How does adenomyosis differ from endometriosis? Classic physical exam finding?
Answer
Adenomyosis: endometrial tissue within the MYOMETRIUM (extension into uterine wall) — SAME uterus. Endometriosis: endometrial tissue OUTSIDE the uterus (ovary, peritoneum, etc).
Presentation: Multiparous woman, late 40s, with heavy painful menses and uniformly enlarged, boggy, tender uterus. Dx: MRI shows thickened junctional zone; definitive dx post-hysterectomy. Tx: OCPs, IUD, hysterectomy (definitive).
Uterine Fibroids (Leiomyomas)
Demographics, hormone dependence, histology, and classic complication?
Answer
Most common gynecologic benign tumor. Estrogen-sensitive — grow during reproductive years, regress after menopause. Higher incidence in Black women.
Histology: Whorled bundles of smooth muscle cells with well-demarcated borders (arise from myometrium).
Presentation: Menorrhagia (#1 cause of iron-deficiency anemia in menstruating women), bulk symptoms, pelvic mass.
Key receptor patterns (ER, PR, HER2), invasive ductal vs lobular features, and key Step 1 mutations?
Answer
Invasive ductal carcinoma (75–80%): firm, fibrous, "stellate" mass with retraction; classic imaging of spiculated lesion. Invasive lobular carcinoma:"Indian file" single-file cells; loss of E-cadherin; often bilateral.
Letrozole:Aromatase inhibitor → ↓ peripheral estrogen → ↑ FSH/LH. Now preferred 1st-line over clomiphene in PCOS (higher live birth rates). Also used for ER+ breast cancer in postmenopausal women.
Key: both work via ↑ gonadotropin secretion but by different mechanisms.
OCPs — Mechanism & AE
How do combined OCPs prevent pregnancy? Risks & benefits?
Answer
Mechanism: Estrogen + progestin → negative feedback on HPO axis → ↓ GnRH, ↓ FSH, ↓ LH → no LH surge → no ovulation. Progestin thickens cervical mucus, thins endometrium.
↑ Risk: VTE (esp. smoking over 35), HTN, hepatic adenoma, cervical cancer (slight). ↓ Risk:Ovarian + endometrial cancers (↓ ovulations), benign breast disease, ectopic pregnancy, dysmenorrhea, PID.
Contraindications: Smoker over 35, migraine with aura, VTE history, HTN, breast CA, pregnancy.
Ectopic Pregnancy
Most common site, risk factors, classic presentation, and diagnostic labs?
Answer
Most common site:ampulla of fallopian tube (>70%) — same site as normal fertilization.
Labs/Dx:β-hCG doesn't double every 48 hrs (abnormal trend); transvaginal US shows no IUP with β-hCG > 1500 discriminatory zone.
Tx: Methotrexate (early, stable) or surgery (ruptured, unstable).
Step 1-Style MCQs: Select the best answer for each question. Your choice locks in immediately and the explanation reveals automatically. Green = correct, Red = incorrect.
Question 1 of 6 — PCOS Hormone Pattern
A 23-year-old nulligravid woman presents with oligomenorrhea (3–4 periods per year), hirsutism, acne, and a BMI of 32. Pelvic US shows multiple subcapsular follicles in both ovaries ("string of pearls"). Which of the following lab patterns is most consistent with her diagnosis?
B — Classic PCOS hormone profile. Persistent GnRH pulsatility favors LH over FSH → LH:FSH > 3. High LH drives theca cells to make androgens (testosterone, androstenedione) → hirsutism/acne. Low SHBG (from insulin resistance) increases free testosterone bioavailability. Peripheral aromatization of excess androgens → chronic unopposed estrone → ↑ endometrial cancer risk (protect with OCPs/IUD). Key metabolic picture: insulin resistance, T2DM risk, dyslipidemia.
Question 2 of 6 — Cervical Cancer Precursor
A 28-year-old woman undergoes routine Pap smear that shows atypical cells consistent with cervical intraepithelial neoplasia (CIN). HPV testing confirms HPV-16. Biopsy shows moderate dysplasia involving 2/3 of the cervical epithelium. Which part of the cervix is most likely affected, and what is the molecular mechanism?
