Reproductive Physiology Practice Questions

Q: Which hormone influences the ferning pattern of cervical mucus?

Estrogen. **Explanation:** The **ferning pattern** (arborization) of cervical mucus is a classic physiological phenomenon driven by **Estrogen**. **1. Why Estrogen is Correct:** During the follicular phase of the menstrual cycle, rising estrogen levels cause the cervical mucus to become thin, watery, and alkaline. High estrogen concentrations increase the **sodium chloride (NaCl)** content of the mucus. When this mucus is spread on a glass slide and allowed to air-dry, the high salt concentration crystallizes in a characteristic palm-leaf or "fern-like" pattern. This pattern is maximal just before ovulation, facilitating sperm penetration. **2. Why Other Options are Incorrect:** * **Progesterone:** This hormone dominates the luteal phase. It makes the cervical mucus thick, tenacious, and cellular. Progesterone inhibits ferning (causing a "beading" pattern), which acts as a barrier to sperm. * **Testosterone:** This is the primary male androgen and does not play a direct role in the cyclical changes of cervical mucus in females. * **Prostaglandins:** These are lipid compounds involved in uterine contractions and inflammation but do not influence the crystallization properties of cervical mucus. **Clinical Pearls for NEET-PG:** * **Spinnbarkeit Phenomenon:** Also induced by **Estrogen**; refers to the elasticity of cervical mucus (it can be stretched into a long thread, usually 8–10 cm, at mid-cycle). * **Fern Test:** Used clinically to assess ovulation or to detect the premature rupture of membranes (amniotic fluid also ferns). * **Progesterone Effect:** If a patient is pregnant or in the luteal phase, the fern test will be **negative** due to the presence of progesterone.

Q: What is the typical time frame for the formation of mature sperm?

70-75 days. **Explanation:** The correct answer is **D (70-75 days)**. This timeframe represents the complete process of **spermatogenesis**, which occurs within the seminiferous tubules of the testes. **1. Why Option D is Correct:** Spermatogenesis is the process by which primitive germ cells (spermatogonia) transform into mature spermatozoa. In humans, this process takes approximately **74 days** (commonly cited as 70–75 days in standard textbooks like Guyton and Ganong). This period includes: * **Spermatocytogenesis:** Mitosis of spermatogonia to form primary spermatocytes. * **Meiosis:** Division of spermatocytes into haploid spermatids. * **Spermiogenesis:** The morphological transformation of spherical spermatids into elongated, motile spermatozoa (formation of the acrosome, condensation of the nucleus, and growth of the tail). **2. Why Other Options are Incorrect:** * **Options A, B, and C:** These timeframes (30–55 days) are too short for the human biological cycle. While spermatogenesis varies across species (e.g., ~35 days in mice), in humans, any duration under 70 days would result in incomplete maturation of the sperm lineage. **3. High-Yield Clinical Pearls for NEET-PG:** * **Spermiogenesis vs. Spermatogenesis:** Do not confuse the two. *Spermiogenesis* is specifically the final phase (differentiation) where no cell division occurs. * **Epididymal Transit:** After the ~74-day testicular phase, sperm move to the **epididymis**, where they spend an additional **12–14 days** to gain functional maturity and motility. * **Sertoli Cells:** Often called "nurse cells," they provide nourishment and are essential for the 74-day maturation process. They also form the **blood-testis barrier**. * **Hormonal Control:** Spermatogenesis is initiated by **FSH** (acting on Sertoli cells) and maintained by high local concentrations of **Testosterone** (produced by Leydig cells under LH stimulation).

Q: Spermatogenesis is maintained by which hormone(s)?

