Eduovisual
Endocrine
Diabetic retinopathy, neuropathy, and nephropathy screening
— Diabetes mellitus (DM) affects ~11% of US adults; microvascular complications (retinopathy, nephropathy, neuropathy) are the leading causes of new-onset blindness, end-stage kidney disease (ESKD), and non-traumatic lower-extremity amputation in working-age adults
— Microvascular disease correlates with hyperglycemia duration and severity (A1c exposure) plus hypertension; macrovascular disease tracks more with lipids, smoking, and BP
— Type 1 DM: begin retinopathy, nephropathy, and neuropathy screening 5 years after diagnosis (microvascular damage rare before then), then annually
— Type 2 DM: begin screening at the time of diagnosis because onset is insidious and patients often have unrecognized hyperglycemia for years
— Gestational DM: screen at 4–12 weeks postpartum with 75-g OGTT, then every 1–3 years for incident DM
— Long-standing poorly controlled DM (A1c persistently >8%)
— Coexisting HTN, dyslipidemia, smoking, obesity, CKD, or known CAD/PAD — clusters predict microvascular damage
— Symptoms: blurred vision, floaters, foot numbness/burning, erectile dysfunction, gastroparesis-type symptoms, frothy urine, edema
— All three complications share chronic hyperglycemia → AGEs, polyol/PKC activation, oxidative stress → endothelial and pericyte dysfunction
— Therefore patients with one microvascular complication almost always have (or will develop) the others — finding retinopathy raises pretest probability of nephropathy and vice versa
Board pearl: A patient with new microalbuminuria but no retinopathy should prompt a search for a non-diabetic cause of kidney disease (e.g., IgA nephropathy, FSGS, hypertensive nephrosclerosis) — diabetic nephropathy nearly always coexists with retinopathy, especially in T1DM.
— Most cases are asymptomatic until advanced — exactly why universal annual screening exists
— Symptomatic clues: gradual blurred vision (macular edema), sudden vision loss/floaters/cobwebs (vitreous hemorrhage from proliferative disease), curtain over vision (tractional retinal detachment)
— Ask about prior laser/anti-VEGF injections, cataract surgery, and date of last dilated exam
— Earliest finding is moderately increased albuminuria (formerly microalbuminuria, 30–300 mg/g) — entirely asymptomatic
— Progression: severely increased albuminuria (>300 mg/g), then declining eGFR, then nephrotic-range proteinuria, edema, HTN worsening, anemia, hyperkalemia
— Ask about ACEi/ARB use, NSAID use, IV contrast exposures, and BP readings at home
— Distal symmetric polyneuropathy (DSPN) — most common; "stocking-glove" numbness, burning, tingling, often worse at night; loss of protective sensation predisposes to foot ulcers
— Autonomic neuropathy — resting tachycardia, orthostatic hypotension without compensatory HR rise, gastroparesis (early satiety, postprandial nausea), neurogenic bladder, erectile dysfunction, gustatory sweating, hypoglycemia unawareness
— Mononeuropathies — CN III palsy (pupil-sparing), median nerve at wrist, foot drop
— Diabetic amyotrophy (lumbosacral radiculoplexus neuropathy) — proximal thigh pain and weakness with weight loss, often after improved glycemic control
— Duration of DM, A1c trajectory, hypoglycemic episodes/unawareness, BP, ACR results, last eye exam, foot self-exam habits, footwear, smoking, lipids
Step 3 management: At every diabetes follow-up visit, document the "ABCs": A1c, BP, Cholesterol/statin status, Aspirin indication, ACR, Annual eye exam, foot exam (Annual + at every visit if neuropathy), And smoking cessation — a structured checklist increases guideline-concordant care and is favored on CCS cases.
