The organ involved here is the ovary, which develops high in the posterior abdominal wall and only later descends.
Because of this embryological origin, its lymphatic drainage remains to the para-aortic (lumbar) lymph nodes, located near the level of L1–L2.

This is a key exam point:
👉 Ovaries drain to para-aortic nodes
👉 Not to pelvic or inguinal nodes

❌ Why the Other Options Are Wrong

Common iliac
❌ Drains cervix and lower uterus, not ovaries.

External iliac
❌ Drains body of uterus, cervix, and upper vagina—not ovaries.

Internal iliac
❌ Drains lower pelvic organs like the cervix, prostate, and bladder.

Superficial inguinal
❌ Drains vulva, skin of perineum, and lower vagina—not ovaries.

The organ described is the ovary, showing multiple cystic follicles typical of PCOS.

The surface of the ovary is lined by a special epithelium called:

👉 Germinal epithelium = simple cuboidal epithelium

This single layer of cuboidal cells covers the ovary and is the epithelium seen where cysts appear on ultrasound.

❌ Why the Other Options Are Wrong

Simple squamous
❌ Lines serous membranes (peritoneum), not the ovary itself.

Stratified columnar
❌ Rare epithelium; not found in the ovary.

Stratified cuboidal
❌ Lines large ducts of glands such as sweat glands—not ovarian tissue.

Stratified squamous
❌ Lines skin and vagina—not the ovary.

In PCOS, the LH : FSH ratio is elevated, which leads to:

1. Failure of the LH surge → No ovulation

FSH is too low to mature follicles properly, so the ovary never reaches the stage where a dominant follicle can respond with a proper ovulatory LH surge.

➡️ Ovulation does not occur → Ovulatory phase is affected

2. No ovulation → No corpus luteum → No progesterone

The luteal phase depends entirely on formation of the corpus luteum, which produces progesterone.

If ovulation doesn’t happen, the corpus luteum never forms.

➡️ Luteal phase is absent or defective

So, the phases affected are:

👉 Ovulatory phase
👉 Luteal phase

❌ Why the Other Options Are Wrong

Luteal and menstrual phase
❌ Menstrual flow may still occur—irregularly—but the key defect is in ovulation, not menstruation.

Menstrual flow and follicular phase
❌ Follicular phase starts normally but fails to progress to ovulation; menstrual flow is not primarily the issue.

Proliferative and ovulatory phase
❌ Proliferative (estrogen-driven) phase is generally intact; the block is at ovulation.

Proliferative and menstrual phase
❌ Neither of these is chiefly impaired in PCOS.

This 14-year-old girl shows the classic cluster of findings seen in PCOS:

• Irregular menstrual cycles (oligomenorrhea, amenorrhea)

• Acne and increased facial hair → signs of hyperandrogenism

• Ultrasound showing multiple cystic follicles

• Elevated LH : FSH ratio, a hallmark of PCOS

The ovaries fail to ovulate, follicles accumulate, and excess androgen production explains the acne and hirsutism.

❌ Why the Other Options Are Wrong

Endometrial polyp
❌ Causes irregular bleeding but does not produce cystic ovaries, acne, or high LH:FSH ratio.

Anovulatory cycles
❌ May cause irregular periods but do not cause hyperandrogenism or cystic ovaries.

Ectopic pregnancy
❌ Causes abdominal pain + missed period — not chronic menstrual irregularity or hirsutism.

Endometrial carcinoma
❌ Occurs in older women and presents with abnormal bleeding, not androgen excess or ovarian cysts.

This patient has vaginismus, a condition where involuntary contraction of pelvic floor muscles occurs due to fear, anxiety, or anticipation of pain with intercourse.
There is no anatomical or gynecological abnormality, which matches the scenario.

Best management:
👉 Psychosexual education, counseling, reassurance, and addressing fear/anxiety
This includes:

• Explaining the condition to both partners

• Reducing fear and misconceptions about intercourse

• Teaching relaxation techniques

• Gradual desensitization (e.g., pelvic floor exercises, dilators when appropriate)

• Couple-oriented therapy

This approach targets the root cause, which is psychological fear and conditioned anxiety.

❌ Why the Other Options Are Wrong

Prescribe short-acting benzodiazepine
❌ Wrong — benzodiazepines may reduce anxiety temporarily but do not treat vaginismus and may worsen avoidance behaviors.

Counsel the couple that there is no major problem and to keep trying
❌ Invalid — merely telling them to “keep trying” can increase fear, pain, and frustration. Structured therapy is needed.

Prescribe painkillers prior to intercourse
❌ Pain is not due to inflammation or physical injury — it is due to involuntary muscle spasm and fear. Analgesics won’t help.

Prescribe a placebo
❌ Unethical and ineffective.

This boy identifies as female despite being biologically male and experiences:

• Persistent distress about his biological sex

• Desire to change genitalia

• Long-standing discomfort since childhood

This fits gender dysphoria, which is defined as:

👉 A marked incongruence between one’s experienced gender and assigned sex, accompanied by significant distress or impairment.

