Male Reproductive Physiology — MCQs
After injecting testosterone in a hypoandrogenic male, which of the following occurs ?
What is the effect of inhibin B hormone?
Enzyme that can be traced in semen sample of 8-10 weeks is:
What is the correct sequential order of sperm formation? 1. Spermatogonia 2. Spermatocyte 3. Spermatids 4. Spermatozoa
Which of the following is a cause of male infertility?
Pseudotumor cerebri is seen in -
What is the most likely consequence of prolonged testosterone treatment on male fertility?
Disruption of the hypothalamic-pituitary portal system will lead to
What is the mechanism by which hyperprolactinemia causes amenorrhea?
Where does meiosis occur in human females?
Male Reproductive Physiology Indian Medical PG Practice Questions and MCQs
Question 1: After injecting testosterone in a hypoandrogenic male, which of the following occurs ?
- A. Decreased LH secretion
- B. Decreased FSH secretion (Correct Answer)
- C. Increased spermatogenesis
- D. None of the options
Explanation: ***Decreased FSH secretion*** - Exogenous testosterone administration leads to **negative feedback** on the hypothalamic-pituitary-gonadal axis, suppressing **GnRH** release, which in turn decreases both **LH** and **FSH** secretion. - FSH suppression is particularly clinically significant because it results in **inhibition of spermatogenesis**, which is a key consideration when using testosterone replacement therapy. - The decrease in FSH, combined with reduced **intratesticular testosterone** (due to LH suppression), impairs Sertoli cell function and sperm production. *Decreased LH secretion* - **This also occurs** with exogenous testosterone administration due to negative feedback on the hypothalamus and pituitary. - Testosterone primarily suppresses **LH** through direct negative feedback at the hypothalamic-pituitary level. - However, in the context of this question focusing on the consequences in a hypoandrogenic male receiving testosterone, the **FSH suppression** and its impact on spermatogenesis is the more clinically emphasized outcome. - **Note:** Both LH and FSH decrease; this question likely emphasizes FSH due to its role in fertility concerns with testosterone therapy. *Increased spermatogenesis* - This is **incorrect**. Exogenous testosterone actually **suppresses spermatogenesis** through multiple mechanisms: - Decreased **FSH** (essential for Sertoli cell function) - Decreased **intratesticular testosterone** concentration (despite high systemic levels) - The high local testosterone concentration within the seminiferous tubules (30-100x serum levels) cannot be achieved by systemic testosterone alone. *None of the options* - This is incorrect because exogenous testosterone administration clearly causes **suppression of gonadotropins** (both LH and FSH) through well-established negative feedback mechanisms.
Question 2: What is the effect of inhibin B hormone?
- A. Stimulates Sertoli cell proliferation
- B. Inhibits FSH secretion from anterior pituitary (Correct Answer)
- C. Directly stimulates seminiferous tubule development
- D. Directly enhances spermatogenesis rate
Explanation: ***Inhibits FSH secretion from anterior pituitary*** - **Inhibin B** is a hormone produced by the **Sertoli cells** in males and **granulosa cells** in females. - Its primary function is to provide **negative feedback** to the anterior pituitary, specifically **inhibiting the release of follicle-stimulating hormone (FSH)**. *Stimulates Sertoli cell proliferation* - **FSH** (not inhibin B) is responsible for stimulating **Sertoli cell proliferation** and differentiation. - **Inhibin B** is produced by mature Sertoli cells, indicating their functional status rather than promoting their growth. *Directly stimulates seminiferous tubule development* - **FSH** and **testosterone** are the primary hormones crucial for the development and maintenance of the **seminiferous tubules**. - **Inhibin B** acts indirectly by regulating FSH, but it does not directly stimulate tubule development. *Directly enhances spermatogenesis rate* - While **inhibin B** production is correlated with the rate of spermatogenesis (it's high when spermatogenesis is active), it does not directly enhance the process. - **FSH** and **testosterone** are the direct hormonal regulators that enhance the rate of **spermatogenesis**.
