The document discusses diseases of the female genital tract, including the cervix and ovaries. It covers topics such as cervicitis, cervical polyps, pre-cancerous and cancerous lesions of the cervix. It discusses screening for cervical cancer with Pap tests and HPV vaccination. It also discusses functional and neoplastic cysts of the ovaries as well as classifications of ovarian tumors. Diseases of the uterus discussed include endometriosis, adenomyosis, and leiomyomas (fibroids). Ectopic pregnancy is also summarized.

1. The Female Genital Tract
Item-20, 21

2. Item No. 20
Diseases of the Cervix
Diseases of the Ovary

3. Diseases of the Cervix
i. Inflammation of the Cervix.
ii. Cervical polyp (Endocervical polyp).
iii. Premalignant and Malignant neoplasm of
cervix.

4. Acute and chronic cervicitis
• Inflammation of the cervix is called cervicitis.
• Some degree of cervical inflammation may
be found in virtually all women and it is
usually of little clinical consequence.
• Infections by E. coli, gonococci, chlamydia,
trichomoniasis and HSV may produce
significant acute or chronic cervicitis.

5. Acute and chronic cervicitis
• Allergic reactions by contraceptive
spermicides or to latex, feminine hygiene
products such as douches or feminine
deodorants also can cause cervicitis.
• Bacterial overgrowth. An overgrowth of some
of the bacteria that are normally present in the
vagina (bacterial vaginosis) can lead to
cervicitis.

6. Acute and chronic cervicitis
Symptoms
• Persistent, unusual vaginal discharge
• Frequent, painful urination
• Pain and discomfort during intercourse.
• Nonmenstrual vaginal bleeding.

7. Defensive mechanism against infection
• Normal vaginal and cervical mucosa has large
number of lactobacilli.
• Lactobacilli produce lactic acid, maintaining
vaginal pH below 4.5, suppressing the growth
of organisms.
• Lactobacilli at lower pH produce bacteriotoxic
hydrogen peroxide (H2O2).

8. Breach of defense causing infection
• Menstrual bleeding, sexual intercourse, vaginal
douching causes decrease H2O2 production by
lactobacilli, permitting the overgrowth of
microorganisms.
• Antibiotic therapy suppress the lactobacilli.
• This altered vaginal and cervical environment
promotes the overgrowth of the microorganism
causing cervicitis.

9. Endocervical Polyp
• Endocervical polyps are common benign polyp
that arise within the endocervical canal that
may protrude through the cervical os.
• they may be the source of irregular vaginal
“spotting” or bleeding causing suspicion of
some more ominous lesion.

10. Premalignant and Malignant
Neoplasm of Cervix
• Worldwide, cervical carcinoma is the third
most common cancer in women.
• The Pap test/ cervical smear test and visual
examination (colposcopy) of cerivix
• And the slow progression from precursor
lesions to invasive carcinoma provides ample
time for screening, detection, and preventive
treatment.

11. Premalignant and Malignant
Neoplasm
• Premalignant condition:
Cervical intraepithelial neoplasia (CIN)
• Malignant tumour:
i. Carcinoma in Situ (CIS)
ii. Squamous cell carcinoma
iii. Adenocarcinoma
iv. Adenosquamous carcinoma
v. Neuroendocrine carcinoma

12. Role of HPV in cervical cancer
• Genital HPV infections are extremely common;
most of them are asymptomatic.
• Most HPV infections are transient and are
eliminated by the immune response in the
course of months.
• HPVs infect immature basal cells of the
squamous epithelium in areas of epithelial
breaks or at the squamocolumnar junction.

13. Role of HPV in cervical cancer
• High risk HPV (HPV strain 16,18, 31, 33, 45) are
considered the single most important factor in
cervical carcinoma.
• High risk HPVs also causes squamous cell
carcinomas of vagina, vulva, tonsil and other
oropharyngeal locations.
• Low risk HPVs (HPV 6 and11) are the cause of
vulvar, perineal and perianal warts.

14. Role of HPV in cervical cancer
• The high risk HPV (HPV 16,18, 31, 33, 45) acts
as a carcinogic agent in cervical carcinoma.
• The ability of HPV to act as a carcinogen
depends on the viral proteins E6 and E7.
• Viral E7 protein binds the active form of tumor
suppressor RB gene and causes its
degradation.