— Visual acuity with Snellen chart at each visit if symptomatic
— Direct ophthalmoscopy by PCP is inadequate for screening — does not replace dilated exam by optometrist/ophthalmologist or validated retinal photography
— Findings on referral exam: microaneurysms, dot-blot hemorrhages, hard exudates, cotton-wool spots (non-proliferative); neovascularization of disc/elsewhere (proliferative); macular thickening (DME)
— 10-g Semmes-Weinstein monofilament at plantar surface of great toe and metatarsal heads — inability to detect = loss of protective sensation (LOPS), the strongest predictor of ulceration
— 128-Hz tuning fork for vibration sense at the dorsal great toe
— Pinprick, ankle reflexes (often absent), proprioception
— Inspect for fissures, calluses, hammertoes, Charcot deformity (midfoot collapse, "rocker-bottom"), web-space maceration, onychomycosis
— Palpate dorsalis pedis and posterior tibial pulses; ABI if absent or claudication
— Orthostatic vitals (BP drop ≥20/10 without appropriate HR rise = neurogenic orthostasis)
— Resting HR >100 suggests cardiac autonomic neuropathy
— Abdominal exam for succussion splash (gastroparesis), bladder distention
— BP measurement at every visit — goal generally <130/80 in DM with albuminuria or high ASCVD risk
— Volume status: JVP, edema, lung crackles (cardiorenal overlap)
— Skin: necrobiosis lipoidica, acanthosis nigricans, eruptive xanthomas
Key distinction: Distal symmetric diabetic polyneuropathy typically has preserved or symmetric pulses with diminished sensation, whereas peripheral arterial disease presents with diminished pulses, dependent rubor, hair loss, and pain with exertion — both commonly coexist in DM and both must be assessed because management differs (offloading vs revascularization).
— Check every 3 months if not at goal or therapy changing; every 6 months if stable and at goal
— Goal individualized: <7% for most non-pregnant adults; <6.5% if achievable without hypoglycemia; <8% for limited life expectancy, severe comorbidity, hypoglycemia unawareness, or advanced complications
— Spot urine albumin-to-creatinine ratio (UACR) on a random sample
— Normal <30 mg/g
— Moderately increased 30–299 mg/g
— Severely increased ≥300 mg/g
— Two of three abnormal UACR samples over 3–6 months required to diagnose albuminuria (transient elevations from exercise, fever, UTI, hyperglycemia, menstruation, HF decompensation)
— Serum creatinine with eGFR (CKD-EPI 2021, race-free) annually; more often if abnormal
— Stage CKD by eGFR + albuminuria (KDIGO heat map) — both axes independently predict progression and CV mortality
— Dilated fundoscopy by optometrist/ophthalmologist annually is gold standard
— Validated retinal fundus photography (with or without AI interpretation) acceptable for screening; abnormal results require referral
— If exam fully normal and well-controlled DM, screening every 1–2 years is acceptable per ADA
— Annual comprehensive foot exam with monofilament + one other modality (vibration, pinprick, temperature, or ankle reflex) — diagnosis is clinical
— Routine EMG/NCS not needed unless atypical features (asymmetry, motor predominance, rapid progression, upper-extremity onset)
— Fasting lipid panel, TSH, B12 (especially on metformin >4 years or symptomatic neuropathy), LFTs before statin
Board pearl: A patient on long-term metformin with new or worsening neuropathy should have vitamin B12 checked — metformin causes B12 malabsorption, and replacing B12 can improve neuropathy that is otherwise blamed on diabetes.
— Referral to ophthalmology triggers: any retinopathy on screening, decreased visual acuity, symptoms of vitreous hemorrhage or detachment, pregnancy with pre-existing DM
— Ophthalmology may use OCT (optical coherence tomography) to quantify diabetic macular edema, fluorescein angiography to identify neovascularization and ischemic zones, B-scan ultrasound if media opacity (vitreous hemorrhage) prevents fundus view
— Clinical clues supporting diabetic nephropathy: long-standing DM (usually >10 y for T1DM), concurrent retinopathy, slowly progressive albuminuria → proteinuria → eGFR decline, bland sediment
— Red flags for non-diabetic kidney disease prompting nephrology referral and possible biopsy:
— Onset of proteinuria <5 y after T1DM diagnosis
— Absence of retinopathy with significant albuminuria
— Active urinary sediment (RBC casts, dysmorphic RBCs)
— Rapidly declining eGFR (>5 mL/min/1.73 m²/yr)
— Nephrotic syndrome with normal-sized kidneys and other systemic clues
— Atypical features → EMG/NCS, plus rule out mimics: B12 deficiency, hypothyroidism, monoclonal gammopathy (SPEP/IFE/free light chains), HIV, HCV, alcohol, paraneoplastic, chemotherapy exposure, hereditary neuropathies, syphilis (RPR if risk factors)
— Autonomic testing (HR variability, tilt table, gastric emptying study with 4-hour solid-phase scintigraphy) for suspected autonomic dysfunction with significant disability
— Probe-to-bone test, plain radiographs, then MRI if osteomyelitis suspected
— Bone biopsy for definitive osteomyelitis diagnosis and culture-guided antibiotics
Step 3 management: When a T2DM patient presents with new severely increased albuminuria, before invoking diabetic nephropathy, order ACR ×2 to confirm persistence, check urine microscopy, screen for monoclonal protein in patients >40, and confirm presence of retinopathy via dilated exam — only then commit to a diabetic etiology without nephrology consult.
