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Male & Female Genital Tract - High Yield Topics

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MALE GENITAL TRACT

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🧬 MIND MAP: Male Genital Tract Overview

MALE GENITAL TRACT
├── PENIS
│   ├── Congenital: Hypospadias (ventral) / Epispadias (dorsal)
│   ├── Phimosis → tight prepuce → ↑ smegma → ↑ carcinoma risk
│   ├── Balanoposthitis (Candida, anaerobes, Gardnerella)
│   └── Tumors
│       ├── Benign: Condyloma acuminatum (HPV 6, 11)
│       └── Malignant: Squamous cell carcinoma
│           ├── HPV-unrelated (verrucous, usual type SCC)
│           └── HPV-related (basaloid, warty)
├── TESTIS & EPIDIDYMIS
│   ├── Congenital: Cryptorchidism
│   ├── Inflammation (epididymis > testis)
│   └── Tumors (95% germ cell)
│       ├── Seminoma (50% of GCTs)
│       ├── Embryonal carcinoma
│       ├── Yolk sac tumor
│       ├── Choriocarcinoma
│       ├── Teratoma
│       └── Spermatocytic tumor (>65y, benign)
└── PROSTATE
    ├── Prostatitis (bacterial, granulomatous)
    ├── BPH (transition zone)
    └── Adenocarcinoma (peripheral zone)

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🗺️ PROSTATE ANATOMY DIAGRAM

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📊 FLOWCHART: Cryptorchidism

Cryptorchidism (undescended testes)
         │
         ▼
  1% of boys at age 1
         │
    ┌────┴────────────────────────────────┐
    │                                     │
Phase 1: Transabdominal descent     Phase 2: Inguinoscrotal descent
  (Mullerian-inhibiting substance)    (Androgen-dependent, CGRP-mediated)
    │                                     │
    └────────────┬────────────────────────┘
                 │
        Arrest anywhere → most common site: inguinal canal
                 │
         ┌───────┴────────────────────┐
         │                            │
  Complications:                Associated with:
  • ↑ testicular cancer (25x)    • Prader-Willi syndrome
  • ↓ fertility                  • Noonan syndrome
  • Torsion                      • Hypospadias

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📋 FLOWCHART: Testicular Germ Cell Tumors (GCTs)

Primordial Germ Cells
         │
         ▼
  Germ Cell Neoplasia In Situ (GCNIS) ──────────────────────────────┐
         │                                                            │
         ▼                                                    NOT associated
  Postpubertal GCTs (type 1)                              Spermatocytic tumor
  Associated with i(12p)                                   (>65y, benign)
         │
    ┌────┴──────────────────────────────────────────┐
    │                                               │
 SEMINOMA (50%)                            NON-SEMINOMATOUS
 4th decade                                        │
 Homogeneous gray-white mass               ┌───────┴──────────────────────┐
 Lymphocytic infiltrate                    │           │                   │
 KIT+, OCT3/4+, podoplanin+        Embryonal Ca  Yolk Sac Tumor    Choriocarcinoma
 hCG mildly ↑ if syncytiotrophoblasts  AFP+        AFP ↑↑           hCG ↑↑↑
                                       CD30+       Schiller-         Hemorrhagic
                                                   Duval bodies      necrosis
                                               │
                                           Teratoma
                                           (mature/immature)
                                           AFP variable

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📊 GLEASON GRADING SYSTEM (Prostate Cancer)

GLEASON GRADE GROUPS
┌─────────────────┬──────────────────────────────────────────────────────────┐
│ Grade Group 1   │ Score ≤6: Well-formed discrete glands only               │
│ Grade Group 2   │ Score 3+4: Predominantly well-formed + minor poorly formed│
│ Grade Group 3   │ Score 4+3: Predominantly poorly formed + minor well-formed│
│ Grade Group 4   │ Score 4+4/3+5/5+3: Only poorly formed/fused/cribriform   │
│ Grade Group 5   │ Score 4+5/5+5: No gland formation (sheets of cells)      │
└─────────────────┴──────────────────────────────────────────────────────────┘