15. Role of HPV in cervical cancer
• Viral proteins E6 and E7 inhibits p21 and p27,
two important cell cycle inhibitors.
• Inhibiting tumor suppressor gene and cell
cycle inhibitors enhances cell cycle
progression
• And also impairs the ability of cells to repair
DNA damage.

16. The risk factors for cervical cancer
1. Persistent infection with a high oncogenic
risk HPV, HPV 16 or HPV18
2. Multiple sexual partners
3. Young age at first intercourse
4. High parity
5. Immunosuppression
6. Use of oral contraceptives
7. Use of nicotine (cigarette, tobacco)

17. Cervical intraepithelial neoplasia (CIN)
• Cervical intraepithelial neoplasia (CIN) is a
precancerous condition of the cervix.
• CIN may exist in the noninvasive stage for as
long as 20 years.
• And shed abnormal cells that can be detected
on cytologic (Paps test) examination.

18. Cervical intraepithelial neoplasia (CIN)
Classified in a variety of ways :
• Mild, moderate and severe dysplasia (Old way).
• Commonly classified as CIN-I, CIN-II and CIN-
III.
• Currently classified as:
i. Low grade squamous intraepithelial lesion
(LSIL/ CIN-I).
ii. High grade squamous intraepithelial lesion
(HSIL/ CIN-II, CIN-III).

19. Cervical intraepithelial neoplasia (CIN)
• The classification is based on expansion of the
immature cell layer from its normal basal
location to upwards toward the superficial
layer.
i. CIN-1 (LSIL )
ii. CIN-2 (HSIL)
iii. CIN-3 (HSIL)

20. Cervical intraepithelial neoplasia (CIN)
• LSIL (CIN-1): If the atypical, immature
squamous cells are confined to the lower one
third of the epithelium.
• HSIL (CIN-2): If the atypical cells expand to two
thirds of the epithelial thickness.
• HSIL (CIN-3): Total replacement of all the layers
of epithelium by atypical cells.

21. CIN-I, II, III

22. CIN: Progression/ Fate
• LSIL (CIN-I): Does not progress directly to
invasive carcinoma and in fact most cases
regress spontaneously.
• HSIL (CIN-II, III): increased cellular proliferation
may become irreversible and lead to a fully
transformed malignancy.
• LSIL (Low grade lesion) are ten times more
common than HSIL (High grade lesion).

23. Carcinoma in Situ (CIS)
• Atypical malignant cells involving whole
thickness of the cervical epithelium but does
not cross the epithelial basement membrane is
called carcinoma in situ.
• It is the malignant condition of the cervix. But
the malignant cells do not cross the basement
membrane.
• If the malignant cells cross the basement
membrane it is called invasive carcinoma not
CIS.

24. CERVICAL CARCINOMA
• Types:
• Squamous cell carcinoma (80%).
• Adenocarcinoma.
• Adenosquamous carcinoma.
• Neuroendocrine carcinoma.

25. Squamous cell carcinoma

26. Cervical Cancer Screening and Prevention
Management of CIN
HPV vaccination
OVARIAN TUMOR

27. Cervical Cancer Screening and Prevention
• The pap test screening is effective in
preventing cervical cancer as cancers arise
from precursor lesions over the years.
• And shed abnormal cells that can be detected
on cytologic examination (Pap test).

28. Cervical Cancer Screening and Prevention
• If Pap test is abnormal, a colposcopic
examination of the cervix is performed to
identify abnormal area.
• The mucosa is examined with a magnifying
glass following application of acetic acid,
which highlights abnormal epithelium as white
spots (acetowhite areas).
• Abnormal appearing areas are biopsied.

29. Cytologic screening by Pap test
• Pap tests are cytologic preparations of
exfoliated cells from the cervical
transformation zone.
• Cells are stained with the Papanicolaou stain
(Pap stain).
• The stained smear can identify the normal,
LSIL and HSIL.
• HPV DNA testing can also be done on cervical
cytology for screening.

30. Pap smear (Normal)

31. Pap smear (LSIL)

32. Pap smear (HSIL)

33. Management of CIN
• Women with LSIL is treated conservatively with
repeat smears with regular follow-up. Some
gynecologists perform local ablation
(cryosurgery).
• HSILs are treated with cervical conization
(superficial Excision).