— DCCT (T1DM) and UKPDS (T2DM) established that tight glycemic control reduces retinopathy, nephropathy, and neuropathy onset/progression
— Each 1% A1c reduction → ~35% relative reduction in microvascular events
— Legacy effect: early intensive control yields benefits decades later
— Target <130/80 in DM with albuminuria, established ASCVD, or high ASCVD risk; <140/90 otherwise (ADA permits individualization)
— First-line agents when albuminuria is present: ACE inhibitor or ARB — slows progression of nephropathy and reduces CV events
— Do not combine ACEi + ARB (no added benefit, increased hyperkalemia and AKI — ONTARGET)
— Moderate-intensity statin for DM age 40–75 regardless of LDL; high-intensity if ASCVD or 10-y risk ≥20%
— Statin before age 40 if additional risk factors or existing complications
— SGLT2i (empagliflozin, dapagliflozin, canagliflozin): reduce CKD progression, HF hospitalization, and CV death; indicated in T2DM with CKD (eGFR ≥20 and UACR ≥200 mg/g) or HF — independent of A1c
— GLP-1 RAs (semaglutide, liraglutide, dulaglutide, tirzepatide): reduce MACE; preferred when ASCVD predominates or weight loss desired
— Smoking cessation (smoking accelerates all microvascular complications, especially nephropathy)
— Mediterranean/DASH diet, 150 min/wk moderate exercise, weight loss 5–10%
— Sodium <2.3 g/day, protein 0.8 g/kg/day in established CKD
Step 3 management: In a T2DM patient with UACR 250 mg/g and eGFR 55, the highest-yield trio is: maximize ACEi/ARB to highest tolerated dose, add SGLT2 inhibitor, and add finerenone (nonsteroidal MRA) if albuminuria persists despite RAS blockade with normal K+ — this stack has the strongest evidence for renal and CV protection in diabetic CKD.
— Metformin — first-line in T2DM; weight neutral, low hypoglycemia risk; hold if eGFR <30, caution 30–45 (do not initiate <45)
— SGLT2 inhibitors — first-line add-on with CKD or HF; cause modest A1c reduction (~0.5–1%), weight loss, BP lowering; renal benefit even at low eGFR
— GLP-1 RAs — strong A1c lowering, weight loss, ASCVD benefit; semaglutide and liraglutide have albuminuria reduction signals
— Avoid or minimize: long-acting sulfonylureas (hypoglycemia in CKD), TZDs in HF
— ACEi or ARB: titrate to maximally tolerated dose if albuminuria or HTN; recheck Cr and K+ within 1–2 weeks; allow Cr rise up to 30% if K+ stable
— Finerenone — nonsteroidal MRA proven to reduce CKD progression and CV events in T2DM CKD (FIDELIO-DKD, FIGARO-DKD); contraindicated if K+ >5.0
— SGLT2i as above
— First-line: duloxetine (SNRI, also helps depression), pregabalin or gabapentin, TCAs (amitriptyline, nortriptyline — avoid in elderly, BPH, glaucoma, arrhythmia)
— Second-line: tapentadol (FDA-approved), topical capsaicin 8% patch, lidocaine patch
— Avoid chronic opioids — minimal long-term efficacy, addiction risk
— Gastroparesis: small frequent meals, low-fat low-fiber; metoclopramide (limit to <12 weeks due to tardive dyskinesia black box); erythromycin short-term
— Orthostatic hypotension: compression stockings, increased salt/water, midodrine, fludrocortisone (caution with HF)
— Erectile dysfunction: PDE5 inhibitors first-line
— Neurogenic bladder: scheduled voiding, intermittent catheterization
Board pearl: Duloxetine and pregabalin are FDA-approved for diabetic neuropathic pain; gabapentin is off-label but commonly used. In a depressed diabetic with painful neuropathy and overweight body habitus, duloxetine addresses both conditions without the weight gain seen with pregabalin or TCAs.
