dL one unit of insulin lowers glucose; correction dose = (current - target) / factor.

ICR 1:10, factor 1u/50, eat 50 g at 200 mg/dL (target 100): 5 u (carb) + 2 u (correction) = 7 units.

Delivers continuous rapid-acting insulin (basal) plus user-triggered meal/correction boluses; no long-acting insulin used.

Store unopened insulin in the refrigerator; in-use vials/pens can stay at room temperature ~28 days; never freeze.

Repeated injection at one spot causes fatty lumps that erratically alter absorption; rotate sites within a region.

GLP-1 receptor agonists (and dual GIP/GLP-1 tirzepatide).

Slows gastric emptying and suppresses glucagon; used with mealtime insulin; risk of hypoglycemia.

Ultra-long: > 42 hours, allowing flexible dosing times.

Combines intermediate + rapid/short insulin in fixed ratio; convenient but less flexible for carb matching.

Most pens stay at room temperature for a labeled number of days (commonly 28); never freeze.

Abdomen (fastest), then arm, thigh, buttock (slowest); keep the body region consistent for a given time of day.

Metformin, DPP-4 inhibitors, SGLT2 inhibitors, GLP-1 agonists, TZDs (low risk); sulfonylureas and insulin DO.

Long-term metformin can lower vitamin B12; monitor periodically, especially with neuropathy or anemia.

Hold during acute illness/dehydration/surgery to reduce euglycemic DKA risk ('SADMANS' / sick-day medication guidance).

ADA recommends them (independent of A1C) for established ASCVD, heart failure, or CKD.

Considered for secondary prevention (established ASCVD); not routine for primary prevention due to bleeding risk.

Inhaled and rapid-acting analogs act fastest; regular is slower; basal insulins act slowest and longest.

Glucocorticoids most raise post-lunch and afternoon glucose; often need added/adjusted insulin.

Insulin pump therapy delivering rapid-acting insulin continuously with mealtime boluses.

Basal covers background hepatic glucose; stopping it (especially in type 1) risks DKA.

Local or systemic reactions can occur; analog insulins reduce immunogenicity vs older preparations.

Insulin can cause weight gain; pair with nutrition/activity, and consider weight-favorable agents (GLP-1, SGLT2).

Can induce type 2 remission/improvement; an option for selected patients with obesity and diabetes.

Standard insulin is U-100 (100 units/mL); always use an insulin syringe/pen matched to concentration.

Deliver more units in less volume for high-dose needs; dosing errors are dangerous — verify the device.

Its onset matches meal absorption; dosing too early or late risks hypo- or hyperglycemia.

Avoid stacking — wait for the prior rapid-insulin dose to act (insulin-on-board) before re-correcting.

Active insulin still working from a prior dose; pumps track it to prevent dose stacking and lows.

Both long-acting basal analogs; glargine ~24 hr, detemir sometimes twice daily; relatively peakless.

NPH's mid-action peak can cause hypoglycemia hours later; time meals/snacks accordingly.

Change the set and site every 2-3 days to prevent absorption problems and infection.

Given before meals, separate from insulin; reduces post-meal glucose spikes.

A rapid-acting mealtime option (Afrezza); contraindicated in asthma/COPD; check lung function.

If A1C remains above target after lifestyle + metformin, add agents based on comorbidities/cost/preference.

With very high A1C/glucose, symptoms of catabolism, or when other agents fail to reach goal.

Titrate based on fasting glucose trends, raising/lowering by small increments to reach the fasting target.

Use post-meal and pre-next-meal glucose; refine the carb ratio and correction factor over time.

> 70% of readings in 70-180 mg/dL, with < 4% below 70 and < 1% below 54.

~15 grams of carbohydrate.

Fill half the 9-inch plate with nonstarchy vegetables, one quarter lean protein, one quarter carbohydrate foods.

Match mealtime insulin to grams of carbohydrate eaten for flexible, accurate dosing.