34. HPV Vaccination
• A new aspect of cervical cancer prevention is
vaccination against high-risk oncogenic HPVs.
• It is now recommended for all girls and boys
by age 11 to 12 years, as well as young men
and women up to age 26 years.
• The vaccines offer protection for up to 10 years

35. Diseases of the Ovary

36. Diseases of the Ovary
Diseases mainly are:
1. Functional or non-neoplastic cysts.
2. Ovarian Tumour.

37. Diseases of the Ovary
• Nonneoplastic and Functional Cysts
are:
1. Follicular cyst.
2. Luteal cyst.
3. Polycystic ovaries.

38. Follicular and Luteal Cysts
• Cystic follicles are very common in the ovary.
• They originate from unruptured graafian
follicles or in follicles that have ruptured and
immediately sealed containing serous fluid.
• These cysts are usually multiple. They range
in size up to 2 cm in diameter, are filled with a
clear serous fluid.

39. Polycystic Ovaries (PCOS)
• Polycystic ovarian syndrome (PCOS) is a
complex endocrine disorder characterized by:
i. Polycystic ovaries
ii. Menstrual abnormalities
iii. Hyperandrogenism
iv. Chronic anovulation
v. Decreased fertility.

40. Polycystic Ovaries (PCOS)
• Formerly called Stein Leventhal syndrome,
affects 6-10% of reproductive age women
worldwide.
• It is also associated with obesity, type 2
diabetes, and premature atherosclerosis.
• Due to an increase in serum estrogen levels,
women with PCOS are at risk for endometrial
hyperplasia and carcinoma.

41. Ovarian tumor
• 80% of ovarian tumor are benign, and these
occur mostly in young women between the
ages of 20 and 45 years.
• Malignant tumors are more common in older
women.
• Ovarian cancer accounts for 3% of all cancers
in females and is the fifth most common cause
of death due to cancer.

42. Ovarian tumor
• Most ovarian cancers have already spread
beyond the ovary by the time of diagnosis.
• Ovarian tumour is categorized into Benign
tumor, Borderline tumor and Malignant tumor.
• Benign tumor is called Cystadenoma and
malignant tumor is called Cystadenocarcinoma

43. Pic: Ovarian tumor

44. Classification of Ovarian tumor
• Primary tumours:
i. SURFACE EPITHELIAL-STROMAL TUMORS
ii. SEX CORD–STROMAL TUMORS
iii. GERM CELL TUMORS
• Secondary metastatic tumour to ovary:
• From Colon, Appendix, Gastric carcinoma.

45. Surface epithelial-Stromal Tumor
1. Serous tumors
i. Benign (cystadenoma)
ii. Borderline tumors (serous borderline tumor)
iii. Malignant (serous adenocarcinoma)
2. Mucinous tumors
3. Endometrioid tumors
4. Clear cell tumors
5. Transitional cell tumors

46. Classification
• Surface epithelial stromal tumors are most
common.
• Among surface epithelial stromal tumors
serous tumors are more common (approx. 40%).
• Mucinous tumors account for about 20% to
25% of all ovarian neoplasms and in more
aggressive then serous tumor.

47. Sex Cord–Stromal Tumors
1. Granulosa tumors
2. Fibromas
3. Fibrothecomas
4. Thecomas
5. Sertoli cell tumors
6. Leydig cell tumors

48. Germ Cell Tumors
1. Teratoma
2. Dysgerminoma.
3. Yolk sac tumor.
4. Mixed germ cell tumour.

49. Teratoma
• Teratomas are the tumors arising from the
component from more than one germ layer.
• Teratomas are bilateral in 10% to 15% of cases
and may cause infirtility.
• Characteristically they are unilocular cysts
containing hair and sebaceous material, bones,
teeth, cartilage.

50. Teratoma Classification
i. Immature (Malignant in nature)
ii. Mature (Benign in nature)
iii. Monodermal or special (struma ovarii)
• Mature :
i. Solid
ii. Cystic (Dermoid cyst) (Mature
Cystic Teratoma

51. Pic: Dermoid Cyst

52. Hormone producing tumors of ovary
Granulosa cell tumor Oestrogen
Thecoma Oestrogen
Leydig cell tumor Androgen
Sertoli cell tumor Androgen, Oestrogen
Struma ovari Thyroxine

53. Diseases of the
Corpus or Body of the
Uterus
(Item-21)

54. Endometriosis
• Presence of endometrial glands and stroma
outside of the uterus is called endometriosis.
• Endometriosis affects approximately 6% to
10% of women.
• It often causes infertility, dysmenorrhea
(painful menstruation), dyspareunia and pelvic
pain.