• Originates in peripheral zone - palpable on DRE
• No capsule on prostate - so pT2 = organ confined, pT3a = extraprostatic extension, pT3b = seminal vesicle invasion
• Metastases: osteoblastic bone lesions (spine, pelvis)
• Hormonal therapy targets androgen receptor (castration-sensitive vs castration-resistant)

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FEMALE GENITAL TRACT

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🧬 MIND MAP: Female Genital Tract Overview

FEMALE GENITAL TRACT
├── INFECTIONS (Lower → Upper)
│   ├── HSV-2 (latent in sacral ganglia, recurrent ulcers)
│   ├── HPV (6,11 → condyloma; 16,18 → cancer)
│   └── PID (N. gonorrhoeae, C. trachomatis → upper tract)
│       └── Complications: Infertility, ectopic pregnancy, TOA, Fitz-Hugh-Curtis
├── VULVA
│   ├── Lichen sclerosus (↑ SCC risk, white plaques, older women)
│   ├── Lichen simplex chronicus (thickening, pruritus)
│   ├── VIN → Vulvar carcinoma (2 pathways: HPV-related & HPV-independent)
│   └── Extramammary Paget disease (intraepithelial adenocarcinoma)
├── VAGINA
│   ├── VAIN → SCC (HPV-related)
│   ├── Clear cell adenocarcinoma (DES exposure in utero)
│   └── Sarcoma botryoides (embryonal RMS - children <5y, "grapelike")
├── CERVIX
│   ├── Squamocolumnar junction (transformation zone) - MOST SUSCEPTIBLE
│   ├── Cervicitis (HPV, Chlamydia, Gonorrhea)
│   ├── LSIL → HSIL → Invasive SCC (HPV-driven)
│   └── Cervical adenocarcinoma (endocervical glands)
├── UTERUS
│   ├── Leiomyoma (most common tumor in women, MED12 mutations)
│   ├── Endometrial hyperplasia → Type I carcinoma (estrogen-driven)
│   │   ├── Without atypia (minimal risk)
│   │   └── Atypical hyperplasia / EIN (↑↑ risk → endometrioid carcinoma)
│   ├── Endometrioid carcinoma (Type I: estrogen, PTEN/PIK3CA mutations)
│   ├── Serous carcinoma (Type II: TP53 mutation, aggressive)
│   └── Carcinosarcoma / Mixed Mullerian tumor
├── FALLOPIAN TUBES
│   ├── Salpingitis → PID → Pyosalpinx / Hydrosalpinx
│   └── STIC (serous tubal intraepithelial carcinoma) → source of high-grade serous ovarian ca
└── OVARIES
    ├── Functional cysts (follicular, luteal)
    ├── PCOS (polycystic ovaries + anovulation + hyperandrogenism)
    ├── Epithelial tumors (65-70%) - see flowchart below
    ├── Germ cell tumors (15-20%)
    └── Sex cord-stromal tumors (5-10%)

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📊 FLOWCHART: HPV → Cervical Cancer Pathway

HPV INFECTION (high-risk: 16, 18, 31, 33)
         │
         ▼
E6 → degrades p53 (↑ genomic instability)
E7 → inactivates Rb (↑ cell cycle progression)
         │
         ▼
   TRANSFORMATION ZONE
   (immature squamous metaplasia most susceptible)
         │
    ┌────┴──────────────────────┐
    │                           │
  LSIL                        HSIL
(CIN 1)                   (CIN 2, 3)
  Low-grade,              High-grade,
  productive              progressive
  HPV infection           deregulation
  Usually regresses     May → Invasive
         │                   Carcinoma
         └──────────────────────┘
                  │
          INVASIVE CARCINOMA
          (Squamous cell >> Adenocarcinoma)
          Spreads: local invasion → lymphatics
          → parametrium → bladder/rectum

