Repro – 2017

Beta-human chorionic gonadotropin (β-hCG) is a glycoprotein hormone secreted during pregnancy, primarily by the syncytiotrophoblast of the placenta. Its levels change in a predictable pattern, which is clinically important for diagnosis and monitoring of early pregnancy.

Key Points:

1. Secretion and Function

   • β-hCG maintains the corpus luteum in early pregnancy, allowing it to continue progesterone production until the placenta can take over (~10–12 weeks).

   • Supports early endometrial maintenance and trophoblast differentiation.

2. Typical Peak Levels

   • β-hCG levels rise rapidly after implantation, doubling approximately every 48–72 hours in early pregnancy.

   • Levels peak around 8–10 weeks of gestation.

   • After this peak, β-hCG levels gradually decline and plateau for the remainder of the pregnancy.

3. Clinical Relevance

   • Used in pregnancy tests, monitoring early pregnancy, and diagnosing ectopic pregnancy or gestational trophoblastic disease.

   • Deviations from the expected peak can indicate abnormal pregnancy.

❌ Why the Other Options Are Incorrect

1. 12 to 15 weeks – False. By this time, β-hCG levels are already declining.

2. 17 to 19 weeks – False. Levels are well past their peak, usually plateauing at lower levels.

3. 20 to 22 weeks – False. Plateau phase; not the peak.

4. 5 to 6 weeks – False. Levels are rising but have not yet reached their maximum.

The prostate gland is highly sensitive to androgens, which regulate its growth, differentiation, and function. Among the androgens, dihydrotestosterone (DHT) plays a central role.

Key Points:

1. Source and Conversion

   • Testosterone from the testes enters prostate stromal cells.

   • Within these cells, 5-alpha reductase converts testosterone into DHT, the more potent androgen.

2. Receptor Binding

   • DHT binds to androgen receptors (AR) in stromal and epithelial cells.

   • The stromal cells mediate paracrine signals to the epithelial cells, regulating growth and secretory function.

3. Clinical Relevance

   • Benign prostatic hyperplasia (BPH) is driven primarily by DHT acting on stromal cells.

   • 5-alpha reductase inhibitors (e.g., finasteride) reduce DHT levels to treat BPH and androgenic alopecia.

❌ Why the Other Options Are Incorrect

1. Androstenedione – False. A weak androgen; not the primary effector in the prostate.

2. Testosterone – False. Testosterone must be converted to DHT to effectively stimulate stromal androgen receptors.

3. Cortisol – False. A glucocorticoid; unrelated to androgen receptor signaling.

4. Estrogen – False. While estrogens influence prostate indirectly, they do not bind androgen receptors.

Milk production (lactation) involves several hormones, each with distinct roles. Understanding which hormone is responsible for actual milk synthesis is crucial.

Key Points:

1. Prolactin ✅

   • Secreted by the anterior pituitary gland.

   • Primary hormone responsible for stimulating the alveolar cells in the mammary glands to synthesize milk (lactogenesis).

   • Its secretion is stimulated by suckling, which inhibits dopamine (prolactin-inhibiting factor) and increases prolactin release.

2. Other Hormones and Their Roles

   • Oxytocin – Responsible for milk ejection (galactokinesis) by contracting myoepithelial cells, not milk synthesis.

   • Progesterone – Supports mammary gland development during pregnancy but inhibits milk secretion during gestation.

   • Estrogen – Stimulates ductal growth in the breast but does not produce milk.

   • Beta hCG – Supports corpus luteum and early pregnancy; unrelated to lactation.

❌ Why the Other Options Are Incorrect

1. Progesterone – False. Essential for breast development, but inhibits full milk secretion until after delivery.

2. Estrogen – False. Promotes ductal growth, not milk production.

3. Oxytocin – False. Controls let-down reflex, not synthesis.

4. Beta hCG – False. Supports early pregnancy only; no role in milk production.

Breastfeeding involves several coordinated physiological processes for milk production, ejection, and mammary development. It is important to distinguish these terms:

Key Lactational Processes:

1. Mammogenesis

   • Growth and development of the mammary glands before pregnancy and during gestation.

   • Hormones involved: estrogen, progesterone, prolactin.

2. Lactogenesis

   • Initiation of milk secretion, usually occurs late in pregnancy.

   • Triggered by prolactin, influenced by falling progesterone after delivery.

3. Galactopoiesis

   • Maintenance of ongoing milk production after lactation has started.

   • Dependent on prolactin and continued suckling.

4. Galactokinesis ✅

   • Milk ejection (let-down reflex).

   • Stimulated by suckling, which triggers oxytocin release from the posterior pituitary.

   • Oxytocin causes contraction of myoepithelial cells around alveoli and ducts, pushing milk into larger ducts for the baby to drink.

5. Involution

   • Regression of the mammary gland after weaning.

❌ Why the Other Options Are Incorrect

1. Galactopoiesis – False. Refers to maintenance of milk production, not the act of ejection.

2. Lactogenesis – False. Refers to initiation of milk secretion, occurs earlier than the ejection process.

3. Mammogenesis – False. Refers to breast development, not milk movement.

4. Involution – False. Refers to regression of the mammary gland after lactation stops.

Turner’s syndrome is a chromosomal disorder affecting females, characterized by complete or partial monosomy of the X chromosome. Recognizing the karyotype is critical for diagnosis.

Key Points:

1. Karyotype in Turner’s Syndrome

   • 45, X (or 45 XO): Only one X chromosome, no second sex chromosome.

