Eduovisual
Endocrine
Diabetes: ADA screening guidelines and diagnostic criteria
— ~38 million US adults have diabetes; ~1 in 5 are undiagnosed
— Another ~98 million have prediabetes; >80% unaware
— Type 2 DM accounts for ~90–95% of cases; type 1 ~5–10%; remainder are monogenic (MODY), pancreatogenic, drug-induced, or gestational
— Primary care owns screening, diagnosis, and longitudinal risk reduction
— Early detection prevents microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (ASCVD, stroke, PAD) disease
— Screening is a USPSTF Grade B recommendation in adults 35–70 with overweight/obesity — translates to insurance coverage without cost-sharing
— Classic triad: polyuria, polydipsia, unintentional weight loss
— Recurrent candidal vulvovaginitis, balanitis, or skin infections
— Acanthosis nigricans, skin tags, or new-onset erectile dysfunction
— Blurry vision from osmotic lens changes
— Incidental glucosuria, hyperglycemia on routine CMP, or HbA1c run as part of pre-op workup
— Recurrent UTIs or slow-healing wounds in middle-aged adults
— Acute presentation: DKA in a lean adult (think type 1 or LADA), HHS in elderly with infection
— Non-Hispanic Black, Hispanic/Latino, American Indian, Asian American, Pacific Islander
— Lower socioeconomic status, food-insecure patients
— Patients with severe mental illness on second-generation antipsychotics
Board pearl: On Step 3, an asymptomatic 42-year-old with BMI 31 presenting for a "physical" is the prototypical screening vignette — the correct answer is order HbA1c (or FPG), not "reassure and recheck in 3 years." The trigger is age ≥35 plus overweight, regardless of family history or symptoms. If the patient is symptomatic with random glucose ≥200, you skip screening logic and move straight to diagnostic confirmation.
— Adult presenting for annual visit, pre-employment physical, or insurance exam
— BMI ≥25 (≥23 in Asian Americans) with ≥1 risk factor, OR age ≥35 regardless of BMI
— Risk factors: first-degree relative with DM, HTN (≥130/80 or on therapy), HDL <35 or TG >250, PCOS, physical inactivity, prior GDM, prior CVD, acanthosis nigricans
— Polyuria/nocturia, polydipsia, polyphagia
— Weight loss despite increased intake (more typical of T1DM/LADA)
— Fatigue, blurred vision, paresthesias
— Recurrent mucocutaneous infections
— DKA: nausea/vomiting, abdominal pain, Kussmaul breathing, fruity breath — classically T1DM but seen in T2DM (ketosis-prone) and SGLT2i users (euglycemic DKA)
— HHS: profound dehydration, altered mentation, often elderly with intercurrent illness
— Family history of DM, autoimmune disease (T1DM clue: vitiligo, Hashimoto, celiac, Addison)
— Obstetric history: GDM, macrosomic infant (>9 lb), stillbirth
— Medication review: glucocorticoids, atypical antipsychotics (olanzapine, clozapine), thiazides, tacrolimus, protease inhibitors, statins (small effect), niacin
— Pancreatic history: chronic pancreatitis, pancreatectomy, hemochromatosis, CF
— Endocrinopathies: Cushing, acromegaly, pheochromocytoma, hyperthyroidism
— Social: diet pattern, physical activity, sleep apnea symptoms, tobacco/alcohol
Key distinction: A lean adult <35 with rapid weight loss, DKA, or strong autoimmune family history should prompt type 1 workup (GAD-65, IA-2, ZnT8, insulin autoantibodies, C-peptide) — not reflexive metformin initiation. LADA is frequently misclassified as T2DM; suspect when "T2DM" fails oral agents within 6–12 months despite adherence and weight loss. Documenting these features changes downstream therapy and screening cadence.
