Endocrinology

A

• Acute Adrenal Crisis — Hydrocortisone First, Aggressive Fluids, and Precipitant Control

  Life-threatening hypotension, hyponatremia, hyperkalemia, and hypoglycemia in patients with adrenal insufficiency or chronic steroid use. Give hydrocortisone immediately with large-volume isotonic fluids and dextrose; treat triggers such as infection or withdrawal; do not delay steroids for labs.
• Acute Adrenal Crisis — Stress-Dose Steroids, Fluids, and Precipitant Control

  Life-threatening cortisol deficiency with hypotension, hyponatremia, hyperkalemia, and hypoglycemia. Treat immediately with hydrocortisone 100 mg IV, aggressive isotonic fluids, and dextrose as needed; do not delay for labs. Identify precipitating illness or medication nonadherence.
• Adrenal Crisis — Immediate Hydrocortisone and Fluids

  Life-threatening adrenal insufficiency with hypotension and shock; give hydrocortisone immediately, aggressive fluids, dextrose as needed, and treat precipitating cause.
• Adrenal Crisis — Recognition & Treatment

  Adrenal crisis is acute glucocorticoid deficiency causing hypotension or shock, volume depletion, gastrointestinal symptoms, electrolyte disturbance, hypoglycemia, and altered mental status. It can complicate primary adrenal insufficiency, secondary adrenal insufficiency, pituitary disease, or suppression from chronic exogenous glucocorticoids. Treatment is clinical and must begin immediately with parenteral hydrocortisone and isotonic fluid. Cortisol testing can be obtained before steroids if it does not d
• Adrenal Crisis — Stress‑Dose Steroids, Triggers, and Disposition

  Life‑threatening cortisol deficiency with hypotension, abdominal pain, hyponatremia/hyperkalemia, and shock. Treat immediately with IV hydrocortisone and isotonic fluids; do not delay for labs. Identify precipitants (infection, missed doses, surgery) and provide sick‑day education.

C

• Cushing Syndrome — Screening & Localization

  Cushing syndrome is chronic pathologic cortisol excess. After endogenous hypercortisolism is confirmed, measure ACTH.
• Cushing’s Syndrome — Diagnosis & Management

  Progressive weight gain with central adiposity, proximal myopathy, violaceous striae, glucose intolerance, and hypertension. Confirm hypercortisolism with high-accuracy testing (late-night salivary cortisol, 1-mg dex suppression, or 24-h UFC) prior to etiologic workup. Distinguish ACTH-dependent vs. ACTH-independent disease; pituitary MRI and inferior petrosal sinus sampling guide localization in Cushing disease. Management targets the source—surgical resection first line, with adjunct medical therapy when

D

• Diabetes in CKD — Medication Choice & Dose Adjustments

  Diabetes management in chronic kidney disease has two goals: achieve individualized glycemic control without hypoglycemia and slow kidney/cardiovascular progression with therapies that work beyond glucose lowering. SGLT2 inhibitors are foundational kidney- and heart-protective therapy for eligible type 2 diabetes with CKD and can generally be initiated down to an eGFR around 20 mL/min/1.73 m² under current guidance.
• Diabetic Ketoacidosis — Adult

  Adult diabetic ketoacidosis is defined by diabetes or hyperglycemia together with ketosis and metabolic acidosis. Treatment is built on isotonic fluid replacement, potassium-guided insulin therapy, treatment of the precipitating cause, and frequent biochemical reassessment. Resolution should be judged by clearance of ketonemia and correction of acidosis rather than glucose alone.
• Diabetic Ketoacidosis — Adult ED Management

  Fluid resuscitation, insulin infusion with careful potassium management, and identification of precipitating cause; transition to subcutaneous insulin after resolution criteria met.
• Diabetic Ketoacidosis — Fluids, Insulin Protocol, and Potassium Strategy

  DKA presents with hyperglycemia, anion gap metabolic acidosis, and ketonemia/ketonuria. Begin isotonic fluids, correct potassium before insulin if K+ <3.3, start insulin infusion when safe, and transition to subcutaneous insulin once gap closes. Identify and treat precipitants.
• Diabetic Ketoacidosis — Fluids, Insulin-Dextrose Pairing, and Electrolytes

  Hyperglycemia, ketonemia, and anion-gap metabolic acidosis. Start isotonic fluids, initiate insulin with potassium-safe thresholds, add dextrose when glucose ~200–250 mg/dL to continue ketone clearance, and correct electrolytes; search for triggers.
• Diabetic Ketoacidosis — Fluids, Insulin, Potassium, and Anion Gap Closure

  DKA presents with hyperglycemia, ketosis, and metabolic acidosis. Begin balanced crystalloids, correct potassium, and start insulin infusion after K+ ≥3.3 mEq/L. Add dextrose as glucose approaches 200 mg/dL and continue insulin until ketoacidosis resolves (anion gap closes). Search for precipitants.
• DKA in Adults — Fluid, Insulin, and Electrolytes

  Diabetic ketoacidosis is a hyperglycemic crisis defined by diabetes or hyperglycemia plus clinically significant ketonemia and metabolic acidosis. Begin isotonic or balanced crystalloid resuscitation, adjusting rate for age, heart failure, kidney disease, sodium, and hemodynamics.

