Endocrine Disorders

Diabetes Mellitus

The single most tested endocrine topic on the LPN/LVN exit exam.

Type 1 DMautoimmune

Cause: Autoimmune destruction of beta cells → NO insulin produced. Usually childhood/adolescence. Often thin. ALWAYS requires insulin — cannot survive without it. HIGH ketosis risk (DKA). Rapid symptom onset (days to weeks).

Type 2 DMinsulin resistance

Cause: Insulin resistance + relative insulin deficiency. Usually adults >40 (increasingly younger). Often overweight/obese. May need insulin but often managed with oral medications first. LOW ketosis risk — more prone to HHS. Gradual symptom onset (months to years).

Classic Symptoms — The 3 P's

• Polyuria — excessive urination (body tries to excrete excess glucose)
• Polydipsia — excessive thirst (due to dehydration from polyuria)
• Polyphagia — excessive hunger (cells can't use glucose for energy)

Diagnostic Criteria

Ranges vary by lab, facility, and textbook — for exams, use the range given in the question. See the full NCLEX-PN lab-value reference & sources →

• Fasting blood glucose ≥126 mg/dL
• HbA1c ≥6.5% (reflects average blood glucose over 2–3 months)
• Random blood glucose ≥200 mg/dL with symptoms
• Normal fasting glucose: 70–100 mg/dL

Hypoglycemia vs Hyperglycemia

Hypoglycemia<70 mg/dL

Onset: Rapid. Symptoms: Shakiness, diaphoresis, tachycardia, confusion, irritability, hunger, pale/cool skin. Treatment: Rule of 15: 15g fast-acting carb → recheck in 15 min → repeat if still <70. If unconscious: glucagon IM or dextrose IV. MORE immediately dangerous — can cause seizures, loss of consciousness, death quickly.

Hyperglycemia>180 mg/dL

Onset: Gradual. Symptoms: 3 P's, blurred vision, fatigue, headache, fruity breath (DKA), Kussmaul respirations (DKA). Treatment: Administer insulin as ordered, fluids, monitor glucose. Dangerous over time; can progress to DKA or HHS.

DKA vs HHS

Both are diabetic emergencies — know how they differ.

DKAType 1, primarily

Blood glucose >300 mg/dL. Ketones PRESENT (body burns fat → ketones). pH acidotic (<7.35) — metabolic acidosis. Kussmaul respirations (deep, rapid — body tries to blow off CO₂). Fruity/acetone breath. Moderate dehydration. Onset hours to days. Lower mortality. Treatment: IV fluids (NS first), IV insulin drip, monitor K⁺.

HHSType 2, primarily

Blood glucose >600 mg/dL (often 800–2000). Ketones absent or minimal. pH normal or slightly low. Normal or shallow breathing. No fruity breath. SEVERE dehydration. Onset days to weeks. Higher mortality (severe dehydration, older patients). Treatment: IV fluids (NS — AGGRESSIVE rehydration), IV insulin drip, monitor K⁺.

Insulin Management

Know the onset, peak, and duration — and what "peak" means for hypoglycemia risk.

Rapid-actingLispro (Humalog), Aspart (NovoLog)

Onset 15 min · Peak 1–2 hrs · Duration 3–5 hrs. Give immediately before meals.

Short-actingRegular (Humulin R, Novolin R)

Onset 30–60 min · Peak 2–4 hrs · Duration 6–8 hrs. Only insulin that can be given IV.

Intermediate-actingNPH (Humulin N)

Onset 1–2 hrs · Peak 6–12 hrs · Duration 18–24 hrs. Cloudy — gently roll before use.

Long-actingGlargine (Lantus), Detemir (Levemir)

Onset 1–2 hrs · No peak (steady) · Duration 24 hrs. Never mix with other insulins.

Critical Insulin Rules

• Peak time = highest hypoglycemia risk — make sure patient has eaten
• Only Regular insulin can be given IV (all others are subQ only)
• When mixing insulins: draw up clear (Regular) before cloudy (NPH) — "Clear before cloudy"
• Do NOT mix Lantus (glargine) with any other insulin
• Rotate injection sites to prevent lipodystrophy; inject within the same body region at the same time of day
• Do NOT shake insulin — gently roll the vial between palms (NPH needs to be mixed)
• Opened insulin vials: good for 28 days at room temperature

Thyroid Disorders

Hypo vs hyper — everything is opposite. Master this comparison.

Hypothyroidismslowed metabolism

Weight GAIN, bradycardia, cold intolerance, dry/coarse skin, fatigue/lethargy, constipation. Lab: TSH HIGH (pituitary overdriving), T3/T4 LOW. Special: myxedema (severe form), goiter possible. Treatment: Levothyroxine (Synthroid) — lifelong.