CEctocervix only; HPV causes direct cell lysis in keratinized epithelium
DUterine fundus; HPV prefers the endometrial functionalis
EVaginal fornix; HPV requires stratified squamous non-keratinized epithelium only
B — Transformation zone; E6/E7 inhibit p53/Rb. The transformation (transition) zone is where stratified squamous (ectocervix) meets simple columnar (endocervix) — the metaplastic cells here are particularly susceptible. High-risk HPV 16/18: E6 promotes p53 degradation; E7 inhibits Rb. Loss of these tumor suppressors allows cell cycle progression → CIN → invasive SCC (80% of cervical cancers). Prevention: Gardasil 9 (9vHPV) before sexual debut. Ectocervix (C) is keratinized in vulva only, not cervix — ectocervix is non-keratinized.
Question 3 of 6 — Menstrual Physiology
A medical student reviewing the menstrual cycle notes that the secretory phase endometrium shows coiled, tortuous glands with prominent spiral arteries, while the proliferative phase shows elongated straight tubular glands. Which hormonal change is primarily responsible for this morphologic transition?
ADecline of estrogen from the degenerating corpus luteum
BFSH surge driving granulosa cell proliferation
CPost-ovulatory rise in progesterone from the corpus luteum
DProlactin-mediated uterine remodeling
EhCG release from the zygote
C — Corpus luteum progesterone drives the secretory transition. After ovulation, the corpus luteum secretes progesterone (primary) + estrogen. Progesterone converts the endometrium from "proliferative" (straight tubular glands, driven by estrogen) to "secretory" (coiled/tortuous glands filled with glycogen-rich secretions; spiral arteries elongate and coil). This maximally prepares the endometrium for implantation ~day 21–24. If no implantation, progesterone withdrawal from CL regression → spiral artery vasospasm → ischemic necrosis → menses.
Question 4 of 6 — Corpus Luteum Rescue
A 26-year-old woman has unprotected intercourse on day 14 of her cycle and her blastocyst implants in the uterus at day 21. By day 28, rather than menstruating, she maintains her uterine lining and has a positive urine pregnancy test. Which hormone, secreted by what structure, is directly responsible for preventing corpus luteum regression in this case?
ALH from the anterior pituitary
BhCG from the syncytiotrophoblast of the implanting blastocyst
CEstrogen from the corpus luteum itself
DProlactin from the anterior pituitary
EProgesterone from the endometrium
B — hCG from the syncytiotrophoblast.hCG (human chorionic gonadotropin) is structurally similar to LH (same α-subunit, different β-subunit) and binds the same LH receptor on the corpus luteum. This prevents CL regression and maintains progesterone output through T1, supporting the decidualized endometrium. Around weeks 8–10, the placenta takes over sex steroid production (corpus luteum-placental shift) and CL gradually involutes. Urine pregnancy tests detect β-hCG (unique to hCG). Normal rise in early pregnancy: β-hCG doubles every 48–72 hours.
Question 5 of 6 — Ovarian Cancer
A 57-year-old woman presents with 6 months of bloating, early satiety, and vague abdominal pain. She has never been pregnant and started her periods at age 11. Physical exam reveals a pelvic mass. CA-125 is markedly elevated; CT shows bilateral ovarian masses with ascites and omental caking. Biopsy shows psammoma bodies within serous tumor cells. Which of the following is the most likely origin of the malignancy?
AGranulosa cells of the ovarian follicle
BTheca cells of the ovarian follicle
CGerminal (surface) epithelium of the ovary
DPrimordial germ cells
EStromal sex cord cells
C — Germinal (surface) epithelium. Most ovarian cancers (65–70%) arise from the germinal epithelium (single layer of simple cuboidal cells covering the ovary). Serous cystadenocarcinoma is the most common subtype — recognized by psammoma bodies (concentric laminated calcifications). Risk factors: nulliparity, early menarche, late menopause, BRCA1/2, Lynch syndrome, family history. Marker: CA-125 (good for monitoring, not screening). Granulosa cell tumor (A): "Call-Exner bodies," estrogen-secreting; Dysgerminoma (D): germ cell origin, LDH+.
Question 6 of 6 — Breast Cancer Histology
A 52-year-old woman has a 2-cm breast mass biopsy showing single-file cells infiltrating the stroma. Immunohistochemistry reveals loss of E-cadherin expression. MRI identifies a contralateral breast lesion with similar features. Which of the following is the most likely diagnosis?
