PART 1 of 5
This is Part 1 of the Reproductive
Endocrinology and Infertility
Fundamentals 11th Edition
Comprehensive Test Bank by
Taylor, Pal, and Seli.
TABLE OF CONTENTS
Chapter 1: Hormone Biosynthesis, Metabolism, and Mechanism of Action — Questions 1–8
Chapter 2: The Ovary: Embryology and Development — Questions 9–15
Chapter 3: The Uterus: Endometrial Physiology and Menstruation — Questions 16–22
Chapter 4: Neuroendocrinology — Questions 23–30
Chapter 5: Regulation of the Menstrual Cycle — Questions 31–38
Chapter 6: Conception: Sperm and Egg Transport, Fertilization, Implantation, and Early
Embryogenesis — Questions 39–45
Chapter 7: The Endocrinology of Pregnancy — Questions 46–50
Q1. A 28-year-old female with polycystic ovary syndrome is being treated with metformin. Which of
the following molecular mechanisms best explains metformin's effect on androgen production in
theca cells?
A. Activation of adenosine monophosphate-activated protein kinase (AMPK) reducing steroidogenic
enzyme expression
B. Inhibition of cytochrome P450 17 alpha-hydroxylase activity
C. Blockade of luteinizing hormone receptors on theca cells
D. Direct suppression of ovarian androgen secretion via insulin receptor antagonism
,Correct Answer: Activation of adenosine monophosphate-activated protein kinase (AMPK) reducing
steroidogenic enzyme expression ✅
Rationale: The correct answer is option A. Metformin activates AMPK, which leads to reduced
expression of key steroidogenic enzymes including CYP17 and CYP11A1 in theca cells, thereby
decreasing ovarian androgen production. This mechanism is particularly relevant in PCOS where
insulin resistance contributes to excessive ovarian androgen synthesis. Option B is incorrect because
metformin does not directly inhibit CYP17 activity; rather, it reduces the expression of the enzyme
through AMPK-mediated signaling. Option C is incorrect because metformin does not block LH
receptors; the elevated LH levels in PCOS are not directly antagonized by metformin. Option D is
incorrect because metformin does not act as an insulin receptor antagonist; it improves insulin
sensitivity by enhancing peripheral glucose uptake and reducing hepatic gluconeogenesis. The
concept tested is the molecular mechanism of insulin sensitizers in modulating ovarian
steroidogenesis.
Q2. A 32-year-old female is found to have elevated serum androstenedione with normal
dehydroepiandrosterone sulfate levels. Which of the following enzyme deficiencies is most likely
responsible for this pattern?
A. 21-hydroxylase deficiency
B. 11 beta-hydroxylase deficiency
C. 3 beta-hydroxysteroid dehydrogenase deficiency
D. 17 alpha-hydroxylase deficiency
Correct Answer: 3 beta-hydroxysteroid dehydrogenase deficiency ✅
Rationale: The correct answer is option C. 3 beta-hydroxysteroid dehydrogenase deficiency
impairs the conversion of dehydroepiandrosterone to androstenedione and of androstenedione to
testosterone, but it also affects the delta-5 pathway more severely than the delta-4 pathway. This
results in elevated DHEA and DHEAS with relatively normal or elevated androstenedione, depending
on the extent of the block. Option A is incorrect because 21-hydroxylase deficiency shunts precursors
into the androgen pathway, causing elevated DHEAS, androstenedione, and testosterone. Option B is
incorrect because 11 beta-hydroxylase deficiency also causes elevated androgens but is typically
associated with hypertension due to mineralocorticoid excess. Option D is incorrect because 17
alpha-hydroxylase deficiency causes decreased sex steroids and hypertension due to
mineralocorticoid excess. The concept tested is the biochemical patterns of steroidogenic enzyme
deficiencies.
,Q3. A 45-year-old female with symptoms of estrogen deficiency is found to have elevated follicle-
stimulating hormone and luteinizing hormone levels. Which of the following molecular mechanisms
best explains the elevated gonadotropin levels in this patient?
A. Loss of negative feedback from ovarian inhibin and estradiol
B. Increased hypothalamic gonadotropin-releasing hormone pulse frequency
C. Pituitary hypersensitivity to gonadotropin-releasing hormone
D. Enhanced activin signaling in the pituitary
Correct Answer: Loss of negative feedback from ovarian inhibin and estradiol ✅
Rationale: The correct answer is option A. In ovarian insufficiency, the loss of negative
feedback from ovarian inhibin and estradiol leads to increased gonadotropin-releasing hormone
pulse amplitude and frequency, resulting in elevated FSH and LH levels. Option B is incorrect because
the increased GnRH pulse frequency is a consequence rather than the primary mechanism; the
fundamental defect is the loss of negative feedback. Option C is incorrect because pituitary
hypersensitivity to GnRH is not the primary mechanism; the pituitary responds normally to increased
GnRH stimulation. Option D is incorrect because activin signaling is not the primary driver of elevated
gonadotropins in ovarian insufficiency. The concept tested is the feedback regulation of the
hypothalamic-pituitary-ovarian axis.