Ranks carbohydrate foods by how quickly they raise blood glucose; lower-GI foods cause a slower rise.

Slows glucose absorption, improves satiety and lipids; aim for whole grains, legumes, vegetables, and fruit.

Individualized, evidence-based nutrition care from a registered dietitian; a core DSMES component.

Alcohol can cause delayed hypoglycemia by suppressing hepatic glucose output; consume with food and monitor.

>= 150 min/week of moderate-intensity activity spread over >= 3 days, with no more than 2 consecutive days off.

Activity increases insulin sensitivity; those on insulin/secretagogues may need carbs or reduced insulin to avoid lows (including delayed/overnight).

Avoid vigorous exercise if glucose > 240-250 mg/dL with ketones — it can worsen hyperglycemia/ketosis.

Fingerstick capillary glucose; timing (fasting, pre/post-meal, bedtime) guides therapy adjustments.

A sensor measures interstitial glucose continuously, showing trends, time in range, and alerts for highs/lows.

Interstitial glucose lags blood glucose ~5-15 min, most noticeable when glucose is changing rapidly.

A CGM and insulin pump communicate via an algorithm to auto-adjust basal insulin (and some boluses).

A CGM-derived estimate of A1C based on average sensor glucose.

Early-morning hyperglycemia from a natural surge of counterregulatory hormones (cortisol, growth hormone).

Overnight hypoglycemia triggering rebound morning hyperglycemia; check ~3 a.m. glucose to distinguish from dawn phenomenon.

Low-carb vegetables (leafy greens, broccoli, peppers) that fill half the plate and minimally raise glucose.

Use Total Carbohydrate (includes fiber and sugars), serving size, and servings per container for carb counting.

Glycemic load accounts for both the GI and the amount of carbohydrate in a typical serving.

Sweeteners (sorbitol, xylitol) with less glycemic impact; excess can cause GI upset/diarrhea.

2-3 sessions/week on nonconsecutive days, in addition to aerobic activity.

If on insulin/secretagogues and glucose is low/borderline, have carbohydrate available to prevent exercise-induced hypoglycemia.

A standardized one-page CGM report summarizing time in range, variability, and glucose patterns.

A measure of glucose variability; target <= 36% (lower = more stable glucose).

When symptoms don't match the reading, during rapid changes, or per device instructions before dosing.

Improves time in range and reduces hypoglycemia by automating basal adjustments using CGM data.

Wide swings increase hypoglycemia and may worsen complications independent of average glucose.

Wash hands, use the side of the fingertip, rotate sites, and don't reuse lancets; first drop may be wiped if dirty.

1-2 hours after the start of the meal, when post-meal targets are a concern (e.g., pregnancy).

Evidence-based patterns emphasizing vegetables, whole grains, lean protein, and healthy fats for diabetes.

Add total grams from all carbohydrate foods; fat/protein can slow absorption and delay the glucose rise.

Fasting/basal driven by overnight hepatic output; postprandial driven by mealtime carbohydrate and bolus timing.

Match the device (CGM, pump, AID) to the person's needs, dexterity, literacy, and access.

Set low/high alerts and use trend arrows to act before reaching dangerous levels.

Record frequency, severity, timing, and likely causes to guide regimen and target changes.

Treat glucose < 70 mg/dL with 15 g fast-acting carbohydrate, recheck in 15 minutes, repeat if still < 70.

Glucose < 70 mg/dL (>= 54) — an alert value requiring fast-acting carbohydrate.

Glucose < 54 mg/dL — clinically significant; sufficient to cause neuroglycopenic symptoms.

Severe cognitive/physical impairment requiring assistance from another person to recover.

For severe hypoglycemia when the person cannot safely swallow; give injectable/nasal glucagon and call for help; position on side.

Loss of warning symptoms from frequent lows; managed by raising targets and avoiding lows for several weeks to restore awareness.

Eat a snack with carbohydrate and protein to sustain glucose until the meal.

