Reproductive Pathology — MCQs

Reproductive Pathology Indian Medical PG Practice Questions and MCQs

Question 111: Which of the following is NOT associated with arrhenoblastoma?

A. CD56
B. Call Exner bodies (Correct Answer)
C. Sex cord stromal tumor
D. Musculanising tumor

Explanation: **Explanation:** **Arrhenoblastoma** (also known as a **Sertoli-Leydig Cell Tumor**) is a rare sex cord-stromal tumor of the ovary [1]. The correct answer is **Call-Exner bodies**, as these are the pathognomonic histological hallmark of **Granulosa Cell Tumors**, not arrhenoblastomas. 1. **Why Call-Exner bodies is the correct answer:** Call-Exner bodies are small, gland-like spaces filled with eosinophilic material and basement membrane components, surrounded by granulosa cells. They are characteristic of adult-type Granulosa Cell Tumors. Their presence in a question regarding arrhenoblastoma represents a classic "distractor" between two different types of sex cord-stromal tumors. 2. **Analysis of Incorrect Options:** * **CD56:** This is a sensitive immunohistochemical marker for sex cord-stromal tumors, including Sertoli-Leydig cell tumors. * **Sex cord-stromal tumor:** Arrhenoblastoma belongs to this category of ovarian neoplasms, which arise from the ovarian mesenchyme (the precursors to Sertoli, Leydig, Granulosa, and Theca cells) [1]. * **Masculinizing tumor:** These tumors typically secrete androgens (testosterone). Clinically, patients present with **defeminization** (atrophy of breasts, amenorrhea) followed by **virilization** (hirsutism, clitoromegaly, and deepening of the voice) [1]. **High-Yield NEET-PG Pearls:** * **Reinke Crystals:** Characteristic rod-shaped inclusions found in the Leydig cell component of these tumors (though only present in about 35% of cases) [1]. * **DICER1 Mutation:** Frequently associated with moderately and poorly differentiated Sertoli-Leydig cell tumors. * **Tumor Marker:** Often associated with elevated **Alpha-fetoprotein (AFP)** in cases with heterologous elements (like hepatoid differentiation). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1037-1038.

Question 112: What is the most common malignant germ cell tumor of the testis?

A. Seminoma
B. Teratoma
C. Choriocarcinoma (Correct Answer)
D. Embryonal carcinoma

Explanation: **Explanation:** The question asks for the most common malignant germ cell tumor (GCT) of the testis. **1. Why the Correct Answer is Right:** **Seminoma (Option A)** is the most common malignant germ cell tumor of the testis, accounting for approximately 50% of all cases [1]. It typically occurs in the 4th decade of life and is characterized by a "fried-egg" appearance on histology (large cells with clear cytoplasm and central nuclei) and fibrous septa containing lymphocytic infiltrates. It is highly radiosensitive and has an excellent prognosis. **2. Why the Other Options are Wrong:** * **Teratoma (Option B):** In adults, pure teratomas are rare and usually considered malignant (unlike in females where they are often benign) [2]. They are less common than seminomas. * **Choriocarcinoma (Option C):** This is the **most aggressive** and highly malignant GCT, but it is the **least common** in its pure form (<1%) [4]. It is characterized by high levels of hCG and early hematogenous spread [4]. * **Embryonal Carcinoma (Option D):** This is a highly aggressive tumor that often presents as part of a mixed germ cell tumor [2]. While common in mixed forms, pure embryonal carcinoma is less frequent than pure seminoma. **3. NEET-PG High-Yield Pearls:** * **Most common GCT overall:** Seminoma [1]. * **Most common GCT in infants/children:** Yolk Sac Tumor (Endodermal Sinus Tumor); characterized by **Schiller-Duval bodies** and elevated **AFP**. * **Most common testicular tumor in elderly (>60 years):** Diffuse Large B-Cell Lymphoma (not a GCT). * **Tumor Marker for Seminoma:** Usually none, but 10% may show mildly elevated hCG (due to syncytiotrophoblasts) [3]. AFP is **never** elevated in pure seminoma. * **Reinke Crystals:** Pathognomonic for Leydig Cell Tumors (Sex cord-stromal tumor). *(Note: There appears to be a discrepancy in the provided prompt's key; medically, Seminoma is the most common, while Choriocarcinoma is the most aggressive/least common.)* **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 979-980. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 512-513. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 980-982. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, p. 982.