The key feature is distress, which separates gender dysphoria from merely identifying differently.

❌ Why the Other Options Are Wrong

Sexual orientation
❌ Refers to attraction (heterosexual, homosexual, bisexual).
Has nothing to do with identity mismatch or desire for gender transition.

Gender identity
❌ This is the internal sense of being male, female, both, or neither.
It may be female in this case, but the disorder is not “gender identity”; it is the distress caused by the mismatch → gender dysphoria.

Sexual identity
❌ Similar to sexual orientation; relates to how one identifies sexually, not gender identity.

Sexual behavior
❌ Refers to sexual acts or activities; not applicable here.

Permanent methods of contraception are those that irreversibly block the reproductive pathway.
In females, the standard permanent method is tubal ligation, where the fallopian tubes are cut, tied, or sealed → preventing sperm from reaching the ovum.

It is commonly offered after multiple C-sections or when the woman desires no future pregnancies.

❌ Why the Other Options Are Wrong

Depo-Provera injection
❌ Long-acting, but temporary. Effect wears off in 3–6 months.

Subdermal implant (Implanon/Nexplanon)
❌ Highly effective and long-acting (3–5 years), but reversible.

Oral pills
❌ Daily, completely reversible.

IUCD (Copper T or hormonal)
❌ Long-term (5–10 years), but reversible once removed.

Only tubal ligation is a permanent contraceptive method.

Orchiopexy is the surgical procedure used to bring an undescended testis into the scrotum and fix it in place.
This is the treatment for cryptorchidism, which is failure of testicular descent.

Why early intervention?

• Prevent infertility

• Reduce risk of torsion

• Reduce risk of testicular cancer

• Allow normal hormonal function

• Make examination easier later in life

Thus, orchiopexy = correction of undescended testis.

❌ Why the Other Options Are Wrong

Hypospadias
❌ Urethral opening on the ventral side of penis; corrected by urethroplasty, not orchiopexy.

Epispadias
❌ Urethral opening on dorsal side; surgical repair, not orchiopexy.

Phimosis
❌ Tight foreskin; treated with circumcision, not orchiopexy.

Torsion
❌ Testicular torsion is treated by detorsion + orchiopexy, but orchiopexy here is done to prevent recurrence in an already descended testis — not the primary condition described.

The question specifically refers to abnormal location of testis, so cryptorchidism is correct.

The case describes gestational choriocarcinoma:

• History of spontaneous abortion followed by curettage

• Microscopy: cytotrophoblast + syncytiotrophoblast

• No chorionic villi (key hallmark)

• Hemorrhage and necrosis

• Early hematogenous spread → nodules in lungs and brain

Despite being highly malignant, gestational choriocarcinoma is very chemosensitive, and with proper evacuation and chemotherapy, the prognosis is usually excellent, with very high cure rates, even in metastatic disease.

That’s why:
👉 “Response to evacuation and chemotherapy is usually excellent” is TRUE.

❌ Why the Other Options Are Wrong

In males this tumor is classified as a sex-cord stromal tumor
❌ In males, choriocarcinoma is a type of germ cell tumor, not a sex-cord stromal tumor. Sex-cord stromal tumors include Leydig and Sertoli cell tumors, not choriocarcinoma.

More than half of these tumors arise in ectopic pregnancies
❌ Most gestational choriocarcinomas arise after:

• Complete mole (most common)

• Spontaneous abortion

• Normal pregnancy
  Ectopic pregnancy is a rare source, not the majority.

Alpha-fetoprotein levels are used to monitor this disease
❌ Choriocarcinoma is monitored with β-hCG, not AFP. AFP is used for yolk sac tumors and some liver conditions.

Ovarian variant of this tumor has a very good prognosis
❌ Non-gestational (ovarian) choriocarcinoma has a worse prognosis than gestational choriocarcinoma and is less responsive to therapy.

A 14-year-old girl with:

• Irregular cycles (oligomenorrhea, amenorrhea)

• Acne

• Hirsutism

• Elevated LH:FSH ratio

This combination is classic for Polycystic Ovarian Syndrome (PCOS).

In PCOS:

• LH is disproportionately elevated → increases androgen production from theca cells

• High androgens → acne + hirsutism

• Irregular cycles → due to chronic anovulation

Thus, PCOS best fits the hormonal pattern and the clinical picture.

❌ Why the Other Options Are Wrong

Endometrial carcinoma
❌ Occurs in older women, not teenagers. Presents with heavy bleeding, not oligomenorrhea.

Anovulatory cycles
❌ Can cause irregular bleeding, but do NOT cause hirsutism or acne, and LH:FSH ratio is usually normal.

Ectopic pregnancy
❌ Causes abdominal pain + missed period; not chronic irregular cycles or hirsutism.