— Intravitreal anti-VEGF injections (ranibizumab, aflibercept, bevacizumab): first-line for center-involving diabetic macular edema and increasingly for proliferative diabetic retinopathy; given monthly initially
— Panretinal photocoagulation (PRP): laser for proliferative diabetic retinopathy when anti-VEGF unsuitable or noncompliant; preserves central vision at expense of peripheral and night vision
— Focal/grid laser: less commonly used now for DME
— Pars plana vitrectomy: vitreous hemorrhage not clearing, tractional retinal detachment, severe fibrovascular proliferation
— When eGFR <30: refer to nephrology for kidney replacement therapy planning (vascular access, transplant referral, dialysis modality counseling)
— Preemptive kidney transplant ideal before dialysis if eligible; simultaneous pancreas-kidney (SPK) transplant option in T1DM with ESKD
— AV fistula creation when eGFR ~15–20 to allow maturation
— Charcot neuroarthropathy: immediate total contact casting and offloading, non-weight-bearing; podiatry/orthopedics referral
— Diabetic foot ulcers:
— Sharp debridement, offloading (total contact cast is gold standard for plantar ulcers), moist wound dressings
— Cultures + empiric antibiotics if cellulitis/osteomyelitis
— Revascularization if PAD with non-healing wound (ABI, angiography, bypass or endovascular)
— Hyperbaric oxygen for select Wagner grade 3+ ulcers
— Amputation as last resort; counseling on contralateral limb risk (≈50% within 5 years)
CCS pearl: On a CCS case of a diabetic foot ulcer, the highest-yield orders are: obtain wound cultures and plain X-ray (then MRI if positive probe-to-bone or persistent ulcer), start empiric broad-spectrum antibiotics covering MRSA and gram-negatives if signs of infection, consult podiatry/vascular surgery, and order ABI. Don't forget tetanus status and glycemic optimization with basal–bolus insulin while admitted.
— A1c goal 7.5–8.0% for most older adults with multiple comorbidities; <8.5% for very limited life expectancy or advanced dementia
— Avoid hypoglycemia at all costs — falls, MI, dementia progression; loosen targets if recurrent hypoglycemia, hypoglycemia unawareness, frailty
— Deprescribe sulfonylureas (especially glyburide — Beers list) and long-acting insulins requiring complex titration in cognitively impaired patients
— Continue retinopathy and foot exams as long as treatment of detected disease would alter management and quality of life
— Consider functional status, life expectancy, and goals of care before initiating aggressive screening in patients with <5–10 y life expectancy
— Metformin: max 1 g/day if eGFR 30–45; contraindicated <30
— SGLT2i: continue down to eGFR 20 for renal/CV indication; do not start <20; do not use in dialysis
— GLP-1 RAs: generally safe across CKD spectrum; semaglutide and liraglutide preferred
— Sulfonylureas: use glipizide (no active renal metabolites) over glyburide; avoid in advanced CKD
— Insulin: requirements often decrease with worsening CKD (reduced renal clearance) — dose reductions to prevent hypoglycemia
— ACEi/ARB: continue even with Cr rise up to 30% if K+ tolerated; hold for AKI, K+ >5.5, or symptomatic hypotension
— Avoid TZDs and consider hepatic dose adjustments for SUs; metformin generally avoided in active hepatic disease due to lactic acidosis risk
Key distinction: Glyburide is on the Beers Criteria for inappropriate medications in older adults due to prolonged half-life and severe hypoglycemia; glipizide is the preferred sulfonylurea in elderly or CKD patients because it lacks active renal metabolites — a common Step 3 swap question.
— Preconception counseling essential: target A1c <6.5% before conception to minimize congenital anomalies (cardiac, neural tube)
— Retinopathy can progress rapidly during pregnancy — dilated eye exam before pregnancy or in T1, then each trimester and 1 year postpartum
— Nephropathy in pregnancy: ACEi/ARB are teratogenic — discontinue before conception or as soon as pregnancy confirmed; switch to labetalol, nifedipine, or methyldopa for HTN
— Tight glycemic control with insulin (preferred); metformin and glyburide cross placenta and are second-line where insulin not feasible
— Aspirin 81 mg from 12 weeks for preeclampsia prevention
— Postpartum 75-g OGTT at 4–12 weeks; repeat screening every 1–3 years
— Lifestyle and metformin for prevention of T2DM; ~50% lifetime risk of T2DM
— T1DM: screen retinopathy, nephropathy, neuropathy starting at age 11 or puberty AND ≥5 years duration
— T2DM in youth: screen at diagnosis and annually (more aggressive course than adult T2DM — TODAY trial)
— BP target adjusted to age/sex/height percentiles; ACEi/ARB for albuminuria
— Higher prevalence and worse outcomes in Black, Hispanic, Native American, and Asian American populations
— Screening uptake barriers: cost, transportation, time off work — telemedicine retinal photography programs address this gap
— Health-literacy-appropriate education improves self-management
Board pearl: A pregnant patient with pre-existing T2DM on lisinopril for albuminuria should have it stopped immediately upon positive pregnancy test (or ideally pre-conception) — ACEi/ARB in 2nd/3rd trimesters cause fetal renal dysgenesis, oligohydramnios, hypocalvaria; substitute labetalol or nifedipine for BP and rely on tight glycemic control for renoprotection.