• Pap smear (cytology) - detects LSIL/HSIL
• HPV co-testing - detects high-risk HPV types
• Colposcopy → biopsy if abnormal

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📊 FLOWCHART: Endometrial Carcinoma - Two Pathways

ENDOMETRIAL CARCINOMA
         │
    ┌────┴──────────────────────────┐
    │                               │
TYPE I (Endometrioid)           TYPE II (Serous)
~80% of cases                    ~10-15% of cases
         │                               │
Estrogen-driven                 Not estrogen-driven
Obesity, PCOS, anovulation      Atrophic endometrium
Prolonged estrogen use          Older women
         │                               │
PTEN mutation (30-80%)          TP53 mutation
PIK3CA, KRAS mutations          HER2 amplification
         │                               │
Preceded by:                    Preceded by:
Endometrial hyperplasia         EIC (endometrial
(atypical = EIN)                intraepithelial
                                carcinoma)
         │                               │
Well-differentiated             Poorly differentiated
Favorable prognosis             Worse prognosis
(Stage I: 90% 5-yr survival)    Spreads early

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🗺️ OVARIAN TUMOR PATHOGENESIS DIAGRAM

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📋 MIND MAP: Ovarian Tumors Classification

OVARIAN TUMORS
├── EPITHELIAL TUMORS (65-70%)
│   ├── Serous (most common epithelial)
│   │   ├── Type I (Low-grade): KRAS/BRAF mutations; borderline → invasive
│   │   └── Type II (High-grade): TP53 mutation; STIC → aggressive
│   ├── Mucinous (pseudomyxoma peritonei if ruptures)
│   ├── Endometrioid (associated with endometriosis)
│   ├── Clear cell carcinoma
│   └── Brenner (transitional cell type; usually benign)
│
├── GERM CELL TUMORS (15-20%)
│   ├── Teratoma
│   │   ├── Mature cystic (dermoid cyst) - BENIGN (hair, teeth, sebaceous material)
│   │   ├── Immature teratoma - MALIGNANT (primitive neuroepithelium)
│   │   └── Monodermal: Struma ovarii (thyroid → hyperthyroidism)
│   │                  Carcinoid (5-HT → carcinoid syndrome without liver mets)
│   ├── Dysgerminoma (= testicular seminoma; KIT mutations, OCT3/4+, i(12p))
│   ├── Yolk sac tumor (AFP ↑↑, Schiller-Duval bodies)
│   └── Choriocarcinoma (hCG ↑↑)
│
└── SEX CORD-STROMAL TUMORS (5-10%)
    ├── Granulosa cell tumor
    │   ├── Estrogen-secreting → endometrial hyperplasia/carcinoma
    │   ├── Call-Exner bodies (coffee bean nuclei)
    │   └── FOXL2 mutation (adult type)
    ├── Fibroma / Thecoma (Meigs syndrome: fibroma + ascites + pleural effusion)
    └── Sertoli-Leydig cell tumor
        ├── Androgen-secreting → virilization
        └── DICER1 mutation

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📊 FLOWCHART: Ovarian Tumor - Clinical Clues

PATIENT PRESENTATION
         │
    ┌────┴────────────────────────────────────────┐
    │                          │                   │
 HORMONAL EFFECTS         MASS EFFECT           TUMOR MARKERS
    │                          │                   │
 Estrogen excess:         Pelvic pain,          CA-125: epithelial
 • Precocious puberty       bloating,              (serous >> mucinous)
 • Endometrial hyper        constipation          AFP: germ cell
 • Postmenopausal                                  (YST, immature teratoma)
   bleeding                                       hCG: choriocarcinoma,
                                                   dysgerminoma
 Androgen excess:                                 Inhibin: granulosa cell
 • Virilization                                   LDH: dysgerminoma