Testosterone. **Explanation:** Spermatogenesis is a complex process primarily regulated by the Hypothalamic-Pituitary-Gonadal (HPG) axis. While multiple hormones are involved, **Testosterone** is the absolute requirement for the maintenance and completion of spermatogenesis. 1. **Why Testosterone is Correct:** Testosterone is produced by the Leydig cells under the influence of LH. It acts on the **Sertoli cells** (via androgen receptors) to stimulate the transition of spermatocytes to spermatids. Without high intratesticular concentrations of testosterone (which are 20–100 times higher than serum levels), spermatogenesis ceases at the meiosis stage. 2. **Why other options are incorrect:** * **FSH (Follicle Stimulating Hormone):** FSH is essential for the *initiation* of spermatogenesis during puberty and increases the production of Androgen Binding Protein (ABP). However, if testosterone levels are adequate, spermatogenesis can be maintained even in the absence of FSH. * **LH (Luteinizing Hormone):** LH does not act directly on germ cells. Its role is indirect; it stimulates Leydig cells to produce the testosterone required for the process. * **Prolactin:** In physiological limits, it may increase LH receptor expression, but pathologically high levels (Hyperprolactinemia) actually inhibit GnRH, leading to infertility. **High-Yield NEET-PG Pearls:** * **Blood-Testis Barrier:** Formed by tight junctions between Sertoli cells; it protects developing germ cells from the immune system. * **Androgen Binding Protein (ABP):** Secreted by Sertoli cells to keep intratesticular testosterone levels high. * **Inhibin B:** Secreted by Sertoli cells; it provides negative feedback specifically to the anterior pituitary to inhibit FSH. * **Spermiogenesis:** The transformation of circular spermatids into mature, motile spermatozoa (no cell division occurs here).

Q: Progesterone is produced by which of the following cells?

Granulosa luteal cells. **Explanation:** The production of progesterone is a hallmark of the luteal phase of the menstrual cycle. Following ovulation, the collapsed follicle undergoes **luteinization** under the influence of Luteinizing Hormone (LH). 1. **Why Option A is correct:** After ovulation, the **Granulosa cells** undergo hypertrophy and accumulate lipid droplets (luteinization) to become **Granulosa luteal cells**. These cells are the primary source of **Progesterone**. While they also produce estrogens, their main function is to secrete high levels of progesterone to prepare the endometrium for potential implantation. 2. **Why the other options are incorrect:** * **Stroma of the ovary (B):** The stroma provides structural support and contains interstitial cells that primarily secrete androgens, not significant amounts of progesterone. * **Theca cells (C):** Theca interna cells primarily produce **Androstenedione** (androgens) under the influence of LH. These androgens are then transferred to granulosa cells to be converted into estrogens via the enzyme aromatase (Two-Cell, Two-Gonadotropin Theory). * **Sertoli cells (D):** These are found in the male testes. Their primary role is to support spermatogenesis and secrete Inhibin B and Anti-Müllerian Hormone (AMH). **High-Yield Clinical Pearls for NEET-PG:** * **The Two-Cell Theory:** Theca cells (LH) produce Androgens $\rightarrow$ Granulosa cells (FSH) convert them to Estrogens. * **Progesterone Source:** In the first trimester of pregnancy, the **Corpus Luteum** is the main source of progesterone. By the 8th–12th week, the **Placenta** takes over (Luteal-Placental shift). * **Marker of Ovulation:** A serum progesterone level >3 ng/mL on day 21 of a 28-day cycle is a reliable indicator that ovulation has occurred.

Q: Capacitation of sperm in the female reproductive tract helps sperm to:

Remove the glycoprotein coat from the acrosomal region. **Explanation:** **Capacitation** is the final step of sperm maturation that occurs within the female reproductive tract (primarily in the isthmus of the fallopian tube). It is a biochemical process lasting 1–7 hours, essential for the sperm to acquire the ability to fertilize an oocyte. **Why Option C is Correct:** The primary mechanism of capacitation involves the **removal of the glycoprotein coat and seminal plasma proteins** from the plasma membrane overlying the acrosomal region of the sperm. This process also involves the efflux of cholesterol, which increases membrane fluidity and permeability to calcium ions. These changes are prerequisites for the subsequent acrosome reaction. **Analysis of Incorrect Options:** * **Option A:** While capacitation leads to "hyperactivated motility" (whiplash-like movement), it is a *result* of the process rather than the definition. The fundamental change is the membrane modification. * **Option B:** Capacitation actually decreases the lifespan of the sperm. Once capacitated, the sperm becomes more fragile and must fertilize the egg quickly or it will perish. * **Option D:** The release of acrosin occurs during the **Acrosome Reaction**, which happens *after* capacitation is complete and the sperm binds to the Zona Pellucida (ZP3 receptor). **High-Yield NEET-PG Pearls:** * **Site:** Capacitation occurs in the female reproductive tract (uterus and fallopian tubes), NOT in the male tract. * **Calcium Role:** Capacitation is dependent on an influx of $Ca^{2+}$ and an increase in intracellular cAMP. * **Sequence:** Spermiogenesis (differentiation) $\rightarrow$ Maturation (Epididymis) $\rightarrow$ Capacitation (Female tract) $\rightarrow$ Acrosome Reaction (on contact with Zona Pellucida). * **In-vitro Fertilization (IVF):** In IVF, capacitation is artificially induced by washing the sperm in a protein-rich medium.

