A 65-year-old male with symptomatic benign prostatic hyperplasia (BPH) is considering treatment options. He asks about the role of finasteride in BPH management. What is the primary mechanism of action of finasteride in the treatment of BPH?

A. Rheumatoid arthritis primarily involves Type 3 hypersensitivity, where immune complexes deposit in the synovial joints to trigger inflammation. While T-cells are present, the formation of rheumatoid factor complexes is a central pathological feature. It represents a systemic autoimmune response characterized by both antibody-mediated and cell-mediated damage, but Type 3 is highly prominent.

B. Systemic lupus erythematosus (SLE) is the prototypical Type 3 hypersensitivity disorder involving the systemic deposition of antigen-antibody complexes. These complexes circulate and lodge in various tissues, such as the kidneys and skin, leading to complement activation and tissue destruction. It is not primarily defined by the delayed, cell-mediated mechanisms of Type IV hypersensitivity.

C. Multiple sclerosis is an autoimmune disorder driven by Type IV hypersensitivity, where autoreactive T-lymphocytes cross the blood-brain barrier to attack the myelin sheath. These T-cells release cytokines that activate macrophages, leading to the destruction of oligodendrocytes in the central nervous system. This delayed, cell-mediated immune response results in the characteristic plaque formation and neurodegeneration.

D. Graves’ disease is a Type 2 hypersensitivity reaction where autoantibodies specifically target and stimulate the thyroid-stimulating hormone (TSH) receptor. This leads to the autonomous overproduction of thyroid hormones, resulting in hyperthyroidism. The pathology is caused by direct antibody-receptor interaction rather than the sensitized T-cell activity that characterizes Type IV hypersensitivity.

A. Correcting fluid and electrolyte disturbances is vital in AKI management to prevent life-threatening complications like hyperkalemia or pulmonary edema. Because the kidneys cannot effectively regulate potassium or sodium, aggressive monitoring and pharmacological intervention are required. Restoring fluid homeostasis supports the metabolic environment necessary for the survival and regeneration of injured tubular cells.

B. Preventing and treating infections is a critical component of care because sepsis is a leading cause of mortality in patients with acute kidney injury. AKI often induces a state of immune dysfunction, increasing the patient's susceptibility to opportunistic pathogens. Prompt antimicrobial therapy and strict aseptic techniques are essential to prevent further systemic decline during the recovery phase.

C. All the choices are correct because the management of AKI is multifaceted and aims to stabilize the internal milieu while the kidneys recover. This includes the simultaneous control of fluid volume, electrolyte balance, blood pressure, and the prevention of secondary infections. Comprehensive supportive care is the only way to minimize multi-organ failure during the acute phase.

D. Managing blood pressure is essential to ensure adequate renal perfusion without causing further barotrauma to the glomerular capillaries. Maintaining a mean arterial pressure high enough to overcome intrarenal resistance facilitates the recovery of the glomerular filtration rate. Both hypotension and extreme hypertension must be avoided to prevent the transition from AKI to chronic disease.