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Reproductive System & Endocrine System — USMLE Step 1 practice questions

23 multiple-choice questions and 7 flashcards on Reproductive System & Endocrine System, about 13% of the USMLE Step 1 bank. Every one carries a written rationale.

Written and maintained by Nick Burton · last updated 2026-08-22 · how we write and review questions

What this chapter covers

Reproductive System & Endocrine System is one of 10 chapters in CoStudy's USMLE Step 1 — Medical Licensing bank, and it holds 23 of the bank's 172 multiple-choice questions — roughly 13% of the total. That proportion is not arbitrary: chapters follow the certifying body's published exam outline, and the number of questions in each is set by that domain's published weight, so the share of your practice time this chapter takes matches the share of the real exam it accounts for.

Studying by chapter is worth doing once you have a diagnostic score. A single overall percentage tells you whether you are close; it does not tell you which domain is dragging. Working a weak chapter in isolation, and re-testing it in isolation, is the fastest way to move a score that has stalled — and it is why the mock exams in CoStudy report by domain rather than as one number.

Free Reproductive System & Endocrine System practice questions

10 questions drawn from this chapter, with the full rationale shown — the controlling principle behind the right answer, and why each wrong option tempts and fails.

Type 1 diabetes mellitus is best characterized by:

  1. Autoimmune destruction of pancreatic β cells leading to absolute insulin deficiency; often presents younger with DKA
  2. Insulin resistance with relative insulin deficiency
  3. Pancreatic exocrine failure alone
  4. Adrenal-gland tumor

Answer: A — Autoimmune destruction of pancreatic β cells leading to absolute insulin deficiency; often presents younger with DKA

A) T1DM pathology. B) T2DM. C/D) Different diagnoses.

A 35-year-old woman has weight loss, heat intolerance, palpitations, and a diffusely enlarged thyroid. TSH is suppressed, free T4 is elevated, and there is proptosis. Which finding would BEST confirm the underlying mechanism?

  1. Elevated thyroglobulin antibodies
  2. Elevated thyroid peroxidase (TPO) antibodies
  3. Elevated TSH-receptor antibodies (stimulating)
  4. Decreased radioactive iodine uptake
  5. Hyperechoic thyroid nodules on ultrasound

Answer: C — Elevated TSH-receptor antibodies (stimulating)

C) Correct: Graves disease is caused by stimulating TSH-receptor antibodies (TSI) that activate the TSH receptor → hyperthyroidism + extrathyroidal features (proptosis from orbital fibroblast TSH receptors). A) Thyroglobulin antibodies can be present but aren't the driver — true-but-irrelevant. B) Anti-TPO is seen in BOTH Graves and Hashimoto, so it's nonspecific — half-right trap. D) Graves shows INCREASED, diffuse RAIU; decreased RAIU suggests thyroiditis — direction reversal. E) Nodules suggest toxic adenoma or multinodular goiter, not Graves.

A 22-year-old presents with weight loss, tremor, anxiety, palpitations, and exophthalmos. Likely diagnosis:

  1. Hashimoto's thyroiditis
  2. Graves' disease (autoimmune hyperthyroidism with TSH receptor-stimulating antibodies)
  3. De Quervain's (subacute) thyroiditis
  4. Hypothyroidism

Answer: B — Graves' disease (autoimmune hyperthyroidism with TSH receptor-stimulating antibodies)

Graves: hyperthyroid + diffuse goiter + ophthalmopathy (exophthalmos, lid lag) + pretibial myxedema. Caused by TSI antibodies. Treat: methimazole, RAI ablation, or surgery.

A 65-year-old man has progressive urinary frequency, hesitancy, and weak stream. DRE reveals a smooth, symmetrically enlarged prostate. PSA is 3.2 ng/mL (slightly elevated for age). Which is the underlying cellular change?

  1. Hyperplasia of the peripheral zone glandular epithelium
  2. Hyperplasia of the transitional zone stromal AND glandular components
  3. Adenocarcinoma of the peripheral zone
  4. Squamous metaplasia of the prostatic urethra
  5. Atrophy of the central zone

Answer: B — Hyperplasia of the transitional zone stromal AND glandular components

B) Correct: BPH is a hyperplasia of BOTH stromal and glandular elements of the transitional zone (periurethral), explaining obstructive symptoms. A) Peripheral zone hyperplasia isn't where BPH originates — off-by-one zonal trap (peripheral zone is where cancer arises). C) Prostate adenocarcinoma typically arises in the peripheral zone and produces an asymmetric, hard nodule, not symmetric smooth enlargement. D) Squamous metaplasia isn't the BPH lesion. E) Atrophy is the opposite of hyperplasia.