Endometrial polyp
❌ Causes spotting, not androgen excess. No effect on LH/FSH.

Estrogen in the bloodstream is not freely floating — most of it is bound to transport proteins.

The main carrier of estrogen is Sex Hormone–Binding Globulin (SHBG).
SHBG binds:

• Estrogen (estradiol)

• Testosterone

Only a small “free” fraction remains biologically active.

A smaller amount of estrogen is also loosely bound to albumin, but the principal high-affinity transporter is SHBG.

❌ Why the Other Options Are Wrong

Ferritin
❌ Binds iron, not hormones.

Cholesterol-binding lipoproteins
❌ Transport lipids and cholesterol, not steroid hormones.

Corticosteroid-binding globulin (CBG)
❌ Transports cortisol and progesterone—not estrogen.

Sex hormone–binding albumin
❌ There is no specific protein called “sex hormone–binding albumin.”
Albumin does bind hormones weakly, but it is not the main carrier and not called this name.

This patient has classic symptoms of a hydatidiform mole (molar pregnancy):

• Missed period

• Severe nausea/vomiting (hyperemesis gravidarum)

• Passage of grape-like vesicles

• Ultrasound showing a “snowstorm” pattern or multiple cysts

• Excessively high hCG levels

Why is hCG so high?

• In a molar pregnancy, trophoblastic tissue proliferates excessively, producing very large amounts of hCG.

• hCG stimulates nausea/vomiting and can even cause ovarian theca-lutein cysts.

So extremely elevated hCG is a key diagnostic marker.

❌ Why the Other Options Are Wrong

Human somatomammotropin (hPL)
❌ Does not rise significantly in molar pregnancy; produced by placenta later in pregnancy.

Progesterone
❌ May be elevated but not excessively high, and not diagnostic.

Estrogen
❌ Usually low in molar pregnancy due to absence of a normal fetus.

GnRH
❌ Not related to molar pregnancy diagnosis.

The menstrual cycle is divided into two main phases regarding the endometrium (uterine lining): the Proliferative Phase and the Secretory Phase. The key to answering this question lies in distinguishing which hormone dominates after ovulation.

• • Before Ovulation (Proliferative Phase): The hormone Estradiol (Estrogen) is dominant. It stimulates the

  • endometrial cells to multiply (proliferate), causing the lining to rebuild and thicken after menstruation.

  • After Ovulation (Secretory Phase): The ruptured follicle transforms into the Corpus Luteum, which secretes high levels of Progesteron

    • Progesterone stops the endometrial cells from multiplying further.

    • Instead, it stimulates the glands to widen, become tortuous, and fill with secretions (glycogen and lipids) to nourish a potential embryo.

    • It also increases blood flow and causes fluid retention (edema) in the tissue.

    • These changes result in the endometrium reaching its maximum thickness and becoming a lush, soft bed suitable for implantation

Why the other options are incorrect

Combined oral contraceptive pills (estrogen + progesterone) prevent pregnancy mainly by stopping ovulation.

How do they do this?

• The synthetic estrogen and progesterone provide negative feedback on the hypothalamus and pituitary.

• This suppresses FSH and LH secretion.

• Without sufficient FSH → follicles do not mature normally.

• Most importantly, there is no LH surge, and therefore no ovulation.

So the key mechanism is the prevention of the LH surge, which is absolutely required for ovulation.

❌ Why the Other Options Are Wrong

Suppressing function of the corpus luteum soon after it forms
❌ The goal is to prevent ovulation, so the corpus luteum doesn’t form in the first place.

Prevention of normal development of the endometrium
❌ This is a secondary effect (makes implantation harder), but not the primary mechanism.

Prevention of development of the ovarian follicles
❌ Follicular development is partially suppressed, but some early follicular growth still occurs. The critical prevention is the LH surge.

Suppressing the function of GnRH
❌ GnRH pulsatility is indirectly suppressed, but this is not the primary explanation tested — the main point is blocking the LH surge.

The liver is the principal site of estrogen synthesis in males because:

• It contains high aromatase activity, the enzyme that converts:

  • Testosterone → Estradiol

  • Androstenedione → Estrone

• It continuously processes large amounts of circulating androgens

• It contributes significantly to systemic (circulating) estrogen levels

According to Guyton & Hall, the majority of estrogen in males arises from peripheral conversion of androgens, with the liver being the most important contributor.

📘 Reference:
Guyton and Hall Textbook of Medical Physiology, 14th Edition, Page 1019

Why the Other Options Are Incorrect

❌ Prostate cells

• The prostate is androgen-dependent, not a major endocrine organ

• While estrogen receptors are present, it does not significantly synthesize estrogen

• Any local conversion is minimal and not physiologically dominant

❌ Leydig cells

• Leydig cells primarily synthesize testosterone

• They possess minimal aromatase activity

• Their role is androgen production, not estrogen formation

❌ Trophoblast

• Trophoblast cells are found in the placenta

• Relevant only in pregnancy, not in male physiology

• Completely unrelated to male estrogen synthesis

❌ Osteoblasts

• Osteoblasts express aromatase and can convert androgens locally

• This estrogen acts paracrinally, mainly for bone health

• They are not the principal systemic source

High-Yield Summary Table

The seminal vesicles develop as outgrowths from the mesonephric (Wolffian) ducts, which themselves arise from the intermediate mesoderm.