   • Occasionally, mosaic patterns occur (e.g., 45,X/46,XX), but the classic form is 45 XO.

2. Clinical Features

   • Short stature

   • Webbed neck

   • Gonadal dysgenesis (streak ovaries → infertility)

   • Cardiovascular anomalies (e.g., coarctation of aorta)

   • Amenorrhea due to primary ovarian failure

3. Hormonal Effects

   • Low estrogen → delayed puberty

   • High gonadotropins (FSH, LH) due to lack of negative feedback

❌ Why the Other Options Are Incorrect

1. 47 XXY – False. This is Klinefelter syndrome, a male disorder with extra X chromosome.

2. 46 XO – False. Human karyotypes require 46 chromosomes; XO notation must indicate 45 chromosomes, as one sex chromosome is missing.

3. 46 XX – False. Normal female karyotype.

4. 46 XY – False. Normal male karyotype.

Progesterone is essential for maintaining pregnancy, primarily by supporting the endometrium and preventing uterine contractions. The source of progesterone changes as pregnancy progresses.

Key Points:

1. Corpus Luteum in Early Pregnancy

   • Formed from the ovulated follicle after fertilization.

   • Produces progesterone and some estrogen.

   • Maintains the endometrium and supports early pregnancy until the placenta is fully developed.

   • This role is critical in the first trimester (~up to 10–12 weeks).

2. Placenta Takes Over Later

   • After the first trimester, the placenta becomes fully functional.

   • It synthesizes progesterone independently of the corpus luteum (luteal-placental shift).

   • By the second and third trimesters, the placenta is the main source of progesterone.

❌ Why the Other Options Are Incorrect

1. Throughout pregnancy – False. The corpus luteum only dominates early pregnancy.

2. 2nd trimester – False. Progesterone is mainly placental in origin by this stage.

3. 3rd trimester – False. Placenta continues to produce the majority of progesterone.

4. None of these – False. First trimester is the correct period for corpus luteum dominance.

The broad ligament is a double layer of peritoneum that supports the female reproductive organs. It has several subdivisions based on which organ or structure it encloses or supports.

Key Points:

1. Subdivisions of the Broad Ligament

   • Mesometrium: Largest part; extends from uterus to pelvic wall. Supports the body of the uterus.

   • Mesovarium: Attaches the ovary to the broad ligament; short peritoneal fold containing vessels and nerves.

   • Mesosalpinx ✅: The portion that encloses and covers the uterine (fallopian) tubes.

     • Forms a sleeve around the uterine tube, extending from the ovary to the mesometrium.

     • Provides structural support and a conduit for blood vessels.

2. Function

   • The mesosalpinx stabilizes the uterine tube and allows the tube to remain mobile while keeping vessels and lymphatics close to the tube.

❌ Why the Other Options Are Incorrect

1. Infundibular ligaments – False. Likely referring to suspensory ligaments of the ovary, which connect the ovary to the pelvic wall; do not cover uterine tubes.

2. Cardinal ligaments – False. Provide lateral support to the cervix, not part of the broad ligament that covers uterine tubes.

3. Mesometrium – False. Covers and supports the uterine body, not the uterine tubes.

4. Mesovarium – False. Connects the ovary to the broad ligament, not the uterine tube.

The broad ligament is a double layer of peritoneum that extends from the sides of the uterus to the lateral pelvic walls, enclosing and supporting several reproductive structures. Understanding its components is essential in female pelvic anatomy.

Key Points:

1. Structure and Parts of the Broad Ligament

   • Mesometrium: Largest part; stretches from uterus to pelvic wall.

   • Mesosalpinx: Superior portion that encloses the fallopian tubes.

   • Mesovarium ✅: Short peritoneal fold that attaches the anterior border of the ovary to the broad ligament.

     • Contains blood vessels, lymphatics, and nerves supplying the ovary.

2. Function

   • Supports the uterus, fallopian tubes, and ovaries.

   • Serves as a conduit for blood vessels and nerves to the reproductive organs.

❌ Why the Other Options Are Incorrect

1. Pubocervical ligaments – False. These are fibromuscular ligaments supporting the bladder and anterior uterus; not part of the broad ligament.

2. Infundibulopelvic ligaments (suspensory ligaments of ovary) – False. Connect the ovary to the lateral pelvic wall; not part of the broad ligament, though they are close to the mesovarium.

3. Uterosacral ligaments – False. Fibrous ligaments supporting the uterus posteriorly; independent of the broad ligament.

4. Cardinal ligaments (transverse cervical ligaments) – False. Provide lateral support to the cervix; not considered part of the broad ligament.

Estrogen replacement therapy (ERT) is commonly used in postmenopausal women to manage symptoms of estrogen deficiency and prevent certain long-term complications. Understanding its effects and risks is crucial.

Key Effects of ERT:

1. Increased risk of endometrial carcinoma if used alone ✅

   • True. Unopposed estrogen stimulates the endometrial lining, increasing the risk of hyperplasia and carcinoma.

   • This is why progestins are added in women with an intact uterus.

2. Reduced osteoporotic fractures ✅

   • True. Estrogen helps maintain bone density, reducing the risk of fractures in postmenopausal women.

3. Increased thromboembolic risk ✅

   • True. Estrogen increases coagulation factors, raising the risk of deep vein thrombosis (DVT) and pulmonary embolism.

4. Breast tenderness ✅

   • True. Estrogen stimulates breast tissue, which can lead to tenderness or engorgement.

❌ Why the Other Option is Incorrect

• Hot flashes – False. Estrogen therapy relieves hot flashes, which are one of the primary indications for treatment.