Diabetic ketoacidosis: mainly type 1; absolute insulin deficiency → hyperglycemia, ketosis, and metabolic acidosis.

Glucose usually > 250 mg/dL, ketones present, pH < 7.3, low bicarbonate, anion-gap acidosis.

Kussmaul (deep rapid) breathing, fruity (acetone) breath, abdominal pain, dehydration, and altered mental status.

IV fluids first, then IV insulin, and potassium replacement/monitoring (insulin drives K+ into cells).

Mainly type 2; extreme hyperglycemia (often > 600 mg/dL), severe dehydration, very high osmolality, minimal/no ketones.

DKA has significant ketosis/acidosis; HHS has profound hyperglycemia and dehydration with little/no ketosis.

Never stop insulin when ill; illness raises glucose (stress hormones). Keep taking basal insulin even if not eating.

Check glucose & ketones more often, stay hydrated, continue insulin, and seek care for persistent ketones/vomiting.

Damage to retinal blood vessels — the leading cause of new adult blindness; screen with annual dilated eye exam.

Annual urine albumin-to-creatinine ratio (UACR) and eGFR; ACE inhibitors/ARBs and SGLT2 inhibitors slow progression.

Distal symmetric peripheral neuropathy (numbness/tingling/pain in feet); raises ulcer and amputation risk.

Gastroparesis, orthostatic hypotension, erectile dysfunction, hypoglycemia unawareness.

Daily inspection, well-fitting shoes, never barefoot, no soaking, lukewarm water, cut nails straight, annual comprehensive foot exam.

ASCVD is the leading cause of death in diabetes; manage BP, lipids (statins), glucose, and smoking cessation.

Generally < 130/80 mmHg for most adults with diabetes (individualize).

Recommended for most adults 40-75 with diabetes for ASCVD risk reduction, regardless of baseline LDL.

Stress hormones (cortisol, epinephrine) increase hepatic glucose production and insulin resistance.

Fat breakdown for fuel when insulin is insufficient; elevated ketones warn of impending DKA.

When glucose is persistently > 240 mg/dL, during illness, or with DKA symptoms (especially in type 1).

Symptoms of hypoglycemia, a low measured glucose, and relief of symptoms when glucose is raised.

Shakiness, sweating, palpitations, hunger, anxiety — from epinephrine release.

Confusion, difficulty concentrating, slurred speech, behavior change, seizures — brain glucose deprivation.

4 glucose tablets, 4 oz (1/2 cup) regular juice or soda, 1 tablespoon honey/sugar — avoid fat (slows absorption).

Their fat slows carbohydrate absorption, delaying glucose recovery.

Check expiration periodically; ensure family knows where it is and how to use it; replace after use.

Continue insulin, check ketones when glucose is high or ill, hydrate, and seek care for persistent ketones.

SGLT2 inhibitors can cause DKA with near-normal glucose; check ketones even when glucose isn't very high.

Delayed stomach emptying causes unpredictable post-meal glucose; consider timing insulin and smaller, low-fat meals.

Progressive joint/bone destruction in the neuropathic foot; a podiatric emergency needing offloading.

Early good control reduces long-term microvascular and macrovascular complications (DCCT/UKPDS legacy effect).

Retinopathy, nephropathy, and neuropathy — small-vessel damage from chronic hyperglycemia.

Coronary artery disease, stroke, and peripheral artery disease — large-vessel atherosclerosis.

A1C, BP, lipids, UACR & eGFR, dilated eye exam, comprehensive foot exam, and vaccinations.

Greatly increases cardiovascular and microvascular risk; cessation counseling is a core part of care.

Insulin and correction of acidosis shift potassium into cells, risking dangerous hypokalemia.

IV isotonic fluids restore volume and improve perfusion before/with insulin therapy.

A serious complication; fluids/correction are managed cautiously to avoid rapid osmotic shifts.

Generally 140-180 mg/dL for most hospitalized patients (avoid tight control that risks hypoglycemia).