— Diabetic macular edema (DME) — leading cause of vision loss in DM; can occur at any stage of retinopathy
— Proliferative diabetic retinopathy (PDR) complications: vitreous hemorrhage, tractional retinal detachment, neovascular glaucoma
— Cataracts develop earlier and progress faster in DM
— Permanent vision loss if untreated; legal blindness affects daily function, driving, employment
— Albuminuria → declining eGFR → ESKD requiring dialysis or transplant
— Comorbid burden: anemia of CKD, secondary hyperparathyroidism, metabolic acidosis, volume overload, 2–3× cardiovascular mortality at any given eGFR compared with non-diabetic CKD
— Hyperkalemia risk amplified by RAS blockade, MRAs, NSAIDs, trimethoprim
— Foot ulceration (lifetime risk ~25% in DM), infection, osteomyelitis, amputation
— Charcot arthropathy — painless joint destruction; missed diagnosis leads to severe deformity
— Falls in elderly due to sensory loss and orthostasis
— Gastroparesis → erratic glycemia, malnutrition, weight loss, bezoar formation
— Cardiac autonomic neuropathy → silent MI, sudden cardiac death, perioperative cardiovascular events
— Hypoglycemia unawareness → severe hypoglycemic events with seizure, coma, MVA
— Anti-VEGF: rare endophthalmitis, retinal detachment, transient IOP rise
— SGLT2i: euglycemic DKA (especially perioperative), genital mycotic infections, volume depletion, rare Fournier gangrene
— Finerenone/ACEi/ARB: hyperkalemia, AKI
— Pregabalin/gabapentin: sedation, edema, weight gain, misuse potential
Step 3 management: Counsel any patient starting an SGLT2 inhibitor to hold the drug ≥3 days before elective surgery (4 days for ertugliflozin) and during acute illness/fasting to prevent euglycemic DKA — a high-yield perioperative pitfall on Step 3.
— Same-day/emergent: sudden vision loss, new floaters with photopsia (possible vitreous hemorrhage or detachment), severe eye pain with vision loss (neovascular glaucoma)
— Within weeks: any retinopathy detected on screening, decreased visual acuity, pregnancy with DM
— Routine annual: all diabetics for screening
— eGFR <30 (CKD G4) — mandatory referral for RRT planning
— Rapidly declining eGFR (>5 mL/min/1.73 m²/yr)
— UACR >300 mg/g despite maximal RAS blockade and SGLT2i
— Diagnostic uncertainty (no retinopathy with significant proteinuria, active sediment, suspected non-diabetic etiology)
— Refractory hyperkalemia, refractory HTN, electrolyte/acid-base disturbances
— Active foot ulcer, Charcot foot, severe deformity needing offloading, suspected osteomyelitis, peripheral arterial disease with non-healing wound or rest pain
— Type 1 DM (especially pediatric/adolescent), uncontrolled DM despite multiple agents, hypoglycemia unawareness, pump/CGM management, pregnancy with DM
— Admit: DKA, HHS, severe hypoglycemia with persistent altered mental status, severe foot infection with sepsis, acute limb ischemia, AKI on CKD with hyperkalemia, severe gastroparesis with dehydration
— ICU: DKA/HHS with hemodynamic instability or severe metabolic derangement, sepsis from limb infection, pulmonary edema from cardiorenal failure
CCS pearl: A diabetic admitted with a foot ulcer and temperature 38.5°C, WBC 18k, lactate 3 needs immediate blood cultures, IV broad-spectrum antibiotics (vancomycin + piperacillin-tazobactam), IV fluids, surgery consult, and admission orders for glucose monitoring q6h with basal-bolus insulin, holding oral agents — sliding scale alone is inadequate for inpatient diabetes management.