  • Hot flashes are a symptom of estrogen deficiency, and ERT typically reduces or eliminates them in postmenopausal women.

Tubal ligation is a permanent method of female sterilization in which the fallopian tubes are occluded to prevent eggs from reaching the uterus. There are several approaches, but the most commonly used today is laparoscopic surgery.

Key Points:

1. Laparoscopic Approach ✅

   • Minimally invasive surgery using small abdominal incisions and a laparoscope.

   • Tubes are coagulated, clipped, or tied, preventing fertilization.

   • Advantages:

     • Short recovery time

     • Minimal scarring

     • Can be done under local or general anesthesia

2. Open Abdominal Approach

   • Laparotomy through a larger incision.

   • Rarely used now; typically reserved for cases requiring concurrent abdominal surgery or when laparoscopy is contraindicated.

3. Other Approaches

   • Pharmacologic: No effective drug exists for permanent tubal occlusion; reversible methods like hormonal contraception are used instead.

   • Intravaginal / Transrectal: Not used for tubal ligation; these approaches do not allow access to the fallopian tubes.

❌ Why the Other Options Are Incorrect

1. Open abdominal – False. Less common today due to higher morbidity and longer recovery.

2. Pharmacologic – False. Drugs cannot achieve permanent tubal blockage.

3. Intravaginal – False. The vagina does not provide direct access to fallopian tubes.

4. Transrectal – False. Not anatomically feasible for tubal ligation.

Peg cells are specialized secretory epithelial cells found in the female reproductive tract, specifically in the fallopian tubes (oviducts). They play an important role in fertility and early embryonic development.

Key Points:

1. Location

   • Found in the epithelium of the fallopian tubes, particularly in the ampulla.

   • Interspersed between ciliated cells that help transport the oocyte.

2. Structure and Function

   • Non-ciliated, columnar secretory cells.

   • Secrete nutrient-rich fluid that:

     • Nourishes the ovum

     • Supports capacitation of sperm

     • Provides an optimal environment for fertilization and early zygote development.

3. Ciliated Cells vs Peg Cells

   • Ciliated cells: Move the ovum toward the uterus.

   • Peg cells: Secrete supportive fluid and enzymes.

❌ Why the Other Options Are Incorrect

1. Uterine cavity – False. Lined by endometrial epithelium, no peg cells.

2. Ovaries – False. Ovarian surface epithelium is simple cuboidal or squamous, no peg cells.

3. Cervix – False. Lined by columnar or squamous epithelium; secretes mucus but does not have peg cells.

4. Vagina – False. Lined by stratified squamous epithelium, no peg cells.

The seminal vesicles are paired tubular glands that contribute to the male reproductive system. Understanding their function is key to reproductive physiology.

Key Points:

1. Structure and Location

   • Paired glands located posterior to the bladder and lateral to the vas deferens.

   • Each seminal vesicle is a highly coiled tube forming part of the ejaculatory duct.

2. Function

   • Accessory sex glands: They secrete seminal fluid, which makes up ~60–70% of semen volume.

   • Seminal fluid is alkaline, rich in fructose (energy for sperm), prostaglandins, and other proteins.

   • This secretion mixes with sperm from the testes during ejaculation.

3. Not the Site of Sperm Production

   • Sperm are produced in the seminiferous tubules of the testes.

   • Seminal vesicles do not mature sperm either; maturation occurs in the epididymis.

❌ Why the Other Options Are Incorrect

1. Site of sperm production – False. This occurs in the testes, not seminal vesicles.

2. Site of sperm maturation – False. Sperm mature in the epididymis, not seminal vesicles.

3. Intramuscular glands – False. Seminal vesicles are tubular glands, not intramuscular.

4. Copulatory organ – False. The penis serves as the copulatory organ, not the seminal vesicles.

The testes are located in the scrotum outside the abdominal cavity for a reason: spermatogenesis is highly temperature-sensitive, requiring a temperature 2–4°C below core body temperature. Elevated testicular temperature can have significant effects on male reproductive function.

Effects of High Testicular Temperature:

1. Spermatogenesis

   • Highly sensitive to heat.

   • Elevated temperature damages germ cells, disrupts meiosis, and leads to poor sperm quality and quantity.

   • Main clinical consequence: infertility.

2. Testosterone Production

   • Leydig cells are less sensitive to moderate heat, so testosterone may remain relatively normal initially.

3. Hormonal Feedback

   • If spermatogenesis declines, there may be slightly elevated FSH, but LH may not rise significantly unless Leydig cells are affected.

   • Inhibin A (produced by Sertoli cells) may decrease, not increase, as spermatogenesis fails.

4. Clinical Scenarios

   • Cryptorchidism (undescended testes)

   • Prolonged fever

   • Tight clothing or occupational heat exposure

❌ Why the Other Options Are Incorrect

1. Low testosterone production

   • False. Leydig cells are relatively resistant to heat; testosterone may remain near normal initially.

2. High levels of LH hormone

   • False. LH may rise only if Leydig cells are chronically damaged, not immediately with short-term heat.

3. High levels of inhibin A

   • False. Inhibin A decreases when Sertoli cells and spermatogenesis are impaired.

4. Normal spermatogenesis

   • False. Heat directly disrupts spermatogenesis, especially meiosis.

Human chorionic gonadotropin (hCG) is a glycoprotein hormone crucial for maintaining early pregnancy, but its source changes over time.

Key Points:

1. Early Pregnancy

   • Initially secreted by the syncytiotrophoblast cells of the developing embryo and early placenta.