55. Endometriosis; Sites:
(1) Ovary (Commonest), if bilateral causes
infertility
(2) Uterine ligaments
(3) Rectovaginal septum
(4) Cul de sac
(5) Pelvic peritoneum
(6) Large and small bowel and appendix;
(7) Mucosa of cervix, vagina and fallopian tubes
(8) Laparotomy scars (Due to inappropriate
surgical toileting after cesarean section).

56. Endometriosis

57. Endometriosis; Theory
• The regurgitation theory (retrograde flow of
menstrual endometrium).
• The benign metastases theory (endometrial
tissue spread via blood vessels and lymphatic
channels).
• The metaplastic theory (arises directly from
mesothelium of pelvis or abdomen)

58. Adenomyosis
• Adenomyosis is the presence of endometrial
glands and stroma in the myometrium.
• Adenomyosis is considered benign (not life-
threatening) condition but the frequent pain
and heavy menstrual bleeding can have a
negative impact on a woman's quality of life.
• Mostly diagnosed in middle-aged women who
is having children and women who have had
prior uterine surgery.

59. Adenomyosis

60. Ectopic Pregnancy
• Implantation of the fetus at any site other than
normal intrauterine location is named ectopic
pregnancy. Occurs about one in every 150
pregnancies.
• The most common site is the extrauterine
fallopian tube (approximately 90% of cases).
• Implantation in fallopian tube will ultimately
rupture the tube and its a medical emergency.

61. Ectopic Pregnancy; Risk factors:
• Prior pelvic inflammatory disease (PID)
resulting in fallopian tube scarring or fibrosis.
• Peritubal scarring and adhesions caused by
appendicitis, endometriosis, and previous
surgery.

62. Ectopic Pregnancy
• Abdominal pain, vaginal bleeding, hemorrhagic
shock with signs of an acute abdomen.
• Despite advances in early diagnosis, ectopic
pregnancy still accounts for 4% to 10% of
pregnancy related deaths.

63. Ectopic Pregnancy
• Sites:
i. fallopian tubes (∼90%)
ii. ovaries
iii. abdominal cavity
iv. intrauterine portion of the fallopian tube.

64. Sites of Ectopic Pregnancy

65. Leiomyoma (Fibroid)
• Uterine leiomyoma is the benign tumour of the
smooth muscle of myometrium.
• Perhaps most common tumor in female.
Leiomyomas may occur singly, but more often
are multiple.
• Can be within the myometrium (intramural),
beneath the endometrium (submucosal) or
beneath the serosa (subserosal)

66. Leiomyoma; Types:
Leiomyoma can be:
i. within the myometrium (intramural)
ii. beneath the endometrium (submucosal)
iii. beneath the serosa (subserosal)

67. Leiomyoma (Fibroid)
• Leiomyomas of the uterus can be asymptomatic.
And may cause:
• Abnormal uterine bleeding.
• Urinary frequency due to compression of the
bladder.
• Sudden pain from infarction of a large or
pedunculated leiomyoma.
• Impaired fertility.

68. Leiomyoma in pregnant women
Leiomyoma in pregnant women may cause:
i. Increase the frequency of spontaneous
abortion.
ii. Fetal malpresentation.
iii. Uterine inertia .
iv. Postpartum hemorrhage.
• Malignant leiomyoma is rare and is called
leiomyosarcoma.

69. Leiomyoma

70. Leiomyoma: Microscopically

71. Abnormal Uterine Bleeding
Dysfunctional Uterine Bleeding

72. Abnormal Uterine Bleeding
• Abnormal uterine bleeding can be caused
by pathologic conditions, such as:
i. Chronic endometritis
ii. Endometrial polyp
iii. Leiomyoma
iv. Endometrial neoplasm.
v. Endometrial hyperplasia

73. Abnormal uterine bleeding
• Prepuberty:
Precocious puberty (hypothalamic, pituitary,
or ovarian origin)
• Adolescence:
i. Anovulatory cycle
ii. Coagulation disorders

74. • Reproductive age:
1. Abortion
2. Ectopic pregnancy
4. Leiomyoma
5. Adenomyosis
6. Trophoblastic disease
7. Endometrial polyps
8. Endometrial hyperplasia
9. Endometrial carcinoma

75. • Perimenopausal and Postmenopausal:
1. Endometrial carcinoma.
2. Endometrial hyperplasia
3. Endometrial polyps
4. Anovulatory cycle
5. Cystic atrophy of the endometrium.