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📊 FLOWCHART: Pelvic Inflammatory Disease (PID)

CAUSATIVE ORGANISMS
         │
    ┌────┴───────────────────────────────┐
    │                                    │
N. gonorrhoeae                  C. trachomatis
(primary ascent)                (primary ascent)
    │                                    │
    └────────────┬───────────────────────┘
                 ▼
         ENDOMETRITIS → SALPINGITIS
                 │
         ┌───────┴──────────────────────┐
         │                              │
   Acute salpingitis              Chronic salpingitis
   (pus in lumen,                 (plicae adhere → fuse →
   edematous plicae)              glandlike spaces)
         │                              │
         ▼                              ▼
   Pyosalpinx                    SEQUELAE:
   Hydrosalpinx                  • Infertility
   Tubo-ovarian abscess (TOA)    • Ectopic pregnancy
                                 • Pelvic pain
                                 • Intestinal obstruction
         │
   Fitz-Hugh-Curtis syndrome
   (perihepatitis - RUQ pain
   from gonococcal/chlamydial
   peritoneal spread to liver
   capsule)

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📊 LEIOMYOMA vs LEIOMYOSARCOMA

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📋 KEY CONCEPTS QUICK TABLE - High Yield

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📊 FLOWCHART: Gestational Trophoblastic Disease (GTD)

ABNORMAL PREGNANCY
         │
    ┌────┴──────────────────────────────┐
    │                                   │
COMPLETE MOLE                   PARTIAL MOLE
46,XX (all paternal)            69,XXY (triploid)
No fetus, no amnion             Fetal tissue present
Snowstorm on US                 Less hCG rise
↑↑↑ hCG                       ↓ malignant potential
↑ risk choriocarcinoma                │
         │                            │
         └───────────────┬────────────┘
                         │
                 Choriocarcinoma
                 (hCG ↑↑↑, hemorrhagic,
                  hematogenous spread -
                  lungs, brain, liver)
                  HIGHLY CHEMO-SENSITIVE
                  Cure rate >90%

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🔑 REMEMBER ASSOCIATIONS (High Yield Mnemonics)

• Choriocarcinoma → hCG
• Ovarian fibroma → Meigs (pleural effusion + ascites)
• Mucinous cystadenoma → pseudomyxoma peritonei (appendix connection)
• Endometrioid → associated with endometriosis
• Granulosa cell → estrogen → endometrial hyperplasia
• Epithelioid tumors = most common ovarian cancers
• Teratoma (dermoid) = most common BENIGN ovarian germ cell
• Serous = most common ovarian MALIGNANT epithelial tumor

• BPH: Transition zone, TURP treatment, Temperature changes (DHT)
• Ca: Peripheral zone, PSA, Postatic acid Phosphatase (PAP), Painful osteoblastic mets

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Top 3 High-Yield Female Genital Tract Topics - Robbins

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TOPIC 1: CERVICAL CARCINOMA

🧬 Mind Map: Cervical Carcinoma

CERVICAL CARCINOMA
│
├── ANATOMY (Key Starting Point)
│   ├── Ectocervix → mature squamous epithelium (RESISTANT to HPV)
│   ├── Endocervix → columnar mucus-secreting cells
│   ├── Squamocolumnar junction = where they meet
│   └── TRANSFORMATION ZONE = where columnar is replaced by
│       squamous metaplasia → MOST SUSCEPTIBLE to HPV
│
├── PATHOGENESIS
│   ├── High-risk HPV (15 types total)
│   │   ├── HPV-16 → 60% of cervical cancers
│   │   ├── HPV-18 → 10% of cervical cancers
│   │   └── Others (31, 33, 45, 52, 58) each <5%
│   ├── E6 protein → binds & degrades p53 (via proteasome)
│   │                → upregulates TELOMERASE → immortalization
│   └── E7 protein → degrades RB + inhibits p21, p27
│                  → cell cycle deregulation
│
├── PRECURSOR LESIONS (SIL)
│   ├── LSIL (CIN 1) = productive HPV infection → usually REGRESSES
│   └── HSIL (CIN 2, 3) = cell cycle deregulation → may progress
│
├── INVASIVE CARCINOMA
│   ├── Squamous cell carcinoma (majority)
│   └── Adenocarcinoma (endocervical gland origin)
│
├── SPREAD
│   ├── Direct: parametrium → bladder/rectum
│   └── Death from ureteral obstruction → pyelonephritis → uremia
│       (NOT usually from distant mets)
│
├── SCREENING
│   ├── Pap test (first at age 21, then q3y)
│   ├── HPV DNA testing (added from age 30, q5y co-test)
│   └── Colposcopy + biopsy if abnormal
│
└── PREVENTION
    └── HPV vaccine → 81% drop in HPV infections,
        40% reduction in SIL