   • Corpus luteum is stimulated by hCG to continue progesterone production, maintaining the endometrium during the first trimester.

2. Late Pregnancy

   • After the first trimester, the placenta becomes fully functional and takes over hormone production.

   • By late pregnancy, the placenta is the major source of hCG, although levels are lower than the peak in the first trimester.

3. Other Structures

   • Yolk sac: Active in early embryonic development, but does not produce hCG in significant amounts.

   • Breasts and amnion: No role in hCG secretion; these tissues are involved in lactation and fetal membranes.

❌ Why the Other Options Are Incorrect

1. Corpus luteum

   • Produces progesterone in early pregnancy, but its activity declines after 10–12 weeks as the placenta takes over. Not the major source of hCG in late pregnancy.

2. Yolk sac

   • Produces early nutrients and some hormones, but not significant hCG.

3. Breasts

   • Function is lactation; they do not secrete hCG.

4. Amnion

   • Part of the fetal membranes; no hCG secretion.

Undescended testes (cryptorchidism) is a condition in which one or both testes fail to descend into the scrotum. This condition has several well-documented complications, primarily due to abnormal positioning and impaired testicular function.

Common Complications:

1. Sertoli cell failure ✅

   • True. High intra-abdominal temperature can impair Sertoli cell function, leading to impaired spermatogenesis.

2. Testicular torsion ✅

   • True. Undescended testes are more mobile, increasing the risk of torsion.

3. Germ cell tumors ✅

   • True. Cryptorchid testes carry a significantly higher risk of testicular cancer, especially seminomas.

4. Infertility ✅

   • True. Impaired spermatogenesis and abnormal testicular development can lead to subfertility or infertility, particularly if bilateral.

❌ Why the Other Option is Incorrect

• Phimosis

  • False. Phimosis is a condition of the foreskin of the penis, unrelated to the position of the testes.

  • It is not a complication of cryptorchidism.

Colostrum is the first milk produced by the mammary glands during the late stages of pregnancy and first few days postpartum. It is specially designed to provide nutrition and immunity to the newborn.

Key Components of Colostrum:

1. Immunoglobulins (IgA)

   • Colostrum is rich in secretory IgA, which provides passive immunity to the neonate and protects the gastrointestinal tract from infections.

2. White Blood Cells

   • Includes neutrophils, macrophages, and lymphocytes, which help in immune protection.

3. Lactoferrin

   • Iron-binding protein with antimicrobial properties, inhibiting bacterial growth in the gut.

4. Vitamin K

   • Present in small amounts; helps in coagulation and preventing hemorrhagic disease of the newborn.

❌ Why the Other Option is Incorrect

• Amiodarone

  • False. Amiodarone is a synthetic antiarrhythmic drug, not a natural component of colostrum.

  • It may be excreted into breast milk if the mother takes it, but it is not naturally present in colostrum.

Anorchism is a medical term referring to the complete absence of one or both testes. It is a rare condition that can be congenital (present at birth) or acquired (after surgical removal or trauma).

Key Points:

1. Definition

   • Anorchism: Total absence of testes.

   • Monorchism: Absence of one testis (unilateral anorchism).

2. Clinical Significance

   • Leads to lack of testosterone production if bilateral.

   • Causes primary hypogonadism, delayed or absent puberty, and infertility.

3. Diagnosis

   • Physical examination: Absence of testes in the scrotum.

   • Ultrasound or MRI: To confirm absence in the inguinal canal or abdominal cavity.

❌ Why the Other Options Are Incorrect

1. Absence of testes from scrotal sac

   • False. This describes cryptorchidism (undescended testes), not complete absence.

2. Small testes

   • False. This is hypogonadism, not anorchism.

3. Large testes

   • False. Usually pathological (e.g., tumors), not related to anorchism.

4. Fused testes

   • False. Rare congenital anomaly, not related to absence.

The uterus is supported in the pelvis by a combination of ligaments and connective tissue structures, which maintain its position and prevent prolapse. Among these, the cardinal ligaments (transverse cervical ligaments) are the primary structural support.

Key Points:

1. Cardinal Ligaments (Transverse Cervical Ligaments)

   • Extend from the lateral sides of the cervix and vagina to the lateral pelvic walls.

   • Contain fibrous connective tissue, smooth muscle, and blood vessels, particularly the uterine artery and vein.

   • Function: Prevent downward displacement of the uterus and maintain its anteverted and anteflexed position.

2. Other Ligaments

   • Broad ligament: Double layer of peritoneum that encloses the uterus, fallopian tubes, and ovaries; mainly a mesenteric support, not a strong suspensory ligament.

   • Round ligament: Runs from the uterine horns to the labia majora; maintains anteversion but does not provide major support.

   • Utero-ovarian ligament (ovarian ligament): Connects ovary to uterus; supports ovary more than the uterus.

   • Sacrospinous ligament: Anchors the coccyx and sacrum to the ischial spine; used in pelvic prolapse surgery but not a primary uterine support.

❌ Why the Other Options Are Incorrect

1. Utero-ovarian ligament – Supports the ovary, not the uterus itself.

2. Sacrospinous ligament – Provides support only if surgically used; anatomically it is not the major support of the uterus.

3. Broad ligament – Suspends the uterus but is peritoneal fold only; weak in providing structural support.

4. Round ligament – Maintains uterine anteversion but offers minimal support against prolapse.

The sacral cornua (or sacral horns) are important anatomical landmarks at the inferior end of the sacrum. They are clinically significant because they are used as landmarks for caudal epidural anesthesia.

