Endocrine
Diabetes Mellitus — Complete
Endocrine

Diabetes Mellitus — Complete

Types, diagnosis, complications (DKA, HHS, neuropathy, nephropathy, retinopathy).

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◆Diagnosis

  • •HbA1c ≥6.5% (diabetes); 5.7–6.4% (prediabetes)
  • •Fasting glucose ≥126 mg/dL
  • •OGTT 2-hr ≥200
  • •Random ≥200 + symptoms
  • •Confirm with repeat test unless symptomatic + clearly elevated

◆Type 1 vs Type 2

  • •Type 1: autoimmune β-cell destruction (anti-GAD, anti-islet); juvenile/lean; insulin-dependent; DKA-prone
  • •Type 2: insulin resistance + relative insulin deficiency; older/obese; HHS-prone; metabolic syndrome
  • •MODY: monogenic; family history with AD inheritance
  • •LADA: latent autoimmune of adulthood; T1DM in T2DM presentation

◆Type 2 treatment ladder

  • •Metformin first-line (UNLESS GFR <30, decompensated HF, acidosis); GI side effects; B12 deficiency long-term
  • •Add SGLT2 (-flozins) if HFrEF, CKD, ASCVD: cardiorenal protection; risk of euglycemic DKA, UTI, mycotic infections, amputation (canagliflozin)
  • •Add GLP-1 (-tides) if ASCVD or obesity: weight loss; ↑ pancreatitis risk; ↑ medullary thyroid CA risk in animals (avoid MEN 2/MTC history)
  • •Other: sulfonylureas (hypoglycemia, weight gain), DPP-4 inhibitors (neutral), TZDs (weight gain, HF, fractures), insulin

◆DKA

  • •Glucose >250 + anion gap acidosis + ketones + pH <7.3 + HCO3 <18
  • •Trigger: infection, MI, missed insulin, new T1DM
  • •Fluids FIRST: NS 1–1.5 L bolus then maintenance
  • •Potassium: <3.3 hold insulin + replete K; 3.3–5.3 start insulin + replete K; >5.3 start insulin no K
  • •Insulin: regular IV infusion; continue until anion gap CLOSES (not when glucose normalizes)
  • •Add D5 to fluids when glucose ~200
  • •Bicarb only if pH <6.9
  • •Cerebral edema is dreaded peds complication (don't drop glucose/Na too fast)

◆HHS (hyperosmolar hyperglycemic state)

  • •Glucose often >600 + osm >320 + minimal/no ketones + AMS
  • •Type 2 elderly; trigger infection
  • •Aggressive IV fluids + insulin + K monitoring
  • •Mortality higher than DKA (older + comorbidities)

◆Chronic complications

  • •Retinopathy: annual dilated exam; nonproliferative (microaneurysms, hard exudates, cotton-wool) → proliferative (neovascularization) → panretinal photocoagulation
  • •Nephropathy: microalbuminuria earliest; ACEi/ARB + SGLT2 protect; eventual ESRD
  • •Peripheral neuropathy: stocking-glove sensory; gabapentin/duloxetine/TCAs for pain; foot care
  • •Autonomic neuropathy: gastroparesis, postural hypotension, ED, neurogenic bladder
  • •Macrovascular: MI, stroke, PVD
  • •Foot ulcers: offloading + debridement; osteomyelitis if probes to bone
  • •Diabetic mononeuropathies: CN III palsy (pupil-SPARING in DM ischemic; pupil-INVOLVING = aneurysm)

◆Hypoglycemia in DM

  • •Triad: Whipple triad (low glucose + symptoms + relief with sugar)
  • •Treat: oral glucose if alert; IV dextrose or IM glucagon if AMS
  • •Sulfonylurea hypoglycemia is prolonged — admit

High-yield pearls

  • ◆Don't stop insulin in DKA until anion gap CLOSES (glucose normalization alone is not enough)
  • ◆Pregnant + DM: insulin only (oral agents not first-line); tight control reduces fetal anomalies
  • ◆Steroids cause hyperglycemia — basal-bolus regimen + sliding scale
  • ◆Somogyi vs dawn: dawn phenomenon = morning hyperglycemia from cortisol surge; Somogyi (controversial) = early AM hypoglycemia → rebound hyperglycemia
  • ◆Newer GLP-1/GIP agonists (semaglutide, tirzepatide) — weight loss + cardiometabolic benefit
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