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📸 Textbook Image: Squamocolumnar Junction (Transformation Zone)

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📸 Textbook Image: Pap Smear Cytology Spectrum

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📊 Flowchart: HPV → Cervical Cancer Step by Step

HPV (high-risk: 16, 18) infects
IMMATURE cells at transformation zone
              │
              ▼
   Viral DNA initially EPISOMAL
   (extrachromosomal) in precursor lesions
              │
              ▼
   Virus INTEGRATES into host genome
   → ↑↑ E6 and E7 expression
   → MYC dysregulation at insertion sites
              │
      ┌───────┴──────────────────────┐
      │                              │
   E6 acts on p53                E7 acts on RB
   → proteasomal degradation     → proteasomal degradation
   → ↑ telomerase                → also inhibits p21, p27
   → no apoptosis                → cells bypass G1 arrest
      │                              │
      └───────────────┬──────────────┘
                      ▼
        ↑ Cell proliferation + ↓ DNA repair
                      │
                      ▼
              LSIL (CIN 1)
         (productive infection, koilocytes)
                      │
               most REGRESS
                      │
              (persistent infection)
                      ▼
              HSIL (CIN 2, 3)
         (progressive atypia, full thickness)
                      │
              (untreated, months-years)
                      ▼
           INVASIVE SQUAMOUS CELL CARCINOMA
           (breaks through basement membrane)

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🔑 Key Concepts Box: Cervical SIL & Carcinoma

• Superficially invasive (microinvasive): 5-yr survival 100%
• Stage I/II confined to pelvis: good prognosis
• Beyond pelvis: <20% 5-year survival

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TOPIC 2: ENDOMETRIAL CARCINOMA