Anything derived from the male internal duct system (epididymis, vas deferens, seminal vesicles, ejaculatory ducts) traces back to the mesonephric duct → intermediate mesoderm.

❌ Why the Other Options Are Wrong

Lateral plate mesoderm
❌ Forms body wall structures, blood vessels, and smooth muscle of organs — not the reproductive ducts.

Paraxial mesoderm
❌ Forms somites → muscles, vertebrae, dermis — no role in male reproductive ducts.

Ectoderm
❌ Forms skin, nervous system — nothing in the seminal vesicles.

Endoderm
❌ Forms lining of GI and respiratory tracts — not male reproductive glands.

In embryology, genital swellings give rise to different external genital structures depending on androgen exposure.

In females (absence of DHT):

• Genital swelling → Labia majora

• Urogenital folds → Labia minora

• Genital tubercle → Clitoris

The genital swellings do not form the vestibule or vaginal opening.

❌ Why the Other Options Are Wrong

Vaginal orifice
❌ From the urogenital sinus, not genital swelling.

The vestibule
❌ Also from urogenital sinus.

Labia minora
❌ From urogenital folds, not genital swellings.

Clitoris
❌ From the genital tubercle.

In Androgen Insensitivity Syndrome (AIS):

• The patient has a 46 XY karyotype.

• SRY gene is present → testes develop (usually undescended or in inguinal canal).

• Sertoli cells in the testes secrete Anti-Müllerian Hormone (AMH) → causes regression of Müllerian structures (uterus, fallopian tubes, upper vagina).

• Androgen receptors are nonfunctional, so the body cannot respond to testosterone or DHT, leading to female external genitalia.

Thus, the ONLY internal genital structure present is the testes.

❌ Why the Other Options Are Wrong

Fallopian tube
❌ Absent — AMH causes Müllerian duct regression.

Prostate
❌ Not present — prostate development requires functioning androgen receptors.

Ovaries
❌ Impossible — the patient is genetically XY, so ovaries cannot form.

Uterus
❌ Absent — AMH from Sertoli cells destroys Müllerian ducts.

The vagina has dual embryological origin:

• Upper 1/3 → Fused paramesonephric (Müllerian) ducts

• Lower 2/3 → Urogenital sinus (via the sinovaginal bulbs forming the vaginal plate)

The fornices also come from the upper portion, therefore from the Müllerian ducts, not the urogenital sinus.

The hymen is formed from the vaginal plate (UG sinus), not the Müllerian ducts.

❌ Why the Other Options Are Wrong

“Vagina upper two-third develops from urogenital sinus”
❌ Wrong — upper 2/3 is Müllerian, lower 1/3 is UG sinus (not the other way around).

“Hymen develops from cells derived from Müllerian duct”
❌ Incorrect — the hymen comes from the UG sinus-derived vaginal plate.

“Vaginal fornices are of urogenital sinus origin”
❌ Fornices belong to the upper vagina → from Müllerian ducts.

“Lower two-third is from surface ectoderm”
❌ No — the lower vagina is from endoderm of the urogenital sinus, not surface ectoderm.

The vagina is lined by non-keratinized stratified squamous epithelium.
The cervical canal (endocervix) is lined by simple columnar epithelium.

The point where these two meet is called the squamocolumnar junction, also known as the transformation zone — the most common site for cervical dysplasia and carcinoma.

So the epithelial transition is:

👉 Stratified squamous (vagina/exocervix)
→ Simple columnar (endocervix)

❌ Why the Other Options Are Wrong

Stratified squamous → stratified columnar
Endocervix is not stratified.

Simple squamous → stratified columnar
Neither epithelium fits the anatomy.

Simple columnar → simple squamous
Simple squamous is not found in the vagina or cervix lining.

Simple squamous → simple columnar
Again, no simple squamous epithelium here.

The prostate gland is lined mainly by simple columnar epithelium, which forms the secretory cells responsible for producing prostatic fluid.
These cells sit within a fibromuscular stroma, a classic identifying feature of the prostate.

Other epithelial types (simple cuboidal, pseudostratified columnar) may appear in small areas, but the dominant and most commonly seen type is simple columnar.

❌ Why the Other Options Are Wrong

Stratified squamous
Not present in the prostate; found in the distal urethra/vagina.

Simple cuboidal
Can appear focally, but it is not the main epithelium.

Simple squamous
Seen in vessels, peritoneum — not in glandular prostate tissue.

Transitional (urothelium)
Lines the prostatic urethra, not the prostatic glands themselves.