Key Points:

1. Location and Structure

   • The sacral cornua are paired bony projections that arise from the inferior articular processes of the fifth sacral vertebra (S5).

   • They project posteriorly and medially, flanking the sacral hiatus.

2. Function

   • Serve as articulating points for the coccyx.

   • Serve as palpable landmarks for needle insertion during caudal epidural block.

❌ Why the Other Options Are Incorrect

1. Foramina through which sacral nerves exit

   • False. These are the anterior and posterior sacral foramina, not the cornua. Cornua are bony projections, not holes.

2. Site of attachment of ligamentum flavum

   • False. The ligamentum flavum connects the laminae of adjacent vertebrae; it does not attach to the sacral cornua.

3. Articular processes for the iliac bone

   • False. The auricular surface of the sacrum forms the sacroiliac joint, not the cornua.

4. Median ridge of the sacrum

   • False. The median sacral crest is the fused spinous processes of S1–S4; it is distinct from the cornua.

The ovarian follicle undergoes distinct developmental stages before and after puberty, and understanding these differences is key in reproductive physiology.

Key Points:

1. Prepubertal Ovarian Follicles

   • Contain primary oocytes arrested in prophase I of meiosis.

   • These oocytes are surrounded by a single layer of flattened granulosa cells (primordial follicle) or cuboidal granulosa cells (primary follicle).

   • Follicles do not mature fully because gonadotropin stimulation is low before puberty.

   • No secondary follicles with stratum granulosum or antral cavity are formed.

2. Postpubertal (Pubertal) Ovarian Follicles

   • After puberty, rising FSH and LH stimulate follicular growth.

   • Follicles develop into secondary follicles, characterized by:

     • Stratum granulosum (multiple layers of granulosa cells)

     • Formation of a fluid-filled antrum

     • Zona pellucida surrounding the oocyte

   • These changes allow for selection of a dominant follicle for ovulation.

❌ Why the Other Options Are Incorrect

1. Prepubertal follicles contain primary oocytes arrested in metaphase

   • False. Primary oocytes are arrested in prophase I, not metaphase. Metaphase arrest occurs only after the LH surge in the secondary oocyte during ovulation.

2. Post puberty, ovarian follicles increase in number

   • False. The total number of follicles is determined at birth. After puberty, follicles undergo selection and atresia, but total primordial numbers decrease with age.

3. Prepubertal follicles contain secondary oocyte

   • False. Secondary oocytes are only formed after meiosis I resumes at ovulation, which occurs post-puberty.

4. Prepubertal follicles contain germ cells

   • False. Germ cells (oogonia) are present during fetal development, not in prepubertal ovarian follicles. By birth, oogonia have differentiated into primary oocytes.

Spermatogenesis is the process by which male germ cells develop into mature spermatozoa. Understanding which cells undergo meiosis I and II is critical in reproductive physiology.

Stepwise Overview of Spermatogenesis:

1. Spermatogonia

   • Diploid stem cells (2n) in the seminiferous tubules.

   • Undergo mitosis to maintain the stem cell population or produce primary spermatocytes.

2. Primary spermatocyte

   • Diploid (2n) cells that enter meiosis I.

   • Result of meiosis I: two haploid secondary spermatocytes (n), each with duplicated chromosomes.

3. Secondary spermatocyte ✅

   • Haploid (n) cells with duplicated chromatids.

   • Undergo meiosis II, dividing sister chromatids to produce spermatids (n).

4. Spermatid

   • Haploid (n) cells resulting from meiosis II.

   • Undergo spermiogenesis to become mature spermatozoa.

5. Germ cell

   • General term for all reproductive cells; not a specific stage that undergoes meiosis II.

❌ Why the Other Options Are Incorrect

1. Primary spermatocyte

   • Undergoes meiosis I, not meiosis II.

   • Produces secondary spermatocytes, which then undergo meiosis II.

2. Spermatogonia

   • Diploid stem cells; undergo mitotic division, not meiosis.

3. Spermatid

   • Result of meiosis II, but does not divide further.

   • Undergoes maturation (spermiogenesis), not meiosis.

4. Germ cell

   • General term for any cell that can give rise to gametes; not a stage in meiosis II.

Prolactin is a hormone secreted by the anterior pituitary (lactotroph cells) and is primarily responsible for stimulating milk production (lactogenesis). It also has significant effects on the hypothalamic-pituitary-ovarian axis, which explains its influence on menstruation.

Mechanism of Action:

1. Inhibition of GnRH:

   • High prolactin levels inhibit hypothalamic secretion of gonadotropin-releasing hormone (GnRH).

   • This reduces pituitary secretion of FSH and LH, which are essential for ovarian follicle development and ovulation.

2. Effect on Ovarian Function:

   • Without adequate FSH and LH, follicular maturation is impaired, and ovulation may not occur.

3. Clinical Outcome:

   • The lack of ovulation leads to amenorrhea (absence of menstrual periods).

   • This is commonly seen in hyperprolactinemia, which can occur due to pituitary tumors (prolactinomas), certain medications, or physiological states like lactation.

❌ Why the Other Options Are Incorrect

1. It leads to prolonged menstrual cycle

   • False. High prolactin generally stops cycles entirely rather than prolonging them.

2. It causes heavy menstrual bleeding

   • False. Hyperprolactinemia typically leads to reduced or absent bleeding, not menorrhagia.

3. It leads to prolonged luteal phase

   • False. Ovulation may not occur at all, so there is no normal luteal phase to prolong.

