A nurse is caring for a patient who has acute gastroenteritis but is able to tolerate oral fluids. The nurse should anticipate providing which of the following types of fluid?

Choice A reason: Serum calcium does not typically decrease in Addisonian crisis. Adrenal insufficiency reduces aldosterone, causing sodium loss and potassium retention, but calcium homeostasis is primarily regulated by parathyroid hormone and vitamin D. Hypocalcemia is not a hallmark of Addisonian crisis, and calcium levels remain normal unless other conditions are present.

Choice B reason: BUN (blood urea nitrogen) may increase, not decrease, in Addisonian crisis due to dehydration from sodium loss and reduced glomerular filtration. Adrenal insufficiency does not directly lower BUN. Elevated BUN reflects hemoconcentration and reduced renal perfusion, making this an incorrect choice for a lab value that decreases in this condition.

Choice C reason: Serum cortisol decreases in Addisonian crisis due to adrenal insufficiency, impairing glucocorticoid production. Cortisol is critical for glucose metabolism and stress response. In primary adrenal insufficiency (Addison’s disease), adrenal glands fail to produce cortisol, leading to hypoglycemia, fatigue, and shock, making low cortisol a key diagnostic feature of the crisis.

Choice D reason: Serum potassium increases, not decreases, in Addisonian crisis. Aldosterone deficiency impairs sodium retention and potassium excretion, leading to hyperkalemia. This can cause cardiac arrhythmias and muscle weakness. Decreased potassium is not associated with Addisonian crisis, as the pathophysiology drives potassium retention, making this choice incorrect.

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.