— Height, weight, BMI, waist circumference (>40" men, >35" women = increased risk)
— Blood pressure both arms; orthostatics if autonomic neuropathy suspected
— Acanthosis nigricans: velvety hyperpigmentation at neck, axillae, groin — marker of insulin resistance
— Skin tags (acrochordons), often co-located with acanthosis
— Necrobiosis lipoidica diabeticorum: yellow-brown atrophic plaques on shins
— Diabetic dermopathy: "shin spots," brown atrophic macules
— Eruptive xanthomas if marked hypertriglyceridemia
— Granuloma annulare, bullosis diabeticorum
— Fundoscopy for retinopathy (microaneurysms, dot-blot hemorrhages, exudates, neovascularization)
— Thyroid exam (autoimmune overlap in T1DM)
— Oral exam for periodontal disease
— Carotid bruits, peripheral pulses (DP, PT), capillary refill
— ABI if claudication or diminished pulses
— Inspection for calluses, ulcers, deformity (Charcot foot, hammer toes)
— 10-g monofilament at 4 sites per foot; vibration with 128-Hz tuning fork; ankle reflexes; pinprick
— Loss of protective sensation = annual or more frequent comprehensive foot care
— Distal symmetric stocking-glove sensory loss
— Autonomic signs: resting tachycardia, orthostasis, gastroparesis clues
Step 3 management: At every diabetes visit, document a foot exam, BP, and BMI; at diagnosis and annually thereafter perform a comprehensive foot exam with monofilament, dilated retinal exam (or validated retinal photography), and screen for albuminuria with urine albumin-to-creatinine ratio plus eGFR. These are heavily tested HEDIS/quality measures and frequent CCS order-set components — missing them on a longitudinal case will cost points.
— HbA1c ≥6.5% — NGSP-certified, DCCT-standardized assay
— Fasting plasma glucose (FPG) ≥126 mg/dL — fasting ≥8 hours
— 2-hour plasma glucose ≥200 mg/dL during 75-g OGTT
— Random plasma glucose ≥200 mg/dL in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis
— In the absence of unequivocal hyperglycemia, diagnosis requires two abnormal results — either two different tests at the same time, or the same test repeated on a separate day
— If two different tests are both diagnostic, no repeat needed
— If two different tests are discordant, repeat the abnormal one
— HbA1c 5.7–6.4%
— Impaired fasting glucose (IFG): FPG 100–125 mg/dL
— Impaired glucose tolerance (IGT): 2-hr OGTT 140–199 mg/dL
— Conditions affecting RBC turnover invalidate HbA1c: hemolytic anemia, recent transfusion, EPO therapy, end-stage CKD, hemoglobinopathies (use fructosamine or glucose-based testing)
— Sickle cell trait/disease: use HbA1c assays validated for variants
— Iron deficiency falsely elevates HbA1c; treat first or use glucose-based testing
— Pregnancy: HbA1c is not used to diagnose GDM (separate criteria)
— Lipid panel, comprehensive metabolic panel, eGFR, urine albumin-to-creatinine ratio
— TSH (especially T1DM), LFTs (NAFLD screen)
— Hepatitis B screening before vaccination per ACIP/ADA
Board pearl: A single HbA1c of 7.2% in an asymptomatic patient is not sufficient — repeat the same test (or order a confirmatory FPG) on a separate day before labeling the patient diabetic. Mislabeling carries insurance and life-event consequences.
— Lean adult, rapid presentation, DKA, family history of autoimmunity → suspect T1DM/LADA
— Multigenerational autosomal dominant DM, onset <25, lean, mild fasting hyperglycemia, no autoimmunity → suspect MODY
— Hyperpigmentation, arthropathy, hepatomegaly, cardiomyopathy → hemochromatosis (check ferritin, transferrin saturation)
— Steatorrhea, weight loss, alcohol use, pancreatic calcifications → pancreatogenic (T3c) DM
— GAD-65 antibodies (highest yield in adults), IA-2, ZnT8, insulin autoantibodies (mainly in children)
— C-peptide (fasting, with simultaneous glucose): low or undetectable supports insulin deficiency
— Positive antibodies + young age + rapid progression → T1DM
— Positive antibodies + adult onset + initial response to orals → LADA
— Genetic testing (HNF1A, GCK, HNF4A most common); refer to endocrinology/genetics
— GCK-MODY: stable mild fasting hyperglycemia, no treatment typically needed, no microvascular complications
— Cushing: late-night salivary cortisol, 1-mg DST, 24-hr UFC
— Acromegaly: IGF-1
— Pheochromocytoma: plasma or 24-hr urinary metanephrines
— Hemochromatosis: iron studies → HFE genotyping
— ASCVD 10-year risk calculation (Pooled Cohort Equations)
— UACR and eGFR (CKD staging)
— Liver enzymes; if elevated or NAFLD risk, FIB-4 to triage for fibrosis
Key distinction: A 28-year-old with "T2DM" failing metformin + sulfonylurea in 6 months and progressively losing weight needs antibody testing and C-peptide, not another oral agent. Reclassifying to LADA changes therapy to insulin and prevents DKA on the next viral illness or SGLT2i prescription.
