MALE AND FEMALE GENITAL TRACT
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This is a powerpoint presentation on the Topic of Male and female genital tract, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics
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MALE AND FEMALE GENITAL TRACT
- 1. WELCOME
- 2. Where are we? • www.facebook.com/pathologybasics • https://www.youtube.com/channel/U CwjkzK-YnJ-ra4HMOqq3Fkw • pathologybasics@gmail.com
- 3. PATHOLOGY OF THE GENITAL SYSTEM Dr. ASHISH JAWARKAR, MD
- 4. OVERVIEW MALE PENIS TESTIS, EPIDIDYMIS LOWER URINARY TRACT (URETHRA, PROSTATE) FEMALE LOWER GENITAL TRACT (CERVIX, VAGINA, URETHRA) UPPER GENITAL TRACT (ENDOMETRIUM, MYOMETRIUM, OVARIES, FALLOPIAN TUBES) GESTATIONAL DISORDERS LESIONS ANATOMIC DEVELOPMENTAL DISORDERS INFECTIONS MALIGNANCIES
- 5. MALE GENITAL SYSTEM TESTIS AND EPIDIDYMIS
- 6. CONGENITAL ANOMALIES - CRYPTORCHID ISMComplete or partial failure of the intra-abdominal testes to descend into the scrotal sac Is common till first year of age, only 1% remain undescended at the end is associated with testicular dysfunction Increased risk of testicular cancer (germ cell tumors like seminoma)Source: Robbins textbook of
- 7. TORSION Twisting of the spermatic cord typically cuts off the venous drainage of the testis If untreated, it frequently leads to testicular infarction Source: Robbins textbook of
- 8. INFECTIONS commonly related to infections in the urinary tract (cystitis, urethritis, prostatitis), which reach the epididymis and the testis through either the vas deferens or the lymphatics of the spermatic cord Childhood – gram negative rods Sexually active – C. trachomatis, N. gonorrhoea Older men – E. coli, pseudomonas Mumps orchitis – seen later on in life, after an attack of mumps parotitis earlier in life
- 9. MALIGNANCI ESBENIGN Lipoma Adenomatoid tumor MALIGNANT Germ cell tumors Aggressive, can be cured Seminomatous Non seminomatous Sex cord stromal tumors Usually benign Sertoli cell Leydig cell Seminoma Source: Robbins textbook of
- 10. SEMINOMA Epidemiology 15-34 years Testicular dysgenesis syndrome – cryptorchidism, hypospadias, poor sperm quality Pathogenesis Arise from precussor lesion called “INTRATUBULAR GERM CELL NEOPLASIA” Source: Robbins textbook of
- 11. SEMINOMA Morphology Gross Large, bulky masses up to 10 times the size of normal testis Homogenous, gray white, fleshy, lobular cut surface Microscopy Sheets of uniform cells divided into poorly demarcated lobules by delicate fibrous septa containing a lymphocytic infiltrate large and round to polyhedral and has a distinct cell membrane; clear or watery-appearing cytoplasm; and Source: Robbins textbook of
- 12. TRIVIA Cryptorchidism is associated with Germ cell tumors Sex cord stromal tumors Embryonal carcinomas Surface epithelial tumors
- 13. TRIVIA Most common organism causing orchitis in sexually active age group is Gonorrhoea Chlamydia E coli Pseudomonas
- 14. TRIVIA Identify the tumor on gross If age is 25 Seminoma If age is 70 Lymphoma Source: Robbins textbook of
- 15. TRIVIA Which of the following is not used as a tumor marker in testicular tumors AFP LDH HCG CEA Yolk sac tumor Germ cell tumor Germ cell tumor Surface epithelial tumors of ovary
- 16. TRIVIA A 25 year old man Presents with testicular mass having high levels of AFP Microscopy – sheets of un-differentitated cells No metastasis What best describes this tumor A. Benign Low grade Low stage B. Benign Low grade High stage C. Malignant High grade Low stage D. Maligant High grade High stage Embryonal carcinoma
- 17. MALE GENITAL SYSTEM PROSTATE
- 18. PROSTATE ANATOMY BENIGN HYPERPLASIA OF PROSTATE ADENOCARCINOMA