Question 113: A 32-year-old male presents with a few weeks' history of progressive breast tissue enlargement. On examination, a painless testicular mass is noted. Hormonal investigations reveal low serum LH and testosterone levels. What is the likely cause in this case?

A. Sertoli cell tumor (Correct Answer)
B. Spermatocytic tumor
C. Androgen resistance state
D. Gonadotropin-secreting tumor

Explanation: ### Explanation The clinical presentation of a **painless testicular mass** associated with **gynecomastia** and suppressed gonadotropins (low LH and testosterone) points toward a sex cord-stromal tumor [1], specifically a **Sertoli cell tumor**. **Why Sertoli Cell Tumor is correct:** Sertoli cell tumors are rare sex cord-stromal tumors. While most are hormonally silent, about 10-15% can produce **estrogens** (via aromatization of androgens) or **inhibin**. Excess estrogen leads to gynecomastia. The high estrogen levels exert **negative feedback** on the hypothalamus and pituitary, leading to the suppression of LH and FSH, which subsequently results in low endogenous testosterone levels. **Analysis of Incorrect Options:** * **B. Spermatocytic tumor:** Formerly called spermatocytic seminoma, these occur in older men (>50 years) and are typically hormonally inactive. They do not cause gynecomastia or LH suppression. * **C. Androgen resistance state:** While this causes gynecomastia, it is a congenital condition (not a new-onset mass) and typically presents with **high** LH and testosterone levels due to the lack of negative feedback at the pituitary level. * **D. Gonadotropin-secreting tumor:** These (like Choriocarcinoma) secrete **hCG**, which acts like LH [1]. This would lead to **high** testosterone levels, not low. **NEET-PG High-Yield Pearls:** * **Leydig Cell Tumors:** The most common sex cord-stromal tumor; often present with precocious puberty (in children) or gynecomastia (in adults) due to androgen/estrogen production [1]. Reinke crystals are the pathognomonic histological finding. * **Sertoli Cell Tumors:** Histologically characterized by hollow or solid tubules lined by columnar cells. * **Gynecomastia in Testicular Tumors:** Most commonly associated with Leydig cell tumors, Sertoli cell tumors, and hCG-secreting germ cell tumors (e.g., Choriocarcinoma) [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 510-514.

Question 114: Which of the following is NOT associated with breast cancer?

A. BRCA 1 & BRCA 2 mutations
B. Apocrine metaplasia (Correct Answer)
C. Atypical ductal hyperplasia
D. All of the above

Explanation: **Explanation:** The risk of developing breast cancer is categorized based on the histological findings of benign breast lesions [1]. **1. Why Apocrine Metaplasia is the correct answer:** Apocrine metaplasia is a feature of **Non-proliferative Breast Disease (Fibrocystic changes)** [1]. In this condition, the cuboidal epithelium of the acini undergoes transformation into large columnar cells with granular eosinophilic cytoplasm (resembling sweat glands). This change, along with simple cysts and fibrosis, carries **no increased risk (Relative Risk 1.0)** for developing invasive carcinoma. **2. Analysis of Incorrect Options:** * **BRCA 1 & BRCA 2 mutations:** These are high-penetrance germline mutations. BRCA1 (Chromosome 17q) and BRCA2 (Chromosome 13q) are tumor suppressor genes involved in DNA repair. Mutations significantly increase the lifetime risk of breast and ovarian cancer. * **Atypical Ductal Hyperplasia (ADH):** This falls under **Proliferative disease with atypia** [2]. It histologically resembles ductal carcinoma in situ (DCIS) but is limited in extent [2]. It carries a **high risk (Relative Risk 4.0–5.0)** of progressing to invasive cancer. **3. High-Yield Clinical Pearls for NEET-PG:** * **No Risk (RR 1.0):** Apocrine metaplasia, cysts, mild hyperplasia, fibroadenoma (without complex features). * **Slightly Increased Risk (RR 1.5–2.0):** Moderate to florid hyperplasia (without atypia), ductal papillomatosis, sclerosing adenosis. * **Significantly Increased Risk (RR 4.0–5.0):** Atypical ductal hyperplasia (ADH) and Atypical lobular hyperplasia (ALH) [2]. * **Highest Risk:** Carcinoma in situ (DCIS/LCIS) carries an RR of 8.0–10.0. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1052. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1054-1056.