HyperthyroidismGraves' Disease · fast metabolism

Weight LOSS, tachycardia/palpitations/A-fib, heat intolerance, warm/moist skin, restlessness/insomnia, diarrhea. Lab: TSH LOW, T3/T4 HIGH. Special: exophthalmos (bulging eyes), goiter, tremors. Treatment: antithyroid drugs (methimazole, PTU), radioactive iodine, thyroidectomy.

Post-Thyroidectomy Nursing Care (Tested!)

• Monitor for hemorrhage: check behind the neck (blood pools posteriorly)
• Keep tracheostomy tray at bedside (laryngeal edema risk)
• Monitor for hypocalcemia (parathyroid glands can be accidentally damaged) — signs: tingling around mouth, Chvostek's sign (facial twitch when tapping cheek), Trousseau's sign (carpopedal spasm with BP cuff inflated)
• Assess voice quality — hoarseness may indicate laryngeal nerve damage
• Support the neck when repositioning

Addison's Disease vs Cushing's Syndrome

One has too little cortisol, one has too much — they are opposites.

Addison's DiseaseTOO LITTLE cortisol

Cause: Autoimmune destruction of adrenal cortex; abrupt steroid withdrawal. Hypoglycemia, hypotension, hyponatremia, hyperkalemia. Weight loss. Bronze/hyperpigmentation skin. Crisis: Addisonian shock. Treatment: Lifelong corticosteroid replacement (hydrocortisone, fludrocortisone). NEVER stop steroids abruptly.

Cushing's SyndromeTOO MUCH cortisol

Cause: Prolonged corticosteroid use (#1); pituitary adenoma. Hyperglycemia, hypertension, hypernatremia, hypokalemia. Weight gain (truncal obesity, moon face, buffalo hump). Thin skin, easy bruising, striae, poor wound healing. Immunosuppressed → infection risk. Treatment: Taper/discontinue steroids if drug-induced; surgery if tumor.

SIADH vs Diabetes Insipidus (DI)

Both involve ADH — one has too much, one has too little.

SIADHToo MUCH ADH

Body RETAINS too much water. Urine output DECREASED (concentrated, dark). Urine specific gravity HIGH (>1.030). Serum sodium dilutional HYPONATREMIA. Serum osmolality LOW (diluted). Fluid OVERLOAD. Weight gain. Symptoms: headache, confusion, nausea (from hyponatremia), possible seizures. Treatment: Fluid RESTRICTION, hypertonic saline (3% NS) for severe hyponatremia, demeclocycline.

Diabetes InsipidusToo LITTLE ADH

Body EXCRETES too much water. Urine output INCREASED — massive polyuria (dilute, pale urine, 5–20 L/day!). Urine specific gravity LOW (<1.005). Serum sodium HYPERNATREMIA. Serum osmolality HIGH. Fluid DEFICIT (severe dehydration). Weight loss. Extreme thirst. Treatment: Fluid REPLACEMENT (oral + IV), desmopressin (DDAVP) — synthetic ADH.

Key Endocrine Medications

Medications you'll see on every endocrine question.

Levothyroxine (Synthroid)hypothyroidism

Take on empty stomach in AM, 30–60 min before food. Monitor HR (tachycardia = too much). Lifelong therapy.

Methimazole / PTUhyperthyroidism

Blocks thyroid hormone production. Monitor WBCs (agranulocytosis risk — report sore throat/fever). PTU preferred in 1st trimester pregnancy.

Metformin (Glucophage)Type 2 DM

First-line oral med. Does NOT cause hypoglycemia when used alone. Hold before contrast dye procedures. Rare but serious: lactic acidosis (report muscle pain, weakness). Avoid alcohol.

Glipizide (Glucotrol)Type 2 DM

Sulfonylurea — stimulates pancreas to release insulin. CAN cause hypoglycemia. Take 30 min before meals.

HydrocortisoneAddison's

Corticosteroid replacement. Never stop abruptly. Increase during stress. Monitor glucose, BP.

Desmopressin (DDAVP)Diabetes Insipidus

Synthetic ADH — decreases urine output. Monitor for water retention, hyponatremia. Nasal spray or injection.

Insulin (all types)Type 1 & Type 2 DM

See insulin table above. Only Regular can be given IV. Monitor for hypoglycemia at peak times.

Frequently Asked Questions

Common student questions on this topic.

Quick-Reference Cheatsheet

Every key point from this guide on a single printable page.