— Screen adults 35–70 with overweight or obesity for prediabetes and T2DM (Grade B)
— Offer or refer those with prediabetes to effective preventive interventions
— Screen all adults beginning at age 35, regardless of BMI
— Screen adults of any age with BMI ≥25 (≥23 in Asian Americans) plus ≥1 risk factor:
— First-degree relative with DM
— High-risk race/ethnicity
— History of CVD, HTN (≥130/80 or treated), HDL <35 and/or TG >250
— PCOS, physical inactivity, acanthosis nigricans
— Prior GDM (screen lifelong, at least every 3 years)
— Patients with prediabetes: rescreen annually
— Patients with HIV: screen at entry to care, before/after ART changes, then annually
— Begin at puberty or age ≥10, whichever earlier, in youth with overweight/obesity plus ≥1 risk factor (maternal GDM, family history, high-risk ethnicity, signs of insulin resistance)
— Repeat every 3 years (more often if BMI rising)
— Every 3 years if results normal; sooner if risk factors change or symptoms develop
— HbA1c, FPG, or 75-g OGTT — all acceptable
— HbA1c preferred for convenience (no fasting); OGTT most sensitive but least practical
— Initiate or escalate screening when starting chronic glucocorticoids, atypical antipsychotics, or post-transplant immunosuppression
Step 3 management: For a 36-year-old with normal BMI, no symptoms, and no risk factors, the ADA still recommends screening starting at age 35. Don't be tricked into "low risk, no screen." If the screen is normal, the correct next-step interval is 3 years, not 1 year. For prior GDM, rescreen at 4–12 weeks postpartum with 75-g OGTT, then at least every 3 years lifelong.
— Diabetes Prevention Program (DPP): structured lifestyle program reduces progression to T2DM by ~58% (vs 31% with metformin) over 3 years
— Goals: 7% weight loss, ≥150 minutes/week moderate-intensity activity
— Refer to CDC-recognized National DPP — Medicare covers (MDPP benefit) for eligible beneficiaries
— Mediterranean, DASH, or plant-forward diets all acceptable; emphasize fiber, whole grains, reduced refined carbs and sugar-sweetened beverages
— Consider in patients with prediabetes who are:
— BMI ≥35
— Age <60
— Women with prior GDM
— Rising HbA1c despite lifestyle, or HbA1c 6.0–6.4%
— Start 500 mg daily with meals, titrate to 1000 mg BID as tolerated
— Monitor B12 annually with long-term use
— Recheck HbA1c (or FPG) annually
— Reassess CV risk factors at each visit; treat HTN and lipids aggressively
— Screen for and treat OSA, NAFLD
— Intensive behavioral therapy (Medicare-covered in primary care)
— Pharmacotherapy (semaglutide, tirzepatide, phentermine/topiramate, naltrexone/bupropion, orlistat) for BMI ≥30 or ≥27 with comorbidity
— Bariatric/metabolic surgery for BMI ≥35 with comorbidity, or ≥30 with poorly controlled DM
— Treat HTN to <130/80 if tolerated
— Statin per ASCVD risk; prediabetes itself is not a statin trigger but often co-occurs with elevated risk
Board pearl: The single most evidence-based intervention for prediabetes is referral to a structured DPP program, not handing the patient a metformin script. On Step 3 vignettes, "refer to lifestyle program" outranks pharmacotherapy unless the patient has the BMI ≥35, age <60, or prior GDM criteria.