Question 115: Koilocytes with perinuclear halo on Pap smear are pathognomic of which condition?

A. HPV infection (Correct Answer)
B. Metaplasia
C. Dysplasia
D. Bacterial vaginosis

Explanation: ### Explanation **Correct Answer: A. HPV infection** **Mechanism and Pathophysiology:** Koilocytes are the hallmark cytological feature of **Human Papillomavirus (HPV)** infection [1]. A koilocyte is a squamous epithelial cell that has undergone specific structural changes due to the viral E6 and E7 oncoproteins [2]. The characteristic **perinuclear halo** is a clear, sharply defined zone around the nucleus caused by the collapse of the cytoplasmic intermediate filaments (cytokeratin). This is accompanied by nuclear changes including enlargement, hyperchromasia, and an irregular "raisinoid" nuclear membrane. **Analysis of Incorrect Options:** * **B. Metaplasia:** Squamous metaplasia in the cervix is a physiological replacement of columnar epithelium with squamous epithelium at the transformation zone. It shows mature squamous cells without the viral nuclear atypia or halos. * **C. Dysplasia:** While HPV causes dysplasia (CIN), koilocytes specifically represent the **cytopathic effect** of the virus, typically seen in Low-grade Squamous Intraepithelial Lesions (LSIL) [1]. High-grade dysplasia (HSIL) often shows more profound nuclear atypia with a loss of the koilocytic halo [1]. * **D. Bacterial Vaginosis:** This is characterized by **"Clue cells"**—squamous epithelial cells covered by coccobacilli (*Gardnerella vaginalis*), giving them a fuzzy, "granular" appearance, not a clear perinuclear halo. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic feature:** Koilocytes = HPV (primarily types 6, 11 for warts; 16, 18 for malignancy). * **Nuclear/Cytoplasmic ratio:** In koilocytes, the N:C ratio is increased compared to normal cells [1]. * **Fried-egg appearance:** Sometimes used to describe the appearance of koilocytes in histology. * **Bethesda System:** Koilocytosis is categorized under **LSIL** (Low-grade Squamous Intraepithelial Lesion) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, p. 1010. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1007-1008.

Question 116: Singnet ring appearance in an ovarian tumour is characteristic of which of the following?

A. Krukenberg's tumour (Correct Answer)
B. Dysgerminoma
C. Granulosa cell carcinoma
D. Papillary cystadenocarcinoma

Explanation: **Explanation:** **Krukenberg’s tumour** is a metastatic signet ring cell carcinoma of the ovary, most commonly originating from a primary site in the **stomach** (diffuse type gastric adenocarcinoma) [1]. The characteristic **"signet-ring" appearance** occurs because intracellular mucin accumulates in the cytoplasm, pushing the nucleus to the periphery of the cell [1]. These tumors are typically bilateral and involve a diffuse infiltration of the ovarian stroma. **Analysis of Incorrect Options:** * **Dysgerminoma:** This is the female counterpart of a seminoma. Histologically, it features large, clear cells with central nuclei and prominent nucleoli, arranged in nests separated by fibrous septa containing lymphocytes. * **Granulosa cell carcinoma:** This sex cord-stromal tumor is characterized by **Call-Exner bodies** (small follicles filled with eosinophilic material) and "coffee-bean" nuclei (longitudinal nuclear grooves) [3]. * **Papillary cystadenocarcinoma:** This is a common surface epithelial tumor. It is characterized by complex papillary projections and the presence of **Psammoma bodies** (laminated calcifications), not signet ring cells [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Site:** While the stomach is the most common primary (70%), Krukenberg tumors can also arise from the colon, breast, or appendix. * **Route of Spread:** Classically thought to be via retrograde lymphatic spread rather than peritoneal seeding. * **Stain:** Signet ring cells are positive for mucin stains like **PAS (Periodic Acid-Schiff)** or **Mucicarmine**. * **Bilateralism:** Krukenberg tumors are almost always bilateral, a key feature distinguishing them from primary ovarian cancers. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 478-480. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 481-482.