Pumps use only rapid insulin, so any interruption can quickly cause hyperglycemia/DKA — have a backup plan.

High triglycerides, low HDL, and small dense LDL — atherogenic; managed with statins and lifestyle.

First-line for hypertension with albuminuria; protects kidneys; monitor potassium and renal function.

Influenza, pneumococcal, hepatitis B, COVID-19, and others per CDC schedule.

Check glucose before driving; treat lows and wait until recovered; keep fast carbs in the vehicle.

Insulin (with glucose) is used to drive potassium into cells to treat hyperkalemia.

Persistent vomiting, dehydration, confusion, Kussmaul breathing, or fruity breath — seek emergency care.

Eat carbohydrate with alcohol, monitor overnight, and know glucagon may be less effective after drinking.

Redness, warmth, drainage, calluses, or a non-healing wound — report promptly to prevent amputation.

A 10-g monofilament screens for protective-sensation loss (peripheral neuropathy) on the feet.

Common from autonomic neuropathy and vascular disease; assess and address sensitively.

Measure BP at every routine visit; confirm elevated readings and treat to target.

Beta-blockers can mask adrenergic warning symptoms (except sweating) — teach extra monitoring.

Infection, missed insulin, new-onset type 1, pump failure, MI, or certain medications.

Infection, dehydration, limited water access (often older adults), and certain medications.

Older, sicker patients with profound dehydration, comorbidities, and delayed recognition.

Once alert and able to swallow, give oral carbohydrate to replenish glycogen; monitor for recurrence.

Resting tachycardia and orthostatic hypotension; raises silent-ischemia and arrhythmia risk.

Retinopathy is often asymptomatic until advanced; early detection allows sight-saving treatment.

Blunted glucagon/epinephrine responses contribute to hypoglycemia unawareness.

Both treat severe hypoglycemia; nasal needs no reconstitution and is easier for caregivers.

Prevent acute and chronic complications while minimizing hypoglycemia and preserving quality of life.

Hyperglycemia first recognized in pregnancy from placental hormones causing insulin resistance; usually 2nd-3rd trimester.

Diabetes Self-Management Education and Support.

At diagnosis, annually/when not meeting goals, when complicating factors develop, and during care transitions.

Healthy Eating, Being Active, Monitoring, Taking Medication, Problem Solving, Healthy Coping, Reducing Risks.

The self-care behavior addressing diabetes distress, burnout, depression, and emotional well-being.

Applying skills to handle hypo/hyperglycemia, sick days, and barriers as they arise.

Precontemplation, Contemplation, Preparation, Action, Maintenance — match the intervention to the stage.

Already checking glucose daily and actively asking how to improve the routine.

A collaborative, person-centered style that elicits the person's own motivation to change; uses open-ended questions and reflective listening.

A person's capacity to obtain, understand, and use health information; teach plainly, use teach-back, avoid jargon.

Have the person explain the instruction in their own words to confirm understanding — not 'Do you understand?'

Care built on the person's values, preferences, and goals through partnership and respect for autonomy.

The emotional burden of living with diabetes; distinct from clinical depression, common, and addressed under Healthy Coping.

Emphasize hands-on practice and return demonstrations rather than written or verbal instruction alone.

Specific, Measurable, Achievable, Relevant, Time-bound — the framework for setting behavior-change goals.

Quality criteria a program must meet to deliver effective, evidence-based diabetes education and support (used for recognition/accreditation).

ADA recommends an A1C < 7% for most children/adolescents with type 1 (individualize).

Fasting < 95 mg/dL, 1-hr postprandial < 140, 2-hr postprandial < 120 mg/dL.

Medical nutrition therapy and activity; insulin is the preferred medication if targets aren't met.

Healthy older adults < 7-7.5%; complex/frail < 8-8.5%; prioritize avoiding hypoglycemia (deintensify when needed).

Higher risk of falls, cognitive impairment, and unawareness; favor agents with low hypoglycemia risk.