— Screen women with risk factors for undiagnosed T2DM at the first prenatal visit using standard non-pregnant criteria (HbA1c, FPG, or OGTT)
— Risk factors: BMI ≥25 (≥23 Asian American), prior GDM, family history, high-risk ethnicity, PCOS, HTN, prior macrosomia
— Diagnosis at this stage = overt diabetes in pregnancy, not GDM
— Two-step approach (most common in US):
— Step 1: 50-g glucose challenge (non-fasting); 1-hr plasma glucose
— Threshold ≥130, 135, or 140 mg/dL (institution-dependent) → proceed to step 2
— Step 2: 100-g 3-hour OGTT (fasting); diagnose GDM if ≥2 values meet/exceed:
— Fasting 95, 1-hr 180, 2-hr 155, 3-hr 140 (Carpenter-Coustan)
— One-step approach (IADPSG/ADA-acceptable):
— 75-g 2-hour OGTT (fasting); diagnose if any one value meets/exceeds:
— Fasting ≥92, 1-hr ≥180, 2-hr ≥153 mg/dL
— Medical nutrition therapy and exercise first-line
— Self-monitored blood glucose: fasting <95, 1-hr postprandial <140, 2-hr <120
— Pharmacotherapy if targets not met: insulin is first-line; metformin and glyburide cross placenta and are second-line
— Fetal surveillance and timed delivery per OB
— 75-g 2-hour OGTT at 4–12 weeks postpartum to reclassify
— Lifelong rescreening every 1–3 years
— Lifetime risk of T2DM ~50–70%; counsel on lactation, weight, contraception, lifestyle
— Encourage breastfeeding (reduces maternal and infant DM risk)
Step 3 management: A patient with prior GDM presenting for her 6-week postpartum visit needs a 75-g 2-hour OGTT, not an HbA1c. HbA1c is unreliable postpartum due to recent pregnancy-related RBC turnover and is not the ADA-recommended postpartum test. After that, transition to standard ADA rescreening at least every 3 years.
— Continue screening per ADA; do not stop based on age alone
— Individualize glycemic targets by health status:
— Healthy, few comorbidities, intact cognition → HbA1c <7.0–7.5%
— Complex/intermediate → <8.0%
— Very complex/poor health, limited life expectancy → <8.5%, avoid symptomatic hyperglycemia
— Avoid overtreatment; deprescribe sulfonylureas and tight insulin regimens in frail elderly
— Falsely low HbA1c: hemolysis, recent transfusion, EPO/iron/B12 therapy, advanced CKD on dialysis, pregnancy, splenomegaly
— Falsely high HbA1c: iron deficiency, B12 deficiency, splenectomy, hyperbilirubinemia, uremia, chronic alcohol use
— Hemoglobinopathies (HbS, C, E) require variant-tolerant assays
— In these cases, use FPG or OGTT; fructosamine and glycated albumin are alternatives but not ADA-diagnostic
— eGFR <30 or dialysis: HbA1c underestimates true glycemia; rely on glucose monitoring, CGM where available
— Screen all CKD patients for DM at diagnosis; manage with renally appropriate agents
— Cirrhosis is associated with high prevalence of "hepatogenous diabetes"
— HbA1c may be falsely low due to splenomegaly/hemolysis; use FPG/OGTT
— Screen pre-transplant; post-transplant DM (NODAT) screen weekly x 4 weeks, then 3, 6, 12 months
— FPG plus OGTT preferred; tacrolimus > cyclosporine for diabetogenicity
Key distinction: A dialysis patient with "HbA1c 6.2%" is not necessarily well-controlled or non-diabetic — HbA1c is unreliable in ESRD. Order FPG, fingerstick patterns, or CGM before drawing conclusions. Similarly, an iron-deficient woman with HbA1c 6.6% deserves iron repletion and repeat testing before being labeled prediabetic.
— Begin at age 10 or onset of puberty, whichever earlier
— Criteria: BMI ≥85th percentile plus ≥1 of:
— Maternal history of DM or GDM during the child's gestation
— Family history of T2DM in first- or second-degree relative
— High-risk race/ethnicity
— Signs of insulin resistance (acanthosis, HTN, dyslipidemia, PCOS, SGA birth weight)
— Repeat every 3 years (more often if BMI rising or risk increasing)
— Use FPG, HbA1c, or 2-hr OGTT
— No routine population screening
— Antibody screening considered in first-degree relatives within TrialNet/research settings
— Target HbA1c <6.5% before conception to reduce congenital anomalies and miscarriage
— Folic acid 400–800 mcg (some recommend higher for DM)
— Switch off teratogens: ACEi/ARB, statins, most non-insulin agents (continue metformin if needed)
— Retinal exam pre-pregnancy and each trimester; baseline UACR, TSH
— Screen for DM/prediabetes at diagnosis with OGTT (preferred) and every 3 years
— Higher prevalence of insulin resistance; screen at entry, before/after ART start or change, then annually
— Older protease inhibitors most diabetogenic
— Baseline FPG/HbA1c, lipids, weight, BP before starting; recheck at 3 months, then annually
— Olanzapine and clozapine highest risk
Board pearl: A 12-year-old with BMI in the 95th percentile, acanthosis nigricans, and a mother with T2DM should be screened now with HbA1c or FPG — pediatric T2DM is increasingly common and frequently tested. The first-line agents approved in pediatric T2DM are metformin, liraglutide, and insulin; sulfonylureas and most other agents are not approved in youth.
