Anatomy of the Ovaries Blood Supply of Ovaries Ovarian Ligaments Microscopic Anatomy Oogenesis Ovarian Cyst Ovarian mass Functional cysts Simple ovarian cyst Risk of Malignancy Index or RMI. Tubo-ovarian abscess Ovarian Endometrioma: Benign tumor malignant tumors

1. Diaa Mohammad Srahin
6th year Medical Student
Al-Quds University
Obstetrics & Gynecology
December/ 2018

2. Anatomy of the Ovaries
The ovaries are oval, flattened, compressible organs, approximately
3 × 2 × 2 cm in size.
Blood supply of ovaries :
 Ovarian artery (directly from aorta)
 Branches of uterine artery ( from internal iliac )
 Ovarian vein
Right: drains directly into inferior vena cava
Left: drains into left renal vein
Lymphatic drainage of the ovaries is through the pelvic and para-aortic
lymph nodes.

3. Blood Supply of Ovaries

4. Ovarian Ligaments
Several paired ligaments support the ovaries:
1. The ovarian ligament connects the uterus and ovary.
2. The posterior portion of the broad ligament forms
the mesovarium
3. The suspensory ligament of the ovary (infundibular
pelvic ligament) attaches the ovary to the pelvic
sidewall and contains the ovarian artery and vein, as
well as nerve supply to the ovary.

5. Ovarian Ligaments

6. • The Cortex is where the follicles
and oocytes at various stages of
development and degeneration.
• The cortex is made of tightly
packed connective tissue. The
stroma of this cortical connective
tissue is composed of fibroblasts.
• The Medulla is where the
ovarian vasculature is found and
is primarily loose stromal tissue.
Microscopic Anatomy

7. Oogenesis
 1° oocytes begin meiosis I during fetal life and complete
meiosis I just prior to ovulation.
 Meiosis I is arrested in prOphase I for years until
Ovulation (1° oocytes).
 Meiosis II is arrested in metaphase II until fertilization
(2° oocytes). “An egg met a sperm.”
 If fertilization does not occur within 1 day, the 2° oocyte
degenerates.

8. Ovarian Cyst
 Ovarian cysts are common, with a reported clinical
prevalence of 15% in premenopausal and 8% in
postmenopausal women.
 Most of these cysts resolve over time without
treatment.
 The causes of benign ovarian tumor will vary with age.

9. Ovarian mass
Ovarian mass
Functional Inflammatory Neoplastic

10. Functional cysts
 It is the most common cause of a simple cystic mass in the
reproductive age years.
 During the reproductive years the ovaries are functionally
active, producing a dominant follicle in the first half of
the cycle and a corpus luteum after ovulation in the
second half of the menstrual cycle.
 Either of these structures, the follicle or the corpus luteum,
can become fluid-filled and enlarged, producing a
functional cyst.

11. Cont.
 COCPs reduce its risk .
 Diagnosis is made when the cyst measures more than
3 cm , simple unilocular in U/S.

12. Functional cysts
Functional
cysts
Follicular
cysts
Corpus
luteal cysts
Theca-
luteal cysts
Polycystic
ovaries

13.  Follicular cyst : develops when an ovarian follicle
fails to rupture.
 Corpus luteal cyst: develop if the corpus luteum
grows to over 3 cm and fails to regress normally
after 14 days.
 Hemorrhagic cyst : form when invasion of
ovarian vessels into the corpus luteal cyst 2 to 3
days after ovulation causes bleeding within the
cyst.

14. Simple ovarian cyst

15.  Theca Lutein Cysts :
 These are benign neoplasms stimulated by high levels of FSH
and β-hCG.
 They are associated with twins and molar pregnancies and
choriocarcinoma.
 Patients undergoing ovulation induction with
gonadotropins, clomiphene, or letrozole may also develop
theca-lutein cysts.
 The natural course of these tumors is postpartum
spontaneous regression.
 Require only conservative management.