Q: Inhibin-A is produced by?

Placenta. **Explanation:** Inhibins are glycoprotein hormones that selectively inhibit the secretion of Follicle-Stimulating Hormone (FSH). They exist in two primary forms: **Inhibin A** and **Inhibin B**. 1. **Why Placenta is Correct:** During pregnancy, the **Placenta** (specifically the syncytiotrophoblast) is the primary source of **Inhibin A**. Its levels rise significantly during the first trimester and are used clinically in the **Quadruple Marker Test** to screen for Down Syndrome (Trisomy 21), where Inhibin A levels are characteristically elevated. In non-pregnant females, Inhibin A is produced by the dominant follicle and the corpus luteum. 2. **Why Other Options are Incorrect:** * **Sertoli Cells:** These cells in the testes primarily produce **Inhibin B**. Inhibin B serves as a marker of spermatogenesis and provides negative feedback on FSH in males. * **Leydig Cells:** These cells are responsible for testosterone production under the influence of LH; they do not produce significant amounts of inhibin. * **Hilus Cells:** Located in the ovarian hilum (homologous to Leydig cells), they secrete androgens and are not a source of inhibin. **High-Yield Clinical Pearls for NEET-PG:** * **Inhibin A:** Think **A**fter ovulation (Corpus Luteum) and **A**bnormal pregnancy screening (Down Syndrome). * **Inhibin B:** Think **B**efore ovulation (Granulosa cells of pre-antral follicles) and **B**oy/Male (Sertoli cells). * **Tumor Marker:** Inhibins are used as specific tumor markers for **Granulosa Cell Tumors** of the ovary. * **Down Syndrome Screening:** The Quadruple screen includes: AFP (low), uE3 (low), hCG (high), and **Inhibin A (high)**.

Q: What is the uteroplacental blood flow per minute?

600 ml/minute. **Explanation:** The correct answer is **600 ml/minute**. In a term pregnancy, the uteroplacental blood flow (UPBF) increases significantly to meet the high metabolic demands of the growing fetus and placenta. At term, the total uterine blood flow is approximately **500–750 ml/min**, which represents about 10–15% of the total maternal cardiac output. Of this, roughly 80–90% (approx. 600 ml/min) specifically supplies the intervillous space (placenta), while the remainder supplies the myometrium. **Analysis of Options:** * **Option A (200 ml/min):** This value is too low for a term pregnancy; it is more representative of uterine blood flow in the mid-second trimester. * **Option B & C (300–400 ml/min):** While blood flow increases progressively throughout pregnancy, these values represent the flow around 28–32 weeks of gestation, not the peak flow at term. * **Option D (600 ml/min):** This is the standard physiological value cited in major textbooks (like Ganong and Guyton) for uteroplacental flow at term. **High-Yield Clinical Pearls for NEET-PG:** * **Regulation:** Uterine blood flow is **not autoregulated**; it depends directly on maternal mean arterial pressure and is inversely proportional to uterine vascular resistance. * **Vascular Remodeling:** The physiological conversion of high-resistance spiral arteries into low-resistance, high-capacity vessels (mediated by trophoblast invasion) is essential for achieving this high flow rate. * **Clinical Correlation:** Failure of this remodeling leads to reduced UPBF, resulting in conditions like **Preeclampsia** and **IUGR** (Intrauterine Growth Restriction). * **Positioning:** Maternal supine position can decrease UPBF due to aortocaval compression (Supine Hypotension Syndrome).

Q: Increased body temperature after ovulation is due to which hormone?