BRCA1/2 mutations significantly increase lifetime risk of:

  1. Lung cancer only
  2. Breast and ovarian cancer (BRCA1 > BRCA2 for ovarian; both elevate breast)
  3. Pancreatic cancer only
  4. Skin cancer only

Answer: B — Breast and ovarian cancer (BRCA1 > BRCA2 for ovarian; both elevate breast)

BRCA1/2 are tumor suppressors involved in homologous-recombination DNA repair. Pathogenic mutations confer high breast-cancer risk; BRCA1 has higher ovarian-cancer risk than BRCA2.

A 30-year-old woman complains of polyuria and polydipsia. Serum sodium is 148, serum osmolality 305, and urine osmolality 150. After desmopressin (DDAVP) administration, urine osmolality rises to 450. Which is the MOST likely diagnosis?

  1. Central diabetes insipidus
  2. Nephrogenic diabetes insipidus
  3. Primary polydipsia
  4. SIADH
  5. Osmotic diuresis from hyperglycemia

Answer: A — Central diabetes insipidus

A) Correct: dilute urine in face of hypernatremia + brisk response to DDAVP = central DI (lack of ADH, kidneys still responsive). B) Nephrogenic DI shows NO response to DDAVP — direction reversal trap (the kidney can't respond regardless of ADH). C) Primary polydipsia causes hyponatremia and low serum osm. D) SIADH is opposite — hyponatremia with inappropriately concentrated urine. E) Osmotic diuresis would show high urine osm (glucose), not low.

Insulin's primary action is to:

  1. Promote cellular uptake of glucose (especially in muscle and adipose tissue via GLUT4), suppress hepatic gluconeogenesis, promote glycogenesis, and anabolic effects (protein synthesis, lipogenesis)
  2. Raise blood glucose
  3. Promote glycogenolysis
  4. Inhibit lipid synthesis

Answer: A — Promote cellular uptake of glucose (especially in muscle and adipose tissue via GLUT4), suppress hepatic gluconeogenesis, promote glycogenesis, and anabolic effects (protein synthesis, lipogenesis)

A) Standard physiology. B/C/D) Each contradicts.

A 50-year-old man has weight gain, central obesity, purple striae, and proximal muscle weakness. 24-hour urine free cortisol is elevated. Plasma ACTH is also elevated. High-dose dexamethasone suppresses cortisol by >50%. Which is the MOST likely diagnosis?

  1. Adrenal adenoma
  2. Cushing disease (pituitary adenoma)
  3. Ectopic ACTH from small cell lung cancer
  4. Exogenous corticosteroid use
  5. Adrenocortical carcinoma

Answer: B — Cushing disease (pituitary adenoma)

B) Correct: ACTH-dependent Cushing's (high ACTH) + suppression with high-dose dexamethasone = pituitary source (Cushing DISEASE) because pituitary corticotrophs retain partial negative feedback. A) Adrenal tumor causes LOW ACTH (feedback suppressed) — wrong axis level. C) Ectopic ACTH (small cell) shows high ACTH that does NOT suppress with high-dose dex — direction reversal trap. D) Exogenous steroids suppress ACTH and endogenous cortisol — opposite picture. E) Adrenocortical carcinoma is ACTH-independent (low ACTH).

What is the mechanism of action of metformin in type 2 diabetes?

  1. Inhibits hepatic gluconeogenesis (and modestly improves insulin sensitivity)
  2. Stimulates insulin secretion
  3. Increases renal glucose excretion
  4. Blocks alpha-glucosidase

Answer: A — Inhibits hepatic gluconeogenesis (and modestly improves insulin sensitivity)

Metformin primarily inhibits hepatic gluconeogenesis (via AMPK activation), reducing fasting glucose. It also enhances peripheral insulin sensitivity. First-line for T2DM; minimal hypoglycemia risk.

A patient with Cushing syndrome typically has:

  1. Hypoglycemia and hyperkalemia
  2. Hyponatremia and hypotension
  3. Hypothermia and bradycardia
  4. Hyperglycemia, hypertension, central obesity, purple striae, proximal muscle weakness — from glucocorticoid excess

Answer: D — Hyperglycemia, hypertension, central obesity, purple striae, proximal muscle weakness — from glucocorticoid excess

D) Cushing's clinical syndrome. A) Adrenal insufficiency picture. B/C) Different endocrinopathies.

Reproductive System & Endocrine System flashcards

4 cards from the 7 in this chapter.

Menstrual cycle phases?

Follicular (proliferative) → Ovulation → Luteal (secretory). LH surge triggers ovulation.

Cushing syndrome?

Cortisol excess. Moon facies, buffalo hump, central obesity, striae, HTN, hyperglycemia.

Diabetic ketoacidosis (DKA)?

Hyperglycemia, ketosis, anion gap acidosis. Type 1 DM, often triggered by infection.

Preeclampsia triad?

Hypertension + proteinuria + edema (after 20 weeks gestation).

Practise the full chapter

These are a sample. The full Reproductive System & Endocrine System chapter runs 30 items with per-chapter progress tracking, on the web and in the iOS app.

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