16.  Luteoma of Pregnancy :
 Luteoma of pregnancy is a rare, non-neoplastic
tumor-like mass of the ovary that emerges
during pregnancy and regresses spontaneously after
delivery.
 It is usually asymptomatic and is found incidentally
during a cesarean section or postpartum tubal ligation.
 It can be hormonally active and produce androgens
resulting in maternal and fetal hirsutism and
virilization.

18.  Polycystic ovarian syndrome :
A functional disorder generally associated with chronic
anovulation, hyperandrogenism, and insulin resistance,
can also produce enlarged ovaries with multiple simple
follicles.

20. Clinical features:
 Usually asymptomatic
 The patient may present with
1. delayed menses
2. abnormal uterine bleeding
3. pelvic pain
Occasionally, a functional cyst may undergo torsion (see below)
or it may rupture, which may produce acute lower abdominal pain
and tenderness and the differential diagnosis must include ectopic
pregnancy, pelvic abscess, or adnexal torsion of an ovarian
neoplasm.

21. Diagnosis:
• First, do B-hCG to rule out pregnancy.
1. Bimanual examination: 5- to 8-cm cystic
adnexal mass
2. Transvaginal ultrasonography
3. confirmed when the lesion regresses over the
course of the next several cycles.
4. In general, a functional cyst is mobile,
unilateral, and not associated with ascites.

22. Treatment:
Observation:
 Follow-up examination should be in 6–8 weeks
 Alerted to the possibility of acute onset of pain
 OCPs can be used to prevent recurrence
Laparoscopy:
 cyst is >7 cm
 Or if patient had been on prior steroid contraception
for at least >= 2 months
Torsion of
adnexal cyst

23. Risk of Malignancy Index or RMI.
 A pelvic ultrasound will confirm the cystic nature of
the mass,
 But it cannot differentiate with certainty between a
functional and a neoplastic tumor.

24. RMI

25. Management:
 If the RMI is low < 200; wait and reexamine the
patient after her next menses
 Low-dose contraceptive agents
 If the RMI is high ;surgical exploration and/or
referral to a gynecologic oncologist is indicated.

26. Inflammatory
Cyst
Tubo-ovarian
abscess
Endometrioma

27. Tubo-ovarian abscess
 Accumulation of pus forming an inflammatory mass of ovaries and
other sites.
 Associated with PID.
 It can developed from other infective causes, e.g: appendicitis or
diverticular disease.
 Symptoms: sever lower abdominal-pelvic pain, back pain, pain with
bowel movements.
 PE: sick, fever, tachycardia, septic shock with hypotension,
peritoneal signs.
 +ve cervical culture, blood culture, WBC, ESR
 US or CT – complex mass

29. Management:
 Tx: Inpatient IV ATB (Clindamycin, Gentamycin)
and surgical drainage.
 Can need TAH and BSO
 Definitive surgery is usually deferred:
Increased risk of systemic infection and difficulty
with inflamed and infected tissue.

30. Ovarian Endometrioma:
 Bening condition, ectopic endometrial tissue within the ovary.
 Ovary is the most common site.
 Chocolate cysts: the presence of altered blood within the ovary.
 Cause : Retrograde menstruation , coelomic metaplasia , autoimmune
, lymphovascular, direct implantation.
 They can reach 10 cm in size
 Have a characteristic ‘ground glass’ appearance on US.
 Dx: Laparoscopy

32. Management:
 If not surgically excised, follow-up should be at least
yearly.
 Pregnancy, Pseudopregnancy: OCPs, or Oral MPA
 Pseudomenopause:
Testosterone derivatives( Danocrine, danazol)
GnRH analog (Leuprolide, lupron)
 Down regulation of Pituitary.
 Cx: menopausal Symptoms after 3-6 mth
 We can use DMPA(depoprovera): doesnt make vasomotor
symptoms

33. Neoplastic
Mass
Benign Malignant Borderline

34. Benign Mass
Germ Cell
Benign
teratoma
(dermoid )
Epithelial
Sex cord
stromal

35. Germ Cell Tumor :
 Most common ovarian tumor in young women
 Occur at any age(early 20s)
 These are slow-growing tumors and half the tumors are
diagnosed in women between 25 and 50 years of age.
 Most common form is mature dermoid cyst