G

• Graves Disease — Antithyroid Drugs, RAI, and Surgery

  Graves disease is autoimmune hyperthyroidism caused by thyroid-stimulating immunoglobulins activating the TSH receptor. Control adrenergic symptoms with a beta blocker when appropriate.

H

• Hashimoto Thyroiditis — Diagnosis & Hypothyroid Transition

  Hashimoto thyroiditis is autoimmune destruction of the thyroid and the most common cause of primary hypothyroidism in iodine-sufficient regions. Levothyroxine is standard replacement.
• HHS — Diagnosis & Management

  Hyperosmolar hyperglycemic state is a severe hyperglycemic emergency characterized by profound dehydration and hyperosmolality with little or no clinically important ketoacidosis. Volume replacement is the first major intervention and often produces a substantial fall in glucose before insulin begins.
• Hypercalcemia of Malignancy — Acute Management

  Hypercalcemia of malignancy is an oncologic emergency when calcium is markedly elevated or causing neurologic, renal, gastrointestinal, or cardiac dysfunction. Restore volume with isotonic fluid, use calcitonin for rapid short-term effect in severe cases, and give denosumab or an IV bisphosphonate for sustained control while treating the underlying cancer.
• Hyperosmolar Hyperglycemic State — Adult

  Hyperosmolar hyperglycemic state is a severe hyperglycemic emergency characterized by marked hyperglycemia, hyperosmolality, profound water deficit, and absent or only mild ketonemia and acidosis. It often evolves over days, particularly in older adults with type 2 diabetes, and commonly presents with dehydration and altered cognition. Treatment prioritizes controlled volume replacement, potassium-guided insulin therapy, gradual reduction in osmolality, identification of the precipitating illness, and caref
• Hyperosmolar Hyperglycemic State — Adult Management

  Hyperosmolar hyperglycemic state is a life-threatening hyperglycemic emergency characterized by severe hyperglycemia, hyperosmolality, profound dehydration, and little or no significant ketoacidosis. Treatment prioritizes controlled restoration of intravascular volume, potassium-guided insulin therapy, careful monitoring of osmolality and sodium, and treatment of the precipitating illness. Rapid osmotic shifts should be avoided because overly aggressive correction can cause neurologic complications.
• Hyperosmolar Hyperglycemic State — Fluid Strategy, Insulin, and Electrolyte Targets

  Profound hyperglycemia with hyperosmolality and minimal ketosis; prioritize isotonic fluids with careful correction of osmolality, low-dose insulin infusion once volume is restored, and aggressive potassium and phosphate management.
• Hypocalcemia — Acute Management

  Acute hypocalcemia can cause neuromuscular irritability, laryngospasm, seizures, hypotension, heart failure, and QT prolongation. Management is driven by symptoms and ECG risk rather than by the calcium number alone. Severe or symptomatic disease requires monitored IV calcium while the clinician simultaneously identifies and treats the underlying cause, especially hypomagnesemia and postsurgical hypoparathyroidism.
• Hypocalcemia — Emergency Management & Long‑Term Care

  Hypocalcemia can range from an incidental laboratory finding to a life-threatening cause of tetany, seizure, laryngospasm, or ventricular dysrhythmia. For tetany, seizure, laryngospasm, prolonged QT with instability, or other severe symptoms, give IV calcium gluconate—commonly 1-2 g of 10% calcium gluconate over about 10-20 minutes with ECG monitoring—and repeat or infuse as needed.
• Hypoglycemia — Adult Emergency Management

  Hypoglycemia is a glucose concentration low enough to cause autonomic or neuroglycopenic dysfunction and is most dangerous when the patient cannot self-treat. Immediate therapy is based on consciousness and swallowing ability, followed by identification of the cause and prevention of recurrence. In adults with diabetes, glucose below 70 mg/dL is the alert threshold, below 54 mg/dL is clinically significant, and severe hypoglycemia is defined by the need for assistance rather than a specific glucose value.
• Hypopituitarism — Recognition & Hormone Replacement

  Hypopituitarism can involve one or multiple anterior pituitary hormones and may coexist with central diabetes insipidus. If adrenal crisis or significant ACTH deficiency is suspected, give stress-dose hydrocortisone immediately after drawing cortisol if this does not delay treatment.

