Secondary Amenorrhea — MCQs
A middle-aged female presents with increasing visual loss, breast enlargement, and irregular menses. What is the most appropriate investigation to diagnose the underlying condition?
At what age is delayed puberty diagnosed in girls if they have not developed any secondary sexual characteristics?
What is the mechanism by which hyperprolactinemia causes amenorrhea?
35 yr old with 4 months amenorrhea with increased FSH, decreased estrogen. What is the diagnosis?
In a patient with secondary amenorrhea, failure to experience withdrawal bleeding after administration of estrogen and progesterone indicates dysfunction of which structure?
Withdrawal bleeding following administration of progesterone in a case of secondary amenorrhea indicates all EXCEPT:
A woman who has secondary amenorrhea experiences withdrawal bleeding following progesterone administration. What is the likely diagnosis?
A mother brought her 16-year-old daughter to Gynaecology OPD with a complaint of not attaining menarche. She gives a history of cyclic abdominal pain. On further examination, a midline abdominal swelling is seen. Per rectal examination reveals a bulging mass in the vagina. Which of the following conditions is most likely responsible for these findings?
A 35 year old female with history of repeated D&C now has secondary amenorrhea. What is your diagnosis?
Which of the following markers is not used in quadruple test for antenatal detection of Down syndrome?
Secondary Amenorrhea Indian Medical PG Practice Questions and MCQs
Question 1: A middle-aged female presents with increasing visual loss, breast enlargement, and irregular menses. What is the most appropriate investigation to diagnose the underlying condition?
- A. S. calcitonin
- B. S. prolactin (Correct Answer)
- C. S. hemoglobin concentration
- D. S. calcium
Explanation: ***S. prolactin*** - **Hyperprolactinemia** is the most likely cause of the presented symptoms: **galactorrhea** (**breast enlargement** with milk production), **amenorrhea** (**irregular menses**), and **visual field defects** due to a pituitary tumor compressing the optic chiasm [1]. - Measuring serum prolactin levels directly confirms or rules out **hyperprolactinemia**, guiding further management, including imaging of the pituitary gland if elevated [1]. *S. calcitonin* - **Calcitonin** is a hormone primarily involved in **calcium regulation** and is typically elevated in medullary thyroid carcinoma. - The presented symptoms (visual loss, breast enlargement, irregular menses) are not characteristic of elevated calcitonin levels or a **medullary thyroid carcinoma**. *S. hemoglobin concentration* - **Hemoglobin concentration** measures the amount of oxygen-carrying protein in red blood cells and is used to diagnose **anemia** or polycythemia. - While general labs might include this, it is not directly relevant to the specific constellation of symptoms pointing towards an **endocrine or pituitary issue**. *S. calcium* - **Serum calcium** levels are checked for disorders of calcium metabolism, such as **hyperparathyroidism** or hypocalcemia. - Though calcium is regulated by hormones, the symptoms of **visual loss**, **breast enlargement**, and **menstrual irregularities** are not typically associated with primary disturbances in calcium levels.
Question 2: At what age is delayed puberty diagnosed in girls if they have not developed any secondary sexual characteristics?
- A. 13 years (Correct Answer)
- B. 18 years
- C. 12 years
- D. 16 years
Explanation: ***Correct: 13 years*** - In girls, **delayed puberty** is diagnosed when there are no signs of **breast development (thelarche) by age 13 years** - This represents the upper limit of normal for the onset of secondary sexual characteristics in girls - Absence of any pubertal development by this age warrants evaluation for underlying causes (e.g., hypogonadism, constitutional delay, chronic illness) - Based on **Tanner staging**, breast development typically begins between ages 8-13 years *Incorrect: 18 years* - This age is well beyond the diagnostic threshold for delayed puberty - By 18 years, puberty should be complete in normal girls - Waiting until this age would delay diagnosis and treatment of potentially reversible causes *Incorrect: 12 years* - 12 years is still within the **normal range for onset of puberty** in girls - Many girls normally begin pubertal development at or after age 12 - Diagnosing delayed puberty at this age would be premature and lead to unnecessary investigations *Incorrect: 16 years* - 16 years is the diagnostic age specifically for **absence of menarche** (primary amenorrhea), not for absence of all secondary sexual characteristics - If secondary sexual characteristics are absent by age 16, this indicates severe delay that should have been investigated years earlier (by age 13)
Question 3: What is the mechanism by which hyperprolactinemia causes amenorrhea?