- 21. PROSTATE (BENIGN HYPERPLASIA OF PROSTATE / NODULAR HYPERPLASIA) Epidemiology Very common after age 50 (20%-40, 70%-60, 90%-80) NOT A PREMALIGNANT LESION Etiology It is believed that hyperplasia mainly stems from impaired cell death, resulting in the accumulation of senescent cells in the prostate Androgens (DHT), which are required for the development of BPH, not only increase cellular proliferation, but also inhibit cell death DHT is formed from testosterone in prostate by action of enzyme 5α reductase 5α reductase inhibitor & castration is a treatment
- 22. PROSTATE (BENIGN HYPERPLASIA OF PROSTATE / NODULAR HYPERPLASIA) Morphology Gross Microscopy FIBRO-MUSCULO-EPITHELIAL HYPERTROPHY Source: Robbins textbook of
- 23. PROSTATE (BENIGN HYPERPLASIA OF PROSTATE / NODULAR HYPERPLASIA) Clinical features Urinary obstruction Bladder hypertrophy Urinary retention Frequent UTI Dribbling Incontinence
- 25. PROSTATIC ADENOCARCINOMA Epidemiology Its incidence increases from 20% in men in their 50s to approximately 70% in men between the ages of 70 and 80 years Androgens, like in BPH, play a crucial role in development, however tumor cells become resistant to androgen blockade Source: Robbins textbook of pathology 9/e
- 26. PROSTATIC ADENOCARCI NOMA Morphology Gross Microscopy Well defined glandular pattern, back to back, uniform sized single uniform layer of cuboidal or low columnar epithelium Outer myoepithelial cell layer is absent IHC marker used for highlighting the myoepithelial cells _HMWCK Source: Robbins textbook of
- 27. PROSTATIC ADENOCARCINO MA Spread Hematogenous – bones (lumbar spine most common, osteoblastic mets) Lymphatic Source: Robbins textbook of
- 28. PROSTATIC ADENOCARCINOMA Grading – Tumor grade is the description of a tumor based on how abnormal the cells look under a microscope As discussed, prostatic cancer cells are usually well differentiated, hence the cancer is graded according to architecture rather than on basis of cellular characteristics – GLEASON SCORE Staging – Staging describes the severity of an individual’s cancer based on the magnitude of the original (primary) tumor as well as on the extent cancer has spread in the body.
- 29. LETS GO BACK!!
- 30. TRIVIA A. BPH arises from Peripheral zone B. Carcinoma arises from Transitional zone True False Source: Robbins textbook of
- 31. BPH NEVER PROGRESSES TO ADENOCARCINOMA TRUE FALSE
- 32. PROSTATE (BENIGN HYPERPLASIA OF PROSTATE / NODULAR HYPERPLASIA) Epidemiology Very common after age 50 (20%-40, 70%-60, 90%-80) NOT A PREMALIGNANT LESION Etiology It is believed that hyperplasia mainly stems from impaired cell death, resulting in the accumulation of senescent cells in the prostate Androgens (DHT), which are required for the development of BPH, not only increase cellular proliferation, but also inhibit cell death DHT is formed from testosterone in prostate by action of enzyme 5α reductase 5α reductase inhibitor & castration is a treatment for BPH
- 33. PROSTATIC METS ARE OSTEOCLASTIC IN NATURE TRUE FALSE
- 34. PROSTATIC ADENOCARCINO MA Spread Hematogenous – bones (lumbar spine most common, osteoblastic mets) Lymphatic Source: Robbins textbook of
- 35. MALE GENITAL SYSTEM PENIS
- 36. CONGENITAL ABNORMALITIES Hypospadias - abnormal urethral opening either on the ventral surface of the penis Epispadias - abnormal urethral opening either on the dorsal surface of the penis Phimosis - When the orifice of the prepuce is too small to permit its normal retraction
- 38. MALIGNANCIES Benign – condyloma accuminata – caused by HPV Malignant - Squamous cell carcinoma Source: Robbins textbook of