75 g 2-hr OGTT at 24-28 weeks; any one abnormal value (fasting >= 92, 1-hr >= 180, 2-hr >= 153) diagnoses GDM.

Adapt nutrition, language, and goals to the person's culture, food traditions, and beliefs.

Behaviors that prevent complications: monitoring, screenings, foot/eye care, immunizations, smoking cessation.

Safe, effective, consistent use of medications, including barriers like cost, access, and adherence.

Incorporating physical activity safely into daily life, individualized to ability and goals.

Tracking glucose, A1C, BP, weight, and other markers, and using the data to guide decisions.

Making informed food choices, understanding portions and carbohydrate, and meal planning.

The person is the primary decision-maker; the specialist provides knowledge, skills, and support.

Use aggregated outcome data (behavioral and clinical) to evaluate and guide program improvement.

Education, support, and care coordination within the specialist's licensure; collaborate for prescribing/diagnosis.

Record assessment, goals, education provided, the person's response, and the follow-up plan.

More common with tight targets; treat promptly and adjust insulin; severe lows risk maternal/fetal harm.

Screen with a 75 g OGTT at 4-12 weeks postpartum; lifelong increased type 2 risk warrants periodic screening.

Requirements rise through the 2nd-3rd trimester (placental insulin resistance) and drop sharply after delivery.

Behavioral: an action the person will take (walk 20 min daily). Clinical: a measurable outcome (A1C < 7%).

A person's confidence in their ability to perform a behavior; building it improves self-management.

'What is the hardest part of living with diabetes for you?' invites the person to share concerns.

Behavior depends on perceived susceptibility, severity, benefits, barriers, cues to action, and self-efficacy.

Conditions like food access, income, housing, and transportation that strongly affect diabetes outcomes.

Limited access to affordable healthy food worsens glycemic control; screen and connect to resources.

Low numeracy impairs dosing/carb math; simplify with visual portions, plate method, or fixed-dose plans.

Both are effective; choose by the person's needs, complexity, learning style, and resources.

Diabetes self-management SUPPORT provides ongoing help to sustain behaviors after initial education.

Use 'person with diabetes,' not 'diabetic'; avoid judgmental terms like 'noncompliant' (use 'barriers').

Aim for < 6% if achievable without significant hypoglycemia (individualize up to < 7%).

For significant diabetes distress, depression, anxiety, disordered eating, or severe coping difficulty.

About twice as common as in the general population; screen and treat, as it impairs self-care.

Renewed periodically (every 5 years) by continuing education or re-examination through CBDCE.

Relax the target (e.g., < 8%) to prioritize safety, especially in frail older adults.

Intensive lifestyle (e.g., DPP): 7% weight loss + 150 min/week activity cuts progression to type 2 (metformin if high risk).

A structured CDC-recognized lifestyle program proven to reduce progression from prediabetes to type 2 diabetes.

Modest weight loss (5-10%) improves glycemia, BP, and lipids; significant loss can drive remission.

Medication/insulin use, glucose monitoring, hypo/hyperglycemia recognition and treatment, and when to seek help.

After survival skills: carb counting, sick-day rules, complication prevention, and lifestyle integration.

Assess behavior change and clinical outcomes (A1C, TIR), not just knowledge gained.

Set goals WITH the person (shared decision-making), not for them, to improve adherence.

Limited life expectancy, advanced complications, severe hypoglycemia history, or extensive comorbidity.

Expands access; effective for DSMES, CGM review, and follow-up support.

Balance complication prevention against hypoglycemia risk based on age, comorbidity, and life expectancy.

Emotional exhaustion from constant self-management; addressed under Healthy Coping with support and simplification.

Engage family for support, especially for hypoglycemia treatment and meal planning, with the person's consent.

Modify portions and preparation of traditional foods rather than eliminating them, to support adherence.

Programs review aggregate outcomes and processes regularly to improve education delivery.

An expert in DSMES who bridges the medical plan and the person's daily self-management.