M

• Male Hypogonadism — Workup & Treatment

  Male hypogonadism requires both compatible symptoms/signs and consistently low testosterone—not a single isolated laboratory value. Treat reversible contributors first when possible.
• Myxedema Coma — Recognition and Treatment

  Myxedema coma is decompensated severe hypothyroidism with altered mental status and multisystem physiologic failure. Actual coma is not required. Hypothermia, hypoventilation, bradycardia, hypotension, hyponatremia, hypoglycemia, and precipitating infection or cardiovascular illness are common. Treatment should begin on clinical suspicion because laboratory confirmation may be too slow for a critically ill patient.
• Myxedema Coma — Steroids First, IV Thyroid Hormone, and Passive Rewarming

  Severe decompensated hypothyroidism with hypothermia, bradycardia, hypotension, hyponatremia, and altered mental status. Treat empirically with stress‑dose glucocorticoids, IV levothyroxine loading (± liothyronine), passive rewarming, careful ventilation, and aggressive search for precipitants (infection, MI, sedatives).

P

• Polycystic Ovary Syndrome (PCOS) — Diagnosis & Management

  Irregular menses with chronic anovulation and hyperandrogenism; apply Rotterdam criteria after excluding mimics, screen for metabolic risk, use combined OCPs or cyclic progestin for cycle control, add metformin for metabolic disease, and use letrozole as first-line ovulation induction for infertility.
• Primary Hyperparathyroidism — Evaluation & Indications for Surgery

  Primary hyperparathyroidism is autonomous PTH secretion causing hypercalcemia, usually from a single parathyroid adenoma. Parathyroidectomy is definitive and is recommended for symptomatic disease and many asymptomatic patients, including those with serum calcium more than 1 mg/dL above the upper limit of normal, osteoporosis or fragility fracture, eGFR below 60, nephrolithiasis/nephrocalcinosis, significant hypercalciuria under current criteria, or age below 50.
• Primary Hypothyroidism — Diagnosis & Management

  Fatigue, weight gain, cold intolerance, constipation, and bradycardia with elevated TSH and low free T4. Confirm primary thyroid failure, evaluate for autoimmune etiology, initiate levothyroxine with weight-based dosing, and titrate to normalize TSH.
• Pseudohypoparathyroidism — PTH Resistance & Albright Hereditary Osteodystrophy

  Pseudohypoparathyroidism and related GNAS-pathway disorders are characterized by target-organ resistance to parathyroid hormone, producing elevated PTH with hyperphosphatemia and often hypocalcemia despite intact hormone production. Albright hereditary osteodystrophy features, imprinting effects, and resistance to additional hormones help define the phenotype, while treatment uses active vitamin D and calcium rather than PTH replacement.

S

• Severe Hypoglycemia — Immediate Treatment and Prevention of Rebound

  Severe hypoglycemia is a glucose-lowering emergency in which neuroglycopenia causes altered behavior, seizure, loss of consciousness, or inability to self-treat. Give rapid glucose or glucagon, identify the medication or illness driving the event, and observe long enough to detect recurrence from long-acting insulin or insulin secretagogues.

T

• Thyroid Storm — Beta-Blockade, Thionamides, Iodine, and Steroids

  Life-threatening hyperthyroidism precipitated by infection, surgery, or withdrawal of antithyroid drugs. Start beta-blockade, administer thionamides (PTU preferred initially), give iodine at least 1 hour later to block release, add glucocorticoids, and treat precipitants; ICU monitoring and active cooling as needed.
• Thyroid Storm — Burch–Wartofsky Score, Stepwise Block-and-Replace

  Life-threatening thyrotoxicosis with fever, delirium, and cardiovascular instability; treat with beta blockade, high-dose thionamides, iodide given after thionamide, stress-dose glucocorticoids, and supportive ICU care.
• Thyroid Storm — Emergency Management

  Life threatening thyrotoxicosis with fever, tachyarrhythmia, CNS and GI symptoms; give beta blockade, thionamide, iodine (after thionamide), steroids, and supportive care.
• Thyroid Storm — Emergency Treatment

  Thyroid storm is life-threatening decompensated thyrotoxicosis characterized by hyperthermia, marked adrenergic activation, central nervous system dysfunction, and organ failure. Diagnosis is clinical and treatment should begin when strongly suspected rather than waiting for thyroid-hormone results. Control adrenergic symptoms, block new thyroid-hormone synthesis, block hormone release, reduce peripheral T4-to-T3 conversion, treat the precipitating illness, and provide ICU supportive care. Give iodine only
• Thyroid Storm — Recognition & Treatment

  Thyroid storm is life-threatening decompensated thyrotoxicosis with systemic organ dysfunction, typically involving fever, marked tachycardia or atrial arrhythmia, heart failure, gastrointestinal or hepatic dysfunction, and central nervous system change. It is a clinical diagnosis and treatment should begin when the syndrome is strongly suspected rather than waiting for thyroid hormone results. Therapy blocks adrenergic effects, new thyroid-hormone synthesis, hormone release, and peripheral conversion while
• Thyroid Storm — Thionamides, Iodine Timing, β-Blockade, and Steroids

  Severe thyrotoxicosis with multiorgan dysfunction. Start β-blockade; give PTU 500–1000 mg load then 250 mg q4h (or Methimazole 20 mg q4–6h), followed by iodine (SSKI) 1–2 h later to block release. Add hydrocortisone 100 mg IV q8h and supportive care including cooling and fluids.