AInvasive ductal carcinoma
BInvasive lobular carcinoma
CMedullary carcinoma
DInflammatory breast carcinoma
EPaget disease of the breast
B — Invasive lobular carcinoma. Two pathognomonic features: single-file ("Indian file") infiltration of tumor cells in the stroma, and loss of E-cadherin (CDH1 gene). E-cadherin normally maintains epithelial cell adhesion — loss allows single-cell dispersion. Clinically notable for bilaterality (often multicentric) and subtle mammographic findings. Contrast with invasive ductal carcinoma (most common, 75–80%) which forms a stellate/spiculated mass with retraction. IHC: lobular is usually ER+/PR+, HER2– (similar triple profiles as ductal in general). Gene associated: CDH1 (hereditary diffuse gastric + lobular breast).
Ordering Drills: Arrange each sequence of steps in the correct physiologic or pathologic order. Drag items to reorder. Click "Check Order" to verify, or "Show Answer" to reveal the correct sequence.
PCOS — From Insulin Resistance to Anovulation
Trace the pathophysiologic cascade from insulin resistance to clinical PCOS features.
Implantation occurs in the tube (most commonly ampulla)
Fertilization in ampulla
Tubal transport impaired (PID, surgery, scar)
Implantation in the tube (commonly ampulla)
Inadequate β-hCG rise + conceptus erodes wall
Amenorrhea + unilateral pain + bleeding
Rupture → hemoperitoneum + shock
Vignette MCQs: Clinical scenarios testing disease recognition and mechanisms. Select your best answer and the explanation appears automatically.
Vignette 1 of 4 — Endometriosis
A 32-year-old nulligravid woman presents with 3 years of dysmenorrhea, dyspareunia, and dyschezia. She has been unable to conceive despite regular unprotected intercourse for 12 months. Pelvic exam shows tender nodules along the uterosacral ligament. MRI reveals a 4-cm "chocolate cyst" in the left ovary. Diagnostic laparoscopy shows powder-burn peritoneal lesions.
AUterine leiomyoma (fibroid)
BAdenomyosis
CEndometriosis with ovarian endometrioma
DOvarian dermoid cyst (mature teratoma)
EPolycystic ovary syndrome
C — Endometriosis. Buzzwords: 3 D's (dysmenorrhea, dyspareunia, dyschezia), infertility, chocolate cyst (blood-filled endometrioma), powder-burn lesions, uterosacral ligament nodules. Pathophysiology: ectopic endometrial tissue — common sites are ovary (most common), broad ligament, cul-de-sac, peritoneum. Laparoscopy is the gold-standard diagnostic test. Tx ladder: NSAIDs → OCPs/IUD → GnRH agonists → surgical excision. Adenomyosis (B) involves endometrium within the myometrium and presents as a boggy tender uterus in parous women.
Vignette 2 of 4 — Uterine Fibroid
A 38-year-old African American G2P2 woman presents with heavy menstrual bleeding, passing large clots, for the past 6 months. She has been getting progressively fatigued and her hematocrit is 28%. Pelvic exam reveals an irregularly enlarged uterus. Pelvic US shows three well-circumscribed intramural masses with acoustic shadowing. Which pathophysiologic feature most directly causes her anemia?
AAutoimmune hemolysis from anti-myometrial antibodies
BMalignant transformation to leiomyosarcoma
CChronic menorrhagia from distortion of uterine cavity + ↑ endometrial surface area
DEndometrial hyperplasia from unopposed estrogen
EInvasion of the posterior vaginal wall with bleeding
C — Chronic menorrhagia. Buzzwords: African American, irregular enlarged uterus, heavy menses with clots, multiple intramural masses. Uterine leiomyomas (fibroids) are the #1 cause of iron-deficiency anemia in menstruating women — they distort the uterine cavity, increase endometrial surface area, and impair contraction/hemostasis during menses → heavy bleeding. Fibroids are estrogen-sensitive — regress after menopause. Sarcomatous transformation (B) is very rare (<0.5%). Tx: NSAIDs, OCPs, IUD, GnRH agonists (preoperative shrink), myomectomy (fertility-preserving), hysterectomy.
Vignette 3 of 4 — MRKH Syndrome
A 16-year-old tall girl with Tanner V breasts and normal pubic hair presents with primary amenorrhea. Pelvic exam reveals a blind-ending vaginal pouch of 3 cm; no cervix is palpable. Pelvic MRI demonstrates absent uterus and upper vagina but normal bilateral ovaries. Karyotype is 46,XX. Renal US shows an absent left kidney. Which of the following best explains her findings?