The description is classic for the ovary:

• Primordial follicles located at the cortex, which is the peripheral region

• Central region (medulla) composed of loose connective tissue with blood vessels, nerves, and lymphatics

This cortex–medulla organization is unique to the ovary among reproductive organs.

❌ Why the Other Options Are Wrong

Fallopian tube
Has mucosal folds, smooth muscle layers, and no follicles.

Vagina
Stratified squamous epithelium with no follicles and no cortex–medulla pattern.

Uterus
Has endometrium + myometrium, no follicles.

Cervix
Has mucous-secreting glands and dense connective tissue — again, no follicles.

The theca interna cells are responsible for steroid hormone synthesis, especially androgens, which later diffuse to granulosa cells for aromatization into estrogen.

Steroid-producing cells rely heavily on the smooth endoplasmic reticulum (SER) because:

• SER contains enzymes for cholesterol → steroid conversion

• It is abundant in all steroidogenic tissues (adrenal cortex, Leydig cells, theca interna cells)

Therefore, the organelle most abundant in theca interna cells is the SER.

❌ Why the Other Options Are Wrong

Golgi apparatus
Important for protein modification and packaging, not for steroid synthesis.

Polyribosomes
Involved in protein synthesis — steroid hormones are not proteins.

Centrioles
Used for cell division; no special role in hormone production.

Lysosomes
Used for digestion and breakdown, unrelated to steroid hormone synthesis.

Human chorionic gonadotropin (hCG) is structurally very similar to LH and shares the same receptor — the LH receptor, a GPCR found on:

• Theca cells

• Leydig cells

• Corpus luteum

This is why hCG can maintain the corpus luteum in early pregnancy and stimulate progesterone production, just like LH would.

❌ Why the Other Options Are Wrong

Follicle stimulating hormone receptor
FSH has its own separate receptor; hCG does not bind to it.

Human placental lactogen receptor
hPL acts through receptors similar to growth hormone and prolactin, not LH receptors.

Prolactin hormone receptor
Used for lactation and breast development; unrelated to hCG action.

Growth hormone receptor
Used for metabolic and growth effects; hCG has no interaction here.

A phenotypic female with tests located in the inguinal canals is classic for Androgen Insensitivity Syndrome (AIS).

Key features of AIS:

• Genetically male (46 XY)

• Testes present (often in inguinal canal or abdomen)

• External genitalia appear female due to lack of androgen receptor response

• No Müllerian structures (AMH still works)

• Often first detected as inguinal hernias in young girls

Thus, the most likely karyotype is 46 XY.

❌ Why the Other Options Are Wrong

47 XXY (Klinefelter syndrome)
Phenotypic male, tall stature, small testes — not female appearance or inguinal testes misidentified as hernias.

47 XYY
Also phenotypic male, no feminization or undescended testes presenting as hernias.

46 XX
Would have ovaries, not testes. Cannot produce testes in inguinal canals.

45 XY
This karyotype is not viable — missing X chromosome is incompatible with life.
(Only 45,X — Turner syndrome — is viable, and that produces ovaries, not testes.)

The SRY (Sex-determining Region of the Y chromosome) gene is the testis-determining gene.
It sits on the short arm of the Y chromosome (Yp11.3) and initiates the pathway that converts the indifferent gonad into a testis.

Once SRY is expressed:

• Sertoli cells develop → secrete AMH

• Leydig cells develop → produce testosterone

• Male differentiation begins

Without SRY → the default pathway is ovarian development.

❌ Why the Other Options Are Wrong

Short arm of chromosome 22
No role in sex determination.

Chromosome 12
Not involved in gonadal differentiation.

Chromosome 8
Unrelated to SRY or testis formation.

Chromosome 6
Contains MHC genes, not the SRY region.

Sertoli cells are supported and activated primarily by Follicle-Stimulating Hormone (FSH).

FSH actions on Sertoli cells include:

• Major trophic hormone → promotes growth and function of Sertoli cells

• Stimulates aromatase enzyme → converts androgens → estrogens

• Increases ABP (androgen-binding protein) production

• Supports spermatogenesis

• Enhances secretion of inhibin B (negative feedback to FSH)

Thus, FSH is the main driver of both Sertoli cell activity and aromatase activity.

❌ Why the Other Options Are Wrong

Testosterone
Important for spermatogenesis but acts mainly via paracrine support. It does not stimulate aromatase or act as the trophic hormone for Sertoli cells.

Melatonin
Unrelated to Sertoli cell regulation.

Inhibin
Produced by Sertoli cells. It inhibits FSH — not the other way around.

LH
Acts on Leydig cells, not Sertoli cells. LH stimulates testosterone synthesis, not aromatase in Sertoli cells.

Testicular feminization syndrome (also called Androgen Insensitivity Syndrome, AIS) occurs when the body produces normal amounts of testosterone, but the target tissues cannot respond due to a defect in the androgen receptor gene (located on the X-chromosome).