76. Dysfunctional Uterine Bleeding (DUB)
• DUB is the uterine bleeding due to hormonal
disturbances not caused by any underlying
organic (structural) abnormality.
1. Anovulatory cycle.
2. Ovulatory dysfunctional bleeding
(inadequate luteal phase).
3. Irregular shedding.

77. Endometrial Polyp
• Endometrial polyps are mass of variable size
that project into the endometrial cavity.
• Endometrial Polyps may be asymptomatic or
may cause abnormal bleeding (intramenstrual,
menometrorrhagia, postmenopausal bleeding).
• Endometrial Polyps can be a cause of
infertility.

78. Endometrial Polyp
• Endometrial polyps have been observed in
association with the administration of
tamoxifen.
• Tamoxifen is often used in the therapy of
breast cancer due to its anti-estrogenic activity
on the breast.

79. Endometrial Polyp

80. Endometrial Hyperplasia

81. Endometrial Hyperplasia
• An increased proliferation of the endometrial
glands, resulting in an increased gland-to-
stroma ratio.
• Endometrial hyperplasia is an important cause
of abnormal uterine bleeding.
• A frequent precursor to the endometrial
carcinoma.

82. Endometrial Hyperplasia
• Endometrial hyperplasia is associated with
prolonged estrogenic stimulation of the
endometrium.
• It is divided into non-atypical and atypical
hyperplasia.

83. Endometrial Hyperplasia; Causes:
i. Chronic anovulation
ii. Increased estrogen production from
endogenous sources.
iii. Obesity.
iv. Polycystic ovarian syndrome.
v. Prolonged administration of estrogenic
substances (estrogen replacement
therapy/ HRT).

84. Malignant tumors of endometrium
Types:
1.Type I or Endometrioid carcinoma
2.Type II or Serous Carcinoma
i.Serous carcinoma.
ii.Clear cell carcinoma.
iii.Malignant mixed mullerian tumour.

85. Fallopian Tube diseases
i. Inflammation (Salpingitis): caused by
Gonococcus, Chlamydiae, Tubercular.
ii. Ectopic pregnancy
iii. Endometriosis
Salphingitis causes scarring and fibrosis which
causes infirtility and ectopic pregnancy.

86. Gestational and Placental
Disorders

87. Gestational and Placental Disorders
1. Disorders of Early pregnancy
2. Disorders of late pregnancy
3. Gestational trophoblastic Disease

88. Gestational and Placental Disorders
1. Disorders of Early pregnancy
i.Spontaneous abortion
ii.Ectopic pregnancy
2. Disorders of late pregnancy
i.Placental implantation abnormalities
ii.Twin placenta
iii.Placental infections
3. Gestational trophoblastic Disease

89. Spontaneous abortion
• Spontaneous abortion (miscarriage) is defined
as pregnancy loss before 20 weeks of
gestation.
• Around 30% of early pregnancies in healthy
women terminate spontaneously, many without
notice.
• Fetal chromosomal anomalies, Maternal
endocrine factors, Physical defects of the
uterus, Infections with protozoa (Toxoplasma),
bacteria (Mycoplasma, Listeria).

90. Placental abnormalities
i. Placenta accreta:
ii. Placenta previa :
iii. Placental inflammation and infections
iv. PreEclampsia and Eclampsia.

91. Placental abnormalities
• Placenta accreta:
Adherence of placenta directly to the
myometrium.
• Placenta previa :
Implantation of placenta in the lower uterine
segment or cervix.
• Placental inflammation and infections:
Placentitis, Villitis, Chorioamnionitis
• PreEclampsia and Eclampsia.

92. Placenta previa

93. Placenta accreta:

94. PreEclampsia
Eclampsia

95. PreEclampsia
• Preeclampsia is a systemic syndrome
characterized clinically with hypertension,
edema and proteinuria due to widespread
maternal endothelial dysfunction.
• Occurs in about 3% to 5% of pregnant women.
• Usually in the last trimester.
• More commonly in primiparas (pregnancy for
the first time).

96. PreEclampsia
• Other complications of preeclampsia and
eclampsia include hypercoagulability, acute
renal failure, and pulmonary edema.
• Systemic endothelial dysfunction, Abnormal
placental dysfunction and coagulation
abnormality contributes the pathogenesis.