Progesterone. **Explanation:** The correct answer is **Progesterone**. **Mechanism:** The slight rise in basal body temperature (BBT)—typically **0.5°F to 1.0°F (0.3°C to 0.6°C)**—following ovulation is a hallmark of the luteal phase. This thermogenic effect is mediated by **Progesterone**, which is secreted in large quantities by the **Corpus Luteum** after the egg is released. Progesterone acts directly on the **hypothalamus**, the body’s thermostat, to increase the set-point temperature. This shift occurs approximately 1–2 days after ovulation and persists until menstruation begins. **Analysis of Incorrect Options:** * **Estrogen (A):** Estrogen actually has a mild **hypothermic** (temperature-lowering) effect. It dominates the follicular phase, which is why BBT is lower before ovulation. * **FSH (C):** Follicle-Stimulating Hormone is responsible for the maturation of ovarian follicles but has no direct effect on the hypothalamic thermoregulatory center. * **LH (D):** While the **LH surge** triggers ovulation, the hormone itself does not cause the temperature rise. The rise is a secondary effect of the progesterone produced by the LH-induced Corpus Luteum. **NEET-PG High-Yield Pearls:** * **Biphasic Pattern:** A normal ovulatory cycle shows a biphasic BBT chart (lower in the follicular phase, higher in the luteal phase). A monophasic chart suggests anovulation. * **Clinical Use:** Tracking BBT is a component of the "Rhythm Method" for contraception or to identify the "fertile window" for conception. * **Metabolism:** Progesterone increases the Basal Metabolic Rate (BMR), which contributes to the rise in body temperature.

Q: What is considered the normal sperm count?

15 million/ml. The correct answer is **D. 15 million/ml**. ### **Educational Explanation** **1. Why 15 million/ml is correct:** The definition of a "normal" sperm count has evolved based on the **World Health Organization (WHO) Laboratory Manual** for the examination and processing of human semen. According to the **WHO 5th Edition (2010)** and the latest **6th Edition (2021)**, the lower reference limit (5th centile) for sperm concentration is **15 million spermatozoa per ml**. Any value below this threshold is clinically defined as **Oligozoospermia**. **2. Why the other options are incorrect:** * **Options A, B, and C (20–80 million/ml):** Historically, 20 million/ml was considered the cutoff (WHO 4th Ed, 1999). While these ranges represent healthy concentrations, they are no longer the "minimum" threshold used for clinical diagnosis. In NEET-PG, when asked for the "normal count," the examiner is looking for the **minimum reference value** established by the most recent WHO guidelines. ### **High-Yield Clinical Pearls for NEET-PG** * **Total Sperm Number:** The minimum normal total count per ejaculate is **39 million**. * **Volume:** The lower reference limit for semen volume is **1.5 ml**. * **Motility:** At least **40%** total motility or **32%** progressive motility is considered normal. * **Morphology:** According to Kruger’s strict criteria, at least **4%** normal forms are required. * **Terminology:** * **Aspermia:** Absence of semen. * **Azoospermia:** Absence of sperm in the ejaculate. * **Asthenozoospermia:** Reduced sperm motility. * **Teratozoospermia:** Increased abnormal morphology.

Question 1

Which of the following is NOT an action of progesterone?

Accepted Answer

Reduction in the tone of uterine contractions

Answer

Increase in the tone of the cervical sphincter

Answer

Sodium and water retention

Answer

Secretory hypertrophy

Question 2

Which hormone influences the ferning pattern of cervical mucus?

Accepted Answer

Estrogen

Answer

Progesterone

Answer

Testosterone

Answer

Prostaglandins

Question 3

What is the typical time frame for the formation of mature sperm?

Accepted Answer

70-75 days

Answer

30-35 days

Answer

40-45 days

Answer

50-55 days

Question 4

Spermatogenesis is maintained by which hormone(s)?

Accepted Answer

Testosterone

Answer

FSH

Answer

LH

Answer

Prolactin

Question 5

Progesterone is produced by which of the following cells?

Accepted Answer

Granulosa luteal cells

Answer

Stroma of the ovary

Answer

Theca cells

Answer

Sertoli cells

Question 6

Capacitation of sperm in the female reproductive tract helps sperm to:

Accepted Answer

Remove the glycoprotein coat from the acrosomal region

Answer

Increase motility

Answer

Increase survival

Answer

Release acrosin

Question 7

Inhibin-A is produced by?

Accepted Answer

Placenta

Answer

Sertoli cell

Answer

Leydig cell

Answer

Hilus cell

Question 8

What is the uteroplacental blood flow per minute?

Accepted Answer

600 ml/minute

Answer

200 ml/minute

Answer

400 ml/minute

Answer

300 ml/minute

Question 9

Increased body temperature after ovulation is due to which hormone?

Accepted Answer

Progesterone

Answer

Estrogen

Answer

FSH

Answer

LH

Question 10

What is considered the normal sperm count?

Accepted Answer

15 million/ml

Answer

20-40 million/ml

Answer

40-60 million/ml

Answer

60-80 million/ml

Reproductive Physiology — MCQs

Reproductive Physiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?