Q2. A 67-year-old man with a 40-pack-year smoking history presents with hematuria and left flank pain. Physical examination reveals a palpable mass in the left flank. Laboratory studies show elevated hemoglobin and hematocrit. Abdominal CT reveals a solid mass in the left kidney.
Which of the following is the most likely mechanism responsible for this patient’s elevated hemoglobin?
A. Increased erythropoietin production by tumor cells
B. Chronic hypoxia leading to secondary polycythemia
C. Decreased renal perfusion activating the RAAS system
D. Bone marrow mutation causing autonomous RBC production
E. Autoimmune destruction of red blood cells
Answer: A
Explanation:
This patient most likely has renal cell carcinoma (RCC). Classic findings include hematuria, flank pain, and a palpable mass. RCC can produce erythropoietin ectopically, leading to secondary polycythemia and elevated hemoglobin. This is a paraneoplastic syndrome.
Why the other answers are incorrect:
B. Chronic hypoxia can cause secondary polycythemia, but this patient’s kidney mass suggests ectopic EPO production.
C. RAAS activation increases blood pressure but does not directly cause polycythemia.
D. A bone marrow mutation describes polycythemia vera, a primary myeloproliferative disorder.
E. Autoimmune destruction of RBCs would cause anemia, not elevated hemoglobin.
Q1. A 24-year-old woman presents to the clinic with fatigue, weight loss, and intermittent diarrhea for 6 months. She reports bloating after meals and has noticed a pruritic rash on her elbows and knees. Physical examination reveals a thin woman with a symmetric vesicular rash on the extensor surfaces of her arms. Laboratory studies show iron-deficiency anemia.
Which of the following is the most likely underlying mechanism of this patient’s condition?
A. IgE-mediated hypersensitivity reaction to dietary proteins
B. Autoimmune destruction of gastric parietal cells
C. T-cell–mediated damage to small intestinal villi
D. Immune complex deposition in the renal glomerulus
E. Mutation in CFTR gene leading to thick secretions
Answer: C. T-cell–mediated damage to small intestinal villi
Explanation:
This patient has celiac disease. Key findings include chronic diarrhea, weight loss, iron-deficiency anemia (due to malabsorption in the proximal small intestine), and dermatitis herpetiformis (a pruritic vesicular rash on extensor surfaces). Celiac disease is triggered by gluten (gliadin), which is deamidated by tissue transglutaminase (tTG). This activates CD4+ T cells and leads to immune-mediated destruction of small intestinal villi, resulting in malabsorption. Dermatitis herpetiformis is caused by IgA deposition in the dermal papillae.
Why the other answers are incorrect:
A. IgE-mediated hypersensitivity reaction to dietary proteins – This describes a type I hypersensitivity reaction (e.g., food allergy).
B. Autoimmune destruction of gastric parietal cells – Seen in pernicious anemia, causing vitamin B12 deficiency.
D. Immune complex deposition in the renal glomerulus – Seen in post-streptococcal glomerulonephritis or lupus nephritis.
E. Mutation in CFTR gene leading to thick secretions – Seen in cystic fibrosis.
Simon R. Downes 