Question 117: What defines true hermaphroditism?

A. Presence of both ovarian and testicular tissues (Correct Answer)
B. Presence of both male and female external genitalia
C. Behavioral sex incongruence with chromosomal sex
D. None of the above

Explanation: **Explanation:** **True Hermaphroditism** (now clinically termed **Ovotesticular Disorder of Sex Development**) is defined strictly by the histological presence of **both ovarian and testicular tissue** in the same individual. This can occur in three patterns: 1. **Lateral:** A testis on one side and an ovary on the other. 2. **Bilateral:** Ovotestes (gonads containing both elements) on both sides. 3. **Unilateral:** An ovotestis on one side and an ovary or testis on the other. **Analysis of Options:** * **Option A (Correct):** The defining feature is the gonadal tissue, not the external appearance. The most common karyotype is **46,XX** (approx. 60%), followed by mosaicism (e.g., 46,XX/46,XY). * **Option B (Incorrect):** Ambiguous external genitalia are common in many Disorders of Sex Development (DSDs), such as Congenital Adrenal Hyperplasia (Female Pseudohermaphroditism) or Androgen Insensitivity Syndrome (Male Pseudohermaphroditism), and are not pathognomonic for true hermaphroditism. * **Option C (Incorrect):** This describes **Gender Dysphoria** or gender identity disorders, which are psychological/behavioral and not defined by gonadal histology. **High-Yield Clinical Pearls for NEET-PG:** * **Most common karyotype:** 46,XX. * **Most common gonad:** The **Ovotestis** is the most frequent finding. * **Internal structures:** Usually follow the adjacent gonad (e.g., a fallopian tube is present on the side of an ovary). * **Malignancy risk:** There is an increased risk of **gonadoblastoma**, especially if a Y chromosome is present. * **Distinction:** Pseudohermaphroditism is defined by a mismatch between *chromosomal/gonadal sex* and *phenotypic sex* (e.g., a 46,XX individual with ovaries but virilized external genitalia).

Question 118: An obese diabetic woman presents with menorrhagia. Endometrial biopsy demonstrates endometrial carcinoma. What is the most probable gene associated with this carcinoma?

A. PTEN (Correct Answer)
B. TP53
C. CDH4
D. C-myc

Explanation: **Explanation:** The clinical presentation of an **obese, diabetic woman** with **menorrhagia** and endometrial carcinoma points toward **Type I (Endometrioid) Endometrial Carcinoma**. This is the most common type of endometrial cancer, typically arising in the setting of excess estrogen (unopposed by progesterone), often seen in obesity due to the peripheral conversion of androgens to estrone [1]. **1. Why PTEN is correct:** The **PTEN (Phosphatase and Tensin homolog)** tumor suppressor gene is the most frequently mutated gene in Type I Endometrioid Carcinoma (occurring in 30-80% of cases). PTEN normally inhibits the PI3K/AKT signaling pathway; its loss leads to increased cell proliferation and survival. PTEN mutations are also frequently found in the precursor lesion, **Endometrial Intraepithelial Neoplasia (EIN)** [1]. **2. Why other options are incorrect:** * **TP53:** Mutations in TP53 are the hallmark of **Type II (Serous) Endometrial Carcinoma**, which occurs in older, thin women, is not estrogen-dependent, and carries a much poorer prognosis [1]. * **CDH4:** This gene (encoding R-cadherin) is not a primary driver in endometrial carcinoma. However, loss of **E-cadherin (CDH1)** is associated with EMT and metastasis in various cancers. * **C-myc:** While an oncogene involved in many cancers, it is not the specific diagnostic molecular marker for Type I endometrial carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Type I Endometrioid Carcinoma:** Associated with PTEN, KRAS, and Microsatellite Instability (MSI). Linked to obesity, diabetes, and hypertension (the "Corpus Cancer Syndrome") [1]. * **Type II Endometrial Carcinoma:** Associated with TP53 mutations and p16 overexpression. Arises from atrophic endometrium [1]. * **Cowden Syndrome:** A germline mutation in **PTEN** that increases the risk of endometrial, breast, and thyroid cancers. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1016-1022.

Question 119: Which of the following causes orchitis without epididymitis?