— Hypertensive retinopathy — AV nicking, flame hemorrhages, cotton-wool spots, papilledema in malignant HTN; often coexists
— Retinal vein occlusion (BRVO/CRVO) — sectoral or whole-retina hemorrhages, more sudden onset, often unilateral
— Age-related macular degeneration (AMD) — drusen, central scotoma in elderly; lacks microaneurysms typical of DR
— Radiation retinopathy — history of head/neck radiation
— Sickle cell retinopathy — sea-fan neovascularization; consider in Black patients with neovascularization out of proportion to DM
— Hypertensive nephrosclerosis — long-standing HTN, mild proteinuria, often coexists
— Ischemic nephropathy from renal artery stenosis — flash pulmonary edema, AKI after ACEi initiation, asymmetric kidneys
— Other diabetic-associated: papillary necrosis (especially with NSAIDs), recurrent pyelonephritis (neurogenic bladder), contrast-induced AKI
— Membranous nephropathy — can coexist in DM with nephrotic syndrome; check PLA2R antibody if suspicion
— Critical limb ischemia / PAD — rest pain, dependent rubor, absent pulses
— Lumbar radiculopathy / spinal stenosis — dermatomal pattern, positional, neurogenic claudication relieved by flexion
— Tarsal tunnel syndrome — distal posterior tibial nerve compression with medial foot/heel pain
— Plantar fasciitis, Morton neuroma — focal anatomic foot pain mimics
— Many diabetics have simultaneous PAD + neuropathy + retinopathy + nephropathy — comprehensive evaluation prevents missed diagnoses
Key distinction: Painful PAD worsens with walking, improves with rest and dependency; diabetic neuropathic pain is worse at night and at rest, often improved by walking — opposite temporal patterns help bedside differentiation.
— Vitamin B12 deficiency — combined sensory + dorsal column loss (proprioception, vibration), macrocytic anemia, possible cognitive changes; check in all metformin users
— Alcohol-related neuropathy — chronic heavy use, often painful, small-fiber predominant
— Hypothyroidism — slowed reflexes, cold intolerance
— CKD/uremic neuropathy — overlaps with diabetic disease in ESKD
— Monoclonal gammopathy/MGUS — order SPEP/IFE in atypical or refractory cases >50 y
— HIV, HCV, Lyme, syphilis — infectious neuropathies
— Chemotherapy-induced (platinums, taxanes, vincristine, bortezomib)
— Heavy metals (lead, arsenic, mercury)
— Hereditary — CMT (high arches, hammer toes, family history)
— CIDP — progressive proximal + distal weakness, treatable with IVIG/steroids
— Orthostatic proteinuria in young patients — absent first-morning sample
— Exercise, fever, UTI, menstruation — transient causes; recheck
— Multiple myeloma — Bence-Jones protein not detected by ACR (only detects albumin); check SPEP/UPEP
— Glomerulonephritides — IgA, lupus, FSGS, membranous — active sediment, systemic features
— HF/cardiorenal — volume-driven proteinuria
— Trauma, shaken baby, anticoagulation excess, leukemia/anemia, endocarditis (Roth spots), HIV retinopathy, CMV retinitis in immunocompromised
— Venous stasis ulcers (gaiter area, weepy, hyperpigmentation), arterial ulcers (punched-out, painful, distal toes), pressure ulcers, vasculitic ulcers, pyoderma gangrenosum
Board pearl: Urine dipstick can be negative for protein when the patient has Bence-Jones proteinuria (light chains) because dipstick detects mainly albumin. In an older diabetic with rising creatinine, anemia, bone pain, or hypercalcemia, order SPEP/UPEP with immunofixation — myeloma is a missable diagnosis hidden behind a "diabetic nephropathy" label.