Q4. A 30-year-old female is being evaluated for infertility. Her serum progesterone level in the mid-
luteal phase is 4 nanograms per milliliter. Which of the following mechanisms best explains the
inadequate progesterone production?
A. Defective luteinization of the follicle
B. Premature luteolysis
C. Abnormal cholesterol side-chain cleavage enzyme activity
D. Inadequate luteinizing hormone surge
Correct Answer: Defective luteinization of the follicle ✅
Rationale: The correct answer is option A. A mid-luteal progesterone level below 10
nanograms per milliliter suggests inadequate luteal function. Defective luteinization of the follicle,
, often due to abnormal granulosa cell function or inadequate LH stimulation during the follicular
phase, results in a corpus luteum that cannot produce adequate progesterone. Option B is incorrect
because premature luteolysis is a consequence of defective luteinization rather than the primary
mechanism. Option C is incorrect because cholesterol side-chain cleavage enzyme activity is not the
primary defect in luteal phase deficiency. Option D is incorrect because an inadequate LH surge
affects ovulation but does not directly explain inadequate progesterone production from a formed
corpus luteum. The concept tested is the pathophysiology of luteal phase deficiency.
Q5. A 35-year-old male with infertility is found to have a serum testosterone level of 150 nanograms
per deciliter and elevated gonadotropins. Which of the following mechanisms best explains this
hormonal pattern?
A. Primary testicular failure
B. Secondary hypogonadism
C. Androgen receptor insensitivity
D. Aromatase excess
Correct Answer: Primary testicular failure ✅
Rationale: The correct answer is option A. Low testosterone with elevated gonadotropins is
the hallmark of primary testicular failure, where the testes cannot produce adequate testosterone
despite maximal gonadotropin stimulation. Option B is incorrect because secondary hypogonadism is
characterized by low testosterone with low or normal gonadotropins. Option C is incorrect because
androgen receptor insensitivity typically presents with elevated testosterone and elevated
gonadotropins. Option D is incorrect because aromatase excess presents with elevated estradiol and
low testosterone with variable gonadotropins. The concept tested is the differential diagnosis of
male hypogonadism based on gonadotropin levels.
Q6. A 28-year-old female is being evaluated for hirsutism. Her serum testosterone is mildly elevated,
and her dehydroepiandrosterone sulfate is normal. Which of the following mechanisms is most likely
responsible?
A. Ovarian theca cell androgen overproduction
B. Adrenal androgen overproduction
C. Peripheral conversion of androgens
D. Increased sex hormone-binding globulin
This is Part 1 of the Reproductive
Endocrinology and Infertility
Fundamentals 11th Edition
Comprehensive Test Bank by
Taylor, Pal, and Seli.
TABLE OF CONTENTS
Chapter 1: Hormone Biosynthesis, Metabolism, and Mechanism of Action — Questions 1–8
Chapter 2: The Ovary: Embryology and Development — Questions 9–15
Chapter 3: The Uterus: Endometrial Physiology and Menstruation — Questions 16–22
Chapter 4: Neuroendocrinology — Questions 23–30
Chapter 5: Regulation of the Menstrual Cycle — Questions 31–38
Chapter 6: Conception: Sperm and Egg Transport, Fertilization, Implantation, and Early
Embryogenesis — Questions 39–45
Chapter 7: The Endocrinology of Pregnancy — Questions 46–50
Q1. A 28-year-old female with polycystic ovary syndrome is being treated with metformin. Which of
the following molecular mechanisms best explains metformin's effect on androgen production in
theca cells?
A. Activation of adenosine monophosphate-activated protein kinase (AMPK) reducing steroidogenic
enzyme expression
B. Inhibition of cytochrome P450 17 alpha-hydroxylase activity
C. Blockade of luteinizing hormone receptors on theca cells
D. Direct suppression of ovarian androgen secretion via insulin receptor antagonism
,Correct Answer: Activation of adenosine monophosphate-activated protein kinase (AMPK) reducing
steroidogenic enzyme expression ✅
Rationale: The correct answer is option A. Metformin activates AMPK, which leads to reduced
expression of key steroidogenic enzymes including CYP17 and CYP11A1 in theca cells, thereby
decreasing ovarian androgen production. This mechanism is particularly relevant in PCOS where
insulin resistance contributes to excessive ovarian androgen synthesis. Option B is incorrect because
metformin does not directly inhibit CYP17 activity; rather, it reduces the expression of the enzyme
through AMPK-mediated signaling. Option C is incorrect because metformin does not block LH
receptors; the elevated LH levels in PCOS are not directly antagonized by metformin. Option D is
incorrect because metformin does not act as an insulin receptor antagonist; it improves insulin
sensitivity by enhancing peripheral glucose uptake and reducing hepatic gluconeogenesis. The
concept tested is the molecular mechanism of insulin sensitizers in modulating ovarian
steroidogenesis.
Q2. A 32-year-old female is found to have elevated serum androstenedione with normal
dehydroepiandrosterone sulfate levels. Which of the following enzyme deficiencies is most likely
responsible for this pattern?