— Retinopathy: leading cause of new blindness in working-age adults; ~21% of T2DM have retinopathy at diagnosis → start dilated exam at diagnosis (T2DM) or within 5 years of diagnosis (T1DM, but after puberty)
— Nephropathy: leading cause of ESRD in US; screen with annual UACR and eGFR starting at diagnosis (T2DM) or 5 years after (T1DM)
— Neuropathy: distal symmetric polyneuropathy, autonomic neuropathy (gastroparesis, orthostasis, ED, silent ischemia), mononeuropathies
— 2–4x increased ASCVD risk; DM is a "CHD risk equivalent" for many treatment decisions
— Stroke, MI, peripheral arterial disease, heart failure (especially HFpEF)
— Neuropathy + PAD + minor trauma → ulceration → infection → amputation
— Annual comprehensive foot exam; refer high-risk patients to podiatry
— DKA: more common in T1DM; precipitants include infection, insulin omission, MI, new T1DM
— HHS: T2DM, elderly, infection; glucose often >600, marked hyperosmolality, minimal ketones
— Euglycemic DKA on SGLT2 inhibitors — hold during illness, surgery, prolonged fasting
— NAFLD/MASH (screen with FIB-4 annually in T2DM)
— Periodontal disease
— Obstructive sleep apnea (bidirectional relationship)
— Cognitive decline, depression (screen annually)
— Infections: emphysematous cholecystitis/pyelonephritis, mucormycosis, necrotizing fasciitis, malignant otitis externa
Step 3 management: At T2DM diagnosis, order lipid panel, UACR, eGFR, LFTs, TSH (if T1DM), and arrange dilated retinal exam and comprehensive foot exam. Do not wait 1–5 years as you would in T1DM — T2DM patients may have had unrecognized hyperglycemia for years and frequently already have complications at diagnosis.
— Suspected DKA: anion gap acidosis, ketonuria/ketonemia, glucose typically >250 (may be lower in euglycemic DKA on SGLT2i or in pregnancy)
— Suspected HHS: glucose >600, serum osm >320, altered mental status
— Severe hyperglycemia with dehydration, vomiting, or inability to tolerate PO
— Hypoglycemia with seizure, coma, or recurrent episodes despite outpatient adjustment
— New T1DM/DKA in a child or adolescent — pediatric admission
— Diabetic foot infection with systemic signs, deep abscess, osteomyelitis, or critical limb ischemia
— Suspected new T1DM/LADA without DKA (endocrinology within days; bridge with basal insulin if symptomatic)
— Pregnancy with new hyperglycemia → MFM + endocrinology
— Severe insulin resistance, atypical features, suspected MODY or monogenic DM
— Persistent HbA1c >9% despite multi-agent oral therapy
— Recurrent severe hypoglycemia or hypoglycemia unawareness
— Ophthalmology for dilated retinal exam
— Registered dietitian / certified diabetes care and education specialist (CDCES) — diabetes self-management education and support (DSMES) is covered by Medicare and most payers at diagnosis, annually, and at transitions
— Podiatry for high-risk feet (neuropathy, deformity, prior ulcer, PAD)
— Dental every 6 months
— Mental health for depression screening positives
— Counsel patient, order labs, schedule follow-up; advance clock 2–4 weeks for medication initiation effects, 3 months for HbA1c reassessment
CCS pearl: On a CCS case of newly diagnosed T2DM, the highest-yield non-pharmacologic orders are DSMES referral, nutrition counseling, retinal exam, foot exam, UACR, lipid panel, and pneumococcal/influenza/hepatitis B/COVID vaccinations. Missing these structured orders loses points even when your metformin and statin are correct.