— A1c at individualized target; consider CGM if hypoglycemia, A1c off-target, or insulin-treated
— Avoid hypoglycemia, especially in CKD, elderly, autonomic neuropathy
— Statin therapy for nearly all DM 40–75; high-intensity if ASCVD or 10-y risk ≥20%; consider ezetimibe and PCSK9i if LDL not at goal
— BP <130/80 with ACEi/ARB if albuminuria
— Aspirin 81 mg daily for secondary prevention in established ASCVD; for primary prevention only in selected DM patients age 40–70 at high CV risk with low bleeding risk (individualized)
— Smoking cessation with pharmacologic support (varenicline, NRT, bupropion)
— SGLT2i and/or GLP-1 RA for any T2DM with CKD, HF, or ASCVD regardless of A1c
— Finerenone added if albuminuria persists on max ACEi/ARB and K+ ≤4.8
— Continue ACEi/ARB even as eGFR falls (do not stop reflexively unless AKI, hyperkalemia, or symptomatic hypotension)
— Annual influenza, pneumococcal (PCV20 or PCV15+PPSV23) for all diabetics ≥19 y, hepatitis B (if <60 unvaccinated; consider if ≥60), COVID-19, RSV ≥60 with risk factors, Tdap, zoster ≥50, HPV if eligible
— Daily self-inspection, well-fitting therapeutic footwear, no barefoot walking, no hot water/heating pads, prompt evaluation of any new lesion
— Podiatry visits every 2–3 months if high-risk (prior ulcer, deformity, LOPS + PAD)
— Screen for depression (PHQ-9) and diabetes distress at least annually
— Diabetes self-management education and support (DSMES) at diagnosis, annually, with new complications, and with care transitions
Step 3 management: Document a comprehensive annual diabetes visit checklist: A1c, BP, lipids/statin, ACR, eGFR, dilated eye exam date, comprehensive foot exam, vaccinations, smoking, depression screen, DSMES referral — this structured care template is the single best driver of guideline-concordant outcomes.
— Stable, at-goal T2DM: every 3–6 months; q3 mo if A1c above goal or therapy changing
— T1DM and complex T2DM: every 3 months
— Post-discharge after DKA/HHS or new complication: within 1–2 weeks
— A1c q3 mo (off-target) or q6 mo (at goal)
— ACR + serum Cr/eGFR annually; more often (q3–6 mo) if CKD or recent therapy changes
— Fasting lipid panel annually or 4–12 weeks after statin initiation/change
— K+ and Cr 1–2 weeks after starting/titrating ACEi/ARB, MRA, or finerenone
— LFTs at statin baseline and if symptoms
— B12 in long-term metformin users with neuropathy or anemia, every 1–2 years
— Annually; q2 yrs if normal exam and well-controlled DM; more often if retinopathy present (frequency set by ophthalmology)
— Comprehensive annual exam; visual foot inspection at every visit in patients with LOPS, prior ulcer, deformity, or PAD
— CGM increasingly standard for insulin users; targets: time in range (70–180) >70%, time below 70 <4%, time <54 <1%
— Cardiac rehab if recent ACS/HF; pulmonary rehab if COPD overlap
— Vision rehabilitation for low-vision patients
— Physical therapy for gait/balance training in neuropathy
— Nutrition consultation, particularly with CKD (protein, K+, phosphate restriction)
— Diabetes self-management education and structured group programs
Board pearl: Time in range (TIR) on CGM correlates with A1c and microvascular complications: a TIR of 70% ≈ A1c of ~7%, and each 10% increase in TIR reduces retinopathy/albuminuria progression — increasingly tested in place of legacy A1c-only questions.
— Glycemic and BP targets must be individualized — shared decision-making required, particularly in elderly or those with limited life expectancy where intensive control may harm more than help
— Consent for anti-VEGF injections, laser, dialysis, transplant all require full disclosure of alternatives including conservative management
— Patients with hypoglycemia unawareness or recent severe hypoglycemia are at risk of motor vehicle crashes
— Counsel on check glucose before driving, keep fast-acting carbs in car; advanced retinopathy with significant visual loss requires visual acuity and field testing; report per state law
— Mandatory reporting of unsafe drivers varies by state (e.g., California requires physicians to report lapses of consciousness); know local laws
— Discharge after DKA/HHS or foot infection: ensure insulin regimen reconciled, prescriptions filled before discharge, follow-up within 1–2 weeks, glucose monitoring supplies provided, primary care and specialist appointments scheduled
— Post-hospital insulin errors are a leading cause of readmission — use teach-back to confirm understanding
— Insulin affordability is a recognized public health issue; check eligibility for patient assistance programs, $35/month insulin caps, and 340B pricing
— Telemedicine retinal imaging in primary care expands access; ensure positive screens have a closed-loop referral pathway
— Hold metformin before iodinated contrast if eGFR <30 or AKI risk; hold SGLT2i around surgery
— Avoid NSAIDs in diabetic CKD; review meds at every visit
— High-risk medication reconciliation at every transition (insulin types easily confused; U-500 vs U-100)
— Relax glycemic targets in hospice/advanced illness; discontinue statins if life expectancy <1 year; avoid causing hypoglycemia in dying patients
Step 3 management: When discharging a newly insulin-dependent patient, directly observe self-injection technique, confirm glucometer use, schedule a follow-up within 7–14 days, and document hypoglycemia counseling including driving precautions — these closed-loop safety steps prevent both readmission and a malpractice exposure.