4. It causes menorrhagia

   • False. Menorrhagia (heavy periods) is inconsistent with prolactin-induced hypogonadism.

Mifepristone is a synthetic steroid that acts primarily as a progesterone receptor antagonist. Its main uses are in medical termination of pregnancy and sometimes in Cushing’s syndrome (due to its glucocorticoid receptor antagonism).

Key Points:

1. Mechanism of Action

   • Blocks progesterone receptors in the uterus → destabilizes the endometrium → prevents implantation and maintenance of early pregnancy.

   • Softens the cervix and increases uterine contractility, facilitating expulsion of the embryo.

2. Clinical Use

   • Used orally, usually in combination with misoprostol (a prostaglandin analog) to induce medical abortion, particularly in early pregnancy (<10 weeks).

   • Highly effective for medical termination of early pregnancy.

❌ Why the Other Options Are Incorrect

1. It is typically used in combination with misoprostol ✅

   • True. Mifepristone alone induces endometrial changes, but misoprostol triggers uterine contractions to expel pregnancy tissue. Combination therapy is standard.

2. It is effective in early pregnancy ✅

   • True. Most effective in first-trimester termination.

3. It is a progesterone antagonist ✅

   • True. Its primary mechanism is blocking progesterone, which is necessary for maintaining early pregnancy.

4. It is used orally ✅

   • True. Convenient and safe for oral administration in medical abortion protocols.

5. It is an anti-abortion drug ❌

   • False. Mifepristone is pro-abortion (induces abortion), not anti-abortion. The statement is the odd one out

During pregnancy, levels of estrogen and progesterone rise significantly. These hormones have profound effects on the mammary glands:

Key Points:

1. Breast Development

   • Estrogen promotes ductal growth and branching.

   • Progesterone promotes lobuloalveolar development.

2. Milk Secretion

   • Despite well-developed mammary tissue, high estrogen and progesterone levels inhibit actual milk secretion.

   • This occurs because these hormones block prolactin action on mammary alveolar cells, preventing lactogenesis during pregnancy.

3. Postpartum Lactation

   • After delivery, estrogen and progesterone levels drop sharply, removing the inhibition.

   • Prolactin, now unopposed, stimulates milk production.

❌ Why the Other Options Are Incorrect

1. Decrease in the fatty substance of the breasts

   • False. Estrogen promotes growth and fat deposition in breasts.

2. Decreased prolactin secretion

   • False. Prolactin levels are actually elevated during pregnancy, but its effect is inhibited by estrogen and progesterone.

3. Increased milk secretion

   • False. Milk secretion does not occur during pregnancy due to hormonal inhibition.

4. Decreased breast growth

   • False. Estrogen and progesterone stimulate breast growth, not decrease it.

Progesterone is a steroid hormone synthesized from cholesterol through a series of enzymatic steps in the ovary, corpus luteum, and adrenal cortex. Understanding its biosynthesis is key to endocrine physiology.

Stepwise Synthesis:

1. Cholesterol → Pregnenolone

   • Catalyzed by desmolase (cholesterol side-chain cleavage enzyme, CYP11A1) in mitochondria.

   • This is the rate-limiting step in steroid hormone synthesis.

2. Pregnenolone → Progesterone

   • Pregnenolone is converted to progesterone via the enzyme 3β-hydroxysteroid dehydrogenase.

   • This makes pregnenolone the immediate precursor of progesterone.

3. Progesterone can then serve as a precursor for androgens, estrogens, glucocorticoids, and mineralocorticoids.

❌ Why the Other Options Are Incorrect

1. Dihydroprogesterone

   • Formed from progesterone, not a precursor. It’s a metabolite, not an upstream molecule.

2. Androstenedione

   • Derived from progesterone or 17-hydroxyprogesterone, a precursor for testosterone and estrogens, not a direct precursor to progesterone.

3. Testosterone

   • A downstream androgen hormone, not a precursor for progesterone.

4. Cholesterol

   • Precursor to pregnenolone, not immediately to progesterone. Progesterone synthesis requires pregnenolone as the intermediate.

Pregnancy → plasma ↑↑ > RBC mass ↑ → physiological anemia

Pregnancy is associated with major physiological cardiovascular adaptations to meet the metabolic demands of the mother and the growing fetus. One key change is disproportionate expansion of plasma volume compared to red blood cell (RBC) mass.

✅ Why this option is correct

• Plasma volume increases by ~40–50%

• Red blood cell mass increases by ~20–30%

• Because plasma increases more than RBC mass, this leads to:

  • Physiological (dilutional) anemia of pregnancy

  • Hemoglobin and hematocrit appear lower, despite increased total RBC mass

📌 This is a normal and expected finding in pregnancy.

❌ Why the other options are wrong

• ❌ Increase in plasma volume less than the increase in red blood cell mass

  • Would cause hemoconcentration → not seen in pregnancy

• ❌ Increase in plasma volume with decreased red blood cell mass

  • RBC mass does not decrease in normal pregnancy

• ❌ Decreased plasma volume and red blood cell mass

  • Opposite of physiological changes in pregnancy

• ❌ Increase in plasma volume only

  • RBC mass also increases (just to a lesser degree)

Mullerian inhibitory factor (MIF), also called anti-Mullerian hormone (AMH), is crucial in male sexual differentiation during embryonic development. Its primary role is to regress the Mullerian ducts, which would otherwise develop into female reproductive structures such as the uterus, fallopian tubes, and upper vagina.

• Source: Sertoli cells of the embryonic testes.