- 39. FEMALE GENITAL SYSTEM ENDOMETRIUM
- 42. MENSTRUAL CYCLE – NORMAL HISTOLOGY The endometrium undergoes dynamic physiologic and morphologic changes during the menstrual cycle in response to sex steroid hormones co- ordinately produced in the ovary Source: Robbins textbook of
- 43. MENSTRUAL CYCLE – HISTOLOGY WITH PHASES
- 44. MENSTRUAL CYCLE Source: Robbins textbook of
- 46. DYSFUNCTIONAL UTERINE BLEEDING Uterine bleeding can be caused by Infections Polyps Leiomyomas Malignancies Bleeding caused by hormonal disturbances is called DUB Anovulatory cycles Inadequate luteal phase
- 47. ANOVULATORY CYCLES Due to hormonal imbalances caused by Thyroid/pituitary disorders Ovarian lesions such as PCOS/hormone producing tumors Obesity/malnutrition etc. Histology shows proliferative changes without secretory changes May lead to endometrial hyperplasia
- 48. INADEQUATE LUTEAL PHASE Inadequate progesterone production during the post-ovulatory period Endometrial biopsy performed at an estimated postovulatory date shows secretory endometrium with features that lag behind those expected for the estimated date
- 49. TRIVIA Most common lesion in uterus that remains asymptomatic in majority and is very commonly detected in autopsies Polyp Leiomyoma Carcinoma Cervicitis
- 50. TRIVIA Hormone responsible for Proliferative phase Oesotrogen Secretory phase Progesterone
- 51. ENDOMETRITIS
- 52. ACUTE ENDOMETRITIS Usually after a miscarriage (incomplete abortion) Bacterial infection of retained products of conception
- 53. CHRONIC ENDOMETRITIS • Pelvic inflammatory disease (PID) • Retained gestational tissue, postpartum or post abortion • Intrauterine contraceptive devices • Tuberculosis, either from miliary spread or, more often, from drainage of tuberculous salpingitis Diagnosis rests on demonstration of plasma cells in stroma
- 54. ENDOMETRIOSIS
- 55. ENDOMETRIOSIS AND ADENOMYOSIS Presence of “ectopic” endometrial tissue at a site outside of the uterus Includes both endometrial glands and stroma It occurs in the following sites, in descending order of frequency: (1) ovaries (2) uterine ligaments (3) rectovaginal septum (4) cul de sac (5) pelvic peritoneum (6) large and small bowel and appendix (7) mucosa of the cervix, vagina, and fallopian tubes, and (8) laparotomy scars In myometrium it is known as ADENOMYOSIS Source: Robbins textbook of
- 56. ENDOMETRIOSIS Clinical features causes infertility, dysmenorrhea (painful menstruation) and pelvic pain Affects women in active reproductive life Pathogenesis Regurgitation theory Benign metastasis theory – via blood and lymph The metaplastic theory – from embryonal mesonephric remnants The extrauterine stem/progenitor cell theory
- 57. ENDOMETRIOSIS Morphology Gross – nodules with a red-blue to yellow- brown appearance organizing haemorrhage causes extensive fibrous adhesions between tubes, ovaries, and other structures and obliterates the pouch of Douglas The ovaries may become markedly distorted by large cystic masses (3 to 5 cm in diameter) filled with brown fluid known as chocolate cysts Microscopy Both endometrial glands and stroma are presentSource: Robbins textbook of
- 58. TRIVIA Identify the lesion Chocolate cyst of the ovary
- 60. ENDOMETRIAL POLYPS Endometrial polyps are exophytic masses of variable size that project into the endometrial cavity
- 61. ENDOMETRI AL POLYPS Polyps may be asymptomatic or may cause abnormal bleeding The glands in polyps may be hyperplastic or atrophic, and may occasionally demonstrate secretory changes, rarely may lead to carcinomas Endometrial polyps have been observed in association with the administration of tamoxifen, which is often used in the therapy ofSource: Robbins textbook of