A. 21-hydroxylase deficiency
B. 11 beta-hydroxylase deficiency
C. 3 beta-hydroxysteroid dehydrogenase deficiency
D. 17 alpha-hydroxylase deficiency
Correct Answer: 3 beta-hydroxysteroid dehydrogenase deficiency ✅
Rationale: The correct answer is option C. 3 beta-hydroxysteroid dehydrogenase deficiency
impairs the conversion of dehydroepiandrosterone to androstenedione and of androstenedione to
testosterone, but it also affects the delta-5 pathway more severely than the delta-4 pathway. This
results in elevated DHEA and DHEAS with relatively normal or elevated androstenedione, depending
on the extent of the block. Option A is incorrect because 21-hydroxylase deficiency shunts precursors
into the androgen pathway, causing elevated DHEAS, androstenedione, and testosterone. Option B is
incorrect because 11 beta-hydroxylase deficiency also causes elevated androgens but is typically
associated with hypertension due to mineralocorticoid excess. Option D is incorrect because 17
alpha-hydroxylase deficiency causes decreased sex steroids and hypertension due to
mineralocorticoid excess. The concept tested is the biochemical patterns of steroidogenic enzyme
deficiencies.
,Q3. A 45-year-old female with symptoms of estrogen deficiency is found to have elevated follicle-
stimulating hormone and luteinizing hormone levels. Which of the following molecular mechanisms
best explains the elevated gonadotropin levels in this patient?
A. Loss of negative feedback from ovarian inhibin and estradiol
B. Increased hypothalamic gonadotropin-releasing hormone pulse frequency
C. Pituitary hypersensitivity to gonadotropin-releasing hormone
D. Enhanced activin signaling in the pituitary
Correct Answer: Loss of negative feedback from ovarian inhibin and estradiol ✅
Rationale: The correct answer is option A. In ovarian insufficiency, the loss of negative
feedback from ovarian inhibin and estradiol leads to increased gonadotropin-releasing hormone
pulse amplitude and frequency, resulting in elevated FSH and LH levels. Option B is incorrect because
the increased GnRH pulse frequency is a consequence rather than the primary mechanism; the
fundamental defect is the loss of negative feedback. Option C is incorrect because pituitary
hypersensitivity to GnRH is not the primary mechanism; the pituitary responds normally to increased
GnRH stimulation. Option D is incorrect because activin signaling is not the primary driver of elevated
gonadotropins in ovarian insufficiency. The concept tested is the feedback regulation of the
hypothalamic-pituitary-ovarian axis.
Q4. A 30-year-old female is being evaluated for infertility. Her serum progesterone level in the mid-
luteal phase is 4 nanograms per milliliter. Which of the following mechanisms best explains the
inadequate progesterone production?
A. Defective luteinization of the follicle
B. Premature luteolysis
C. Abnormal cholesterol side-chain cleavage enzyme activity
D. Inadequate luteinizing hormone surge
Correct Answer: Defective luteinization of the follicle ✅
Rationale: The correct answer is option A. A mid-luteal progesterone level below 10
nanograms per milliliter suggests inadequate luteal function. Defective luteinization of the follicle,
, often due to abnormal granulosa cell function or inadequate LH stimulation during the follicular
phase, results in a corpus luteum that cannot produce adequate progesterone. Option B is incorrect
because premature luteolysis is a consequence of defective luteinization rather than the primary
mechanism. Option C is incorrect because cholesterol side-chain cleavage enzyme activity is not the
primary defect in luteal phase deficiency. Option D is incorrect because an inadequate LH surge
affects ovulation but does not directly explain inadequate progesterone production from a formed
corpus luteum. The concept tested is the pathophysiology of luteal phase deficiency.
Q5. A 35-year-old male with infertility is found to have a serum testosterone level of 150 nanograms
per deciliter and elevated gonadotropins. Which of the following mechanisms best explains this
hormonal pattern?
A. Primary testicular failure
B. Secondary hypogonadism
C. Androgen receptor insensitivity
D. Aromatase excess
Correct Answer: Primary testicular failure ✅
Rationale: The correct answer is option A. Low testosterone with elevated gonadotropins is
the hallmark of primary testicular failure, where the testes cannot produce adequate testosterone
despite maximal gonadotropin stimulation. Option B is incorrect because secondary hypogonadism is
characterized by low testosterone with low or normal gonadotropins. Option C is incorrect because
androgen receptor insensitivity typically presents with elevated testosterone and elevated
gonadotropins. Option D is incorrect because aromatase excess presents with elevated estradiol and
low testosterone with variable gonadotropins. The concept tested is the differential diagnosis of
male hypogonadism based on gonadotropin levels.
Q6. A 28-year-old female is being evaluated for hirsutism. Her serum testosterone is mildly elevated,
and her dehydroepiandrosterone sulfate is normal. Which of the following mechanisms is most likely
responsible?
A. Ovarian theca cell androgen overproduction
B. Adrenal androgen overproduction
C. Peripheral conversion of androgens
D. Increased sex hormone-binding globulin