— Elevated glucose during acute illness (sepsis, MI, stroke, trauma, burns, surgery)
— Does not diagnose diabetes; recheck after recovery with FPG or HbA1c
— HbA1c at admission helps distinguish: elevated → preexisting DM; normal → stress hyperglycemia (still confers future DM risk — rescreen in 3–6 months)
— Glucocorticoids — predominantly postprandial; afternoon/evening fingersticks miss morning normoglycemia
— Atypical antipsychotics — olanzapine, clozapine, quetiapine
— Calcineurin inhibitors (tacrolimus > cyclosporine), sirolimus
— Thiazides (dose-dependent, usually modest), beta-blockers (mild)
— Protease inhibitors, especially older agents
— Niacin, pentamidine, interferon, checkpoint inhibitors (can cause autoimmune T1DM)
— Chronic pancreatitis, prior pancreatectomy, pancreatic cancer, hemochromatosis, CF-related DM
— Often brittle control with both hyper- and hypoglycemia due to loss of glucagon
— Check fecal elastase if exocrine insufficiency suspected
— Cushing syndrome — central obesity, striae, proximal weakness, easy bruising
— Acromegaly — coarse features, ring/shoe size change, sweating
— Pheochromocytoma — episodic HTN, headaches, palpitations
— Hyperthyroidism — usually mild glucose elevation
— Glucagonoma — necrolytic migratory erythema, DM, weight loss
— Suspect: onset <25, autosomal dominant family pattern, lean, mild hyperglycemia, negative antibodies, preserved C-peptide
— GCK-MODY: stable mild hyperglycemia, often discovered incidentally; no treatment, no complications
Key distinction: A patient on high-dose prednisone with normal fasting glucose but elevated post-lunch glucose has steroid-induced hyperglycemia, best detected with mid-afternoon or pre-dinner fingersticks, not fasting glucose. Mirror this pattern with NPH insulin dosed with the steroid.
— Diabetes insipidus (central or nephrogenic): dilute urine, hypernatremia tendency, normal glucose
— Primary polydipsia: psychogenic; low serum osm, dilute urine
— Diuretic use
— Hypercalcemia, hypokalemia (nephrogenic DI physiology)
— SIADH does not cause polyuria — opposite picture
— Hyperthyroidism — heat intolerance, tremor, tachycardia, elevated free T4, suppressed TSH
— Malignancy — age-appropriate cancer screening; constitutional symptoms
— Malabsorption (celiac, IBD, chronic pancreatitis) — diarrhea, deficiencies
— Adrenal insufficiency — hyperpigmentation, hyponatremia, hyperkalemia
— Depression, eating disorders
— HIV, tuberculosis
— Anemia (iron, B12)
— Hypothyroidism
— OSA — overlapping with metabolic syndrome
— Immunodeficiency
— Chronic kidney or liver disease
— B12 deficiency (PPI use, metformin use, vegan diet)
— Alcohol-related neuropathy
— Hypothyroidism
— Heavy metal toxicity
— HIV, syphilis, paraneoplastic
— Chemotherapy-induced (platinum, taxanes, vincristine, bortezomib)
— Hypertensive retinopathy
— Radiation retinopathy
— Sickle cell retinopathy
— Branch retinal vein occlusion
Board pearl: A patient with polyuria/polydipsia, dilute urine, normal HbA1c, and hypernatremia after water deprivation has diabetes insipidus, not diabetes mellitus. The shared "diabetes" name causes confusion on test day — anchor on the urine and serum osm, not the symptom triad.