- 63. ENDOMETRIAL HYPERPLASIA Endometrial hyperplasia is associated with prolonged estrogenic stimulation of the endometrium, which can be due to anovulation, increased oestrogen production from endogenous sources, or exogenous oestrogen. Associated conditions include: • Obesity (peripheral conversion of androgens to oestrogens) • Menopause • Polycystic ovarian syndrome • Functioning granulosa cell tumors of the ovary • Excessive ovarian cortical function (cortical stromal hyperplasia) • Prolonged administration of estrogenic substances (estrogen replacement therapy)
- 64. CARCINOMA OF THE ENDOMETRIU MMost common cancer of FGT in US (Ca Cervix mc in India) Two types, completely different pathogenesis and causes
- 65. CA ENDOMETRIUM – MOLECULAR DIFFERENCES
- 66. CA ENDOMETRIUM – TYPE I (MORPHOLOGY) Source: Robbins textbook of pathology 9/e
- 67. CA ENDOMETRIUM – TYPE II - MORPHOLOGY Arise in small atrophic uteri, may form large bulky masses Source: Robbins textbook of
- 68. CARCINO- SARCOMA (MALIGNANT MIXED MULLERIAN TUMOR) Endometrial adenocarcinomas with a malignant mesenchymal component Sarcomatous components may also mimic extrauterine tissues (e.g., striated muscle, cartilage, adipose tissue, and bone)
- 69. LETS TEST OURSELVES!! Identify menstrual phases from histology Menstrual phasePremenstrual phase Secretory phaseProliferative phase Source: Robbins textbook of
- 70. ENDOMETRIOSIS Presence of endometrial glands at a site outside of the uterus True False Source: Robbins textbook of
- 71. CA ENDOMETRIUM - TYPES
- 72. FEMALE GENITAL SYSTEM MYOMETRIUM
- 74. LEIOMYOMA S Uterine leiomyoma (commonly called fibroids) is the most common tumor in women, arise from smooth muscle cell More often are multiple They can occur within the myometrium (intramural), just beneath the endometrium (submucosal) or beneath the serosa (subserosal)
- 75. LEIOMYOMA Morphology Gross sharply circumscribed, discrete, round, firm, gray-white Whorled tumors Microscopy uniform in size and shape and have the characteristic oval nucleus and long, slender bipolar cytoplasmic processes
- 76. ENDOMETRIAL STROMAL SARCOMA Source: Robbins textbook of pathology 9/e
- 77. FEMALE GENITAL SYSTEM CERVIX
- 78. CERVIX ANATOMY CERVICAL CARCINOMA CERVICAL CANCER SCREENING – PAP SMEAR
- 80. SQUAMOUS METAPLASIA OF THE TRANSFORMATION ZONE Source: Robbins textbook of
- 82. CERVICAL CARCINOMA Epidemiology Pathogenesis Cervical intraepithelial neoplasia Cervical carcinoma Cancer detection and screening
- 83. EPIDEMIOLOGY Worldwide, cervical carcinoma is the third most common cancer in women Fifty years ago, carcinoma of the cervix was the leading cause of cancer deaths in women, but the death rate has declined by two third mainly due to screening practices
- 84. PATHOGENESIS HPV 16 and 18 are implicated as the cause of Squamous cell carcinoma 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 immature metaplastic squamous cells present at the squamo-columnar junction The ability of HPV to act as a carcinogen depends on the viral proteins E6 and E7, which interfere with the activity of tumour suppressor proteins
- 86. Source: Robbins textbook of
- 87. LSIL VS HSIL LSIL is associated with a productive HPV infection LSIL does not progress directly to invasive carcinoma and in fact most cases regress spontaneously; only a small percentage progress to HSIL For these reasons, LSIL is not treated like a premalignant lesion
- 88. LSIL VS HSIL In HSIL, on the other hand, there is a progressive deregulation of the cell cycle by HPV Derangement of the cell cycle in HSIL may become irreversible and lead to a fully transformed malignant phenotype, and thus all HSIL are considered to be at high risk for progression to carcinoma