Because the receptors don’t work:

• Testosterone has no effect

• External genitalia develop along the female pathway

• Patients have 46,XY karyotype with undescended testes

• High testosterone converts to estrogen → breast development occurs

So the core issue is androgen receptor dysfunction.

❌ Why the Other Options Are Wrong

Testosterone 5-alpha reductase
Deficiency → cannot convert testosterone to DHT, leading to ambiguous genitalia, not complete feminization. Testosterone receptor still works.

Androgen-binding protein
Produced by Sertoli cells to concentrate testosterone in seminiferous tubules. Defect affects spermatogenesis, not external genital development.

Estrogen receptor
Has no role in male external genital differentiation. Mutation doesn’t cause feminization of a genetic male.

Inhibin
Regulates FSH secretion. No role in androgen action or sexual differentiation abnormalities like AIS.

After ovulation, the corpus luteum forms and secretes progesterone.
Progesterone acts on the endometrium, causing it to become thick, vascular, and glandular — preparing for implantation.
This uterine stage is called the secretory phase, which corresponds exactly to the luteal phase of the ovarian cycle.

❌ Why the Other Options Are Wrong

Proliferative phase
Occurs before ovulation and corresponds to the follicular phase, driven mainly by estrogen, not progesterone.

Follicular phase
This is an ovarian phase, not a uterine one — and it aligns with the proliferative phase, not the luteal phase.

Ovulatory phase
A brief event triggered by the LH surge, not a uterine phase.

Menstrual phase
Occurs when progesterone levels fall after corpus luteum degeneration — after the luteal phase, not during it.

A newborn’s lungs are fluid-filled and collapsed before birth. To inflate them for the first breath, the baby must create a very large negative intrapleural pressure to overcome high surface tension and open the alveoli. Research shows this pressure is roughly –60 mmHg, which allows the initial air entry and lung expansion.

❌ Why the Other Options Are Wrong

–100 mmHg
Too extreme. Newborns generate high negative pressure, but not this high physiologically.

–15 mmHg
Not enough to overcome the high surface tension of fluid-filled, collapsed alveoli.

–5 mmHg
Normal quiet breathing range in adults—far too small for the first breath.

–2 mmHg
Represents minimal breathing effort; completely insufficient to open newborn lungs.

The menstrual cycle follows a very predictable physiological sequence:

1️⃣ Menstruation

Shedding of the endometrium marks Day 1.

2️⃣ FSH Rise

FSH increases to recruit follicles.

3️⃣ LH Surge

High estrogen from the dominant follicle triggers the LH surge.

4️⃣ Ovulation

Occurs ~36 hours after the LH surge.

5️⃣ Luteal Phase

Corpus luteum forms and secretes progesterone.

This matches the option:

✔ Menstruation → FSH rise → LH surge → Ovulation → Luteal phase

Why the other options are incorrect

❌ Follicular phase, luteal phase, FSH rise, ovulation, menstruation
FSH rise occurs before follicular phase ends and definitely before luteal phase.

❌ Luteal phase → menstruation → FSH rise → ovulation → follicular phase
Ovulation happens before luteal phase.

❌ FSH rise → ovulation → LH surge → luteal phase → menstruation
LH surge must happen before ovulation.

❌ FSH rise → menstruation → LH surge → luteal phase → ovulation
Ovulation must occur before luteal phase.

The uterine (fallopian) tube has four parts from medial to lateral:

1. Interstitial (intramural) – passes through uterine wall

2. Isthmus – narrow portion

3. Ampulla – widest part; site of fertilization

4. Infundibulum – funnel-shaped end opening into the peritoneal cavity with fimbriae

Therefore, the part that opens into the peritoneal cavity is:

✔ Infundibulum

This is the structure that picks up the ovulated oocyte using its fimbriae.

Why the other options are incorrect

❌ Interstitial / Intramural
Located inside the uterine wall; does not open into the peritoneal cavity.

❌ Isthmus
Narrow segment medial to ampulla; internal, not open-ended.

❌ Ampulla
Largest section, but not the opening into the peritoneal cavity.

❌ Isthmus
(Repeated) Also does not open externally.

The correct pathway of sperm from their site of storage to exiting the body is:

1️⃣ Epididymis

Sperm mature and are stored here.

2️⃣ Ductus (vas) deferens

Transports sperm during ejaculation.

3️⃣ Ejaculatory duct

Formed by the union of vas deferens + seminal vesicle duct; empties into urethra.

4️⃣ Penis

Sperm exit through the urethra during ejaculation.

So the order is:

✔ Epididymis → ductus deferens → ejaculatory duct → penis

Why the other options are incorrect

❌ Options with reversed or incorrect sequences
Many list vas deferens before epididymis or penis before the ducts — all anatomically incorrect.

The navicular fossa is a dilated portion of the spongy (penile) urethra located within the glans penis, just before the external urethral meatus.