A. Syphilis (Correct Answer)
B. Tuberculosis
C. Gonorrhoea
D. Chlamydia trachomatis

Explanation: In male reproductive pathology, the route of infection is the key to distinguishing between different types of inflammatory conditions. [1] **Why Syphilis is the correct answer:** Syphilis (caused by *Treponema pallidum*) is unique because it typically involves the **testis first**, often sparing the epididymis. [1] This occurs because the infection is **hematogenous** (spread via the bloodstream). In the late stages (Tertiary Syphilis), it manifests as either a diffuse interstitial inflammation with plasma cell infiltration or as a "Gumma"—a localized area of coagulative necrosis. **Why the other options are incorrect:** * **Gonorrhoea and Chlamydia (Options C & D):** These are the most common causes of scrotal inflammation in men under 35. [1] They follow an **ascending route** of infection (from the urethra to the vas deferens). [2] Consequently, they always cause **epididymitis first**, which may later spread to the testis (epididymo-orchitis). [1] * **Tuberculosis (Option B):** Similar to pyogenic bacteria, TB typically involves the **epididymis first**. [1] It presents with classic granulomatous inflammation and caseous necrosis. While it can spread to the testis, isolated orchitis without epididymal involvement is not seen. **NEET-PG High-Yield Pearls:** * **Rule of Thumb:** Most bacterial infections (E. coli, Gonorrhoea, TB) affect the **Epididymis first**. [1] * **Exceptions:** **Syphilis** and **Mumps** are the two classic conditions that cause **Orchitis first** (Primary Orchitis). [1], [3] * **Mumps Orchitis:** Usually occurs in post-pubertal males; it is typically unilateral but can lead to seminiferous tubule atrophy and infertility if bilateral. [3] * **Microscopic Hallmark of Syphilis:** Obliterative endarteritis with a prominent plasma cell infiltrate. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 977-978. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 515-516. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 509-510.

Question 120: What is the most common type of testicular tumor?

A. Seminoma (Correct Answer)
B. Teratoma
C. Sertoli cell tumor
D. Choriocarcinoma

Explanation: **Explanation:** Testicular tumors are broadly classified into **Germ Cell Tumors (GCTs)**, which account for approximately 95% of all cases, and Sex Cord-Stromal Tumors [1]. **Why Seminoma is correct:** Among all testicular neoplasms, **Seminoma** is the most common single histological type, accounting for roughly 50% of all germ cell tumors [1]. It typically occurs in the 4th decade of life (ages 30–40). Grossly, it presents as a bulky, painless, homogenous gray-white mass without hemorrhage or necrosis. Microscopically, it is characterized by "clear cells" (due to cytoplasmic glycogen) arranged in lobules separated by fibrous septa containing lymphocytic infiltrates [2]. **Why the other options are incorrect:** * **Teratoma:** While common in children (pre-pubertal), it is less frequent than seminomas in adults [1]. In adults, pure teratomas are rare and are often part of a "Mixed Germ Cell Tumor" [3]. * **Sertoli cell tumor:** These fall under Sex Cord-Stromal tumors. They are rare (approx. 1%) and usually benign, making them significantly less common than GCTs. * **Choriocarcinoma:** This is the most aggressive but also one of the rarest pure forms of testicular GCT [5]. It is characterized by high levels of hCG and early hematogenous spread [5]. **High-Yield Clinical Pearls for NEET-PG:** * **Tumor Markers:** Seminomas are usually negative for AFP and hCG (though 10% may show mild hCG elevation) [2]. **AFP is never elevated in a pure seminoma.** * **Radiosensitivity:** Seminomas are highly radiosensitive and have the best prognosis among GCTs. * **Risk Factor:** Cryptorchidism (undescended testis) is the most significant risk factor. * **Equivalent:** The ovarian counterpart of a Seminoma is the **Dysgerminoma** [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 979-980. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 980-982. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 512-513. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1140-1141. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, p. 982.

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Diseases of Male Genital Tract

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Testicular Tumors

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Cervical Pathology and Neoplasia

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Endometrial Pathology

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Ovarian Diseases and Tumors

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Gestational Trophoblastic Disease

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Placental Pathology

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Sexually Transmitted Infections

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