Endocrinology USMLE Practice Questions

A. Elevated hepcidin

This option implies increased iron sequestration and decreased absorption (as in anemia of chronic disease), BUT transfusional iron overload typically suppresses hepcidin to allow iron utilization; the key lab is elevated ferritin from massive stores, not hepcidin elevation.

C. Decreased transferrin saturation

This option implies iron deficiency (low iron, many empty binding sites), BUT this patient has chronic transfusions and classic iron overload signs (hyperpigmentation, hepatomegaly, endocrinopathy), so transferrin saturation would be increased, not decreased.

D. Elevated transferrin

This option suggests the body is trying to scavenge more iron, as in iron deficiency, BUT in iron overload transferrin levels are normal/low with high saturation; the hallmark is high ferritin, not elevated transferrin.

E. Decreased haptoglobin

This option implies intravascular hemolysis (free hemoglobin binds haptoglobin), which can occur in hemolytic anemias, BUT the question is specifically targeting chronic iron overload from transfusions (organ deposition, hyperpigmentation, diabetes, hepatomegaly) rather than acute hemolysis markers.

F. Elevated iron-binding capacity

This option corresponds to increased TIBC, typical of iron deficiency (liver makes more transferrin), BUT transfusional iron overload leads to high iron and ferritin with normal or decreased TIBC, not elevated.

A. External orbital radiation

This option implies local immunosuppressive therapy to the orbit, which is used to improve moderate–severe thyroid eye disease, NOT to worsen it.

B. Selenium supplementation

This option implies antioxidant therapy, which has been shown to improve mild thyroid eye disease in some patients, NOT exacerbate symptoms.

C. Smoking cessation

This option implies removal of a major risk factor; smoking worsens Graves ophthalmopathy, BUT stopping smoking reduces progression risk rather than worsening symptoms.

D. Systemic corticosteroids

This option implies systemic immunosuppression, which is standard treatment to reduce inflammation and swelling in active thyroid eye disease, not to transiently worsen it.

A. Pyridoxine levels

This option implies vitamin B6 toxicity or deficiency, which typically causes neuropathy or sideroblastic anemia, BUT does not explain polyuria, polydipsia, constipation, and abdominal pain with normal glucose.

B. Niacin levels

This option implies vitamin B3 excess or deficiency; deficiency causes pellagra (dermatitis, diarrhea, dementia), BUT these findings are absent, and it does not classically cause polyuria or constipation.

D. Hemoglobin A1C

This option implies evaluation for chronic hyperglycemia/diabetes mellitus, which would cause polyuria and polydipsia, BUT her current glucose is normal and GI constipation/abdominal pain with supplement use points more toward hypercalcemia.

E. Free T4 levels

This option implies thyroid dysfunction. Hyperthyroidism causes weight loss, heat intolerance, diarrhea, and sometimes polyuria, BUT she has constipation, abdominal pain, and no weight change, which are more consistent with hypercalcemia from supplements.

A. Postpartum thyroiditis

This option implies transient autoimmune thyroid inflammation causing hyper- then hypothyroidism, which causes high TSH when hypothyroid, BUT this patient has low TSH and low T4 plus failure to lactate and hypoglycemia, pointing to panhypopituitarism, not isolated thyroid disease.

B. Lactotrophic adenoma

This option implies a prolactinoma that causes galactorrhea and amenorrhea from excess prolactin, BUT this patient has decreased milk production and multiple pituitary hormone deficiencies after hemorrhage, incompatible with a prolactin-secreting tumor.

C. Adrenal hemorrhage

This option implies primary adrenal failure (e.g., Waterhouse-Friderichsen) with hyperpigmentation and high ACTH, BUT here thyroid function is also low, and there is postpartum hemorrhage with low TSH/T4 and failed lactation, indicating central (pituitary) rather than primary adrenal pathology.

D. Hypothalamic infarction

This option implies damage to hypothalamic releasing hormones, which could mimic pituitary failure, BUT Sheehan syndrome classically results from direct ischemia of the enlarged anterior pituitary after obstetric hemorrhage; there is no specific reason here to target the hypothalamus instead of the pituitary.

A. Elevated serum thyroxine concentration

This option implies hyperthyroidism, which can cause weight loss, heat intolerance, tremor, and tachycardia, BUT the patient’s only systemic issues are polyuria/polydipsia plus acanthosis nigricans, which point to insulin resistance, not thyroid excess.

C. Elevated serum prostate-specific antigen

This option implies prostate pathology (e.g., BPH or prostate cancer), which can cause urinary frequency and nocturia, BUT it would not explain marked polydipsia or acanthosis nigricans, and usually causes obstructive symptoms (weak stream, hesitancy), which are not described.

D. Positive urinary leukocyte esterase

This option implies a urinary tract infection, which often presents with dysuria, urgency, suprapubic pain, or fever, BUT the stem lacks any pain, burning, or systemic infectious signs and instead shows chronic metabolic signs (acanthosis nigricans).

E. Low urine osmolality

This option implies diabetes insipidus or primary polydipsia, which cause dilute urine, BUT there is a strong clue to insulin resistance (acanthosis nigricans) and sugary drink intake, and diabetes mellitus better ties together all findings and predicts high HbA1c rather than focusing on urine osmolality.