36. Dermoid Cyst :
“Cystic teratoma”
 Most common benign ovarian neoplasm in the
premenopausal woman
 Can take on a great variety of forms with virtually all adult
tissues, composed primarily of ectodermal tissue (such as
sweat and sebaceous glands, hair follicles, and teeth), with
some mesodermal and rarely endodermal elements.
 10- 15 % teratomas are bilateral.
 Thyroid tissue can also be identified, and if it comprises more than
50% of the dermoid, then the condition of struma ovarii is identified

38. Diagnosis:
 Most commonly its an incidental finding
 15% present acutely with torsion
• MRI is the most helpful due to high fat content .

39. Ovarian tortion:
 Ovarian cyst that has grown in size to the point at which it turns over on
itself,
 twisting the suspensory ligament of the ovary and cutting off blood
supply.
 Intense, severe, sudden-onset pain in the RLQ or LLQ
 US - decreased or absent Doppler flow to the ovary
 Emergent surgery to reverse the torsion, hopefully in time to avoid
necrosis of the tissue.
 Untwist

40.  Cystectomy. If revitalization occurs, an ovarian
cystectomy can be performed with preservation of the
ovary.
• Oophorectomy. If the ovary is necrotic, a unilateral
salpingo-oophorectomy is performed.
F/o after 4 Wks  routine examination , then yearly

42. Management of dermoid cyst:
 Depend on the type of neoplasm, the patient’s age, and
her desire for future childbearing
 Premenopausal:
An ovarian cystectomy with preservation of the ovary
 Postmenopausal :
at least unilateral salpingooophorectomy
The contralateral ovary should be carefully inspected to
exclude a bilateral lesion

43. Epithelial
Serous
cystadenoma
Mucinous
cystadenoma
Brenner
tumor

44. Epithelial Ovarian Neoplasms
 Derived from the mesothelial cells lining the surface of the ovary
 Occur more commonly in older age.
 Include:
1- Serous cystadenoma : the lining of the fallopian tubes.
2- Mucinous cystadenoma : cytological resembles the
endocervical epithelium
3- Endometrioid neoplasm: resembles the endometrium
4- Brenner tumor: resemble transitional cells of the bladder
 The most common is serous cystadenoma.

45. Serous tumors:
 Resemble the lining of the fallopian tubes
 Bilateral in about 10% of cases, usually unilocular
 It can be :
 Benign about 70% .
 Malignant 20-25%
 Borderline malignant potential 5-10% .
 Depending largely on the patient’s age.
 Serous tumors characteristically form psammoma bodies

47. Mucinous tumors
 Ccytological resembles the endocervical epithelium.
 Bilateral in 10% of cases , Multiloculated
• Often associated with a mucocele of the appendix.
 Can result in pseudomyxoma peritonei -
intraperitoneal accumulation of mucinous material.
 85%are benign.

49. Gross appearance of a mucinous (A) and serous (B)
cystadenoma of the ovary. The mucinous type is generally
multiloculated and can be quite large

50. Brenner tumor:
 Uncommon.
 Small, smooth solid ovarian neoplasm.
 Epithelioid cells that resemble transitional cells of the
bladder.
 The majority are benign, but can be malignant.
 Often found incidentally.

51. Sex cord
stromal
Thecoma Fibroma

52. Sex Cord–Stromal Ovarian
Neoplasms
 Feminine differentiation , becomes a
granulosa-cell tumor, a theca-cell tumor, or, a
mixed granulosa-theca cell tumor.
 Masculine differentiation become Sertoli-
Leydig cell tumors. (less common).
 Ovarian fibroma, developing from mature
fibroblasts in the ovarian stroma.

53. Clinical findings:
 The granulosa-theca cell tumors promote feminizing signs and
symptoms.
1. Precocious menarche.
2. Precocious thelarche.
3. Premenarchal uterine bleeding during infancy and childhood.
4. Menorrhagia.
5. Postmenopausal bleeding.
6. Endometrial hyperplasia, endometrial cancer.
 Sertoli-Leydig cell tumors :
1. Hirsutism.
2. Temporal baldness0.
3. Deepening of the voice.