— HbA1c <7% for most non-pregnant adults
— <6.5% if achievable without hypoglycemia (young, short duration, no CVD)
— <8% in limited life expectancy, advanced complications, severe hypoglycemia history
— Time-in-range (CGM) ≥70% (70–180 mg/dL) where applicable
— Goal <130/80 in most patients with DM; first-line ACEi or ARB if albuminuria or CKD
— Moderate-intensity statin for DM age 40–75 (no other risk factors)
— High-intensity statin for DM with ASCVD, multiple risk factors, or 10-yr risk ≥20%
— Consider statin in 20–39-year-olds with DM and risk factors
— Aspirin: secondary prevention always; primary prevention only in select high-risk DM patients after bleeding-risk discussion
— GLP-1 RA (semaglutide, liraglutide, dulaglutide) for ASCVD or high CV risk
— SGLT2 inhibitor (empagliflozin, dapagliflozin) for HFrEF/HFpEF, CKD with albuminuria, or established CVD
— Add independently of HbA1c if indications present
— GLP-1 RA, dual GIP/GLP-1 (tirzepatide), bariatric surgery
— Annual influenza
— Pneumococcal (PCV15 + PPSV23 or PCV20)
— Hepatitis B series in adults <60 with DM (shared decision in ≥60)
— COVID-19 per ACIP
— Tdap, zoster (≥50), RSV per age
— Annual depression and diabetes distress screening
— Smoking cessation at every visit
Step 3 management: A T2DM patient with HbA1c 6.9% but HFpEF and stage 3a CKD with albuminuria should still get an SGLT2 inhibitor — the indication is cardiorenal, not glycemic. Don't withhold based on "good" A1c.
— Every 3 months if not at goal or after therapy change
— Every 6 months if stable and at goal
— Weight, BP, foot inspection (quick visual)
— Review home glucose logs / CGM data
— Medication adherence, side effects, hypoglycemia history
— Tobacco, alcohol, sleep, mood, sexual health
— Comprehensive foot exam with monofilament
— Dilated retinal exam (every 1–2 years if no retinopathy and well-controlled)
— UACR and eGFR
— Lipid panel (more often if started or changed therapy)
— Liver enzymes; FIB-4 for MASH risk
— TSH in T1DM (and as indicated in T2DM)
— B12 in patients on long-term metformin (especially with neuropathy or anemia)
— Depression and diabetes distress screening
— Dental exam every 6 months
— At diagnosis
— Annually for assessment of education, nutrition, emotional needs
— When complicating factors arise (new complication, transition, medication change)
— When transitions of care occur
— Patients on insulin: fingersticks 4+ times daily or CGM
— Non-insulin patients: structured SMBG as needed
— Sick-day rules: continue insulin, hydrate, check glucose/ketones q2–4h, hold SGLT2i and metformin during dehydration/illness
— Counsel insulin users to check glucose before driving; treat <70 before driving; carry rapid carbs
CCS pearl: On a longitudinal CCS case, advance the clock 3 months after starting or changing therapy and reorder HbA1c, UACR, BP, weight, and adherence assessment. Forgetting to reassess at 3 months is a common point-loser. After goal is achieved and stable, push to 6-month intervals.
— Glycemic target individualization requires explicit discussion of hypoglycemia risk vs microvascular benefit — document the conversation
— Bariatric and metabolic surgery counseling: realistic expectations, lifelong follow-up, vitamin replacement, mental health screening
— Pregnancy and contraception counseling in reproductive-age women with DM — preconception A1c <6.5%; effective contraception until ready
— Commercial drivers (CDL) with insulin-treated DM require federal exemption with documented hypoglycemia awareness and clinician attestation
— Pilots, law enforcement, and military have role-specific medical standards
— DM is a protected disability under the ADA; reasonable accommodations (breaks for glucose checks, snacks) are required by employers
— School-aged children with T1DM are protected under Section 504; care plans must be in place
— Some states require reporting of severe hypoglycemia causing loss of consciousness or motor vehicle crashes to the DMV — know your state's law
— Child neglect: missed insulin or repeat DKA admissions in a minor may trigger CPS evaluation
— Hospital discharge: reconcile home insulin regimen, ensure scripts and supplies (pen needles, glucometer strips, glucagon), schedule follow-up within 1–2 weeks
— High-alert medications: insulin is a top cause of inpatient medication errors — use weight-based, structured order sets
— Avoid sliding-scale-only insulin in hospitalized DM — pair with basal
— Provide written sick-day rules, hypoglycemia treatment plan, and after-hours contact
— Avoid the label "diabetic"; use person-first language
— Genetic testing for MODY: discuss implications for family members
— Address social determinants: food insecurity (Hunger Vital Sign), insulin cost (assistance programs, $35 cap for Medicare), transportation
Board pearl: A patient with a recent severe hypoglycemic episode behind the wheel triggers a driving safety conversation, glucose monitoring before driving, and possible DMV notification depending on state law — and a regimen change to lower hypoglycemia risk (often switching from sulfonylurea/insulin to GLP-1 RA or SGLT2i).