- 89. LSIL VS HSIL
- 90. MORPHOLOGY The diagnosis of SIL is based on identification of nuclear atypia characterized by nuclear enlargement, hyperchromasia (dark staining), coarse chromatin granules, and variation in nuclear size and shape The nuclear changes are often accompanied by cytoplasmic “halos.” At an ultrastructural level, these “halos” consist of perinuclear vacuoles, a cytopathic change created in part by an HPV-encoded protein called E5 that localizes to the membranes of the endoplasmic reticulum. Nuclear alterations with an associated perinuclear halo are termed koilocytic atypia Source: Robbins textbook of
- 92. CERVICAL SCREENING – PAP SMEAR Cytologic cancer screening has significantly reduced mortality from cervical cancer. In countries where such screening is not widely practiced, cervical cancer continue to exact a high toll. The reason that cytologic screening is so effective in preventing cervical cancer is that most cancers arise from precursor lesions over the course of years. These lesions shed abnormal cells that can be detected on cytologic examination. Using a spatula or brush, the transformation zone of the cervix is circumferentially scraped and the cells are smeared or spun down onto a slide. Following fixation and staining with the Papanicolaou method, the smears are screened microscopically by eye or (increasingly) with automated image analysis systems. The cellular changes seen on the Pap test, illustrating the spectrum from
- 95. FEMALE GENITAL SYSTEM OVARIES
- 96. OVARIES CYSTS TUMORS • Non neoplastic/ functional cysts • Polycystic ovarian syndrome • Surface epithelial tumors • Sex cord stromal tumors • Germ cell tumors • Metastases
- 97. CYSTS
- 98. FOLLICLE LUTEAL CYST FOLLICULAR CYST NON NEOPLASTIC / FUNCTIONAL CYSTS Source: Robbins textbook of pathology 9/e
- 100. PCOS
- 101. TRIVIA PCOS is due to excess Estrogen Androgens
- 102. TUMORS
- 107. SEROUS – CYSTADENOMA (BORDERLINE) Source: Robbins textbook of
- 108. MUCINOUS – CYSTADENOMA Source: Robbins textbook of
- 109. MUCINOUS – CYSTADENOMA (BORDERLINE) Source: Robbins textbook of
- 110. ENDOMETRIOID CYSTADENOMA - BORDERLINE Source: Robbins textbook of pathology 9/e
- 112. LOW GRADE AND HIGH GRADE MALIGNANT SEROUS CARCINOMAS Source: Robbins textbook of
- 113. SEROUS CARCINOMAS Risk factors Age >40 Nulliparity Family history Heritable mutations Protective OC pills Tubal ligation Bilaterality is common (66%) Surface involvement is common Source: Robbins textbook of
- 114. SEROUS CARCINOMAS Morphology Marked nuclear atypia, including pleomorphism, atypical mitotic figures, and multinucleation Psammoma bodies Source: Robbins textbook of
- 115. MUCINOUS CARCINOMAS Mucinous tumors differ from serous in that The surface of the ovary is rarely involved Rarely bilateral They are multiloculated tumors filled with sticky, gelatinous fluid rich in glycoproteins These tumors must be distinguished from metastatic mucinous adenocarcinomas (from colon and appendix) Source: Robbins textbook of
- 116. PSEUDOMYX OMA PERITONEI Extensive mucinous ascites Cystic epithelial implants on the peritoneal surfaces, Adhesions, Frequent involvement of the ovaries (first the surface) Source is usually appendix Source: Robbins textbook of
- 117. CLINICAL COURSE All ovarian carcinomas produce similar clinical manifestations, most commonly lower abdominal pain and abdominal enlargement The serum marker CA-125 is used in patients with known disease to monitor disease recurrence/progression.
