What complication occurs when a person has Cushing syndrome?

A. Primary immunodeficiency involves a developmental failure in the bone marrow or thymus, impairing immune system development. This aligns with the question, as primary immunodeficiencies, such as severe combined immunodeficiency or DiGeorge syndrome, result from genetic defects affecting lymphocyte development, crucial for meeting physiological needs in Maslow’s hierarchy.

B. Secondary immunodeficiency results from external factors like infections or malnutrition, not developmental failure in the bone marrow or thymus. This does not fit the question, as it lacks a congenital basis.

C. Autoimmune disorders arise from immune system dysfunction attacking self-tissues, not developmental failure in immune organs. This is unrelated to the question’s focus on developmental defects.

D. Infections are a consequence of primary immunodeficiency due to impaired T-cell or B-cell function, increasing susceptibility to recurrent bacterial, viral, or fungal infections. This fits the question, as immunodeficiency predisposes individuals to infections.

E. Allergies result from immune overreactions to harmless substances, not a direct consequence of developmental immune defects. This does not align with the question’s focus on immunodeficiency outcomes.

F. Autoimmune diseases involve immune attacks on self-tissues, not a primary outcome of developmental immune failure. This is incorrect for the question’s context.

G. Malignancies are a known complication of primary immunodeficiencies, as impaired immune surveillance increases cancer risk, particularly lymphomas or leukemias. This aligns with the question’s focus on outcomes of immunodeficiency.

H. Chronic pain is not a direct result of immunodeficiency or developmental failure in the bone marrow or thymus. This does not fit the question’s scope.

I. Recurrent infections are a hallmark of primary immunodeficiency, as defective immune components fail to protect against pathogens. This aligns with the question, as it directly results from immune system developmental failure.

Choice A reason: Graves’ disease, a form of hyperthyroidism, does not typically cause decreased calcium. It may lead to hypercalcemia due to increased bone resorption from elevated thyroid hormone levels, which enhance osteoclast activity, making decreased calcium an incorrect laboratory finding for this condition.

Choice B reason: Graves’ disease is characterized by increased thyroid hormone production, including elevated T4 due to autoimmune stimulation of the thyroid. Decreased T4 is associated with hypothyroidism, not hyperthyroidism, making this choice incorrect as it contradicts the pathophysiology of Graves’ disease.

Choice C reason: Increased TSH is seen in primary hypothyroidism, where the thyroid is underactive. In Graves’ disease, TSH is typically decreased due to negative feedback from elevated thyroid hormones (T3 and T4), making this choice incorrect for the expected laboratory profile.

Choice D reason: Graves’ disease causes hyperthyroidism, with increased production of thyroid hormones, including T3, due to autoantibodies stimulating TSH receptors. Elevated T3 levels drive metabolic symptoms like weight loss and tachycardia, making this the correct laboratory finding for Graves’ disease.