97. Risk factors of PreEclampsia

98. Eclampsia
• More severe form of Preeclampsia associated
with convulsions termed as Eclampsia.
• The onset is typically characterized by
hypertension and edema with proteinuria.
• Headache and visual disturbances are serious
events with convulsions and patient eventually
goes into coma.

99. Management of preeclampsia/Eclampsia
• For term pregnancies, delivery is the treatment
of choice regardless of disease severity.
• Eclampsia, severe preeclampsia with maternal
end-organ dysfunction, fetal compromise, are
indications for delivery regardless of
gestational age.
• Proteinuria, Hypertension, Convulsion
disappear within 1 to 2 weeks after delivery.

100. Gestational and Placental Disorders
1. Disorders of early pregnancy
2. Disorders of late pregnancy
3. Gestational trophoblastic Disease

101. Gestational Trophoblastic Disease
• Gestational trophoblastic disease (GTD) is a
group of diseases in which abnormal
trophoblastic cells grow inside the uterus after
conception.
• GTD is made of trophoblast cells which help
connect the fertilized egg to the wall of the
uterus and form part of the placenta.

102. Trophoblast cells help connect the
fertilized egg to the wall of uterus

103. Gestational Trophoblastic Disease
• A pregnancy before 20 or after 35 years of age.
• A previous molar pregnancy affect the risk of
GTD.
• Severe nausea and vomiting during pregnancy.
• Abnormal vaginal bleeding and a uterus that is
larger than normal.
• A very high level of beta human chorionic
gonadotropin (β-hCG) in blood.

104. Gestational trophoblastic Disease:
Classification
1. Hydatidiform mole (Molar Pregnancy):
i. Complete mole
ii. Partial mole
iii. Invasive mole
2. Choriocarcinoma.
3. Placental site trophoblastic tumor
(PSTT)

105. Gestational trophoblastic Disease

106. Hydatidiform mole (Molar Pregnancy)
• HM or molar pregnancy, results from abnormal
fertilization of the oocyte (egg) resulting in
formation of an abnormal fetus.
• The placenta grows normally with little or no
growth of the fetal tissue. The placental tissue
forms a mass in the uterus.
• A molar pregnancy may seem like a normal
pregnancy at first.

107. Signs and Symptoms
• Dark brown to bright red vaginal bleeding
during the first trimester.
• Sometimes vaginal passage of grape-like
cystic structure.
• Severe nausea and vomiting.
• The uterus is too large for the stage of
pregnancy
• High blood pressure.
• Anaemia.
• High beta HcG level in blood.

108. Hydatidiform mole (Molar Pregnancy)
• Hydatidiform moles are associated with an
increased risk of recurrent molar pregnancy
and rarely choriocarcinoma.
• Usually diagnosed during early pregnancy
(average 9 weeks).
• Risk increases in teens and between the ages
of 40 and 50 years.

109. Complete mole

110. Complete mole
• Complete mole results from fertilization of an
egg that has lost its chromosomes and the
genetic material is completely paternally
derived.
• 90% have a 46,XX karyotype and also 46, XY
karyotype, derived from duplication of the
genetic material of one sperm.
• In complete mole, the embryo dies very early in
development and therefore is usually not
identified.

111. Partial mole

112. Partial mole
• Partial moles result from fertilization of an egg
with two sperm.
• In these moles the karyotype is triploid
(69,XXY) or even occasionally tetraploid
(92,XXXY).
• Some fetal tissues are present. But pregnancy
could not be continued.

113. Partial mole VS Complete mole

114. Invasive mole
• Invasive Mole is that molar pregnancy which
penetrate the myometrium and may even
perforate the uterine wall. May causing uterine
rupture.
• As invasive mole is locally destructive, can
invade parametrial tissue and blood vessels.
• Hydropic villi of Invasive mole may embolize
to distant sites such as lungs and brain.

115. Choriocarcinoma
• Choriocarcinoma is a malignant neoplasm of
trophoblastic cells.
• Choriocarcinoma is rapidly invasive and
metastasizes widely.
• But once identified responds very well to
chemotherapy.
• The chemotherapy result is nearly 100%
remission and a high rate of cures.

116. Question??
• Tell a tumor marker which is elevated in normal
physiological condition, in benign tumor and in
malignant tumor???
Ans: Beta HcG
Physiological: Pregnancy,
Benign: Molar pregnancy,
Malignant: Choriocarcinoma

117. Thank You