Question 3: Enzyme that can be traced in semen sample of 8-10 weeks is:
- A. CPK enzyme
- B. LDH
- C. ALP test
- D. Acid phosphatase test (Correct Answer)
Explanation: ***Acid phosphatase test*** - The **acid phosphatase (AP) test** is a crucial forensic test for identifying seminal fluid, even in aged or degraded samples. - While detectable for months, it remains a reliable indicator in semen samples for at least **8-10 weeks** due to its relative stability. *CPK enzyme* - **Creatine phosphokinase (CPK)** is primarily associated with muscle and brain tissue damage, not a specific marker for semen. - It is not routinely traced in semen samples for forensic analysis due to its low specificity. *LDH* - **Lactate dehydrogenase (LDH)** is an enzyme found in various tissues throughout the body, reflecting general cellular damage or metabolism. - It lacks the specificity to be a reliable forensic marker for the presence of semen. *ALP test* - **Alkaline phosphatase (ALP)** is commonly used in clinical settings to assess liver and bone health. - It is not a principal enzyme marker used for the forensic identification of seminal fluid due to its widespread distribution in the body.
Question 4: What is the correct sequential order of sperm formation? 1. Spermatogonia 2. Spermatocyte 3. Spermatids 4. Spermatozoa
- A. 2314
- B. 3214
- C. 1234 (Correct Answer)
- D. 3124
Explanation: **1234** - The correct order of sperm formation begins with **spermatogonia**, which are germline stem cells that differentiate into **spermatocytes**. - Spermatocytes then undergo meiosis to become **spermatids**, which finally mature into **spermatozoa** (mature sperm). *2314* - This order is incorrect because it places spermatocytes before spermatogonia and then incorrectly places spermatogonia before spermatids. - **Spermatogonia** are the initial stem cells, preceding spermatocytes in the process. *3214* - This sequence is incorrect as it starts with spermatids, which are an intermediate stage, not the beginning of sperm formation. - **Spermatocytes** develop from spermatogonia and precede spermatids. *3124* - This order incorrectly places spermatids before spermatocytes in the sequence of maturation. - **Spermatocytes** are the cells that undergo meiosis to form spermatids.
Question 5: Which of the following is a cause of male infertility?
- A. Idiopathic
- B. Yq11 microdeletion
- C. Varicocele
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Idiopathic**, **varicocele**, and **Yq11 microdeletion** are all recognized causes of male infertility, making this the most comprehensive and correct answer. - Male infertility can stem from a variety of factors, including genetic, structural, hormonal, and unexplained (idiopathic) causes. *Idiopathic* - Refers to cases where no specific cause for infertility can be identified despite thorough investigation, accounting for a significant proportion of male infertility. - This diagnosis is made by **exclusion** after ruling out other known causes. *Varicocele* - A common and treatable cause of male infertility, characterized by **dilated veins in the pampiniform plexus** of the scrotum. - Varicoceles can impair sperm production and function due to **increased scrotal temperature** and oxidative stress. *Yq11 microdeletion* - Refers to deletions in the **azoospermia factor (AZF) region** on the long arm of the Y chromosome, which are genetic causes of severe spermatogenic failure. - These deletions disrupt genes essential for sperm production, leading to conditions ranging from **oligozoospermia** (low sperm count) to **azoospermia** (absence of sperm).
Question 6: Pseudotumor cerebri is seen in -
- A. Obese women in the age group 20-40 yrs. (Correct Answer)
- B. Obese males 20-40 yrs.
- C. Thin males 50-60 yrs.
- D. Thin females 50-60 yrs.
Explanation: ***Obese women in the age group 20-40 yrs.*** - **Pseudotumor cerebri** (also known as idiopathic intracranial hypertension) is most commonly seen in **obese women** of childbearing age, typically between **20 and 40 years old** [1]. - Risk factors include **obesity** and certain medications like **tetracyclines**, **excess vitamin A**, or **oral contraceptives** [1]. *Obese males 20-40 yrs.* - While obesity is a risk factor, **males** are significantly less commonly affected by pseudotumor cerebri than females [1]. - The disease has a strong predilection for the female gender in this age group. *Thin males 50-60 yrs.* - **Pseudotumor cerebri** is rarely observed in individuals who are **thin** and in older age groups like **50-60 years old**. - This demographic does not align with the typical patient profile for this condition. *Thin females 50-60 yrs.* - Similar to thin males, **thin females** in the **50-60 year age group** are not typically affected by pseudotumor cerebri. - The condition primarily impacts young to middle-aged obese women.
Question 7: What is the most likely consequence of prolonged testosterone treatment on male fertility?
