Reproductive tract disorders
Female and male reproductive disorders: uterus, cervix, ovary, prostate and testis
Reproductive pathology for FCPS Part 1: uterus, cervix, ovary, early pregnancy, pelvic infection, prostate and testis. Each lesion is linked to its mechanism and its ultrasound or MRI appearance.
One of the most tested topics in past papers
Uterus in pregnancy and after delivery
- Pregnancy enlarges the uterus mainly by hypertrophy of smooth muscle cells (oestrogen driven), with some hyperplasia. By about 4 months the decidua capsularis fuses with the decidua parietalis, obliterating the uterine cavity. After delivery the uterus shrinks by atrophy (autophagy).
- Cervical ectropion in pregnancy, the pill and adolescence: oestrogen everts the columnar endocervical epithelium onto the ectocervix.
- Primary postpartum haemorrhage: commonest cause uterine atony (tone), then trauma, tissue (retained products) and thrombin (coagulopathy); bleeding from the placental bed is normally stopped by myometrial contraction (living ligatures).
- Progestogens (or pregnancy) decidualise the endometrium: abundant plump stroma with few, inactive glands.
Uterine lesions
- Fibroids (leiomyomas): monoclonal smooth muscle tumours (MED12), oestrogen-dependent. Submucous ones bleed most. Degenerations: hyaline (commonest), red in pregnancy, cystic, calcific.
- Lipoleiomyoma: a fat-density mass (about −90 HU) arising within the myometrium; always find the organ of origin of a fatty pelvic mass (ovarian dermoid is the commoner fatty mass).
- Adenomyosis: junctional zone over 12 mm on MRI; boggy tender uterus.
- Endometrial hyperplasia: unopposed oestrogen (anovulation, PCOS, obesity, tamoxifen, granulosa cell tumour) causes heavy irregular bleeding.
| Endometrial cancer | Type I (endometrioid) | Type II (serous) |
|---|---|---|
| Patient | Obese, perimenopausal | Thin, elderly |
| Gene | PTEN; mismatch repair (Lynch) | p53 |
| Outlook | Good | Poor |
- Endometrial cancer spreads mainly by direct myometrial invasion and lymphatics; blood spread is late and least likely. A young woman with endometrial cancer, a mother with the same and a brother with colon cancer has Lynch syndrome (mismatch repair genes, e.g. MLH1, MSH2).
- Asherman syndrome: curettage destroys the stratum basalis.
- Uterine arteriovenous malformation: after curettage or miscarriage; hCG negative, empty cavity, tubular anechoic spaces in the myometrium with turbulent, high-velocity, low-resistance flow. Retained products instead show a vascular echogenic mass in the cavity with positive hCG.
- IUCD perforation: threads missing, pregnancy test negative, empty cavity on ultrasound but the device seen on an abdominal radiograph; copper devices are removed laparoscopically because they cause adhesions.
Cervix
- HPV 16 and 18: E6 degrades p53, E7 inactivates Rb; koilocytes. Cancer begins in the transformation zone.
- Diagnosis: screening cytology or HPV test; abnormal smear (dyskaryosis) is followed by colposcopy with biopsy, and CIN 2–3 is treated by large loop excision of the transformation zone (LLETZ). Invasive cancer is diagnosed by biopsy (histology).
- Carcinoma in situ on cytology: high nuclear to cytoplasmic ratio, hyperchromatic irregular nuclei throughout the epithelium.
- Spread: parametrium (ureteric obstruction), pelvic then para-aortic nodes.
Pelvic infection and vaginitis
- Tubo-ovarian abscess: fever, pain and cervical motion tenderness with a thick-walled multilocular adnexal mass; infection ascends from the cervix through the uterus and tube (gonococcus, chlamydia, anaerobes). It can mimic an ovarian tumour.
- Trichomonas vaginalis: frothy yellow-green discharge, strawberry cervix, motile flagellates on wet mount; no cyst stage, spread sexually; treat both partners with metronidazole.