🧬 Mind Map: Endometrial Carcinoma

ENDOMETRIAL CARCINOMA
│
├── EPIDEMIOLOGY
│   ├── Most common gynecologic malignancy in developed world
│   ├── Peak incidence: postmenopausal (55-65 years)
│   ├── Symptom: POSTMENOPAUSAL BLEEDING → early detection
│   └── Lynch syndrome: 3-5% of endometrial cancers
│       (DNA mismatch repair gene mutations → ALSO high colon ca risk)
│
├── TYPE I: ENDOMETRIOID CARCINOMA (~80%)
│   │
│   ├── RISK FACTORS (all = excess estrogen)
│   │   ├── Obesity → peripheral conversion of androgens → estrogens
│   │   ├── Polycystic ovary syndrome (PCOS) → anovulation
│   │   ├── Functioning granulosa cell tumor → estrogen secretion
│   │   ├── Exogenous estrogen (HRT without progesterone)
│   │   └── Nulliparity, late menopause
│   │
│   ├── PRECURSOR: Endometrial Hyperplasia
│   │   ├── Without atypia: ↑ gland-to-stroma ratio (minimal cancer risk)
│   │   └── Atypical hyperplasia (EIN): crowded glands + cytologic atypia
│   │       → 30% progress to carcinoma if untreated
│   │
│   ├── MOLECULAR ALTERATIONS
│   │   ├── PTEN mutation (30-80%) → ↑ PI3K/AKT → EARLIEST alteration
│   │   ├── PIK3CA mutation
│   │   ├── KRAS mutation
│   │   ├── DNA mismatch repair defects (MSI)
│   │   └── POLE mutation (proofreading defect → ultra-mutated)
│   │
│   └── MORPHOLOGY
│       ├── Grade 1: Well-formed glands, <5% solid areas
│       ├── Grade 2: 5-50% solid areas
│       └── Grade 3: >50% solid areas (highest risk)
│
└── TYPE II: SEROUS CARCINOMA (~10-15%)
    │
    ├── Background: Atrophic endometrium (NOT estrogen-related)
    ├── Older women than Type I
    │
    ├── PRECURSOR: Endometrial Intraepithelial Carcinoma (EIC)
    │   (malignant cells confined to surface epithelium)
    │
    ├── MOLECULAR
    │   ├── TP53 mutation (>90%) → early, present in EIC
    │   ├── HER2 amplification
    │   └── Chromosomal instability + copy number alterations
    │
    └── BEHAVIOR
        ├── Exfoliates → travels through fallopian tubes → peritoneal spread
        ├── ALL classified as HIGH-GRADE (regardless of architecture)
        └── Poor prognosis even with superficial involvement

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📊 Flowchart: Two-Pathway Model of Endometrial Carcinoma

      ESTROGEN EXCESS                    ATROPHIC ENDOMETRIUM
     (obesity, PCOS, HRT)               (older postmenopausal)
            │                                    │
            ▼                                    ▼
   ENDOMETRIAL HYPERPLASIA              ENDOMETRIAL INTRAEPITHELIAL
   (without atypia → minimal risk)       CARCINOMA (EIC)
            │                                    │
            ▼                                    │
   ATYPICAL HYPERPLASIA (EIN)                   │
   PTEN mutation early                          │
            │                                    │
            ▼                                    ▼
   TYPE I CARCINOMA                    TYPE II CARCINOMA
   (Endometrioid)                      (Serous)
   PTEN, PIK3CA, KRAS                  TP53 >90%, HER2
   Well-differentiated                 Always high-grade
   Favorable prognosis                 Peritoneal spread early
   Stage I: ~90% 5-yr survival         Poor prognosis

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📸 Textbook Image: Endometrioid Carcinoma Gross & Histology

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📋 Staging of Endometrial Carcinoma

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🔑 Key Differentiator: Endometrioid vs Serous

---

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TOPIC 3: OVARIAN TUMORS

🧬 Master Mind Map: Ovarian Tumors

OVARIAN TUMORS (WHO Classification)
│
├── EPITHELIAL TUMORS (65-70%) ← Most common overall
│   ├── Serous (most common epithelial)
│   │   ├── Low-grade (Type I): KRAS/BRAF mutations
│   │   │   cystadenoma → borderline → low-grade carcinoma
│   │   └── High-grade (Type II): TP53 mutation
│   │       BRCA1/2 (hereditary) → STIC → carcinoma
│   ├── Mucinous → pseudomyxoma peritonei if ruptures
│   ├── Endometrioid → associated with endometriosis
│   ├── Clear cell → worst prognosis in advanced stage
│   └── Brenner (transitional) → usually benign, urothelium-like nests
│
├── GERM CELL TUMORS (15-20%) ← Most common in young women/girls
│   ├── Mature cystic teratoma (DERMOID CYST) → MOST COMMON benign
│   │   46,XX karyotype; hair, teeth, sebum; 1% → malignant (SCC)
│   ├── Immature teratoma → MALIGNANT, young women (mean age 18)
│   │   primitive neuroepithelium; graded I-III
│   ├── Dysgerminoma → = testicular seminoma
│   │   KIT mutation, i(12p), OCT3/4+; radiosensitive
│   ├── Yolk sac tumor → AFP ↑↑↑, Schiller-Duval bodies
│   └── Choriocarcinoma → hCG ↑↑↑, poor response to chemo
│
└── SEX CORD-STROMAL TUMORS (5-10%) ← Functionally active
    ├── Granulosa cell tumor
    │   ├── ESTROGEN secreting → endometrial hyperplasia
    │   ├── Call-Exner bodies (coffee bean nuclei, rosettes)
    │   ├── FOXL2 mutation (adult type)
    │   └── Inhibin marker
    ├── Fibroma / Thecoma
    │   └── MEIGS SYNDROME: fibroma + ascites + right pleural effusion
    └── Sertoli-Leydig cell tumor
        ├── ANDROGEN secreting → virilization
        └── DICER1 mutation