B — MRKH (Müllerian agenesis). Buzzwords: 46 XX, normal breasts AND normal pubic hair (ovaries function), absent uterus + upper vagina, blind vagina, renal anomaly. The Müllerian ducts fail to develop, but ovaries (mesoderm) are unaffected → estrogen drives normal 2° sex characteristics. Distinguish from CAIS: MRKH is 46 XX with normal pubic hair; CAIS is 46 XY with scant pubic hair. Renal anomalies (unilateral agenesis, horseshoe) are common — same mesodermal intersection. Tx: vaginal dilator or reconstruction; IVF with gestational surrogate for pregnancy.
Vignette 4 of 4 — Ovarian Cancer + BRCA
A 48-year-old woman presents with 4 months of abdominal bloating, early satiety, and a 10-pound weight loss. Her mother died of ovarian cancer at 58; her sister had breast cancer at 42. Exam shows ascites and a palpable adnexal mass. CA-125 is 542 U/mL (markedly elevated). CT reveals bilateral ovarian masses with omental caking. Genetic testing confirms a pathogenic variant. Which gene is MOST likely involved, and what is its primary cellular function?
ATP53 — G1/S checkpoint regulation
BBRCA1/BRCA2 — homologous recombination DNA repair
CHER2/ERBB2 — tyrosine kinase receptor signaling
DAPC — Wnt pathway regulation
ECDH1 — cell-cell adhesion via E-cadherin
B — BRCA1/BRCA2 — DNA repair. Buzzwords: strong family history (mother with ovarian CA, sister with breast CA), premenopausal onset, bilateral ovarian masses, ↑ CA-125, omental caking. BRCA1 (chr 17q21) and BRCA2 (chr 13q12) are tumor suppressors involved in homologous recombination repair of dsDNA breaks. Loss of function → genomic instability → ↑ breast + ovarian cancer risk. BRCA1 has stronger link to triple-negative breast + high-grade serous ovarian CA. Prevention: risk-reducing salpingo-oophorectomy at 35–40. Most ovarian cancers arise from the germinal (surface) epithelium; histology: psammoma bodies in serous cystadenocarcinoma. Tx: cytoreduction + platinum-based chemo + PARP inhibitors (olaparib exploits HRD).
Step 1 Traps: Common false statements that appear plausible but are incorrect. Choose the correct answer to reveal the trap explanation.
Trap 1 of 7
In PCOS, the ovaries fail to develop follicles because FSH is markedly suppressed.
In PCOS, many follicles DO develop — they just never reach dominance. The "string of pearls" on US is many subcapsular follicles arrested in early growth. FSH is normal or slightly low, while LH is ELEVATED, giving the classic LH:FSH > 3. High LH drives theca androgen production → hyperandrogenism (hirsutism, acne). Anovulation is from failure of any follicle to pass the estrogen threshold → no LH surge.
Trap 2 of 7
Cervical cancer arises primarily in the endocervix because that's where HPV preferentially infects columnar cells.
Cervical cancer arises in the transformation (T) zone — the junction between stratified squamous (ectocervix) and simple columnar (endocervix) epithelium. This is where metaplastic squamous cells are particularly susceptible to HPV 16/18 infection. Most cervical cancers are squamous cell carcinoma (80%), arising from these metaplastic cells. Pap smears specifically sample the T-zone. Adenocarcinoma (from endocervical columnar cells) makes up the remaining 20%.
Trap 3 of 7
In the 2-cell model of ovarian steroidogenesis, LH stimulates granulosa cell aromatase, while FSH stimulates theca cell androstenedione production.
The functionalis of the endometrium regenerates itself after menstruation; that's why menstruation can repeat cyclically.
The functionalis is what SHEDS during menstruation — it cannot regenerate itself because it's gone. The BASALIS is preserved and provides the stem cells that regenerate the functionalis in the proliferative phase. If the basalis is destroyed (e.g., by aggressive D&C or infection → Asherman syndrome), the patient develops amenorrhea and infertility because there is no source for functionalis regeneration. Spiral (coiled) arteries serve functionalis; straight arteries serve basalis.
Trap 5 of 7
The follicular phase of the menstrual cycle is fixed at 14 days, but the luteal phase varies in length.
Reversed. The LUTEAL phase is FIXED at ~14 days (determined by corpus luteum lifespan — degenerates after ~14 days unless rescued by hCG). The FOLLICULAR phase is VARIABLE — this is why cycle length differs between women. Clinical implication: ovulation occurs ~14 days BEFORE the next menstrual period, not 14 days after the last one. In PCOS, the follicular phase is often prolonged → long, irregular cycles.