— HbA1c: normal <5.7, prediabetes 5.7–6.4, DM ≥6.5
— FPG: normal <100, IFG 100–125, DM ≥126
— 2-hr OGTT: normal <140, IGT 140–199, DM ≥200
— Random glucose ≥200 with symptoms = DM
— All adults from age 35
— Any age with BMI ≥25 (≥23 Asian American) plus risk factor
— Prior GDM: postpartum OGTT at 4–12 weeks, then ≥ every 3 years lifelong
— Pediatric: age 10 / puberty if BMI ≥85th percentile + risk factor
— HbA1c unreliable in hemoglobinopathies, hemolysis, recent transfusion, ESRD, pregnancy, iron deficiency
— Iron deficiency falsely raises HbA1c
— Pregnancy: do not use HbA1c to diagnose GDM
— GAD-65 highest yield in adult-onset autoimmune diabetes (LADA)
— Young, lean, autosomal dominant, antibody-negative, mild hyperglycemia
— GCK-MODY needs no treatment
— Steroids → postprandial hyperglycemia; check pre-dinner glucose
— Olanzapine/clozapine → weight gain and DM
— Tacrolimus > cyclosporine
— Statins slightly increase DM risk; benefit outweighs in indicated patients
— 7% weight loss + 150 min/week activity = 58% relative risk reduction over 3 years
— HbA1c, BP, statin use, eye exam, foot exam, kidney screening — all HEDIS metrics
— HepB in DM adults <60; consider ≥60
— Annual flu, pneumococcal, COVID-19
Step 3 management: When in doubt on a screening vignette, the right answer is usually HbA1c, repeated if abnormal, with lifestyle referral and annual rescreen of prediabetes. Reserve OGTT for pregnancy, postpartum reclassification, and high-suspicion cases with normal HbA1c.
— "42-year-old, BMI 31, no symptoms, here for physical." → Order HbA1c (or FPG). Trigger is age ≥35 or BMI ≥25 + risk factor.
— "HbA1c 6.7% in asymptomatic patient." → Repeat HbA1c or confirm with FPG on a separate day before diagnosing.
— Patient with sickle cell trait, recent transfusion, ESRD, or iron deficiency with discordant HbA1c. → Use FPG or OGTT.
— "8 weeks postpartum, history of GDM." → 75-g 2-hour OGTT, not HbA1c.
— Failed oral therapy, weight loss, family history of autoimmunity. → GAD-65 antibodies, C-peptide; treat as T1DM/LADA with insulin.
— Patient on prednisone with normal fasting but elevated afternoon glucose. → Mid-afternoon/pre-dinner glucose monitoring; add NPH or basal insulin timed to steroid.
— HbA1c 6.0% in 45-year-old with BMI 30. → Intensive lifestyle (DPP); add metformin if BMI ≥35, age <60, or prior GDM.
— DM with HFpEF, CKD with albuminuria, or established ASCVD. → Add SGLT2i and/or GLP-1 RA regardless of HbA1c.
— 11-year-old BMI 97th percentile, acanthosis, family history. → Screen now with HbA1c/FPG; rescreen every 3 years.
— 22-year-old, lean, mild stable fasting hyperglycemia, multigenerational DM, antibody-negative. → Genetic testing; GCK-MODY needs no therapy.
— Glucose 220 in ICU, no DM history. → Treat hyperglycemia inpatient; recheck HbA1c/FPG after recovery.
Key distinction: Step 3 stems frequently test what to do next, not "what is the diagnosis." Recognize the screening trigger, the confirmation rule, the unreliable-A1c situation, and the cardiorenal "treat-the-comorbidity" rule, and you will capture the majority of diabetes-screening items.
Diabetes is diagnosed by HbA1c ≥6.5%, FPG ≥126, 2-hr OGTT ≥200, or random glucose ≥200 with symptoms — confirmed by a second abnormal test in asymptomatic patients — and ADA recommends screening all adults starting at age 35 (or any age with BMI ≥25 plus a risk factor), with prediabetes managed by intensive lifestyle ± selective metformin.
Board pearl: If you remember just three numbers — 6.5, 126, 200 — and one age — 35 — you can answer the majority of Step 3 diabetes screening and diagnosis stems correctly.