55. The ovarian fibroma:
 Most common
 Not hormonally active
 Often present with torsion in older women.
 May be associated with Meigs syndrome, (ascites
and hydrothorax in association with an ovarian
fibroma).
 spontaneously resolve when the fibroma has been
removed.

56. Management:
 Depend on: the type of neoplasm, the patient’s age,
and her desire for future childbearing.
 Most benign-appearing ovarian cysts may be observed
and followed with ultrasonography.
 If they are symptomatic or enlarging, laparoscopic
management is usually appropriate.
 Laparotomy is usually indicated if the mass is
suspicious for malignancy.

57. ovarian
cancer

58. Ovarian cancer:
 2nd most common gynecologist malignancy.
 1st gynecogogist tumor causing death in females
 Incidence: 1.4%
 mean age of presentation is 69 yrs.
 more in developed countries
 higher in caucasian.

59. Theories of cancer
 Incessant ovulation theory: This relates to
continuous ovulation causing repeated trauma to the
ovarian epithelium leading to genetic mutation and
development of a cancer.
 This is supported by an increased incidence of EOC in
nulliparous women, women with early menarche or
late menopause and a reduction in incidence of EOC
in multiparous women and in women who have used
oral contraception.
 Excess gonadatrophin secretion: This promotes
higher levels of oestrogen which in turn leads to
epithelial proliferation and malignant transformation
of the ovarian epithelium.

60. Risk Factors:
Decreased risk of ovarian cancer Increased risk of ovarian cancer
Multiparity Nullparity
OCPs IUD
Tubal ligation Endometriosis
Hysterectomy Cigarette smoking
Breast-feeding Obesity
Chronic anovulation
Short reproductive life

61. Genetic factors in ovarian
cancer:
About 10-15% of ovarian cancer
3 main types of genes include:
BRCA1, BRCA2, Lynch syndrome
Usually associated with other cancers
(breast, colorectal).

62. classification of Ovarian cancer:
Epithelial tumor (80%) Serous
Mucinous
Endometroid
Clear cell
Undifferentiated
Germ cell tumor(15%) Dysgerminoma
Endodermal sinus
teratoma
choriocarcinoma
mixed
Stromal tumor (5%) Granulosa cell
Sertoli cell
Gynandroblastoma
Metastatic tumor Including Krukenberg

65. Epithelial cell
 Most common type
 Postmenopausal women
 Most common malignant tumor is Serous
 Usually symptomatic with non specific symptoms
 persistent pelvic and abdominal pain;
 increased abdominal size/persistent bloating;
 difficulty eating and feeling full quickly.

66. Germ cell tumor:
 Predominantly occurs in
teenagers, large
 Most common malignant
form is dysgerminoma
 Uniquley X ray sensitive

67. Stromal tumors:
 Functionally active
 Granulosa-theca cell tumor secret estrogen, so bleeding from
endometrial hyperplasia
 Sertoli -leyding cell tumor secrete testosteron. So produce
musculinization syndrome
 Pt Usually come early
 Tx:
 Oophorectomy of involved adnexa( desire for fertility)
 TAH or BSO(nodesire)
 If mets(rarely): it requires Chemotherapy(vincristine, actinomycin,
cytoxan)

68. Metastatic disease:
 Most common sources is :
Endometrium, GI, Breast
 Krukenberg tumors : are mucin producing tumor
from stomach to ovaries.

69. Clinical Features:
 Pelvic and abdominal examination:
Fixed hard pelvic mass
Ascites : Highly indicative
• Chest examination:
Pleural fluid
• Neck and groin: palpable LNs.