- A. Inhibition of adrenal steroidogenesis
- B. It causes hypogonadotropic hypogonadism
- C. Inhibition of GnRH pulse secretion (Correct Answer)
- D. It leads to decreased ovarian function due to low FSH and LH levels
Explanation: ***Inhibition of GnRH pulse secretion*** - **Hyperprolactinemia** directly inhibits the pulsatile release of **gonadotropin-releasing hormone (GnRH)** from the hypothalamus. - This disruption of GnRH pulsatility subsequently impairs the release of **luteinizing hormone (LH)** and **follicle-stimulating hormone (FSH)** from the pituitary, leading to **anovulation** and **amenorrhea**. *Inhibition of adrenal steroidogenesis* - High prolactin levels do not primarily inhibit **adrenal steroidogenesis**; instead, they interfere with the **hypothalamic-pituitary-gonadal (HPG)** axis. - Adrenal steroidogenesis largely involves the production of **androgens**, **glucocorticoids**, and **mineralocorticoids**, which is a separate endocrine pathway. *It causes hypogonadotropic hypogonadism* - While **hyperprolactinemia** *does* lead to **hypogonadotropic hypogonadism**, this option describes the *result* or *consequence* rather than the specific *mechanism* of how it causes amenorrhea. - The fundamental mechanism involves the direct disruption of **GnRH pulsatility** at the hypothalamic level, which then leads to the reduced secretion of gonadotropins. *It leads to decreased ovarian function due to low FSH and LH levels.* - This statement is a downstream effect, not the primary mechanism, just like the previous option. **Low FSH and LH levels** are indeed caused by the initial inhibition of GnRH. - **Decreased ovarian function** is a direct consequence of insufficient **gonadotropin stimulation**, preventing follicular development and estrogen production, which ultimately results in amenorrhea.
Question 4: 35 yr old with 4 months amenorrhea with increased FSH, decreased estrogen. What is the diagnosis?
- A. Premature ovarian failure (Correct Answer)
- B. Pituitary dysfunction
- C. Hypothalamic dysfunction
- D. Polycystic Ovary Syndrome
Explanation: ***Premature ovarian failure*** - The combination of **amenorrhea** for 4 months in a 35-year-old, with **increased FSH** and **decreased estrogen**, is characteristic of premature ovarian failure, indicating the ovaries are no longer responding to FSH stimulation. - This condition signifies the cessation of ovarian function before the age of 40, leading to menopausal symptoms and infertility. *Pituitary dysfunction* - Pituitary dysfunction might lead to **decreased FSH** (hypogonadotropic hypogonadism) due to insufficient stimulation of the ovaries, not increased FSH. - In cases of pituitary adenomas, increased prolactin can cause amenorrhea, but FSH would not be elevated in the manner described. *Hypothalamic dysfunction* - Hypothalamic dysfunction, such as **functional hypothalamic amenorrhea**, typically presents with **low or normal FSH and LH levels** (hypogonadotropic hypogonadism) due to reduced GnRH pulsatility. - This condition is often associated with stress, excessive exercise, or low body weight, and would not cause elevated FSH as seen here. *Polycystic Ovary Syndrome* - **Polycystic Ovary Syndrome (PCOS)** is characterized by **anovulation**, resulting in amenorrhea or oligomenorrhea, but typically involves **elevated androgens** and a **high LH-to-FSH ratio**, with FSH levels generally normal or low, and estrogen levels often normal or slightly elevated. - It would not present with simultaneously high FSH and low estrogen, which points to ovarian failure rather than anovulation with intact ovarian reserve.
Question 5: In a patient with secondary amenorrhea, failure to experience withdrawal bleeding after administration of estrogen and progesterone indicates dysfunction of which structure?