• Timing: Secreted early in fetal life (around 7–8 weeks gestation in humans).

• Function: Causes regression of Mullerian ducts in males, allowing male reproductive tract development.

❌ Why the Other Options Are Incorrect

1. Theca interna cells

   • These cells in the ovary produce androgens that are later converted to estrogens by granulosa cells, but they do not secrete MIF.

2. Granulosa cells

   • In females, granulosa cells produce estrogens and inhibin, but they do not secrete MIF.

3. Leydig cells

   • Leydig cells produce testosterone, which supports Wolffian duct development, but they do not secrete MIF.

4. Pituicytes

   • Pituicytes are supporting cells of the posterior pituitary; they have no role in sexual differentiation.

Progesterone is a steroid hormone secreted primarily by the corpus luteum after ovulation. Its main function is to prepare the endometrium for implantation and maintain early pregnancy. Let’s examine its effects on the uterine endometrium:

🧠 Key Effects of Progesterone on the Endometrium:

1. Increases glycogen deposition in the glandular epithelium ✅

   • True. Progesterone stimulates secretory activity of the endometrial glands, leading to glycogen-rich secretions that provide nutrients for the developing embryo.

   • This effect is part of the secretory phase of the menstrual cycle.

❌ Why the Other Options Are Incorrect

1. It works synergistically with estrogen to increase proliferation

   • False. Estrogen is responsible for proliferation of the endometrium (thickening and growth of glands and stroma).

   • Progesterone actually counteracts excessive proliferation, stabilizing and differentiating the endometrium rather than promoting growth.

2. It converts glands from coiled to tubular forms

   • False. Progesterone transforms tubular glands into coiled, secretory glands, not the other way around.

3. It causes regression of spiral arteries

   • False. Progesterone supports spiral artery development during the secretory phase. Regression occurs if pregnancy does not occur, when progesterone levels fall.

4. It increases myometrial excitability

   • False. Progesterone actually reduces myometrial excitability, promoting uterine quiescence during pregnancy.

Let’s analyze the statements about male and female genital glands:

✅ Correct Statements

1. Prostatic hyperplasia occurs in the transitional zone

   • True. Benign prostatic hyperplasia (BPH) primarily affects the transitional zone of the prostate, which surrounds the prostatic urethra.

2. Seminal vesicles secrete fructose for the sperm

   • True. Seminal vesicles produce a fructose-rich fluid, which serves as an energy source for sperm motility.

3. Seminal vesicles secrete an alkaline fluid

   • True. The alkalinity of the seminal vesicle fluid neutralizes the acidic environment of the male urethra and female vagina, aiding sperm survival.

4. Bartholin’s glands open into the vestibule

   • True. Bartholin’s glands (greater vestibular glands) in females secrete mucus to lubricate the vestibule, and their ducts open near the posterolateral vaginal orifice.

❌ Incorrect Statement

• Ducts of Cowper’s glands open into membranous urethra

  • False. Bulbourethral (Cowper’s) glands are paired glands located inferior to the prostate.

  • Their ducts open into the spongy (penile) urethra, not the membranous urethra.

  • They secrete a pre-ejaculate alkaline mucus that lubricates the urethra and neutralizes residual acidity before sperm passage.

💡 Hint (Critical Thinking Prompt)

Think about the anatomical course of the bulbourethral glands’ ducts relative to the urethral segments and the prostate. Which segment do they actually reach?

Let’s analyze each statement about testosterone carefully:

✅ Statements Correctly Describing Testosterone or DHT

1. It is converted to dihydrotestosterone by 5-alpha reductase

   • True. Testosterone is converted to DHT, a more potent androgen, by 5-alpha reductase, especially in the prostate, skin, and hair follicles.

2. Dihydrotestosterone is more potent than testosterone

   • True. DHT has a higher affinity for androgen receptors and is more potent in androgenic effects, like prostate growth and male pattern hair growth.

3. It causes epiphyseal plate closure

   • True. Testosterone is aromatized to estradiol in bone, which leads to epiphyseal plate closure during puberty.

4. It regulates male libido

   • True. Testosterone is the primary androgen responsible for sexual desire in males.

❌ Odd One Out

• Anabolic synthetic steroids have a shorter half-life

  • This is not generally true.

  • Synthetic anabolic steroids are chemically modified derivatives of testosterone designed to increase half-life and anabolic activity, often administered orally or intramuscularly, sometimes with longer half-lives than endogenous testosterone.

  • Hence, this statement is inconsistent with natural physiology of testosterone and its synthetic derivatives.

The levator prostatae (levator prostate) muscle is a thin layer of striated muscle that forms part of the male pelvic floor and surrounds the prostate gland. It functions to support the prostate, compress the prostatic urethra during ejaculation, and assist in urinary continence.

• Origin: Fibers are derived mainly from the levator ani muscle, specifically the pubococcygeus portion.

• Insertion: Blends with the fibrous capsule of the prostate.

• Function: Elevates the prostate, compresses the prostatic urethra, assists in ejaculation.

Thus, the levator ani muscle is the primary contributor to the formation of the levator prostatae.

🧠 Why the Other Options Are Incorrect

1. Transverse perineal muscle

   • Stabilizes the perineal body but does not contribute fibers to the levator prostatae.

2. Obturator internus

   • Forms the lateral pelvic wall, mainly acts on the thigh, and does not participate in the pelvic floor musculature around the prostate.

3. Ischiocavernosus

   • Covers the crura of the penis; assists in penile erection, not in forming the levator prostatae.