- A. Decreased sperm motility
- B. Azoospermia (Correct Answer)
- C. Decreased spermatogenesis
- D. Decreased gonadotropins
Explanation: ***Azoospermia*** - Prolonged exogenous testosterone administration suppresses the **hypothalamic-pituitary-gonadal (HPG) axis**, leading to decreased **gonadotropin-releasing hormone (GnRH)**, then reduced **luteinizing hormone (LH)** and **follicle-stimulating hormone (FSH)**. - Reduced FSH is critical for **spermatogenesis** in the seminiferous tubules, causing a severe reduction or complete absence of sperm in the ejaculate, known as azoospermia. *Decreased spermatogenesis* - While testosterone treatment does lead to decreased spermatogenesis, azoospermia represents the most severe and complete form of this reduction, indicating a total absence of sperm. - Spermatogenesis refers to the general process of sperm production, whereas **azoospermia** specifically describes the clinical outcome of no sperm. *Decreased sperm motility* - Poor sperm motility (**asthenozoospermia**) can occur due to various factors, but prolonged exogenous testosterone primarily affects **sperm production** rather than sperm movement. - Although sperm quality might decline, the most pronounced effect is on the **number of sperm** produced, potentially leading to complete absence. *Decreased gonadotropins* - Decreased gonadotropins (LH and FSH) are an **intermediate step** in the cascade, not the most likely direct consequence on sperm. - The suppression of LH and FSH then leads to the more direct testicular effect of reduced sperm production, ultimately culminating in **azoospermia**.
Question 8: Disruption of the hypothalamic-pituitary portal system will lead to
- A. Increased follicular development due to elevated circulating levels of PRL.
- B. Ovulation with subsequent increase in circulating progesterone levels.
- C. Increased FSH levels due to reduced ovarian inhibin levels.
- D. High circulating levels of PRL, low levels of LH and FSH, leading to ovarian atrophy. (Correct Answer)
Explanation: ***High circulating levels of PRL, low levels of LH and FSH, leading to ovarian atrophy.*** - Disruption of the **hypothalamic-pituitary portal system** impairs the transport of **gonadotropin-releasing hormone (GnRH)** to the anterior pituitary, leading to decreased **luteinizing hormone (LH)** and **follicle-stimulating hormone (FSH)**. - This disruption also prevents **dopamine** from reaching the anterior pituitary, leading to uncontrolled **prolactin (PRL)** secretion (disinhibition), which suppresses GnRH and **gonadotropin** release, contributing to **ovarian atrophy**. *Increased follicular development due to elevated circulating levels of PRL.* - Elevated **prolactin (PRL)** levels typically **inhibit** ovarian function and **suppress follicular development**, rather than promoting it. - **Hyperprolactinemia** causes **hypogonadism** by interfering with **GnRH** pulsatility and directly affecting ovarian responsiveness to **gonadotropins**. *Ovulation with subsequent increase in circulating progesterone levels.* - Disruption of the portal system leads to decreased **LH** and **FSH**, which are essential for **follicular development** and **ovulation**. - Without ovulation, a **corpus luteum** cannot form, and therefore, there will be no significant increase in **progesterone** levels. *Increased FSH levels due to reduced ovarian inhibin levels.* - Reduced **FSH** and **LH** levels, resulting from the disruption, would lead to impaired **follicular development** and thus **reduced estrogen** and **inhibin** production by the ovaries. - While reduced inhibin usually leads to increased FSH (negative feedback), the primary impairment in this scenario is at the **hypothalamic-pituitary axis**, directly causing low **gonadotropin** levels, overriding the inhibin effect.
Question 9: 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 10: Where does meiosis occur in human females?
- A. In the adult ovary (Correct Answer)
- B. At birth in the ovary
- C. In the adult testis
- D. In the prepubertal testis
Explanation: ***In the adult ovary*** - **Meiosis I** in oocytes starts during fetal development but arrests in prophase I. It resumes and completes in the **adult ovary** just before ovulation in response to hormonal signals. - **Meiosis II** begins after the completion of Meiosis I and arrests in metaphase II. It is only completed upon **fertilization** by a sperm, also occurring within the adult reproductive tract. *At birth in the ovary* - At birth, female ovaries contain primary oocytes that have entered **meiosis I** but are arrested in prophase I; actual meiotic divisions promoting maturation do not occur at this stage. - The completion of meiosis I and the initiation of meiosis II are processes that are **post-puberty** and occur in response to hormonal changes leading to ovulation. *In the adult testis* - The testis is the male gonad, and it is the site of **spermatogenesis**, the process of sperm production involving meiosis in males. - **Oogenesis**, the formation of female gametes, occurs exclusively in the **ovaries** of females. *In the prepubertal testis* - In the prepubertal testis, spermatogenesis has not yet begun, and thus **meiosis does not occur** at this stage in males. - Meiosis in males usually begins during **puberty** under the influence of hormones like testosterone.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free