Early pregnancy on ultrasound
| Finding | Meaning |
|---|---|
| Eccentric sac with double decidual rings and yolk sac | True intrauterine pregnancy |
| Central cavity-shaped fluid with a single rim, no yolk sac, hCG 3000 IU/L, adnexal mass | Pseudogestational sac (decidual cast of an ectopic) |
| Live intrauterine pregnancy plus an adnexal ring with yolk sac after IVF | Heterotopic pregnancy; hCG cannot be used to follow the ectopic |
Ovary and adnexa
- Functional cysts: follicular, corpus luteum (ring of fire).
- Paraovarian cyst: thin-walled cyst in the broad ligament (mesonephric remnant) with a normal ovary seen separately that moves away from it under probe pressure; does not change with the cycle.
- Fetal ovarian cyst: in a female fetus in the third trimester, maternal and placental hormones (hCG, oestrogen) stimulate follicles; most regress after birth; a complex cyst with a fluid level may have torted.
| Origin | Tumours | Point |
|---|---|---|
| Surface epithelium | Serous, mucinous, endometrioid, clear cell | Serous: psammoma; transcoelomic spread (malignant ascites) |
| Germ cell | Mature cystic teratoma, dysgerminoma, yolk sac (AFP) | Young women |
| Sex cord–stromal | Granulosa (oestrogen), fibroma (Meigs), Sertoli–Leydig (androgen) | Hormonal effects |
| Metastatic | Krukenberg (stomach) | Bilateral |
- Ovarian fibroma (and Brenner tumour, uterine fibroids) is very dark on T2, like muscle, because of dense collagen with little free water; enhances slowly.
- OHSS: hCG-driven VEGF capillary leak.
Prostate
| Zone | Disease |
|---|---|
| Peripheral | Carcinoma (about 70%) |
| Transition | Benign hyperplasia |
- A normal adult prostate weighs about 20 g (about 20 mL).
- MRI: the normal peripheral zone is bright on T2 because its glands are full of fluid; cancer is dark because packed tumour cells replace the fluid-filled glands, and it restricts diffusion. Prostatitis and post-biopsy blood can mimic it.
- Finasteride (5α-reductase inhibitor) roughly halves PSA after 6–12 months, so double the measured value; a rising PSA on it is suspicious.
- Castration-resistant cancer: the tumour makes its own androgens. Abiraterone inhibits CYP17 (17α-hydroxylase/17,20-lyase), blocking androgen synthesis in adrenals and tumour; it is given with prednisolone because blocked cortisol synthesis raises ACTH and mineralocorticoids (hypokalaemia, hypertension).
- Chronic bacterial prostatitis: recurrent E. coli UTIs and perineal pain; drugs must be lipid soluble (fluoroquinolones, trimethoprim) to cross the prostatic epithelium into acidic prostatic fluid. Calcifications harbour bacteria.
- Spread to the spine via the vertebral venous plexus; sclerotic metastases.
Testis and scrotum
| Tumour | Marker and stains | Point |
|---|---|---|
| Seminoma | AFP normal; OCT3/4 and PLAP positive, CD30 negative | Sheets of large clear cells, central nuclei, fibrous septa with lymphocytes; radiosensitive |
| Embryonal carcinoma | OCT3/4 and CD30 positive | Heterogeneous |
| Yolk sac | AFP | Children under 3 |
| Choriocarcinoma | hCG | Gynaecomastia |
- Gynaecomastia with a testicular tumour: very high hCG acts on LH receptors and stimulates Leydig cells to make oestradiol (aromatase); it can also cause hyperthyroidism.
- Burned-out tumour: retroperitoneal nodes and raised hCG with only a small scar and coarse calcification in the testis.
- Testis lymph drains to para-aortic nodes; scrotal skin (chimney sweep's soot carcinoma) drains to superficial inguinal nodes on the same side.
- Torsion: high transverse testis, absent cremasteric reflex, absent Doppler flow, twisted cord; salvage depends mainly on time since the onset of pain (best within 6 hours). Never let imaging delay exploration.
- Undescended testis: most often in the inguinal canal; retractile testes can be brought down. Seminoma risk persists after orchidopexy.
- Encysted hydrocele of the cord: a transilluminating cyst above the testis that moves with traction on it: the middle segment of the processus vaginalis stays patent while both ends close (canal of Nuck cyst in girls).