- 118. TRIVIA Following statements represent which form of tumors (benign/borderline/malignant) 1. Increased epithelial atypia and presence of stromal invasion 2. Composed of well-differentiated epithelial cells with minimal proliferation 3. Increased cell proliferation, but lack stromal invasion
- 119. TRIVIA Most common tumor leading to pseudomyxoma peritonei 1. Signet ring cell adenocarcinoma of colon 2. Adenocarcinoma of appendix 3. Adenocarcinoma of stomach
- 120. TRIVIA Serous carcinomas are bilateral and don't show surface involvement Mucinous carcinomas are unilateral and show surface involvement
- 121. GERM CELL TUMORS
- 123. TERATOMA Teratomas are germ cell tumors commonly composed of multiple cell types derived from one or more of the 3 germ layers 15-20% of all ovarian tumors Children and young adults Types Mature (Benign) Immature (Malignant) Monodermal teratoma
- 124. BENIGN CYSTIC TERATOMA (DERMOID CYST) Contents are mature (usually derived from ectodermal and mesodermal structures, but well differentiated) Mostly cystic Lined by skin, contain hair and sebaceous material May contain bone, cartilage, thyroid and neural tissue Source: Robbins textbook of
- 125. MONODERMAL TERATOMA (STRUMA OVARII OR CARCINOID) Struma ovarii is composed entirely of mature thyroid tissue, which may be functional and cause hyperthyroidism The ovarian carcinoid, which presumably arises from intestinal tissue found in teratomas, they can produce sufficient 5- hydroxytryptamine to cause the carcinoid syndrome Source: Robbins textbook of
- 126. IMMATURE TERATOMA Differ from benign teratomas in that the component tissues resemble embryonal and immature fetal tissue On microscopic examination there are varying amounts of immature neuroepithelium, cartilage, bone, muscle, and other elements Source: Robbins textbook of
- 127. DYSGERMINOMA Ovarian counterpart of seminoma Arises from follicular oocytes Solid yellow-white to gray-pink appearance and are often soft and fleshyIt is composed of large vesicular cells having a clear cytoplasm, well- defined cell boundaries, and centrally placed regular nuclei. The tumor cells grow in sheets or cords separated by scant fibrous stroma, which is infiltrated by mature lymphocytes and may contain occasional granulomas Source: Robbins textbook of
- 128. YOLK SAC TUMORThe immature ova originate from cells from the dorsal endoderm of the yolk sac Similar to the normal yolk sac, the tumor cells elaborate α- fetoprotein Its characteristic histologic feature is a glomerulus-like structure composed of a central blood vessel enveloped by tumor cells within a space that is also lined by tumor cells (Schiller-DuvalSource: Robbins textbook of
- 130. TRIVIA Which ovarian tumor can present with flushing, diarrhoea and bronchoconstriction?
- 131. TRIVIA A 10 year old child develops a ovarian mass and undergoes oophrectomy. On cut section mass shows variety of appearances and colors. Histologically many different tissue seen including cartilage, thyroid and neural tissue. A small focus of clear cut squamous cell carcinoma is seen. Which of the following is most appropriate classification of this tumor? Dermoid cyst Teratoma with malignant transformation Immature teratoma Solid mature teratoma
- 132. TRIVIA Name the small round blue cell tumors you know Ewing's sarcoma, peripheral neuroectodermal tumor, rhabdomyosarcoma, synovial sarcoma, non-Hodgkin's lymphoma, retinoblastoma, neuroblastoma, hepatoblastoma, and nephroblastoma or Wilms' tumor Immature teratoma
- 133. TRIVIA Rosettes
- 135. SEX CORD STROMAL TUMORS Granulosa cell tumors Sertoli Leydig cell tumors Fibromas and Thecomas
- 136. SEX CORD STROMAL TUMORS The undifferentiated gonadal mesenchyme eventually produces specific types of cells in both male (Sertoli and Leydig) and female (granulosa and theca) gonads Tumors resembling all of these cell types can be identified in the ovary. Because some of these cells normally secrete estrogens (granulosa and theca cells) or androgens (Leydig cells), their corresponding tumors may be either feminizing (granulosa/theca cell tumors) or masculinizing (Leydig cell tumors).
