PA29.4 | Ovarian Tumors — Summary & Reflection

REFLECT

You have just covered one of the most marker-rich topics in pathology. Before you close this SDL, take 3 minutes to test your recall without looking back:

1. Name the four WHO categories of ovarian tumors and their cells of origin.
2. What are psammoma bodies, and which tumor type are they classically associated with?
3. What is the genetic hallmark of high-grade serous carcinoma? And of low-grade serous carcinoma?
4. A young girl with an ovarian mass and AFP of 3,000 ng/mL — what is the most likely diagnosis?
5. What is pseudomyxoma peritonei, and what is its most common primary origin?
6. Name the marker for granulosa cell tumor and the microscopic finding that is pathognomonic.
7. What are the three components of Meigs syndrome, and which tumor causes it?
8. Define Krukenberg tumor precisely — it is not just "any metastatic ovarian tumor."

If you could answer 7–8 of these from memory, you are examination-ready on this topic. For any you hesitated on, go back to that block and re-read the key paragraph. Then re-test tomorrow (spaced retrieval).

KEY TAKEAWAYS

Ovarian tumors — Integrated Summary for PA29.4

Classification (WHO — by cell of origin):
• Surface epithelial (65–70%): serous (most common lethal; HGSC = TP53 + BRCA; psammoma bodies; LGSC = KRAS), mucinous (pseudomyxoma peritonei from appendix), endometrioid (endometriosis + Lynch), clear cell (hobnail/clear cells; ARID1A; chemo-resistant), Brenner (transitional epithelium; coffee-bean nuclei)
• Germ cell (15–20%): mature teratoma = dermoid = most common benign in young women (Rokitansky protuberance, torsion risk); immature teratoma (AFP); dysgerminoma (PLAP, LDH — seminoma equivalent; radiosensitive); yolk sac tumor (AFP, Schiller-Duval bodies); choriocarcinoma (hCG)
• Sex cord–stromal (5–10%): granulosa cell (estrogen, Call-Exner bodies, coffee-bean nuclei, inhibin, FOXL2; late recurrence); thecoma-fibroma (Meigs syndrome); Sertoli-Leydig (androgen, virilization, inhibin)
• Metastatic (~5%): Krukenberg (bilateral solid; signet-ring cells in fibromatous stroma; from stomach)

Risk/protective: BRCA1/2, nulliparity, endometriosis (EAOC) → risk; OCP, multiparity → protective

Spread: transcoelomic (dominant) → omental caking, peritoneal studding, ascites; lymphatic → para-aortic nodes

Staging (FIGO): 75% present Stage III–IV (silent peritoneal spread)

Tumor markers: CA-125 (serous), AFP (yolk sac), hCG (choriocarcinoma), inhibin (granulosa cell), PLAP/LDH (dysgerminoma)

Complications: torsion (most common for benign), chemical peritonitis (dermoid rupture), ascites, malignant transformation (<1% dermoid)

Prognosis: Stage > histological type; BRCA carrier HGSC paradoxically chemo-sensitive; PARP inhibitors exploit BRCAness