- Low-flow priapism in sickle cell disease: sickled cells block venous outflow from the corpora; dark, hypoxic, acidotic blood and no arterial flow; urgent aspiration.
- Breaching the blood–testis barrier (vasectomy) causes antisperm antibodies.
Remember Peripheral zone for prostate cancer, transition zone for hyperplasia; collagen makes pelvic masses dark on T2.
Exam trap A pseudosac in the uterus with an adnexal mass is an ectopic pregnancy, not an early intrauterine one.
Exam trap Never biopsy a testicular mass through the scrotum; it opens a new lymphatic route.
How FCPS asks about this
- Commonest cause of primary PPH: uterine atony.
- Endometrial hyperplasia cause: unopposed oestrogen; endometrial cancer with family colon cancer: Lynch syndrome.
- Abiraterone mechanism: CYP17 inhibition of androgen synthesis.
- PSA on finasteride: double the value.
- Stains supporting seminoma: OCT3/4 and PLAP.
- Scrotal skin cancer in a chimney sweep: superficial inguinal nodes.
- Factor predicting testicular salvage in torsion: time since onset of pain.
Test yourself on this topic
5 of the 206 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 62-year-old man has a raised prostate-specific antigen (PSA) of 12 ng/mL. What is the normal physiological function of this protein?
Answer: Protease that liquefies the semen clot
Prostate-specific antigen is a serine protease of the kallikrein family made by prostatic epithelial cells and secreted into semen. After ejaculation, semenogelins from the seminal vesicles form a gel, and PSA cleaves them over 15 to 30 minutes, liquefying the semen and freeing the sperm. Small amounts leak into the blood, and more leaks when the gland architecture is disrupted by cancer, inflammation, enlargement or instrumentation. PSA is therefore organ-specific but not cancer-specific.
PSA
- Kallikrein serine protease
- Cleaves semenogelins
- Liquefies the semen clot
- Organ-specific, not cancer-specific
Remember PSA dissolves the clot that the seminal vesicles make.
Exam trap Prostatitis, urinary retention and catheterisation also raise PSA.
Why the other options are wrong
- Hormone that drives prostate growth Growth is driven by dihydrotestosterone, not PSA.
- Source of fructose for sperm motility Fructose comes from the seminal vesicles.
- Protein that coagulates fresh semen Coagulation is caused by semenogelins from the seminal vesicles.
- Acid phosphatase that frees zinc Acid phosphatase is a different prostatic enzyme and does not liquefy semen.
A 14-year-old boy has sudden severe left testicular pain with vomiting. The testis lies high and transverse and the cremasteric reflex is absent. Which factor best predicts whether the testis can be saved at surgery?
Answer: Time since the onset of pain
Torsion twists the spermatic cord, first blocking venous return and then arterial inflow, so the testis becomes ischaemic. Germ cells are the most sensitive to ischaemia, and the chance of saving the testis falls steeply with time: salvage is very likely within about 6 hours but drops sharply after 12 to 24 hours. This is why suspected torsion is explored urgently and imaging should not delay surgery. Both testes are fixed at operation because the bell-clapper anomaly is usually bilateral.
Testicular torsion
- Venous then arterial occlusion
- Germ cells die first
- Salvage best within 6 hours
- Fix both testes at surgery
Remember In torsion, time is testis.
Exam trap Never let imaging delay surgical exploration when torsion is clinically likely.
Why the other options are wrong
- Size of the reactive hydrocele A reactive hydrocele does not determine viability.
- Volume of the affected testis Testicular size does not predict salvage.
- Side of the torsion Either side behaves the same way.
- Presence of a bell-clapper on the other side The other side is fixed to prevent future torsion, but it does not affect this testis.
A 32-year-old man has a painless, firm testicular swelling. After orchidectomy, histology shows sheets of large cells with clear cytoplasm and central nuclei, divided by fibrous septa containing lymphocytes. Which immunohistochemical profile supports the diagnosis?