Therefore, it lies in the:

✔ Terminal part of the penile urethra

Why the other options are incorrect

❌ Initial part of penile urethra
This lies near the bulb of the penis, not where the fossa is located.

❌ Intramural part of urethra
Short segment inside the bladder neck; no fossa here.

❌ Membranous urethra
Narrowest part, passes through urogenital diaphragm—no dilatation.

❌ Prostatic urethra
Contains sinuses and the ejaculatory duct openings—not the navicular fossa.

The perineal spaces are divided into:

• Superficial perineal pouch

• Deep perineal pouch

These two spaces are separated by the:

✔ Perineal membrane

(a strong fascial sheet that forms the inferior boundary of the deep pouch and the superior boundary of the superficial pouch)

This membrane is part of the urogenital triangle and plays a key role in supporting pelvic structures.

Why the other options are incorrect

❌ Urogenital diaphragm
Older term; relates to deep pouch contents but not the dividing structure itself.

❌ Perineal pouch
These are the spaces being divided, not the divider.

❌ Colles’ fascia
Forms the inferior boundary of the superficial pouch, not the divider.

❌ Skin
Superficial covering—not involved in division of perineal spaces.

The suspensory ligament of the ovary is also known as the:

✔ Infundibulopelvic ligament (IP ligament)

This ligament extends from the ovary to the lateral pelvic wall and contains:

• Ovarian vessels (artery & vein)

• Lymphatics

• Nerves

It is an important structure surgically because it must be ligated during oophorectomy to control bleeding.

Why the other options are incorrect

❌ Transverse ovarian ligament
Not an anatomical structure.

❌ Utero-ovarian ligament
Attaches the ovary to the uterus (medially), not the suspensory ligament.

❌ Pubocervical ligament
Supports the cervix, unrelated to ovarian suspension.

❌ Uterosacral ligament
Connects the uterus to the sacrum, part of pelvic support.

The conversion of testosterone → estradiol requires the enzyme:

✔ Aromatase (CYP19)

Aromatase is found primarily in:

• Granulosa cells of the ovary

• Adipose tissue

• Placenta

• Brain

It catalyzes the aromatization of the A-ring of androgens, converting them into estrogens.

Why the other options are incorrect

❌ Dehydrogenase
Involved in oxidation/reduction reactions, not estrogen synthesis.

❌ Oxygenase
General class of enzymes; not specific to this conversion.

❌ Isomerase
Changes molecular structure within a molecule; not applicable here.

❌ Lyase
Breaks chemical bonds without hydrolysis; does not produce estrogens.

Right after menstruation, the ovary enters the follicular (proliferative) phase.
During this time, estrogen levels rise rapidly.

✔ The major source of estrogen at this stage is the developing (growing) ovarian follicles, specifically their granulosa cells.

Under FSH stimulation:

• Theca cells make androgens

• Granulosa cells convert these androgens → estrogen via aromatase

This estrogen is responsible for:

• Regeneration and proliferation of the endometrium

• Preparation for ovulation

Why the other options are incorrect

❌ Anterior pituitary gland
Releases FSH and LH, but not estrogen.

❌ Stromal cells of ovaries
Do not produce significant estrogen.

❌ Corpus luteum
Produces progesterone and some estrogen, but only after ovulation, not at the end of menstruation.

❌ Endometrium
Responds to estrogen but does not produce it.

In a prepubertal girl, the ovaries contain:

✔ Primordial follicles

These are the earliest and most basic follicular structures, consisting of:

• A primary oocyte (arrested in prophase I)

• A single layer of flattened (squamous) follicular cells

These follicles remain dormant until puberty, when FSH stimulates some of them to begin maturing.

Why the other options are incorrect

❌ Primary follicles
A few may begin forming before puberty, but the dominant and characteristic follicle type in a young girl is the primordial follicle.

❌ Secondary follicles
These develop only after puberty, under hormonal stimulation.

❌ Atretic follicles
These occur mostly after puberty during the menstrual cycle.

❌ Secondary oocyte
This forms only after ovulation, which occurs after puberty.

This 22-year-old woman presents with the classic triad of PCOS:

1️⃣ Irregular periods

— due to anovulation

2️⃣ Weight gain

— associated with insulin resistance

3️⃣ Thickened facial hair (hirsutism)

— due to excess androgens

Together, these features strongly point toward PCOS, the most common endocrine disorder in reproductive-aged women.

Why the other options are incorrect

❌ Endometrial cancer
Occurs later in life; symptoms include postmenopausal bleeding, not hirsutism.

❌ Cervical dysplasia
Usually asymptomatic; linked to HPV infection and detected via Pap smear.

❌ Uterine fibroids
Cause heavy menstrual bleeding, pelvic pressure—not hirsutism or weight gain.

❌ Pelvic pain
A symptom, not a diagnosis; does not explain her hormonal features.

The testes originate in the abdomen during embryological development, near the kidneys.
Even after descending into the scrotum, they retain their original lymphatic drainage.