- 137. GRANULOSA CELL TUMORS These tumors may elaborate large amounts of estrogen causing Precocious puberty Proliferative breast disease Endometrial hyperplasia Endometrial carcinoma Associated with increased serum levels of Inhibin Source: Robbins textbook of pathology 9/e
- 138. MORPHOLOGY Gross usually unilateral solid, and cystic encapsulated masses yellow coloration to their cut surfaces, due to intracellular lipids Microscopy The tumor cells are arranged in sheets punctuated by small follicle-like structures (Call-Exner bodies) IHC Positive for Inhibin
- 139. FIBROMAS/THECOMAS Tumors arising in the ovarian stroma that are composed of either fibroblasts (fibromas) or plump spindle cells with lipid droplets (thecomas) Source: Robbins textbook of
- 140. MEIGS SYNDROME 1. Hydrothorax, usually only on the right side 2. Ovarian tumor (Fibroma) 3. Ascites Source: Robbins textbook of
- 142. TISSUES OF MULLERIAN ORIGIN Source: Robbins textbook of
- 143. KRUKENBERG TUMOR Source: Robbins textbook of
- 144. FEMALE GENITAL SYSTEM GESTATIONAL DISORDERS
- 145. GESTATIONAL DISORDERS Working anatomy and physiology Disorders of early pregnancy Spontaneous abortion Ectopic pregnancy Disorders of late pregnancy Twin placentas Abnormal implantation Placental infections Preeclampsia and eclampsia Gestational trophoblastic disease Hydatidiform mole Choriocarcinoma Placental site trophoblastic tumor
- 147. Source: Robbins textbook of
- 149. ECTOPIC PREGNANCY
- 150. ECTOPIC PREGNANCY Refers to implantation of the fetus in a site other than the normal intrauterine location Sites Fallopian tube (90%) Ovary Abdominal cavity Causes PID IUCD Peri tubal scarring due to endometriosis or previous surgery
- 151. ECTOPIC PREGNANCY First step when a period is missed is to get a UPT done If its positive, get a USG done to determine that the pregnancy is intrauterine If no USG is done, the pregnancy may continue in tube and eventually rupture and give rise to hemoperitoneum
- 152. ECTOPIC PREGNANCY Morphology Growth of the gestational sac distends the fallopian tube causing thinning of the wall Source: Robbins textbook of pathology 9/e
- 154. PREECLAMPSIA AND ECLAMPSIA Pre eclampsia Systemic syndrome during pregnancy characterized by Widespread maternal endothelial dysfunction Presenting with hypertension, edema, and proteinuria And Hypercoagubility Eclampsia Above features + convulsions HELLP SYNDROME H – hemolytic anemia EL – Elevated liver enzymes (SGPT, SGOT, ALP) LP – low platelets
- 155. PRE ECLAMPSIA Mechanisms Placental ischemia The ischemic placenta releases factors into the maternal circulation that cause an imbalance in circulating angiogenic and anti- angiogenic factors; This in turn leads to systemic maternal endothelial dysfunction Hypercoagulability is likely related to the reduced endothelial production of PGI2, a potent antithrombotic factor Source: Robbins textbook of
- 158. HYDATIDIFORM MOLE Hydatid – derived from Greek “hudat” meaning water – hydatidiform – water containing vesicle Mole - a small burrowing mammal Source: Robbins textbook of pathology 9/e
- 159. HYDATIDIFORM MOLE Moles are diseases of the placenta - characterized histologically by cystic swelling of the chorionic villi, accompanied by variable trophoblastic proliferation They are usually diagnosed during early pregnancy (average 9 weeks) The risk is higher at the two ends of reproductive life, in teenagers and between the ages of 40 and 50 yearsSource: Robbins textbook of pathology 9/e
- 160. CLINICAL FEATURES AND DIAGNOSIS The normal placenta produces beta HCG which is used to diagnose pregnancy Mole produces HCG at an alarming rate, much higher than that of normal placenta Diagnosis is done by – A positive UPT Alarming rate of rise in HCG in blood USG showing hydropic changes in the placenta Source: Robbins textbook of pathology 9/e
- 161. TYPES Complete mole Incomplete mole Source: Robbins textbook of
- 162. MORPHOLOGY Gross mass of thin-walled, translucent, cystic, grapelike structures consisting of swollen edematous (hydropic) villi Microscopy The chorionic villi are enlarged, scalloped in shape with central cavitation (cisterns), and are covered by extensive trophoblast proliferation Source: Robbins textbook of
- 163. CHORIOCARCINOMA Gestational choriocarcinoma is a malignant neoplasm of trophoblastic cells derived from a previously normal or abnormal pregnancy Choriocarcinoma is rapidly invasive and metastasizes widely (to lungs, vagina, liver, brain) through blood, but once identified responds well to chemotherapy
- 164. MORPHOLOGY Gross Choriocarcinoma is a soft, fleshy, yellow- white tumor that usually has large pale areas of necrosis and extensive hemorrhage Microscopy It does not produce chorionic villi and consists entirely of proliferating syncytiotrophoblasts and cytotrophoblasts The tumor invades the underlying myometrium, frequently penetrates blood vessels Source: Robbins textbook of