Trap 6 of 7
Ectopic pregnancy occurs most commonly in the isthmus of the fallopian tube.
The ampulla is the most common site of ectopic pregnancy (>70%) — not the isthmus. This is the same site where fertilization normally occurs. Rank: Ampulla > isthmus > fimbria > ovary > abdomen > cervix. Risk factors: prior PID (leading cause of tubal scarring), prior ectopic, IUD, tubal surgery, endometriosis, smoking. Classic presentation: amenorrhea + unilateral pain + vaginal bleeding. β-hCG doesn't double every 48h.
Trap 7 of 7
Bartholin gland homologues in the male are the prostate glands, which secrete a similar mucus-like fluid.
Swapped. Bartholin glands (greater vestibular) are homologous to the bulbourethral (Cowper) glands — both secrete lubricating mucus. Skene glands (paraurethral) are homologous to the prostate. Both homologous pairs derive from the urogenital sinus. Clinical: Bartholin cysts at 5 & 7 o'clock of vaginal introitus; in postmenopausal women, any Bartholin mass should be biopsied to rule out vulvar adenocarcinoma.
Reference Tables: Quick-lookup tables for gyn pathology, menstrual cycle pharmacology, and breast/ovarian tumors. Print-friendly format.
Medical abortion (+ misoprostol); Cushing syndrome
Cramping, bleeding, incomplete abortion
Combined OCPs
Estrogen + progestin — suppress HPO axis
Contraception; cycle regulation; ↓ ovarian/endometrial CA
VTE, HTN, ↑ cervical CA risk (slight); CI: smoker >35
Progestin-only (POP)
Thickens cervical mucus, thins endometrium
Contraception (breastfeeding, VTE risk)
Irregular bleeding
Trastuzumab
Anti-HER2 monoclonal antibody
HER2+ breast cancer
Cardiotoxicity (monitor LVEF)
High-Yield Testing Notes: Key patterns to recognize on exams. Badges indicate trap concepts, buzzword clusters, and testing-focused insights.
TESTING 2-Cell / 2-Gonadotropin Model — The Core Ovarian Endocrine Unit
The most testable pre-ovulation concept: LH stimulates THECA cells to produce androstenedione. The androgen diffuses into granulosa cells, where FSH-induced aromatase converts it to estrogen. Reverse the question: aromatase inhibitors (anastrozole, letrozole) shut off granulosa conversion → less estrogen. This also explains why PCOS (high LH) → high androgens / hirsutism. Mnemonic: "LH likes L-theca; FSH feeds F-granulosa."
TRAP Corpus Luteum Hormone Switch
Pre-ovulation: granulosa = estrogen; theca = androstenedione (2-cell model). Post-ovulation: granulosa LUTEIN = PROGESTERONE; theca LUTEIN = ESTROGEN. The hormonal outputs swap. This is how the corpus luteum supports the secretory phase (progesterone dominant) while maintaining background estrogen. If pregnancy: hCG from syncytiotrophoblast acts like LH → rescues CL through week ~10, when the placenta takes over (corpus luteum-placental shift).
BUZZWORD PCOS — Classic Vignette Cluster
USMLE PCOS picture: obese young woman + oligomenorrhea + hirsutism/acne + insulin resistance. Labs: LH:FSH > 3, ↑ testosterone, ↓ SHBG. US: "string of pearls" bilateral ovaries. Rotterdam criteria (2 of 3): oligo/anovulation, hyperandrogenism, polycystic ovaries. Remember: ↑ risk endometrial CA (unopposed estrogen). Tx ladder: weight loss → OCPs → metformin → clomiphene/letrozole for fertility.
TESTING HPV Molecular Hook — E6 and E7
High-yield: HPV 16/18 (high-risk) express E6 (degrades p53) and E7 (inhibits Rb) → loss of cell cycle control → CIN → cervical cancer. Location: transformation zone (squamocolumnar junction). Step 1 loves to ask "which tumor suppressor is degraded by E6?" (p53) or which cell cycle phase loses control (G1/S, via Rb). Low-risk HPV (6, 11) causes genital warts — different mechanism, no malignant transformation. Gardasil 9 prevents both.