70. Investigations:
 CBC, urea, electrolyte, LFT,
 Tumor markers
 US: most useful non invasive test for suspected
malignancy
 others:
 Paracentesis if ascites present.
 CT, MRI of abdomen
 barium enema and colonoscopy
 Biopsy

71. Tumor markers:
Tumor marker Tumor type Uses
Ca 125 Epithelial ovarian cancer
(serous), borderline
ovarian tumors
Preoperative, follow up
Ca 19-9 Epithelial ovarian cancer
(mucinous), borderline
ovarian tumors
Preoperative, follow up
Inhibin Granulosa cell tumours Follow up
B-hCG Dysgerminoma,
choriocarcinoma
Preoperative, follow up
AFP Endodermal yolk sack,
teratoma
Preoperative, follow up
Estrogen, Testosteron Stromal tumors Preoperative, follow up

72. Serous CEA , CA-125
Mucinous Ca19-9
Dysgerminoma LDH , B-hCG
Sertoli-Leydig Testosterone
Granulosa Estrogen , Inhibin
Endodermal sinus (Yolk Sac), Teratoma AFP
Choriocarcinoma B-hCG

73. staging:
 Staging is surgical.
 Stage I: Spread limited to the ovaries
 IA. Limited to one ovary, capsule intact, negative cytology
 IB. Limited to both ovaries, capsules intact, negative cytology
 IC. One or both ovaries but ruptured capsule, positive
cytology
 Stage II: Extension to the pelvis
 IIA. Extension to uterus or tubes
 IIB. Extension to other pelvic structures
 IIC. Extension to pelvis with positive cytology

74. Stage III: Peritoneal metastases or positive nodes.
This is the most common stage at diagnosis.
 IIIA. Microscopic peritoneal metastases
 IIIB. Macroscopic peritoneal metastases ≤2 cm
 IIIC. Macroscopic peritoneal metastases >2 cm
Stage IV: Distant metastases
 IVA. Involves bladder or rectum
 IVB. Distant metastasis

75. Management:
 .A surgical exploration should follow preoperative
studies and medical evaluation
 At the time of surgery, a unilateral salpingo-
oophorectomy (USO) is done and sent for frozen
section
 If abdominal or pelvic CT scan shows no evidence of
ascites or spread to the abdominal cavity, and if the
surgeon is an experienced laparoscopist, evaluation
could be performed laparoscopically

76. Benign Histology
 If the patient is not a good surgical candidate or the
patient desires to maintain her uterus and
contralateral ovary, a USO is sufficient treatment.
 If the patient is a good surgical candidate, then a TAH
and BSO

77. Malignant Histology
 Debulking procedure (cytoreduction) .
 TAH and BSO, omentectomy, and bowel resection, if
necessary.
 Postoperative chemotherapy (carboplatin and Taxol)
should be administered.

78. Prognostic factors in ovarian
cancer
Stage of disease
Volume of residual disease post-
surgery
Histological type and grade of tumour
Age at presentation
FIGO Stage 5-year
survival
(%)
I 70–90
II 80
III 30
IV 10–20

79. Follow-Up
 If the final pathology report was benign: the patient
can be followed up in the office yearly for regular
examination.
 If the pathology report was carcinoma, follow up every
3 months for the first 2 years
 then every 6 months for the next 2 years with follow-
up of the CA-125 tumor marker

80. Borderline Cancers
 Also known as tumors of low malignant potential.
 No invasion of the basement membrane
 Tx:
• Conservative surgery. A patient desires further fertility with a
unilateral borderline cancer of the ovary can be treated with a
USO with preservation of the uterus and the opposite adnexa.
• Aggressive surgery. patient has completed her family then
treatment would be a TAH and BSO.
• Chemotherapy. Not requires unless metastasis, and this is a
rare occurrence.

81. Adnexal Mass With Ascites
 Abdominal accumulation of fluid in the peritoneal
cavity
causes of ascites:
 heart, kidney , liver disease and ovarian cancer.
 Meigs syndrome is the triad of ascites, pleural
effusion, and benign ovarian fibroma.

82.  An abdominal pelvic CT scan should be ordered for
evaluation of the upper abdomen.
 The most common method of ovarian carcinoma spread is
by peritoneal dissemination (exfoliation) .
 commonly metastatic to the omentum and to the GI tract.
 Most common cause of death in advanced ovarian
carcinoma is bowel obstruction.
 Treatment as mentioned.