- A. Pituitary
- B. Hypothalamus
- C. Ovary
- D. Endometrium (Correct Answer)
Explanation: ***Endometrium*** - If the **endometrium** fails to respond to **estrogen and progesterone therapy**, it suggests a problem with the uterine lining itself, such as **Asherman's syndrome** or severe endometrial atrophy. - In such cases, despite adequate hormonal stimulation, there is **no withdrawal bleeding** because the target tissue (endometrium) cannot proliferate or shed. *Pituitary* - A **dysfunctional pituitary gland** would typically cause secondary amenorrhea by failing to produce adequate **gonadotropins (LH and FSH)**, which in turn leads to ovarian dysfunction. - However, in this scenario, if the pituitary were the primary issue, providing exogenous **estrogen and progesterone** would likely still induce withdrawal bleeding if the uterus is responsive. *Hypothalamus* - The **hypothalamus** controls pituitary function by releasing **GnRH**. Hypothalamic dysfunction (e.g., due to stress, extreme exercise, or weight loss) causes **hypogonadotropic hypogonadism**. - While it's a common cause of secondary amenorrhea, exogenous **estrogen and progesterone** should still induce withdrawal bleeding if the uterus is healthy and responsive. *Ovary* - **Ovarian failure** (e.g., premature ovarian insufficiency) leads to low **estrogen** and **high FSH/LH** levels. - If the ovaries are the cause, administering **estrogen and progesterone** would typically induce withdrawal bleeding because the uterus is usually functional and responsive to these hormones.
Question 6: Withdrawal bleeding following administration of progesterone in a case of secondary amenorrhea indicates all EXCEPT:
- A. Defect in pituitary gland (Correct Answer)
- B. Absence of pregnancy
- C. Endometrium is responsive to estrogen
- D. Production of endogenous estrogen
Explanation: ***Defect in pituitary gland*** - While withdrawal bleeding after progesterone suggests the problem lies at the **hypothalamic-pituitary level** (anovulation with adequate estrogen), it does **not definitively rule out all pituitary defects**. - The pituitary may still produce sufficient **FSH to stimulate ovarian estrogen production** but have defective **LH surge mechanism** (WHO Group II anovulation). - Examples include **hyperprolactinemia** or **functional hypothalamic amenorrhea** where estrogen production is preserved despite pituitary-hypothalamic dysfunction. - This is the **EXCEPT answer** because the other options are more definitively confirmed by withdrawal bleeding. *Absence of pregnancy* - Withdrawal bleeding after progesterone administration **definitively confirms absence of pregnancy**. - Pregnancy would prevent withdrawal bleeding due to sustained progesterone production by the corpus luteum and placenta. - This is a key diagnostic exclusion in the evaluation of **secondary amenorrhea**. *Endometrium is responsive to estrogen* - The occurrence of withdrawal bleeding **definitively demonstrates** that the endometrium has been exposed to adequate estrogen and has proliferated. - This proliferative endometrium then sheds when progesterone is withdrawn, confirming **normal endometrial responsiveness to hormonal stimulation**. - This rules out **Asherman syndrome** and other uterine factors. *Production of endogenous estrogen* - Withdrawal bleeding **definitively confirms** that there has been sufficient **endogenous estrogen production** to prime the endometrium. - The estrogen causes endometrial thickening, which then sheds when progesterone is withdrawn. - This indicates **adequate ovarian function** in terms of estrogen synthesis and rules out **hypergonadotropic hypogonadism** (ovarian failure).
Question 7: A woman who has secondary amenorrhea experiences withdrawal bleeding following progesterone administration. What is the likely diagnosis?
- A. Anovulation (Correct Answer)
- B. Asherman's syndrome
- C. Premature ovarian failure
- D. Hypothalamic amenorrhea
Explanation: ***Anovulation*** - Withdrawal bleeding after progesterone indicates that the **endometrium was adequately primed with estrogen** but there was no ovulation to produce progesterone. - This scenario points to **anovulation** as the underlying cause of secondary amenorrhea, where estrogen is present, but a corpus luteum does not form to secrete progesterone. *Asherman's syndrome* - This condition involves **intrauterine adhesions** that prevent endometrial shedding, even in the presence of hormones. - A woman with Asherman's syndrome would typically **not experience withdrawal bleeding** after progesterone, as the endometrium is damaged or absent. *Premature ovarian failure* - In **premature ovarian failure**, the ovaries stop functioning, leading to **low estrogen levels**. - Without sufficient estrogen to prime the endometrium, administering progesterone would **not result in withdrawal bleeding**. *Hypothalamic amenorrhea* - This type of amenorrhea is characterized by **low estrogen levels** due to dysfunction in the hypothalamus. - Similar to premature ovarian failure, a lack of estrogen would mean the endometrium is not prepared, and **progesterone withdrawal bleeding would not occur**.
Question 8: A mother brought her 16-year-old daughter to Gynaecology OPD with a complaint of not attaining menarche. She gives a history of cyclic abdominal pain. On further examination, a midline abdominal swelling is seen. Per rectal examination reveals a bulging mass in the vagina. Which of the following conditions is most likely responsible for these findings?