Answer: OCT3/4 and PLAP positive
Large clear cells in sheets separated by fibrous septa with lymphocytes are classical seminoma, the commonest testicular germ cell tumour, peaking in the fourth decade. Seminoma cells express OCT3/4, placental alkaline phosphatase and KIT (CD117), and they are usually negative for CD30 and only weakly or not positive for cytokeratin. Embryonal carcinoma expresses CD30 and cytokeratin, yolk sac tumour expresses AFP and glypican-3, and sex cord-stromal tumours express inhibin and calretinin.
Seminoma
- Commonest germ cell tumour, 30s
- Clear cells, fibrous septa with lymphocytes
- OCT3/4, PLAP, KIT positive
- CD30 negative (unlike embryonal)
Remember Seminoma: clear cells, lymphocytes, OCT3/4 and PLAP.
Exam trap OCT3/4 is also positive in embryonal carcinoma, so use it with CD30 and morphology.
Why the other options are wrong
- CD30 and cytokeratin positive Typical of embryonal carcinoma.
- AFP and glypican-3 positive Typical of yolk sac tumour.
- Inhibin and calretinin positive Typical of Sertoli and Leydig cell tumours.
- Chromogranin and synaptophysin Markers of neuroendocrine tumours.
A 3-year-old boy has a smooth, painless swelling in the right groin above the testis. It transilluminates, moves down when the testis is gently pulled, and does not change with crying or straining. The testis below it is normal. What is its developmental basis?
Answer: Patent middle segment of processus vaginalis
The processus vaginalis normally obliterates from the internal ring down to just above the testis, leaving only the tunica vaginalis around the testis. If a middle segment stays open while both ends close, fluid collects in it as an encysted hydrocele of the cord. It lies above the testis, moves with traction on the testis and does not communicate with the peritoneum, so it does not change with crying. A fully patent processus causes a communicating hydrocele or an indirect inguinal hernia.
Encysted hydrocele of the cord
- Middle segment of processus vaginalis stays open
- Both ends closed
- Lies above the testis, moves with traction
- No change with crying
Remember A cyst on the cord that follows the testis: encysted hydrocele.
Exam trap In girls the same anomaly gives a cyst of the canal of Nuck in the labium majus.
Why the other options are wrong
- Fully patent processus vaginalis to peritoneum Gives a communicating hydrocele or hernia that changes in size.
- Persistent remnant of the gubernaculum The gubernaculum becomes the scrotal ligament and does not form cysts.
- Dilated tubules of the efferent ductules Gives an epididymal cyst or spermatocele above and behind the testis.
- Remnant of the paramesonephric duct Gives the appendix testis, a small pedunculated body.
A 16-year-old boy with sickle cell disease has a painful erection lasting 6 hours. Blood aspirated from the corpora is dark, hypoxic and acidotic. What is the mechanism?
Answer: Sickled cells blocking venous outflow
In sickle cell disease, slow flow and low oxygen in the corpora cavernosa cause red cells to sickle, block the venous outflow and trap blood. Stasis worsens hypoxia and acidosis, which promote further sickling, so the erection persists and becomes painful (ischaemic, low-flow priapism). Aspirated blood is dark, hypoxic and acidotic, unlike the bright red blood of arterial priapism. It is a urological emergency because prolonged ischaemia causes fibrosis and permanent erectile dysfunction.
Ischaemic priapism
- Sickled cells block venous outflow
- Painful, rigid corpora
- Dark, hypoxic, acidotic blood
- Emergency: fibrosis if delayed
Remember Painful, dark blood: ischaemic priapism.
Exam trap High-flow priapism after perineal trauma is painless and not an emergency in the same way; the blood gas separates the two.
Why the other options are wrong
- Arteriocavernous fistula from trauma Causes painless high-flow priapism with bright red, well-oxygenated blood.
- Spinal reflex after cord injury Spinal cord injury causes reflex erections, not this ischaemic picture.
- Excess arterial inflow from a shunt Arterial priapism is painless and gives bright red blood.
- Fibrosis of the tunica albuginea Fibrosis is a late result of ischaemia, not the cause.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Abdominal, renal and reproductive disorders, Female and male reproductive disorders: uterus, ovary, cervix, prostate, testis
Read next
Drug dose pages
Doses, cautions and practical tips for drugs in this chapter.