4. Bulbospongiosus

   • Covers the bulb of the penis; assists in ejaculation and urethral emptying, but is distinct from the levator prostatae.

To achieve pregnancy, two key events must happen:

1. Fertilization — usually occurs in the ampulla of a patent (open) uterine tube.

2. Implantation — occurs in the uterus, but only if a fertilized ovum arrives there.

Let’s analyze the situation:

1️⃣ Left uterine tube removed

• The left ovary still releases an ovum, but the left tube (required to pick it up) is gone.

• Very rarely, the contralateral tube can pick up the ovum across the peritoneal cavity, but this requires the remaining tube to be functional and open.

2️⃣ Right uterine tube has isthmus contraction (blockage)

• The right tube is functionally obstructed.

• This means:

  • Sperm cannot reach the ampulla

  • Ovum cannot pass through the tube

  • Fertilization cannot occur

Since fertilization does NOT occur → implantation cannot occur.

❌ Why the Other Options Are Incorrect

Implantation can occur but no fertilization

Impossible — implantation requires a fertilized ovum.

Both fertilization and implantation occur

Not possible due to blockage.

Fertilization occurs but not implantation

Fertilization itself cannot occur here.

None of these

One option is correct, so this is wrong.

The development of the testes in an embryo requires the activation of a specific gene found on the Y chromosome.

That gene is:

👉 SRY (Sex-determining Region of Y)

The SRY gene produces the testis-determining factor (TDF), a protein that triggers:

• Differentiation of the bipotential gonad into testes

• Development of Sertoli cells → production of Müllerian inhibiting factor

• Development of Leydig cells → production of testosterone

Without the SRY gene, even if other pathways are intact, the gonad develops into an ovary.

Thus, SRY is the master switch for testicular development.

❌ Why the Other Options Are Incorrect

WNT-1

Involved in neural tube and brain development—not sex determination.

SHOX

Controls skeletal development, especially height and limb formation.
Mutations cause short stature (e.g., Turner syndrome), not testis development.

SHH (Sonic Hedgehog)

A key morphogen for body patterning.
Important in limb development and neural tube patterning, but not for determining gonadal sex.

FGF (Fibroblast Growth Factors)

Involved in cell growth and differentiation in many tissues.
Do not determine testis differentiation.

Tubal ligation is a permanent method of female sterilization that involves blocking or cutting the fallopian tubes to prevent fertilization.

The most common and widely performed method is:

👉 Laparoscopic tubal ligation

This technique uses a laparoscope inserted through small abdominal incisions. It is preferred because it is:

• Minimally invasive

• Quick to perform

• Associated with faster recovery

• Highly effective

Common techniques include bipolar coagulation, clips, or rings applied laparoscopically.

❌ Why the Other Options Are Incorrect

Hysteroscopic sterilization

• Includes methods like Essure (now discontinued in many regions).

• Not the most common and not currently widely used due to safety concerns.

Hysterosalpingography

• An imaging procedure used to evaluate tubal patency—not a sterilization method.

Culdocentesis

• A diagnostic procedure involving needle aspiration from the cul-de-sac.

• Not related to tubal ligation.

Amniocentesis

• A prenatal diagnostic test.

• Completely unrelated to sterilization.

Turner’s syndrome is a chromosomal disorder that occurs when one of the X chromosomes is partially or completely missing. The most classic and common karyotype associated with this condition is:

👉 45, XO

This means the individual has:

• 45 chromosomes total

• Only one X chromosome

• No second sex chromosome (no X or Y partner)

This chromosomal pattern leads to the characteristic clinical features of Turner’s syndrome, such as:

• Short stature

• Streak ovaries → infertility

• Primary amenorrhea

• Webbed neck

• Coarctation of the aorta

❌ Why the Other Options Are Incorrect

46, XXY

• This is Klinefelter syndrome, seen in males with feminizing features and small testes.

• Not consistent with Turner’s syndrome.

46, XXX

• This is Triple X syndrome, usually with mild or no physical abnormalities.

• Does not match the features of Turner’s syndrome.

46, XX

• Normal female karyotype.

• Not associated with the clinical presentation in Turner’s syndrome.

46, XY

• Normal male karyotype.

• Completely inconsistent with Turner’s presentation.

This patient is:

• 31 years old

• Pregnant (G2P1+0)

• Known case of uterine fibroids

• Presenting with lower abdominal pain for 5 days

• Examination reveals a tender uterus

These features are classic for red degeneration of a fibroid, also called carneous degeneration.

Why?

During pregnancy, fibroids can outgrow their blood supply because of increased estrogen levels.
This leads to:

• Hemorrhage into the fibroid

• Acute severe pain

• Uterine tenderness

• Sometimes fever or leukocytosis

This condition is most common in pregnancy, especially in the second trimester, but can present at any time during gestation in a patient with fibroids.

❌ Why the Other Options Are Incorrect

Abruptio placentae

• Characterized by vaginal bleeding, abdominal pain, and uterine hypertonicity.

• Also presents with fetal distress.

• Not just tenderness; more acute and severe presentation.

Gray degeneration

• Another form of fibroid degeneration but not painful and not associated with pregnancy.

• The uterus is typically not tender in this condition.

Ectopic pregnancy

• Causes lower abdominal pain but is associated with amenorrhea, positive pregnancy test, possibly bleeding, and adnexal tenderness—not uterine tenderness.

Ovarian torsion

• Severe unilateral pelvic pain with nausea/vomiting.

• Pain is lateralized, not generalized uterine tenderness.

• Ovary, not uterus, is tender.