- A. Vaginal agenesis
- B. Transverse vaginal septum
- C. Imperforate hymen (Correct Answer)
- D. Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome
Explanation: ***Imperforate hymen*** - An **imperforate hymen** obstructs the outflow of menstrual blood, leading to its accumulation in the vagina (**hematocolpos**) and uterus (**hematometra**), causing **cyclic abdominal pain** and a bulging mass (due to accumulated blood) in the vagina. - The patient presents with **primary amenorrhea** (not having attained menarche) and cyclical abdominal pain caused by the inability of menstrual blood to exit the body. *Transverse vaginal septum* - A **transverse vaginal septum** can also cause primary amenorrhea and cyclic abdominal pain due to obstruction of menstrual flow. However, it is a less common cause than an imperforate hymen. - While it can lead to hematocolpos, the characteristic bulging mass on per rectal examination is more strongly associated with an imperforate hymen presenting at the vaginal introitus. *Vaginal agenesis* - **Vaginal agenesis** (complete absence of the vagina) would present with primary amenorrhea, but there would be no cyclic abdominal pain if the uterus is also absent or rudimentary. If a uterus is present, there would be no accumulation of blood in the vagina or a bulging mass per rectum as there is no vaginal canal. - This condition is typically associated with a rudimentary or absent uterus, leading to an inability to menstruate rather than obstructed flow. *Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome* - **MRKH syndrome** is characterized by congenital aplasia of the uterus and the upper two-thirds of the vagina, with normal ovaries and external genitalia. - Patients present with **primary amenorrhea** but typically do not experience **cyclic abdominal pain** or a bulging vaginal mass because there is no functional uterus to produce menstrual blood or a vaginal canal for blood accumulation.
Question 9: A 35 year old female with history of repeated D&C now has secondary amenorrhea. What is your diagnosis?
- A. Asherman's syndrome (Correct Answer)
- B. Hypothyroidism
- C. Kallman syndrome
- D. Sheehan's syndrome
Explanation: ***Asherman's syndrome*** - This syndrome is characterized by the formation of **intrauterine adhesions** or scar tissue following uterine trauma, often from repeated **Dilation and Curettage (D&C)** procedures. - The adhesions can prevent the normal growth and shedding of the **endometrial lining**, leading to **secondary amenorrhea** and infertility. *Hypothyroidism* - While hypothyroidism can cause menstrual irregularities, including **amenorrhea**, it would not typically be linked to a history of **repeated D&C procedures**. - The mechanism involves **hormonal imbalances** (e.g., elevated **TRH leading to elevated prolactin**), not scarring of the uterus. *Kallman syndrome* - This is a rare genetic condition causing **hypogonadotropic hypogonadism** and **anosmia** (loss of smell), leading to **primary amenorrhea**. - It does not involve uterine scarring and is not associated with D&C procedures or **secondary amenorrhea**. *Sheehan's syndrome* - Sheehan's syndrome is **postpartum hypopituitarism** caused by **ischemic necrosis of the pituitary gland** after severe hemorrhage during or after childbirth. - It would present with symptoms like **lactation failure** and could cause **secondary amenorrhea**, but it is not related to repeated D&C procedures.
Question 10: Which of the following markers is not used in quadruple test for antenatal detection of Down syndrome?
- A. Inhibin
- B. Estradiol (Correct Answer)
- C. AFP
- D. ss-hCG
Explanation: ***Estradiol*** - **Estradiol** is a primary **estrogen** produced by the ovaries and placenta but is **not** one of the four markers included in the **quadruple screen** for Down syndrome. - The quadruple screen typically measures levels of **alpha-fetoprotein (AFP)**, **unconjugated estriol (uE3)**, **human chorionic gonadotropin (hCG)**, and **inhibin A**. *Inhibin* - **Inhibin A** is one of the four components of the **quadruple screen** for Down syndrome. - In pregnancies affected by Down syndrome, inhibin A levels are typically **elevated**. *AFP* - **Alpha-fetoprotein (AFP)** is a key component of the **quadruple screen**. - In a Down syndrome pregnancy, maternal serum AFP levels are typically **lower** than normal. *ss-hCG* - **Beta-human chorionic gonadotropin (β-hCG)** is a specific subunit of hCG and is one of the four markers in the **quadruple screen**. - In pregnancies with Down syndrome, maternal serum β-hCG levels are usually **elevated**.
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