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📸 Textbook Image: Ovarian Epithelial Tumor Pathogenesis Diagram

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📊 Flowchart: Ovarian Epithelial Tumors - Type I vs Type II

        TYPE I PATHWAY                    TYPE II PATHWAY
    (Slow, step-wise)                 (Rapid, de novo)
           │                                 │
    ENDOMETRIOSIS /                  FALLOPIAN TUBE FIMBRIAE
    CYSTADENOMA                      (or inclusion cysts)
           │                                 │
           ▼                                 ▼
    BORDERLINE TUMOR              STIC (Serous Tubal
    (no stromal invasion)         Intraepithelial Carcinoma)
           │                                 │
    KRAS / BRAF mutations            TP53 mutation
    ERBB2 mutations                  Chromosomal instability
    NO TP53                          BRCA1/2 (hereditary)
           │                                 │
           ▼                                 ▼
   LOW-GRADE CARCINOMA            HIGH-GRADE SEROUS CARCINOMA
   (serous, endometrioid,          (most common ovarian malignancy)
    mucinous)                       Psammoma bodies
   Better prognosis                 Stage III/IV at diagnosis
                                    CA-125 ↑↑, BRCA testing

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📊 Ovarian Tumor Markers & Associations

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📊 Flowchart: Approach to Ovarian Mass by Age

PATIENT AGE
     │
┌────┴───────────────────────────────────┐
│                                        │
PREMENOPAUSAL                       POSTMENOPAUSAL
     │                                   │
┌────┴──────────────────┐           ALL masses suspicious
│                       │           → rule out epithelial ca
<20 years           20-45 years
     │                  │
Germ cell tumors    Epithelial tumors
(most common)       (functional cysts,
Dermoid cyst        endometrioma,
Dysgerminoma        serous cystadenoma)
Yolk sac tumor           │
                    Sex cord-stromal
                    (if hormonal symptoms)

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🔑 High-Yield One-Liners for Ovarian Tumors

• Most common ovarian tumor overall = Serous cystadenoma (benign epithelial)
• Most common ovarian malignancy = High-grade serous carcinoma (Type II)
• Most common benign ovarian germ cell tumor = Mature cystic teratoma (dermoid cyst)
• Most common malignant ovarian tumor in children = Yolk sac tumor (AFP ↑↑↑)
• Schiller-Duval bodies = Yolk sac tumor (glomeruloid structures)
• Call-Exner bodies = Granulosa cell tumor (coffee bean nuclei + rosettes)
• Meigs syndrome = Ovarian fibroma + ascites + right pleural effusion
• Pseudomyxoma peritonei = Mucinous tumor rupture (usually appendiceal primary)
• BRCA1/2 mutation = Prophylactic salpingo-oophorectomy (not just oophorectomy)
• STIC = Serous Tubal Intraepithelial Carcinoma = fallopian tube precursor of high-grade serous carcinoma
• Psammoma bodies = High-grade serous carcinoma (and papillary thyroid carcinoma)
• Bilateral ovarian tumors = Think metastatic (Krukenberg = gastric primary with signet ring cells)

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