TRAP Luteal Phase is FIXED — Follicular is Variable
Students often assume the 28-day cycle splits evenly. Wrong. The luteal phase is always ~14 days (determined by corpus luteum lifespan). The follicular phase varies — ovulation happens 14 days BEFORE the next period, not 14 days AFTER the last one. In PCOS, follicular phase is prolonged → long irregular cycles. Clinical use: "withdrawal bleeding after progesterone challenge confirms the endometrium has been primed by estrogen" — a test used for secondary amenorrhea workup.
BUZZWORD Invasive Lobular CA — "Indian File" + Lost E-cadherin
High-yield pathology: invasive lobular carcinoma is recognized by (1) single-file ("Indian file") infiltration of tumor cells and (2) loss of E-cadherin (CDH1 mutation). E-cadherin loss disrupts cell-cell adhesion → single-cell dispersion pattern. Often bilateral and subtle on mammo. Contrast with invasive ductal (most common, 75–80%) — forms a stellate/spiculated mass with retraction. Hereditary CDH1 mutations cause diffuse gastric cancer + lobular breast cancer syndrome.
TESTING Endometrial Cancer — Type I vs Type II
Two pathways. Type I (80%, endometrioid):estrogen-driven; precursor = endometrial hyperplasia. Risk factors = anything giving unopposed estrogen: obesity (aromatization), PCOS, nulliparity, late menopause, tamoxifen, HRT (estrogen-only), Lynch syndrome. Better prognosis. Type II (20%, serous/clear cell): non-estrogen; p53 mutations; older, thinner women; worse prognosis. Both present with postmenopausal bleeding — ALWAYS workup. Dx: endometrial biopsy. Tx: TAH-BSO ± adjuvant.
Clinical Correlates: Review key disease profiles and clinical connections. Click "Show" to reveal comparison details.
Primary Amenorrhea Workup
MRKH vs CAIS vs Turner vs Swyer — The "No Period Ever" Differential
Four distinct entities to differentiate in an adolescent with primary amenorrhea:
MRKH (46 XX, Müllerian agenesis): Normal ovaries (functional!) + absent uterus/upper vagina. Normal breasts, normal pubic hair, blind vagina. Renal anomalies common (unilateral agenesis).
CAIS (46 XY): Defective androgen receptor. Testes (abdominal) + normal breasts (aromatization) + scant pubic hair (no AR signaling) + blind vagina + NO uterus (MIS intact).
Cervical, Endometrial, Ovarian & Breast — Screening Essentials
USMLE-testable screening & prevention:
Cervical cancer: Pap smear (q3y starting age 21) or Pap + HPV co-test (q5y from 30–65). Gardasil 9 (9–45 yo) prevents HPV 16/18 and others. Screening samples the transformation zone.
Endometrial cancer: NO screening for average risk; postmenopausal bleeding always warrants endometrial biopsy. Lynch syndrome carriers: annual endometrial biopsy + consider risk-reducing hysterectomy.
Ovarian cancer: NO screening for average risk (CA-125 not sensitive/specific enough). BRCA1/2 carriers: risk-reducing salpingo-oophorectomy at 35–40.
Breast cancer: Mammogram starting 40 (annual) or 50 (biennial) per society; earlier if strong FHx / BRCA. BRCA carriers: MRI + mammogram starting 25–30, risk-reducing mastectomy option.
Clinical red flags requiring workup:
• Postmenopausal bleeding → endometrial biopsy (endometrial CA until proven otherwise)
• Postcoital bleeding → cervical cancer workup
• Bloating + early satiety in a postmenopausal woman → ovarian cancer (often late presentation)
• Bartholin mass in woman over 40 → biopsy (rule out vulvar adenocarcinoma)
• Amenorrhea + unilateral pelvic pain → ectopic pregnancy (check β-hCG!)
Female Repro Histology Synthesis
Key Histology-Clinical Correlations
Histology directly informs clinical pathology:
Germinal epithelium of ovary: Source of most ovarian cancers (serous cystadenocarcinoma with psammoma bodies). BRCA1/2 increase risk.
Transformation zone of cervix: Squamocolumnar junction — site of HPV infection and cervical cancer. Pap smear samples here.
Endometrium: Functionalis sheds with menses (spiral arteries vasoconstrict); basalis regenerates. Asherman syndrome = destruction of basalis → amenorrhea/infertility.
Fallopian tube (ampulla): Most common site of fertilization AND ectopic pregnancy. Cilia + peg cells (estrogen-dependent) transport the zygote.