— T1DM: 5 years after diagnosis (≥age 11 if pediatric)
— T2DM: at diagnosis
— Pregnancy with pre-existing DM: pre-conception, then each trimester
— Normal <30 mg/g; moderately increased 30–299; severely increased ≥300
— Confirm with 2 of 3 samples over 3–6 months
— DM + albuminuria → ACEi/ARB + SGLT2i + finerenone
— DM + HF → SGLT2i + GLP-1 RA + ACEi/ARB + MRA
— DM + ASCVD → GLP-1 RA or SGLT2i + statin + aspirin (secondary)
— DM + obesity → GLP-1 RA (semaglutide, tirzepatide)
— Microaneurysms = earliest retinopathy finding
— Cotton-wool spots = nerve fiber layer infarcts
— Neovascularization = proliferative DR → PRP or anti-VEGF
— DME = leading cause of vision loss → anti-VEGF
— "10-128-Pulse-Inspect": 10-g monofilament, 128-Hz tuning fork, pulses, inspection
— Metformin → B12 deficiency, lactic acidosis with AKI
— SGLT2i → euglycemic DKA, mycotic infections, Fournier
— TZDs → weight gain, edema, HF, fractures
— Sulfonylureas → hypoglycemia, weight gain; avoid glyburide in elderly
— Pregabalin → edema, weight gain, sedation
— Stop ACEi/ARB; switch to labetalol, nifedipine, methyldopa
— Eye exam each trimester
— Influenza, pneumococcal, Hep B if <60, COVID, RSV ≥60, Tdap, zoster ≥50
Board pearl: When you see "diabetic patient with proteinuria but no retinopathy," the answer is almost never "diabetic nephropathy" — search for alternative renal disease and consider nephrology referral with possible biopsy, especially in T1DM where retinopathy nearly always precedes nephropathy.
— T1DM × 3 y with new 2.5 g/day proteinuria, BP 140/90, no retinopathy on dilated exam. Best next step? → Refer to nephrology / consider biopsy for non-diabetic kidney disease (NOT "intensify glycemic control")
— 52 yo with new T2DM (A1c 8.2%). When to screen for retinopathy? → Now (at diagnosis) — not in 5 years
— Overweight diabetic with painful stocking distribution neuropathy and PHQ-9 of 15. Best agent? → Duloxetine (treats both, weight-neutral vs pregabalin/TCA)
— Long-standing T2DM on metformin 8 y, MCV 102, worsening neuropathy. Next test? → Serum vitamin B12
— Diabetic on empagliflozin scheduled for elective surgery. What to do? → Hold ≥3 days preoperatively to prevent euglycemic DKA
— T2DM patient on lisinopril discovers she is 6 weeks pregnant. Next step? → Stop lisinopril, switch to labetalol or nifedipine
— T2DM, A1c 7.2%, eGFR 55, UACR 350 on max-dose losartan and empagliflozin, K+ 4.4. Next step? → Add finerenone
— Diabetic with plantar ulcer, probe-to-bone positive, normal X-ray. Next imaging? → MRI for osteomyelitis
— 82 yo on glyburide with recurrent hypoglycemia. Action? → Stop glyburide (Beers); switch to glipizide or non-SU agent; relax A1c target to 7.5–8%
— Diabetic with severe NPDR/early PDR loses central vision, asks about driving. Action? → Counsel against driving, refer for ophthalmology and visual field testing, comply with state reporting requirements
Step 3 management: Step 3 stems repeatedly test the add-on hierarchy in diabetic CKD: maximize ACEi/ARB → add SGLT2i → add finerenone (if K+ allows) → optimize glycemia with GLP-1 RA — internalize this stepwise stack.
Diabetes microvascular complications are largely silent until late, so every diabetic needs structured annual screening — dilated eye exam, spot UACR with eGFR, and comprehensive foot exam with monofilament — combined with aggressive glycemic, BP, and lipid control plus disease-modifying SGLT2 inhibitors, GLP-1 RAs, ACEi/ARBs, and finerenone to prevent blindness, kidney failure, and amputation.
Board pearl: The single highest-yield reflex for Step 3 is to pair every microvascular finding with the matching guideline action — retinopathy on screening → ophthalmology referral; UACR ≥30 confirmed → ACEi/ARB + SGLT2i; LOPS on monofilament → therapeutic footwear, daily inspection, podiatry — structured, closed-loop responses define guideline-concordant ambulatory diabetes care.