✔ Testicular lymph drains into

Para-aortic (lumbar) lymph nodes, located at L1–L2.

This is clinically important for:

• Testicular cancer staging

• Understanding patterns of metastasis

Why the other options are incorrect

❌ Superficial inguinal lymph nodes
Drain scrotal skin, penis, perineum—but not the testes.

❌ Deep inguinal lymph nodes
Drain deep tissues of the lower limb—not the testes.

❌ Femoral lymph nodes
Drain structures of the thigh—not testes.

❌ None of these
Incorrect, because para-aortic lymph nodes are correct.

A day-21 blood test is typically performed in women with a 28-day menstrual cycle to determine whether ovulation has occurred.

✔ The best indicator of an ovulatory cycle is:

Progesterone level on day 21

Why?

• Ovulation → formation of corpus luteum

• Corpus luteum → secretes progesterone

• Progesterone peaks around day 21 in a normal 28-day cycle

• High progesterone (>3–5 ng/mL) confirms ovulation

If the cycle is anovulatory, progesterone remains low.

Why the other options are incorrect

❌ FSH
Varies during cycle, not specific for ovulation.

❌ LH
LH surge precedes ovulation, but day-21 level does not reflect ovulation.

❌ Prolactin
Related to lactation; not relevant to ovulatory status unless pathologically high.

❌ Estradiol
High before ovulation but drops afterward; not reliable on day-21.

This 15-year-old girl presents with:

• Cyclical lower abdominal pain → suggests menstruation is occurring internally

• Suprapubic swelling → due to accumulated menstrual blood (hematometra/hematocolpos)

• Bluish bulge in the vestibule → classic sign of imperforate hymen

These clinical findings strongly indicate outflow obstruction, specifically:

✔ Imperforate hymen

A congenital condition where the hymen lacks an opening → menstrual blood cannot escape → causes:

• Cyclical pain

• Abdominal/pelvic swelling

• Bulging bluish membrane at hymen due to trapped blood (hematocolpos)

Why the other options are incorrect

❌ Congenital adrenal hyperplasia
Causes virilization; does not cause menstrual outflow obstruction or bluish bulging.

❌ XY gonadal dysgenesis (Swyer syndrome)
Patients do not menstruate at all (no cyclical pain and no hematocolpos).

❌ Müllerian agenesis (MRKH syndrome)
Absence of uterus and upper vagina → no menstruation, no blood retention, no bulge.

❌ Turner syndrome
Causes primary amenorrhea but no cyclic pain and no hematocolpos.

The ampulla of the fallopian tube is the most common site of ectopic pregnancy.

Why the ampulla?

• It is the widest part of the tube

• Fertilization normally occurs here

• If transport of the embryo is delayed, implantation may occur prematurely in the ampulla

Approximately 70–80% of ectopic pregnancies occur in this region.

Why the other options are incorrect

❌ Infundibulum
Accounts for a smaller percentage of tubal ectopics.

❌ Isthmus
Second most common site, but less than ampulla.

❌ Uterus
Normal site of implantation, not ectopic.

❌ Cervix
Rare site of ectopic implantation.

The platypelloid pelvis is characterized by:

• Wide transverse diameter

• Short anteroposterior (AP) diameter

• A flat, kidney-shaped inlet

This makes it the pelvis type in which the transverse diameter of the outlet is greater than the AP diameter.

It is the least common pelvic type and can be associated with labor difficulties due to the shortened AP dimension.

Why the other options are incorrect

❌ Dolicocephalic pelvis
Not a recognized obstetric pelvic type; refers to skull shape, not pelvis.

❌ Mesatipellic pelvis
Intermediate pelvis; balanced AP and transverse diameters.

❌ Gynecoid pelvis
The typical female pelvis—rounded, with better AP diameter; most favorable for childbirth.

❌ Android pelvis
Male-type pelvis—heart-shaped inlet, narrower transverse diameter.

✅ Correct Answer: Transpulmonary pressure

Explanation:

• Transpulmonary pressure (P_tp) is defined as the difference between alveolar pressure (P_A) and pleural pressure (P_pl):

• Role:
  • It is the pressure that keeps the lungs inflated and prevents collapse.
  • A positive transpulmonary pressure ensures lung distention during inspiration.
• Clinical relevance:
  • In conditions like pneumothorax, pleural pressure rises, reducing transpulmonary pressure, which can lead to lung collapse.

Why the other options are incorrect:

• Airway opening pressure: ❌
  → Pressure at the mouth or airway entry, does not directly distend the alveoli.
• Airway closing pressure: ❌
  → Pressure at which small airways collapse, relevant in atelectasis, not lung distention.
• Transthoracic pressure: ❌
  → Difference between alveolar and body surface pressure, reflects the chest wall contribution, not the lungs themselves.
• Alveolar pressure: ❌
  → Pressure inside alveoli, needs to be considered relative to pleural pressure to cause distention.