A patient with a 20-year history of hypothyroidism who has not been compliant with taking thyroid replacement therapy is brought into the ED with a diagnosis of myxedema coma. Which symptoms are consistent with this life-threatening event? (Select all that apply)

Choice A reason: Potassium is contraindicated in Addisonian crisis, as adrenal insufficiency causes hyperkalemia due to aldosterone deficiency, impairing potassium excretion. Administering potassium would worsen hyperkalemia, risking cardiac arrhythmias. Treatment focuses on cortisol replacement and fluids to correct hypotension and hyponatremia, not potassium, which is already elevated.

Choice B reason: Hypotonic saline is not appropriate for Addisonian crisis. Patients have hyponatremia and hypotension due to aldosterone deficiency, requiring isotonic saline (e.g., 0.9% NaCl) to restore sodium and volume. Hypotonic fluids could worsen hyponatremia by further diluting serum sodium, exacerbating neurological symptoms like confusion.

Choice C reason: Insulin is irrelevant in Addisonian crisis, which involves cortisol and aldosterone deficiency, not hyperglycemia. Hypoglycemia may occur due to low cortisol, but glucose is administered if needed, not insulin. The focus is on hydrocortisone to replace deficient glucocorticoids, addressing the underlying adrenal insufficiency and stabilizing the patient.

Choice D reason: Hydrocortisone IV is the cornerstone of Addisonian crisis treatment, replacing deficient glucocorticoids due to adrenal insufficiency. It corrects hypoglycemia, hypotension, and metabolic dysfunction, improving symptoms like weakness and confusion. Rapid administration restores stress response and stabilizes hemodynamics, critical for reversing the life-threatening crisis and preventing shock.

Choice A reason: DIC is not caused by the immune system attacking platelets. This describes conditions like immune thrombocytopenic purpura (ITP). In DIC, widespread clotting consumes platelets and clotting factors, leading to bleeding. The immune system is not the primary driver; rather, it’s triggered by conditions like sepsis or trauma.

Choice B reason: DIC results from abnormal activation of the clotting cascade, often triggered by sepsis, trauma, or malignancy. This causes microclots to form in small vessels, consuming clotting factors and platelets, leading to bleeding. Organ damage occurs from microthrombi, and depletion of coagulation components causes hemorrhage, accurately describing DIC’s pathophysiology.

Choice C reason: Hemolytic processes destroying erythrocytes describe hemolytic anemia, not DIC. While hemolysis may occur in DIC due to microangiopathic changes, it is not the primary cause. DIC involves widespread clotting and factor consumption, not primarily red cell destruction, making this an inaccurate explanation of its etiology.

Choice D reason: DIC is not primarily a complication of autoimmune diseases attacking cells. It is triggered by conditions like sepsis, cancer, or obstetric complications, activating the clotting cascade. Autoimmune diseases like lupus may rarely contribute, but DIC’s hallmark is coagulopathy from external triggers, not autoimmunity, making this explanation incorrect.